(Oxford Library of Psychology) Theodore P. Beauchaine, Sheila E. Crowell - The Oxford Handbook of Emotion Dysregulation-Oxford University Press (2020)

The Oxford Handbook of Emotion Dysregulation
Oxford Library of Psychology
Area Editors:
Clinical Psychology
David H. Barlow
Cognitive Neuroscience
Kevin N. Ochsner and Stephen M. Kosslyn
Cognitive Psychology
Daniel Reisberg
Counseling Psychology
Elizabeth M. Altmaier and Jo-Ida C. Hansen
Developmental Psychology
Philip David Zelazo
Health Psychology
Howard S. Friedman
History of Psychology
David B. Baker
Methods and Measurement

Todd D. Little
Neuropsychology
Kenneth M. Adams
Organizational Psychology
Steve W. J. Kozlowski
Personality and Social Psychology

Kay Deaux and Mark Snyder
OXFORD L I B R A RY OF PSYCHOLOGY
The Oxford Handbook

of Emotion
Dysregulation
Edited by
Theodore P. Beauchaine
Sheila E. Crowell
1
2020
1
Oxford University Press is a department of the University of Oxford. It furthers
the University’s objective of excellence in research, scholarship, and education
by publishing worldwide. Oxford is a registered trade mark of Oxford University
Press in the UK and certain other countries.
Published in the United States of America by Oxford University Press

198 Madison Avenue, New York, NY 10016, United States of America.
© Oxford University Press 2020
All rights reserved. No part of this publication may be reproduced, stored in

a retrieval system, or transmitted, in any form or by any means, without the
prior permission in writing of Oxford University Press, or as expressly permitted
by law, by license, or under terms agreed with the appropriate reproduction
rights organization. Inquiries concerning reproduction outside the scope of the
above should be sent to the Rights Department, Oxford University Press, at the
address above.
You must not circulate this work in any other form

and you must impose this same condition on any acquirer.
Library of Congress Cataloging-in-Publication Data

Names: Beauchaine, Theodore P., editor. | Crowell, Sheila E. (Sheila Elizabeth), editor.
Title: The Oxford handbook of emotion dysregulation /
edited by Theodore P. Beauchaine, Sheila E. Crowell.
Description: New York, NY : Oxford University Press, [2020] |
Series: Oxford library of psychology | Includes bibliographical references and index. |
Identifiers: LCCN 2019031334 (print) | LCCN 2019031335 (ebook) |
ISBN 9780190689285 (hardback) | ISBN 9780190689308 (epub) |
ISBN 9780190689292
Subjects: LCSH: Emotions—Handbooks, manuals, etc. | Psychology, Pathological—
Handbooks, manuals, etc. | Affect (Psychology)—Handbooks, manuals, etc.
Classification: LCC RC455.4.E46 O94 2020 (print) |
LCC RC455.4.E46 (ebook) | DDC 616.89—dc23
LC record available at https://lccn.loc.gov/2019031334
LC ebook record available at https://lccn.loc.gov/2019031335
9 8 7 6 5 4 3 2 1
Printed by Integrated Books International, United States of America
C O N T R I B U TO R S
Molly Adrian, PhD Patricia A. Brennan, PhD

Department of Psychiatry and Department of Psychology
Behavioral Sciences Emory University
Seattle Children’s Hospital April L. Brown, MPH
Kenneth J. D. Allen, AM Department of Psychology
Department of Psychology Emory University
Harvard University Mindy Brown, BS
Ananda B. Amstadter, PhD Department of Psychology
Virginia Institute for Psychiatric and The University of Utah
Behavioral Genetics Alexander L. Chapman, PhD, RPsych
Virginia Commonwealth University Department of Psychology
Michael F. Armey, PhD Simon Fraser University
Department of Psychiatry and Dante Cicchetti, PhD
Human Behavior Institute of Child Development
Warren Alpert Medical School University of Minnesota
Brown University Pamela M. Cole, PhD
Rachel M. Atchley, PhD, MCR Department of Psychology
Center on Mindfulness and Integrative The Pennsylvania State University
Health Intervention Development Lindsey C. Conkey, PhD
(C-MIIND) Department of Psychological and
The University of Utah Brain Sciences
Theodore P. Beauchaine, PhD University of Massachusetts Amherst
Department of Psychology Elisabeth Conradt, PhD
The Ohio State University Department of Psychology
Lane Beckes, PhD The University of Utah
College of Liberal Arts and Sciences Geoffrey W. Corner, BS
Bradley University Department of Psychology
Spencer Bell, PhD University of Southern California
Department of Physiology/Pharmacology Sheila E. Crowell, PhD
Wake Forest University Health Sciences Department of Psychology
Ziv E. Bell, MA The University of Utah
Department of Psychology Katherine L. Dixon-Gordon, PhD
The Ohio State University Department of Psychological and
Michele Berk, PhD Brain Sciences
Psychiatry and Behavioral Sciences - Child University of Massachusetts Amherst
and Adolescent Psychiatry and Child Anna R. Docherty, PhD
Development University Neuropsychiatric Institute
Stanford University University of Utah Health Sciences Center
Grace Binion, MS Weston Layne Edwards, MA
Department of Psychology Department of Psychology
University of Oregon Bradley University
ix
S H O RT C O N T E N T S
About the Editors vii
Contributors ix
Table of Contents xiii
Chapters 1–486
Index 487
v
A B O U T T H E E D I TO R S
Theodore P. Beauchaine, PhD, earned his undergraduate degree in psychology

from Portland State University, and his PhD in clinical psychology, with a quan-
titative minor, from Stony Brook University. He completed his clinical internship
at the University of California at San Diego School of Medicine. He is past recip-
ient of both the American Psychological Association Distinguished Scientific
Award for Early Career Contributions to Psychology and the American
Psychological Association Mid-Career Award for Outstanding Contributions to
Benefit Children, Youth, and Families. He has served on numerous editorial
boards, and as Associate Editor for Development and Psychopathology and
Psychophysiology. He served on the National Institute of Mental Health National
Advisory Council Workgroup on Tasks and Measures for the Research Domain
Criteria (RDoC). His research addresses neural underpinnings of and develop-
ment of behavioral impulsivity, emotion dysregulation, and intentional self-injury
in children, adolescents, and adults.
Sheila E. Crowell earned her PhD in child clinical psychology from the
University of Washington. She completed her clinical internship at Seattle
Children’s Hospital through the University of Washington Psychology Internship
Program. Dr. Crowell has expertise in emotion dysregulation across the lifespan,
including infants, children, adolescents, and adults. Her work on emotion dys-
regulation extends across a number of diverse clinical populations, such as depres-
sion, substance use disorders, trauma, personality disorders, and self-injury.
Dr. Crowell is also a licensed clinical psychologists with expertise in Dialectical
Behavior Therapy (DBT), an evidence-based treatment for diagnoses character-
ized by emotion dysregulation. Dr. Crowell has served on study sections for the
National Institutes of Health and as a reviewer or editorial board member for
several journals. She has received funding for her research from the National
Institutes of Mental Health and the American Foundation for Suicide Prevention.
A primary goal of Dr. Crowell’s research is to prevent suicide and the development
of psychopathology through enhanced identification of those at risk and early in-
tervention.
vii
Margaret A. Fields-Olivieri Hooria Jazaieri, PhD
Department of Psychology Kellogg School of Management
The Pennsylvania State University Northwestern University
Courtney N. Forbes, MEd Parisa R. Kaliush, BA
The University of Toledo The University of Utah
Brett Froeliger, PhD Niranjan S. Karnik, MD, PhD
Department of Neuroscience Department of Psychiatry
Medical University of South Carolina Rush Medical College
Eric L. Garland, PhD, LCSW Erin A. Kaufman, BA
Center on Mindfulness and Integrative Health Department of Psychology
Intervention Development (C-MIIND) The University of Utah
The University of Utah Christiane Kehoe, PhD
Kim L. Gratz, PhD Department of Psychiatry
Department of Psychology The University of Melbourne
The University of Toledo Patricia K. Kerig, PhD
James J. Gross, PhD Department of Psychology
Department of Psychology The University of Utah
Stanford University Mona Khaled, MA
Hunter Hahn, MA Department of Psychology
Department of Psychology University of Southern California
The Ohio State University Joseph C. Leshin, BS
Nathaniel Haines, BA Department of Psychology & Neuroscience
The Center for Cognitive and The University of North Carolina
Brain Sciences at Chapel Hill
The Ohio State University Kristen A. Lindquist, PhD
Greg Hajcak, PhD Department of Psychology & Neuroscience
Department of Psychology The University of North Carolina at
Florida State University Chapel Hill
Lauren A. Haliczer, MA Christina Gamache Martin, PhD
Department of Psychological and Department of Psychology
Brain Sciences University of Oregon
University of Massachusetts Amherst Whitney I. Mattson, PhD
Sophie Havighurst, PhD Brain Development and Social
Department of Psychiatry Cognition Lab
The University of Melbourne Nationwide Children’s Hospital
Sage E. Hawn, BA Kateri McRae, PhD
Virginia Institute for Psychiatric and Department of Psychology
Behavioral Genetics University of Denver
Virginia Commonwealth University Michele A. Morningstar, PhD
Nora H. Hope, PhD, RPsych Brain Development and Social
Department of Psychology Cognition Lab
Simon Fraser University Nationwide Children’s Hospital
Sarah A. Horvath, MA Eric E. Nelson, PhD
Department of Psychology Center for Biobehavioral Health
Ohio University Nationwide Children’s Hospital
Camelia E. Hostinar, PhD Emily Neuhaus, PhD
University of California, Davis University of Washington
x Contributors
Jacqueline O’Brien, MS Ross A. Thompson, PhD
University of Oregon University of California, Davis
Cassie Overstreet, MA Matthew T. Tull, PhD
Virginia Commonwealth University The University of Toledo
Ruchika Shaurya Prakash, PhD Andero Uusberg, PhD
The Ohio State University University of Tartu
Sarah E. Racine, PhD Helen Uusberg, PhD
McGill University University of Tartu
K. Ashana Ramsook, MA Robert D. Vlisides-Henry, BA
The Pennsylvania State University The University of Utah
Lance M. Rappaport, PhD Gemma T. Wallace, BA
Virginia Institute for Psychiatric and Department of Psychiatry
Behavioral Genetics University of Utah School
Virginia Commonwealth University of Medicine
Julia R. Richmond, MA Sara F. Waters, PhD
Department of Psychology Department of Human Development
The University of Toledo Washington State University,
Darby Saxbe, PhD Vancouver
Department of Psychology Linnie E. Wheeless, JD
University of Southern California Department of Psychology
Heather T. Schatten, PhD The University of Toledo
Department of Psychiatry and Patrick Whitmoyer, MA
Human Behavior Department of Psychology
Brown University The Ohio State University
Tiffany M. Shader, MA Dominika A. Winiarski, PhD
The Ohio State University Rush University
Brittany C. Speed, MA Maureen Zalewski, PhD
Stony Brook University University of Oregon
Sarah A. Stoycos, MA Paree Zarolia, PhD
University of Southern California The University of Denver
Contributors xi
TA B L E O F C O N T E N T S
1. Functionalist and Constructionist Perspectives on Emotion

Dysregulation 1
Theodore P. Beauchaine and Nathaniel Haines
2. Emotions as Regulators of Motivated Behavior 13
Eric E. Nelson, Michele A. Morningstar, and Whitney I. Mattson
3. Emotions as Regulators of Social Behavior 27
Lane Beckes and Weston Layne Edwards
4. Cognition and Emotion in Emotion Dysregulation 39
Kateri McRae and Paree Zarolia
5. What Emotion Dysregulation Looks Like: Inferences from
Behavioral Observations 53
K. Ashana Ramsook, Pamela M. Cole, and Margaret A. Fields-Olivieri
6. Emotion Dysregulation and Aging 69
Patrick Whitmoyer and Ruchika Shaurya Prakash
7. Emotion Generation, Regulation, and Dysregulation as Multilevel
Transdiagnostic Constructs 85
Sheila E. Crowell, Robert D. Vlisides-Henry, and Parisa R. Kaliush
8. Development of Emotion Dysregulation in Developing Relationships 99
Ross A. Thompson and Sara F. Waters
9. Operant Reinforcement and Development of Emotion Dysregulation 115
Christina Gamache Martin, Maureen Zalewski, Grace Binion, and
Jacqueline O’Brien
10. Cognitive Processes and Risk for Emotion Dysregulation 127
Hooria Jazaieri, Helen Uusberg, Andero Uusberg, and James J. Gross
11. Interpersonal Processes and the Development of Emotion
Dysregulation 141
Sarah A. Stoycos, Geoffrey W. Corner, Mona Khaled, and Darby Saxbe
12. Respiratory Sinus Arrhythmia as a Transdiagnostic Biomarker of
Emotion Dysregulation 153
Theodore P. Beauchaine and Ziv E. Bell
13. Event-Related Potentials and Emotion Dysregulation 167
Brittany C. Speed and Greg Hajcak
14. Neuroimaging of Emotion Dysregulation 183
Joseph C. Leshin and Kristen A. Lindquist
15. Behavioral and Molecular Genetics of Emotion Dysregulation 203
Lance M. Rappaport, Sage E. Hawn, Cassie Overstreet, and
Ananda B. Amstadter
xiii
16. Epigenetic Foundations of Emotion Dysregulation 221
Mindy Brown, Elisabeth Conradt, and Sheila E. Crowell
17. Emotion Dysregulation and Externalizing Spectrum Disorders 237
Tiffany M. Shader and Theodore P. Beauchaine
18. Emotion Dysregulation and Internalizing Spectrum Disorders 249
Camelia E. Hostinar and Dante Cicchetti
19. Emotion Dysregulation and Childhood Trauma 265
Patricia K. Kerig
20. Emotion Dysregulation in Autism Spectrum Disorder 283
Emily Neuhaus
21. Emotion Dysregulation and Psychosis Spectrum Disorders 299
Gemma T. Wallace and Anna R. Docherty
22. Emotion Dysregulation in Addiction 313
Eric L. Garland, Spencer Bell, Rachel M. Atchley, and Brett Froeliger
23. Emotion Dysregulation and Eating Disorders 327
Sarah E. Racine and Sarah A. Horvath
24. Emotion Dysregulation and Self-Inflicted Injury 345
Erin A. Kaufman and Sheila E. Crowell
25. Emotion Dysregulation and Borderline Personality Disorder 361
Katherine L. Dixon-Gordon, Lauren A. Haliczer, and Lindsey C. Conkey
26. Behavioral Assessment of Emotion Dysregulation 377
Molly Adrian and Michele Berk
27. Self-Report Assessment of Emotion Dysregulation 395
Kim L. Gratz, Courtney N. Forbes, Linnie E. Wheeless,
Julia R. Richmond, and Matthew T. Tull
28. Assessment of Emotion Dysregulation Using Ecological Momentary
Assessment 411
Heather T. Schatten, Kenneth J. D. Allen, and Michael F. Armey
29. Treating Emotion Dysregulation in Externalizing Disorders 427
Dominika A. Winiarski, April L. Brown, Niranjan S. Karnik,
and Patricia A. Brennan
30. Treating Emotion Dysregulation in Internalizing Disorders 443
Christiane Kehoe and Sophie Havighurst
31. Dialectical Behavior Therapy and Treatment of Emotion
Dysregulation 463
Alexander L. Chapman and Nora H. Hope
32. Future Directions in Research and Treatment of Emotion
Dysregulation 477
Theodore P. Beauchaine, Hunter Hahn, and Sheila E. Crowell
Index 487
xiv Table of Contents

CH A PTE R
Functionalist and Constructionist
1 Perspectives on Emotion
Dysregulation
Theodore P. Beauchaine and Nathaniel Haines
Abstract
Two theoretical perspectives—functionalism and constructionism—predominate modern research on

emotion. This introductory chapter describes these perspectives and offers points of convergence and
divergence. It pays special attention to common misconceptions about functionalism and to strengths
and limitations of each perspective. Functionalism, which draws in part from phylogenetic accounts of
emotion and motivation, is limited by difficulties drawing inferences about human emotion from animal
research, even though animal research is conducted using very precise methods of high spatial and
temporal resolution. In contrast, constructionism is limited by difficulties falsifying its core propositions
given reliance on research using functional magnetic resonance imaging, which has poor temporal
resolution. These limitations notwithstanding, both functionalism and constructionism have much to
offer current interpretations of and future research on emotion dysregulation. Thus, pitting the
perspectives against one other is counterproductive.
Keywords: constructionism, emotion, emotion dysregulation, functionalism, psychopathology
Work on this chapter was supported by grant DE025980 from the National
Institutes of Health, and by the National Institutes of Health Science of
Behavior Change (SoBC) Common Fund.
Introduction editing this volume, Sheila Crowell and I (TPB)

It is an honor and a privilege to coedit this Oxford learned more about emotion dysregulation than we
Handbook, in which contributors describe diverse otherwise could have known, and we are indebted
perspectives on emotion dysregulation. We were to a brilliant team of contributors. We hope readers
fortunate to receive contributions from internation- find the diversity of topics useful in advancing their
ally renowned experts in affective science, who to- thinking about emotion dysregulation and its mul-
gether summarize contemporary approaches to and tiple determinants across the lifespan. In this chap-
future directions in emotion dysregulation research. ter, we summarize functionalist and constructionist
Chapters are grouped into six sections: (1) concep- perspectives on emotion, which sets the stage for
tual issues; (2) cognitive, behavioral, and social chapters to follow.
approaches; (3) neurobiological approaches; (4) psy- Over the past two decades, emotion regulation
chopathology; (5) assessment and treatment; and has received burgeoning attention as a scientific
(6) future directions. Collectively, these sections de- construct, as evidenced by foundational articles,
scribe effects of emotion dysregulation on core dedicated volumes, and extended scientific debate
aspects of human function across levels of analysis (e.g., Aldao, Nolen-Hoeksema, & Schweizer, 2010;
including genes, neural networks, electrophysiol- Cole, Martin, & Dennis, 2004; Gross, 1998, 2014).
ogy, and behavior. During 3 years of planning and Although emotion dysregulation has received more
1
circumscribed attention, it is of considerable inter- One common use of the term functionalism as-
est to developmentalists, psychopathologists, and sumes evolutionary selection of at least some human
other invested parties (e.g., Beauchaine, 2015; emotions. Such accounts presume that broad classes
Bradley et al., 2011; Gratz, Rosenthal, Tull, Lejuez, of emotion evolved to motivate adaptive, survival-
& Gunderson, 2006; Linehan, 1993). In this volume, related functions including approach, avoidance,
we place primary emphasis on emotion dysregulation and social affiliation (e.g., Keltner & Gross, 1999).
and how it compromises adaptive human func- According to evolutionary functionalist perspectives,
tioning through its effects on initiating, maintain- emotions that subserve these functions are preserved
ing, and modulating diverse human behaviors (cf. across species and experienced by all mammals, in-
Campos, Mumme, Kermoian, & Campos, 1994; cluding humans, because they were selected in our
Thompson, 1990). Given our objective of convey- environments of adaptation (e.g., Panksepp, 2011,
ing contemporary perspectives on emotion dysregu- 2016). For example, approach emotions (e.g., want-
lation, both emotion and emotion regulation must ing, enthusiasm) elicit consummatory behaviors
be discussed. However, they are not primary foci (e.g., foraging, food seeking); avoidance emotions
given widespread coverage in other sources. Interested (e.g., anxiety, fear) elicit precaution (e.g., passive
readers are referred to excellent recent reviews (Aldao avoidance, suppression of approach); and affiliative
et al., 2010; Barrett, 2017a; Braunstein, Gross, & emotions (e.g., compassion, affection) elicit proso-
Ochsner, 2017; Gross, 2014; Gross & Barrett, 2011). cial behaviors (e.g., group cohesion, pair bonding).
Without emotions motivating approach, avoidance,
Variants of Functionalism and affiliative behaviors, likelihood of survival in
When defining emotion dysregulation, one must our environments of adaptation would presumably
first consider what emotions are, and the day-to-day have been lower. Evolutionary functionalist perspec-
functions they serve and do not serve in both their tives have a long history in animal, human, and
ordinary and extreme forms. From this perspective, comparative research on emotion and suggest that
affect dysregulation cannot be defined by overt ex- emotion and motivation are inextricable facets of
pressions of emotion without first specifying the human function, despite being separated in the his-
contexts in which such expressions occur, then tory of behavioral science (see, e.g., Beauchaine &
evaluating whether the emotion expressed and the Zisner, 2017; Gray & McNaughton, 2000; Panksepp,
intensity of its expression are context appropriate, 2011; Porges, 1997).
inappropriate, or neutral vis-à-vis social and cultural An important corollary of this perspective is
norms. For example, intense expressions of anger that humans sometimes behave at the behest of
toward others may be fully functional if the safety of their emotions. Such is especially likely when
one’s offspring is threatened, but similarly intense environmental contingencies are extreme and pull
displays of anger interfere with adaptive behavior in strongly for survival-relevant actions (e.g., in situ-
most social and cultural contexts. Although often ations of food deprivation, threats to physical
not considered, it is also important to note that in safety to oneself or one’s kin). Strong emotional
some situations expressions of anger are afunctional. reactions to these situations motivate urgent be-
Even moderately intense solitary displays of anger, havioral responses that override ongoing activities
for example, such as those elicited by frustration (see, e.g., Corr, 2004). Notably, however, evolu-
while driving, may serve no function or dysfunction tionary functionalist accounts do not imply that
whatsoever. Thus, whether particular displays of all or even most emotional reactions are survival
emotion are functional, dysfunctional, or afunc- relevant. In fact, evolutionary theorists have long
tional, and whether they are regulated, dysregu- recognized that (1) over any extended period of
lated, or unregulated, depends in large part on time individual differences in emotional and be-
eliciting contextual events, and match or mismatch havioral response tendencies confer probabilistic
between context and expressive intensity (e.g., Aldao, rather than deterministic effects on adaptive fit-
2013). Furthermore, given two common uses of ness, and (2) some behavioral response tendencies
the term functionalism that partly but do not fully are coincidental byproducts of evolution—not
overlap (see immediately below), classifying emo- direct outcomes of adaptive selection (Beauchaine,
tions as functional or dysfunctional, regulated or 1999; Buss, Haselton, Shackelford, Bleske, &
dysregulated, is not as straightforward as it might Wakefield, 1998; Gould, 1991). In the latter case,
first appear (e.g., Barrett, 2017b). such response tendencies have no bearing on
2 Functionalist and Constructionist Perspectives

adaptive fitness. Despite its name, evolutionary circuitry is a difficult proposition (see Barrett, 2017b).
functionalism therefore does not imply that all or These observations contributed to modern construc-
even most emotional experiences or expressions tionist accounts of emotion, which eschew several
are functional, a point we return to in later sec- assumptions of traditional functionalist theories, as
tions (see “Points of Divergence and Convergence described in the next section.
in Functionalism and Constructionism”). A common although not universal assumption
In a second common use of the term functional- of evolutionary functionalism is that at least some
ism, experiences and expressions of emotions are emotions or subsets of emotions represent categories
linked to outcomes in our day-to-day lives, with in nature. This notion follows from seemingly
limited if any consideration of our evolutionary
different classes of behavior—including approach,
environments of adaptation (see Keltner & Gross, avoidance, and social affiliation—that specific emo-
1999). Among children, for example, emotionally tions seem to support (see earlier; Beauchaine &
complaisant, well-mannered behavior in the class- Zisner, 2017; Gray & McNaughton, 2000; Panksepp,
room is seen as functional and adaptive, whereas 2011; Panksepp & Watt, 2011). Furthermore, many
emotionally exuberant, impulsive behavior is seen as evolutionary accounts presume that either rudi-
dysfunctional and maladaptive. Notably, however, ments of or fully formed approach, avoidance, and
exuberance and impulsivity were likely not maladap- affiliative emotions (1) are present across mamma-
tive in our evolutionary environments of adaptation lian species, (2) are experienced by human infants
and may have conferred selective advantages in cer- at birth, and (3) transcend human cultures (Ekman
tain environmental niches (see Mead, Beauchaine, & Cordaro, 2011; Ekman & Friesen, 1971). These
& Shannon, 2010). Thus, whether specific emotions theories articulate phylogenetically old, subcortical
and behaviors are functional or dysfunctional in our neural networks that subserve basic emotions (see,
modern-day lives may have nothing to do with their e.g., Beauchaine, Neuhaus, Zalewski, Crowell, &
phylogenetic adaptive value. Our intent here is to Potapova, 2011; Panksepp, 2016).
call readers’ attention to the important distinction Full articulation of anatomical and functional
between these two common uses of the term func- characteristics of these subcortical structures is
tionalism, the latter of which is especially prone to beyond the scope of this introductory chapter, but
circular reasoning in definitions of adaptation. both are specified in extensive reviews of the animal
Given potential confusion brought about by and human literatures (e.g., Beauchaine et al., 2011;
different uses of the term functionalism, and given Ikemoto, Yang, & Tan, 2015; Koob & Volkow, 2010;
other issues described in foundational articles across Panksepp, 2016; Tovote, Fadok, & Lüthi, 2015). In
the affective sciences (e.g., Campos et al., 1994; brief, early work on subcortical neural circuits of
Cole et al., 2004; Keltner & Gross, 1999; Thompson, approach and avoidance derived from studies of
1990), coeditor Sheila Crowell and I (TPB) encour- associative learning, motivation, and addiction in
aged authors to adopt a common definition of rodents and nonhuman primates. This work, in-
emotion dysregulation as “a pattern of emotional cluding lesion studies, single cell recording experi-
experience and/or expression that interferes with ments, and pharmacological manipulations, identi-
appropriate goal-directed behavior” (Beauchaine, 2015, fied subcortical neural systems of appetitive and
p. 876, emphasis added; see also Cole, Hall, & aversive motivation that are largely preserved across
Hajal, 2017). Here, we chose the word appropriate species. These systems include (1) the medial fore-
instead of adaptive to avoid teleological undertones. brain bundle—particularly projections from the
Teleological explanations are those that define phe- ventral tegmental area to the nucleus accumbens—
nomena based on specific purposes they serve, in- as integral to appetitive motivation and approach
cluding assumptions that specific emotions either emotions (Sagvolden Johansen, Aase, & Russell,
(1) evolved to serve highly specialized functions or 2005; Schultz, 2002; Wise, 2004) and (2) the septo-
(2) always serve an immediate function. As already hippocampal system—including the hippocampus
noted, many displays of emotion are afunctional, and its afferent projections from the amygdala—as
and in Western culture, situations that require “ap- integral to aversive motivation and associated avoid-
propriate” dampening of strong emotions are far ance emotions (Corr, 2013; Gray & McNaughton,
removed from our evolutionary environments of 2000; Strange, Witter, Lein, & Moser, 2014).
adaptation. Moreover, testing evolutionary func- Although general consensus exists regarding the
tions of emotions and emotion-subserving neural primary roles these systems play in approach and
Beauchaine and Haines 3

avoidance motivation and emotion (for reviews see 2008; Galvan et al., 2006). Differential neuromatu-
Beauchaine, 2001; Beauchaine & Zisner, 2017), it is ration of subcortical and cortical brain regions is a
also well recognized that the systems interact struc- likely contributor to the impetuous, impulsive, and
turally and functionally (e.g., Corr, 2013; Corr & emotionally labile behaviors common to adoles-
McNaughton, 2016). For example, neurons in the cence (e.g., Casey & Caudle, 2013). As prefrontal
nucleus accumbens (NAcc) respond to punishment neuromaturation completes in early adulthood,
as well as reward, and the amygdala responds to self- and emotion regulation improve markedly.
reward as well as punishment (e.g., Sauder, Derbidge, Notably, children and adolescents show stronger
& Beauchaine, 2016; Schultz, 2016). Both are there- subcortical responses to incentives than adults, yet
fore intricately involved in associative learning. their prefrontal cortex responding is weaker and
Moreover, the NAcc and the amygdala share inter- more diffuse (Macdonald, Goines, Novacek, &
connections via the paraventricular nucleus and the Walker, 2016). Furthermore, adolescents with im-
stria terminalis (e.g., Dong, Li, & Kirouac, 2017; pulse control problems show blunted frontal neuro-
Tovote et al., 2015). Thus, although the distinction maturation (De Brito et al., 2009).
between appetitive and aversive subcortical systems Finally, deficits in functional connectivity
is useful heuristically, subcortical CNS networks of between cortical and subcortical structures are

approach and avoidance interact complexly and are observed in both impulse control and anxiety

not functionally independent (see also Beauchaine disorders, which are characterized by excessive

& Constantino, 2017; Beyeler, 2016). approach- and avoidance-related emotions, respec-
tively. For example, reduced functional connectiv-
Implications for Emotion Regulation ity between the anterior cingulate and dorsal stria-
and Dysregulation tum is observed among externalizing adolescents
Functionalists often distinguish between bottom- (e.g., Shannon, Sauder, Beauchaine, & Gatzke-
up, subcortically mediated emotion generation pro- Kopp, 2009), and reduced functional connectivity
cesses and top-down, cortically mediated emotion between the amygdala and the orbitofrontal cortex
regulation processes (e.g., Beauchaine, 2015; Gross is associated with compulsive behavior and emo-
& Barrett, 2011). According to such perspectives, tional lability (e.g., Churchwell, Morris, Heurtelou,
subcortical neural circuits that initiate strong emo- & Kesner, 2009; Hilt, Hanson, & Pollak, 2011).
tional responses are modulated by cortical functions Notably, although findings are complex and not
(see also Hare et al., 2008). This literature is volumi- fully consistent, several studies show improved
nous and cannot be reviewed comprehensively, yet cortical–subcortical connectivity following effec-
several findings are noteworthy. First, cortical structive treatment for internalizing and externalizing
tures, particularly in prefrontal and orbitofrontal disorders (for a recent review see Beauchaine,
regions, have long been implicated in executive Zisner, & Hayden, 2019). Collectively, these find-
function and self-regulation (see Beauchaine & ings lend support to the notion that emotion regu-
Zisner, 2017; Etkin, Büchel, & Gross, 2015; lation is subserved by top-down cortical control over
Heatherton, 2011). Modern neuroimaging studies subcortical neural responding, and that disruptions
identify functional subdivisions of the prefrontal, in frontal cortical function and cortical–subcortical
anterior cingulate, and insular cortices as integral connectivity characterize emotion dysregulation
to effortful downregulation of negative affect (e.g., (see also Beauchaine, Constantino, & Hayden,
Tone, Garn, & Pine, 2016; Zilverstand, Parvaz, & 2018).
Goldstein, 2017). In fact, volitional reappraisal of
negative emotion elicits increased neural respond- Constructionism
ing across a distributed network of frontal struc- An alternative to functionalist perspectives is con-
tures, including the dorsolateral, medial, and ven- structionist theory. Constructionists assert that what
trolateral prefrontal cortices; the lateral orbitofrontal humans perceive as discrete emotions are not en-
cortex; the inferior frontal gyrus (IFG); and the coded by specific brain regions, but rather con-
insular cortex (e.g., Goldin, McRae, Ramel, &
structed through learning processes that are highly
Gross, 2008). individualized. According to this perspective, emo-
Second, subcortical structures reach volumetric tions and other experiential states, including per-
and functional maturity many years before cortical ception and cognition, emerge from interactions
neural structures (e.g., Brain Development among more primitive sensory and neural mecha-
Cooperative Group, 2012; Casey, Getz, & Galvan, nisms, which humans interpret and categorize

based on prior experience (see Barrett, 2009). construed in critical discussions concerning its
Constructionist theory identifies core affective pro- merits. This creates an artificial distinction between
cesses, including valence and arousal, which tran- functionalist and constructionist views on emotion.
scend multiple emotional states. Through repeated We view functionalism and constructionism as
visceral pairings of these core affective processes largely compatible, so long as one avoids teleologi-
with sensory and neural input elicited by our envi- cal misconceptions of evolution and acknowledges
ronments, we learn to associate instances of core interactive complexities and functional dependencies
affect with higher order, discrete representations of of neural responding within and across subcortical
emotion such as happiness and sadness (e.g., Russell and cortical networks. In sections to follow, we
& Barrett, 1999). Neural mechanisms of core affec- briefly outline our reasoning.
tive states are presumed to be present at birth, uni-
versal among humans, and supported by the same Implications for Emotion Dysregulation
neural networks as other psychological processes Constructionist accounts now rival functionalist
and states, such as perception and decision making perspectives as explanatory theories of emotion, yet
(see Duncan & Barrett, 2007). constructionists have written far less than function-
Constructionists make a clear distinction be- alists about emotion dysregulation per se. This may
tween core affective processes and emotions. be because constructionist approaches, including
Whereas core affective processes refer to general the theory of constructed emotion (TCE; Barrett,
experiences of positivity–negativity (valence) and 2017a, 2017b; Lindquist, 2013), view emotions as
activation–deactivation (arousal), emotions are more emergent properties of complex neuro-architectures,
specific experiential states, such as sadness, anger, which exhibit individualized affect-imbuing re-
fear, and shame (Ekman, 1992; Ekman & Cordaro, sponse patterns that are byproducts of unique
2011). Thus, despite being experienced discretely, all learning histories. These learning histories produce
emotions can be characterized along dimensions of cognitive–affective schemas, attributional biases,
valence and arousal (Barrett, 2016). According to and stimulus–response associations that contribute
constructionist theory, we rely on learning and collectively to emotional experience. From this
memory from prior experience to infer the meaning standpoint, emotion dysregulation is emotion, be-
of core affect in current situations. In this way, we cause it arises through the same highly individual-
construct context-dependent emotion representa- ized neural processes and unique learning histories
tions (Barrett, 2017a). Of note, core affective pro- (see, e.g., Papa & Epstein, 2018).
cesses, similar to basic emotions, can motivate be- According to TCE, emotion dysregulation
havioral response tendencies. For example, Pavlovian emerges at least in part from neural mechanisms of
bias is a “hard-wired” tendency to approach posi- core affective processes (e.g., valence, arousal) and
tively valenced stimuli and avoid negatively valenced disruptions in situated conceptualization (Barrett,
stimuli (Guitart-Masip et al., 2011). In some cases, Wilson-Mendenhall, & Barsalou, 2013). Situated
Pavlovian bias is so strong that organisms cannot conceptualization refers to “the brain [as] a situated
learn stimulus–response contingencies that require processing architecture, designed to process situa-
avoidance to attain reward (Hershberger, 1986). tions in the moment and to simulate non-present
Constructionists have been critical of functional- situations in thought” (Barsalou, 2016, p. 6). This
ist theories on a number of grounds. Although we includes evaluating what eliciting events represent,
cannot review all such critiques here, three espe- how to act upon those events, and the nature of core
cially important issues concern (1) teleological argu- affective processes to expect. Barrett et al. (2013)
ments concerning adaptive evolution of emotion, as suggest that emotion dysregulation could emerge
outlined earlier (see “Variants of Functionalism”); from highly canalized, inflexible conceptualizations
(2) opposition to the notion that specific neural that are not situational. In turn, nonsituational con-
structures and networks subserve particular emo- ceptualizations could arise from disruptions to one
tional states and functions; and (3) disagreement on or more among several processes, including memory
the extent to which animal research on reward retrieval, autonomic regulation, and attention, to
learning, fear learning, and motivation informs our name but a few. As reviewed by Barrett and Satpute
understanding of human emotion. Although we (2013), many such deficits correlate with abnormal-
agree that these points warrant consideration when ities in connectivity among intrinsic neural net-
evaluating functionalist theories, we argue that works, including the salience network and the
functionalism is often oversimplified and thus mis- fronto-parietal network, as seen in diverse forms of

psychopathology. Thus, disrupted connectivity A second critique of functionalism concerns
plays a central role in both functionalist and con- its linking of emotional states to specific brain
structionist theories of emotion dysregulation. regions and networks. As outlined under “Variants
of Functionalism,” for example, functionalist theo-
Points of Divergence and Convergence in ries often link (1) appetitive emotions to neural re-
Functionalism and Constructionism sponding in the medial forebrain bundle, including
As already noted, teleological explanations are those projections from the ventral tegmental area to the
that define phenomena based on the specific purposes nucleus accumbens (Sagvolden et al., 2005; Schultz,
they serve. The notion that emotions were designed 2002; Wise, 2004), and (2) aversive emotions to
by evolution to serve specific, adaptive functions is neural responding in the septo-hippocampal system,
therefore teleological (Barrett, 2017b). Basic emo- including the hippocampus and its afferent pro-
tion theory identifies approximately six discrete jections from the amygdala (Corr, 2013; Gray &
emotions (happiness, sadness, fear, surprise, anger, McNaughton, 2000; Strange et al., 2014). According
and disgust) that are shared across cultures, some to such accounts, basic emotions are presumed to
of which are documented in other mammals be initiated/generated by localized, phylogenetically
(Chevalier-Skolnikoff, 1973; Ekman & Friesen, old neural structures that are largely preserved
1971). A teleological explanation takes cross-species across mammals and, in some cases, other verte-
and cross-cultural expressions of affect as evidence brates (Panksepp, 2011, 2016). As already noted,
that discrete emotions evolved to facilitate adaptive these conclusions are based on decades of extensive
behaviors (e.g., fear evolved with the purpose of sig- research with animals (rodents and nonhuman pri-
naling organisms to danger). In other words, evolu- mates). This research includes localized lesion stud-
tion by natural selection purposefully designed basic ies, pharmacological manipulations, and implanted
emotional states to preserve the organism. electrode stimulation and recording experiments
Here it is important to note that purposeful that are highly precise both spatially and temporally
design has been explicitly eschewed as a mechanism (e.g., Gray, 1982; Olds & Milner, 1954).
of evolution since Darwin (1859) wrote On the Most studies of this nature cannot be conducted
Origin of Species. Thus, even though evolutionary with humans for obvious ethical reasons. As a con-
psychologists have at times appealed to purposeful sequence, neural studies of human emotion rely pri-
design, evolutionary biologists rejected the notion marily on functional magnetic resonance imaging
over a century ago (see Beauchaine, 1999; Buss et al., (fMRI), which evolved more recently. When fMRI
1998; Gould, 1991). A more accepted approach technology was first applied in emotion research,
among evolutionary theorists is to infer function region-of-interest (ROI) and effective connectivity
from the consequences of emotions throughout analyses predominated. Most early ROI and con-
evolutionary history (Wright, 1973). For example, nectivity studies were deductive (top-down), with
we may infer that the function of fear is to alert an ROIs specified a priori based on theory. Early meta-
organism of immediate danger because fear in the analyses of these studies revealed modest evidence
face of danger creates conditions that are conducive for emotion localization, consistent with animal re-
to survival. By way of natural selection, the most search (e.g., Murphy, Nimmo-Smith, & Lawrence,
likely consequence of an emotion is therefore the 2003; Phan, Wager, Taylor, & Liberzon, 2002).
function of that emotion specifically in our environ- More recently, inductive (bottom-up) ap-
ments of evolutionary adaptation (see Wright, 1973). proaches that capture coactivated neural circuitry
Provided such inferences are supported by observa- have ascended to prominence in the fMRI litera-
ble, biological mechanisms, they are not dubious ture. These approaches show that distributed pat-
philosophically (e.g., Barrett, 2017b; Neander, 1991). terns of neural activity account for more variance
This Darwinian (1872) perspective is infused in in basic emotions than specific brain regions
contemporary thinking about emotion (see Keltner (Celeghin, Diano, Bagnis, Viola, & Tamietto,
& Gross, 1999), despite terminology that some- 2017; Saarimäki et al., 2016). Such findings are
times leads to confusion. Indeed, even in biology, sometimes cited as evidence against functionalism
where most scientists decry language implying that (Kober et al., 2008; Lindquist, Wager, Kober,
evolution proceeds with goal-directed intention, Bliss-Moreau, & Barrett, 2012; Touroutoglou,
some nevertheless use such language as a literary Lindquist, Dickerson, & Barrett, 2015). It is im-
device (e.g., Hanke, 2004). portant to note, however, that linking basic

e motions to specific brain structures oversimplifies In contrast, functionalist accounts suggest that
the functionalist perspective. In fact, functionalists regulated emotions should be associated with (1)
have long recognized that multiple emotional subcortically generated responses to eliciting events
states activate common brain regions (see, e.g., that are (2) modulated by cortical responses via
Gray & McNaughton, 2000), and that complex (3) strong cortical–subcortical connectivity (e.g.,
neural circuits and interacting cortical–subcortical Beauchaine, Constantino, et al., 2018; Beauchaine,
networks generate and regulate affective responses Zisner, et al., 2018). If such is the case, we would
(e.g., Beauchaine, 2015; Beauchaine & Zisner, expect to find distributed neural activity for any
2017; Braunstein et al., 2017; Etkin et al., 2015; given instance of emotion due to the limited tempo-
Goldin et al., 2008; Gray & McNaughton, 2000; ral resolution of fMRI. From this perspective,
Gross & Barrett, 2011). Indeed, functional defi- prominent functionalist accounts look much like
ciencies in cortical–subcortical connectivity char- contructionist ones—both assume that primary-
acterize several psychiatric disorders for which process emotions (core affective states) that promote
emotion dysregulation plays a prominent role (see, approach and avoidance behaviors are subserved by
e.g., Beauchaine, Constantino, et al., 2018; Shannon phylogenetically old structures (primarily subcorti-
et al., 2009; Tone et al., 2016). cal structures), and that cortical networks interact
It should also be noted that neural signals prop- with these subcortical networks to produce what
agate across brain regions and networks at much we consciously experience as emotional states (see
faster rates than fMRI is capable of resolving. For Panksepp, 2011).
example, reactivity to reward cues by midbrain Finally, the locationist basic emotion perspective
dopamine neurons—as assessed via direct electrode of functionalism is only a single perspective—albeit
placement in primates—peaks at about 0.2 seconds a pervasive one in certain areas of research. Other
and returns to baseline at about 0.7 seconds functionalist perspectives focus on the dimen-
(e.g., Lak, Stauffer, & Schultz, 2016). In contrast, sional nature of emotions and various contextual
the fMRI blood oxygen level–dependent (BOLD) factors that influence our experience of affect (cf.
signal peaks between 4 and 5 seconds poststimulus Campos et al., 1994; Haines et al., 2019), similar to
and returns to baseline after 10 seconds (e.g., constructivist ideas. In sum, although language
Lohrenz, Kishida, & Montague, 2016). Thus, the used to describe functionalist and constructivist
BOLD signal is a sluggish indicator of neural re- theories is quite different, underlying ideas are more
sponding and is not well suited for detecting rapidly similar than some recent discourse in the literature
propagating patterns of neural responding that suggests.
originate in the subcortex and project to both corti- A final critique concerns the utility of animal
cal and other subcortical structures. Although research for making inferences about human emo-
modern imaging sequences provide whole-brain tion. Because evolutionarily functionalism is a phy-
coverage of slices at well under 1-second resolution logenetic account of emotion, many functionalists
(e.g., Uğurbil et al., 2013), this does not circumvent assume that neural structures implicated in gener-
sluggishness of the BOLD signal being measured. It ating basic emotions among humans should over-
is important to recognize this limitation when eval- lap considerably (if not fully) with their vertebrate
uating strengths and weaknesses of modern imaging homologues. As noted earlier under “Variants of
techniques that characterize and correlate widely Functionalism,” such arguments are most persua-
distributed patterns of BOLD coactivation with at- sive when applied to subcortical regions that are
tentional and emotional processes (e.g., Yoo et al., structurally similar across species. Nevertheless,
2018). It remains quite possible that among humans, some constructivists have taken a strong stance
at least some emotional states arise from patterns of against comparative research on emotion, noting
neural reactivity that originate in the very subcorti- that functionalist accounts often fail to specify
cal structures identified in decades of animal re- mechanisms adequately, and that it cannot be as-
search. As described earlier, several functionalist sumed that emotions are experienced by animals in
accounts suggest that vulnerability to emotion dys- the same way as they are by humans (see Barrett,
regulation occurs when rapid subcortical responses 2017b; LeDoux, 2012).
to eliciting events are not modulated effectively Given (1) overwhelming structural differentiation
by cortical reactivity (e.g., Beauchaine, 2015; Casey of the human cortex, (2) the phenomenon of human
& Caudle, 2013; Etkin et al., 2015). consciousness, and (3) the role that language plays in

shaping human experience of emotion, this critique We look forward to research from both perspectives
also holds merit. Here again, however, prominent in upcoming years, and we hope this chapter pro-
functionalists have made the same point. Indeed, Jaak vides a framework for readers as they digest the
Panksepp, who spearheaded functionalist emotion re- many interesting chapters to follow.
search with rodents, was very clear in describing qual-
itative differences between animal and human experi- References
ences of emotion: “Are the various affects—diverse Aldao, A. (2013). The future of emotion regulation research:
Capturing context. Perspectives on Psychological Science, 8,
feelings of positive and negative valences (‘good’ and 155–172.
‘bad’ feelings in the vernacular)—identical across Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
species? Of course not! Evolution persistently gener- Emotion regulation strategies and psychopathology: A meta-
ates abundant differences, but always on top of analysis. Clinical Psychology Review, 30, 217–237.
conserved-homologous foundational principles at Barrett, L. F. (2009). The future of psychology: Connecting
mind to brain. Perspectives on Psychological Science, 4,
genetic, neural and primal psychological levels” 326–339.
(Panksepp, 2011, p. 1796). Barrett, L. F. (2016). Navigating the science of emotion. In
Our contention is that interspecies differences H. Meiselman (Ed.), Emotion measurement (pp. 31–63).
in emotion notwithstanding, basic animal research Cambridge, UK: Woodhead Publishing.
offers extensive insights into neural substrates and Barrett, L. F. (2017a). The theory of constructed emotion: An
active inference account of interoception and categorization.
representations of emotion, as discussed in previous Social Cognitive and Affective Neuroscience, 12, 1–23.
sections. Models of dopamine reward prediction Barrett, L. F. (2017b). Functionalism cannot save the classical
error signaling in nonhuman primates provide view of emotion. Social Cognitive and Affective Neuroscience,
one example (Schultz, Dayan, & Montague, 1997). 12, 34–36.
These models capture moment-to-moment affective Barrett, L. F., & Satpute, A. (2013). Large-scale brain networks in
affective and social neuroscience: Towards an integrative
states among humans (Rutledge, Skandali, Dayan, architecture of the human brain. Current Opinion in
& Dolan, 2014) and extend further to explain indi- Neurobiology, 23, 1–12.
vidual differences in mood states, including positive Barrett, L. F., Wilson-Mendenhall, C. D., & Barsalou, L. W.
affectivity, irritability, and anhedonia (e.g., Eldar, (2013). A psychological construction account of emotion
Rutledge, Dolan, & Niv, 2016; Laakso et al., 2003; regulation and dysregulation: The role of situated
conceptualizations. In J. J. Gross (Ed.), Handbook of emotion
Zisner & Beauchaine, 2016). With continued devel- regulation (2nd ed., pp. 447–465). New York, NY: Guilford
opment of computational models of emotion gen- Press.
eration and regulation (e.g., Etkin et al., 2015), we Barsalou, L. W. (2016). Situated conceptualization offers a
expect that many more such examples will become theoretical account of social priming. Current Opinion in
realized in the near future. Psychology, 12, 6–11.
Beauchaine, T. P. (1999). Definitions and levels of analysis.
American Psychologist, 54, 439–440.
Beauchaine, T. P. (2001). Vagal tone, development, and Gray’s
Conclusions
motivational theory: Toward an integrated model of
In this chapter, we introduce functionalist and con- autonomic nervous system functioning in psychopathology.
structionist theories of emotion, discuss their impli- Development and Psychopathology, 13, 183–214.
cations for understanding emotion dysregulation, Beauchaine, T. P. (2015). Future directions in emotion
and consider points of divergence and convergence dysregulation and youth psychopathology. Journal of Clinical
Child and Adolescent Psychology, 44, 875–896.
across perspectives. Although constructionist theo-
Beauchaine, T. P., & Constantino, J. N. (2017). Redefining the
ries have gained remarkable traction in affect re- endophenotype concept to accommodate transdiagnostic
search and offer key insights into the complex indi- vulnerabilities and etiological complexity. Biomarkers in
viduality of emotion, we argue that functionalist Medicine, 11, 769–780.
perspectives still hold value, especially when they Beauchaine, T. P., Constantino, J. N., & Hayden, E. P. (2018).
Psychiatry and developmental psychopathology: Unifying
are not oversimplified. Functionalist perspectives
themes and future directions. Comprehensive Psychiatry, 87,
derive from a long tradition of painstaking neuro- 143–152.
science research, including elegant experiments Beauchaine, T. P., Neuhaus, E., Zalewski, M., Crowell, S. E., &
with animals using techniques of very high spatial Potapova, N. (2011). Effects of allostatic load on neural
and temporal resolution. Although such techniques systems subserving motivation, mood regulation, and social
affiliation. Development and Psychopathology, 23, 975–999.
are not available to those who test constructionist
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion
theories with humans, fMRI studies yield insights regulation, and the latent structure of psychopathology:
into the roles that widely distributed neural net- An integrative and convergent historical perspective.
works play in emotion and emotion dysregulation. International Journal of Psychophysiology, 119, 108–118.

Beauchaine, T. P., Zisner, A. R., & Hayden, E. P. (2019). De Brito, S. A., Mechelli, A., Wilke, M., Laurens, K. R., Jones,
Neurobiological mechanisms of psychopathology and A. P., Barker, G. J., . . . Viding, E. (2009). Size matters:
treatment action. In T. H. Ollendick, S. W. White, & Increased grey matter in boys with conduct problems and
B. A. White (Eds.), The Oxford handbook of clinical child and callous-unemotional traits. Brain, 132, 843–852.
adolescent psychology (pp. 699–723). New York, NY: Oxford Dong, X., Li, S., & Kirouac, G. J. (2017). Collateralization of
University Press. projections from the paraventricular nucleus of the thalamus
Beyeler, A. (2016). Parsing reward from aversion. Science, 354, to the nucleus accumbens, bed nucleus of the stria terminalis,
558. and central nucleus of the amygdala. Brain Structure and
Bradley, B., DeFife, J. A., Guarnaccia, C., Phifer, J., Fani, N., Function, 222, 3927–3943.
Ressler, K. J., & Westen, D. (2011). Emotion dysregulation Duncan, S., & Barrett, L. F. (2007). Affect is a form of
and negative affect: Association with psychiatric symptoms. cognition: A neurobiological analysis. Cognition and
Journal of Clinical Psychiatry, 72, 685–691. Emotion, 21, 1184–1211.
Brain Development Cooperative Group. (2012). Total and regional Ekman, P. (1992). An argument for basic emotions. Cognition
brain volumes in a population-based normative sample and Emotion, 6, 169–200.
from 4 to 18 years: The NIH MRI Study of Normal Brain Ekman, P., & Cordaro, D. (2011). What is meant by calling
Development. Cerebral Cortex, 22, 1–12. emotions basic. Emotion Review, 3, 364–370.
Braunstein, L. M., Gross, J. J., & Ochsner, K. N. (2017). Explicit Ekman, P., & Friesen, W. V. (1971). Constants across cultures
and implicit emotion regulation: A multi-level framework. in the face and emotion. Journal of Personality and Social
Social Cognitive and Affective Neuroscience, 12, 1545–1557. Psychology, 17, 124–129.
Buss, D. M., Haselton, M. G., Shackelford, T. K., Bleske, A. L., Eldar, E., Rutledge, R. B., Dolan, R. J., & Niv, Y. (2016). Mood
& Wakefield, J. C. (1998). Adaptations, exaptations, and as representation of momentum. Trends in Cognitive Sciences,
spandrels. American Psychologist, 53, 533–548. 20, 15–24.
Campos, J. J., Mumme, D. L., Kermoian, R., & Campos, R. G. Etkin, A., Büchel, C., & Gross, J. J. (2015). The neural bases of
(1994). A functionalist perspective on the nature of emotion. emotion regulation. Nature Reviews Neuroscience, 16, 693–700.
Monographs of the Society for Research on Child Development, Galvan, A., Hare, T. A., Parra, C. E., Penn, J., Voss, H., Glover, G.,
59, 284–303. & Casey, B. J. (2006). Earlier development of the accumbens
Casey, B. J., & Caudle, K. (2013). The teenage brain: Self-control. relative to orbitofrontal cortex might underlie risk-taking
Current Directions in Psychological Science, 22, 82–87. behavior in adolescents. Journal of Neuroscience, 26,
Casey, B. J., Getz, S., & Galvan, A. (2008). The adolescent brain. 6885–6892.
Developmental Review, 28, 62–77. Goldin, P. R., McRae, K., Ramel, W., & Gross, J. J. (2008).
Celeghin, A., Diano, M., Bagnis, A., Viola, M., & Tamietto, M. The neural bases of emotion regulation: Reappraisal and
(2017). Basic emotions in human neuroscience: Neuroimaging suppression of negative emotion. Biological Psychiatry, 63,
and beyond. Frontiers in Psychology, 8, 1432. 577–586.
Chevalier-Skolnikoff, S. (1973). Darwin and facial expression. In Gould, S. J. (1991). Exaptation: A crucial tool for an evolutionary
P. Ekman (Ed.), Darwin and facial expression (pp. 11–90). psychology. Journal of Social Issues, 47, 43–65.
New York, NY: Academic Press. Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., &
Churchwell, J. C., Morris, A. M., Heurtelou, N. M., & Kesner, Gunderson, J. G. (2006). An experimental investigation of
R. P. (2009). Interactions between the prefrontal cortex and emotion dysregulation in borderline personality disorder.
amygdala during delay discounting and reversal. Behavioral Journal of Abnormal Psychology, 115, 850–855.
Neuroscience, 123, 1185–1196. Gray, J. A. (1982). The neuropsychology of anxiety: An enquiry
Cole, P. M., Hall, S. E., & Hajal, N. J. (2017). Emotion into the functions of the septo-hippocampal system. Oxford,
dysregulation as a vulnerability to psychopathology. In UK: Oxford University Press.
T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent Gray, J. A., & McNaughton, N. (2000). The neuropsychology of
psychopathology (3rd ed., pp. 346–386). Hoboken, NJ: anxiety (2nd ed.). New York, NY: Oxford University Press.
Wiley. Gross, J. J. (1998). The emerging field of emotion regulation: An
Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion integrative review. Review of General Psychology, 2, 271–299.
regulation as a scientific construct: Methodological challenges Gross, J. J. (2014). Emotion regulation: Conceptual and
and directions for child development research. Child empirical foundations. In J. J. Gross (Ed.), Handbook of
Development, 75, 317–333. emotion regulation (pp. 3–20). New York, NY: Guilford.
Corr, P. J. (2004). Reinforcement sensitivity theory and personality. Gross, J. J., & Barrett, L. F. (2011). Emotion generation and
Neuroscience and Biobehavioral Reviews, 28, 317–332. emotion regulation: One or two depends on your point of
Corr, P. J. (2013). Approach and avoidance behaviour: view. Emotion Review, 3, 8–16.
Multiple systems and their interactions. Emotion Review, Guitart-Masip, M., Fuentemilla, L., Bach, D. R., Huys, Q. J. M.,
5, 285–290. Dayan, P., Dolan, R. J., & Duzel, E. (2011). Action dominates
Corr, P. J., & McNaughton, N. (2016). Neural mechanisms of valence in anticipatory representations in the human
low trait anxiety and risk for externalizing behavior. In striatum and dopaminergic midbrain. Journal of Neuroscience,
T. P. Beauchaine & S. P. Hinshaw (Eds.), The Oxford 31, 7867–7875.
handbook of externalizing spectrum disorders (pp. 220–238). Haines, N., Bell, Z., Crowell, S. E., Hahn, H., Kamara, D.,
New York, NY: Oxford University Press. McDonough-Caplan, H., . . . Beauchaine, T. P. (2019). Using
Darwin, C. (1859). On the origin of species by means of natural automated computer vision and machine learning to code
selection. London, UK: Murray. facial expressions of affective valence and arousal:
Darwin, C. (1872). The expression of the emotions in man and Implications for emotion dysregulation research. Development
animals. London, UK: Murray. and Psychopathology, 31, 871–886.

Hanke, D. (2004). Teleology: The explanation that bedevils brain. Journal of Comparative and Physiological Psychology, 47,
biology. In J. Cornwell (Ed.), Explanations: Styles of explanation 419–427.
in science (pp. 143–156). Oxford, UK: Oxford University Press. Panksepp, J. (2011). The basic emotional circuits of mammalian
Hare, T. A., Tottenham, N., Galvan, A., Voss, H. U., Glover, brains: Do animals have affective lives? Neuroscience and
G. H., & Casey, B. J. (2008). Biological substrates of Biobehavioral Reviews, 35, 1791–1804.
emotional reactivity and regulation in adolescence during Panksepp, J. (2016). The psycho-neurology of cross-species
an emotional Go-No-go task. Biological Psychiatry, 63, affective/social neuroscience: Understanding animal affective
927–934. states as a guide to development of novel psychiatric treatments.
Heatherton, T. F. (2011). Neuroscience of self and self-regulation. Current Topics in Behavioral Neuroscience, 30, 109–125.
Annual Review of Psychology, 62, 363–390. Panksepp, J., & Watt, D. (2011). What is basic about basic
Hershberger, W. A. (1986). An approach through the looking- emotions? Lasting lessons from affective neuroscience.
glass. Animal Learning and Behavior, 14, 443–451. Emotion Review, 3, 387–396.
Hilt, L. M., Hanson, J. L., & Pollak, S. D. (2011). Emotion Papa, A., & Epstein, E. (2018). Emotions and emotion
dysregulation. In B. B. Brown & M. J. Prinstein (Eds.), regulation. In S. C. Hayes & S. G. Hofmann (Eds.), Process-
Encyclopedia of adolescence (Vol. 3, pp. 160–169). New York, based CBT (pp. 137–152). Oakland, CA: New Harbinger.
NY: Elsevier. Phan, K. L., Wager, T., Taylor, S. F., & Liberzon, I. (2002).
Ikemoto, S., Yang, C., & Tan, A. (2015). Basal ganglia circuit Functional neuroanatomy of emotion: A meta-analysis of
loops, dopamine and motivation: A review and enquiry. emotion activation studies in PET and fMRI. Neuroimage,
Behavioural Brain Research, 290, 17–31. 16, 331–348.
Keltner, D., & Gross, J. J. (1999). Functional accounts of Porges, S. W. (1997). Emotion: An evolutionary by-product of
emotions. Cognition and Emotion, 13, 467–480. the neural regulation of the autonomic nervous system.
Kober, H., Barrett, L. F., Joseph, J., Bliss-Moreau, E., Lindquist, Annals of the New York Academy of Sciences, 807, 62–77.
K., & Wager, T. D. (2008). Functional grouping and Russell, J. A., & Barrett, L. F. (1999). Core affect, prototypical
cortical-subcortical interactions in emotion: A meta-analysis emotional episodes, and other things called emotion:
of neuroimaging studies. Neuroimage, 42, 998–1031. Dissecting the elephant. Journal of Personality and Social
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of Psychology, 76, 805–819.
addiction. Neuropsychopharmacology, 35, 217–238. Rutledge, R. B., Skandali, N., Dayan, P., & Dolan, R. J. (2014).
Laakso, A., Wallius, E., Kajander, J., Bergman, J., Eskola, O., A computational and neural model of momentary subjective
Solin, O., . . . Hietala, J. (2003). Personality traits and striatal well-being. Proceedings of the National Academy of Sciences,
dopamine synthesis capacity in healthy subjects. American 111, 12252–12257.
Journal of Psychiatry, 160, 904–910. Saarimäki, H., Gotsopoulos, A., Jääskeläinen, I. P., Lampinen, J.,
Lak, A., Stauffer, W. R., & Schultz, W. (2016). Dopamine neurons Vuilleumier, P., Hari, R., . . . Nummenmaa, L. (2016).
learn relative chosen value from probabilistic rewards. eLife, Discrete neural signatures of basic emotions. Cerebral Cortex,
5, e18044. 26, 2563–2573.
LeDoux, J. E. (2012). Rethinking the emotional brain. Neuron, Sagvolden, T., Johansen, E. B., Aase, H., & Russell, V. A. (2005).
73, 653–676. A dynamic developmental theory of attention-deficit/
Lindquist, K. A. (2013). Emotions emerge from more basic hyperactivity disorder (ADHD) predominantly hyperactive/
psychological ingredients: A modern psychological impulsive and combined subtypes. Behavioral and Brain
constructionist model. Emotion Review, 5, 356–368. Sciences, 28, 397–419.
Lindquist, K. A., Wager, T. D., Kober, H., Bliss-Moreau, E., & Sauder, C. L., Derbidge, C. M., & Beauchaine, T. P. (2016). Neural
Barrett, L. F. (2012). The brain basis of emotion: A meta- responses to monetary incentives among self-injuring adolescent
analytic review. Behavioral and Brain Sciences, 35, 121–143. girls. Development and Psychopathology, 28, 277–291.
Linehan, M. M. (1993). Cognitive-behavioral treatment for Schultz, W. (2002). Getting formal with dopamine and reward.
borderline personality disorder. New York, NY: Guilford. Neuron, 36, 241–263.
Lohrenz, T., Kishida, K. T., & Montague, P. R. (2016). BOLD Schultz, W. (2016). Dopamine reward prediction-error signaling:
and its connection to dopamine release in human striatum: A two-component response. Nature Reviews Neuroscience, 7,
A cross-cohort comparison. Philosophical Transactions of 183–195.
the Royal Society of London B: Biological Sciences, 371, Schultz, W., Dayan, P., & Montague, P. R. (1997). A neural
20150352. substrate of prediction and reward. Science, 275, 1593–1599.
Macdonald, A., Goines, K., Novacek, D., & Walker, E. (2016). Shannon, K. E., Sauder, C., Beauchaine, T. P., & Gatzke-Kopp,
Prefrontal mechanisms of comorbidity from a transdiagnostic L. (2009). Disrupted effective connectivity between the
and ontogenic perspective. Developmental Psychopathology, medial frontal cortex and the caudate in adolescent boys with
28, 1147–1175. externalizing behavior disorders. Criminal Justice and
Mead, H. K., Beauchaine, T. P., & Shannon, K. E. (2010). Behavior, 36, 1141–1157.
Neurobiological adaptations to violence across development. Strange, B. A., Witter, M. P., Lein, E. S., & Moser, E. I. (2014).
Development and Psychopathology, 22, 1–22. Functional organization of the hippocampal longitudinal
Murphy, F. C., Nimmo-Smith, I., & Lawrence, A. D. (2003). axis. Nature Reviews Neuroscience, 15, 655–669.
Functional neuroanatomy of emotions: A meta-analysis. Thompson, R. A. (1990). Emotion and self-regulation. In
Cognitive, Affective, and Behavioral Neuroscience, 3, 207–233. R. A. Thompson (Ed.), Nebraska Symposium on Motivation:
Neander, K. (1991). The teleological notion of “function.” Vol. 36. Socioemotional development (pp. 383–483). Lincoln,
Australasian Journal of Philosophy, 69, 454–468. NE: University of Nebraska Press.
Olds, J., & Milner, P. (1954). Positive reinforcement produced by Tone, E. B., Garn, C. L., & Pine, D. S. (2016). Anxiety
electrical stimulation of septal area and other regions of rat regulation: A developmental psychopathology perspective. In

D. Cicchetti (Ed.), Developmental psychopathology, Vol. 2: Wright, L. (1973). Functions. Philosophical Review, 82,
Developmental neuroscience (3rd ed., pp. 523–556). Hoboken, 139–168.
NJ: Wiley. Yoo, K., Rosenberg, M. D., Hsu, W.-T., Zhang, S., Li, C.-S. R.,
Touroutoglou, A., Lindquist, K. A., Dickerson, B. C., & Barrett, Scheinost, D., . . . Chun, M. M. (2018). Connectome-based
L. F. (2015). Intrinsic connectivity in the human brain does predictive modeling of attention: Comparing different
not reveal networks for “basic” emotions. Social Cognitive functional connectivity features and prediction methods
and Affective Neuroscience, 10, 1257–1265. across datasets. NeuroImage, 167, 11–22.
Tovote, P., Fadok, J. P., & Lüthi, A. (2015). Neuronal circuits for Zilverstand, A., Parvaz, M. A., & Goldstein, R. Z. (2017).
fear and anxiety. Nature Reviews Neuroscience, 16, 317–331. Neuroimaging cognitive reappraisal in clinical populations
Uğurbil, K., Xu, J., Auerbach, E. J., Moeller, S., Vu, A. T., to define neural targets for enhancing emotion regulation.
Duarte-Carvajalino, J. M., . . . WU-Minn HCP Consortium. A systematic review. NeuroImage, 151, 105–116.
(2013). Pushing spatial and temporal resolution for functional Zisner, A., & Beauchaine, T. P. (2016). Neural substrates of trait
and diffusion MRI in the Human Connectome Project. impulsivity, anhedonia, and irritability: Mechanisms of
NeuroImage, 80, 80–104. heterotypic comorbidity between externalizing disorders and
Wise, R. A. (2004). Dopamine, learning and motivation. Nature unipolar depression. Development and Psychopathology, 28,
Reviews Neuroscience, 5, 483–494. 1179–1210.

CH A PT E R
Emotions as Regulators of
2 Motivated Behavior
Eric E. Nelson, Michele A. Morningstar, and Whitney I. Mattson
Abstract
Emotions, when viewed from the affective neuroscience perspective, arise from organized patterns of
brain activity, which function to generate adaptive behavioral responses. Behavior that emerges from
emotional brain engagement can almost always be characterized as motivated. Thus, emotion and
motivation are highly interdependent concepts, particularly when it comes to behavioral expression.
However, emotions do not always generate behavior, and behavioral outcomes of emotional
engagement—that is, motivated behavior—are not always adaptive. The intersection and dissociation
of emotion and motivation are reviewed in this chapter from an affective neuroscience perspective
that is heavily influenced by the work of Jaak Panksepp.
Keywords: affect, neuroscience, psychopathology, bottom-up, translational
This chapter is dedicated to Jaak Panksepp (1943–2017), a mentor, scholar, and

provocateur, who brought emotions into the brain and the animal spirit into
humanity. Jaak was originally slated to write this chapter but his untimely death
prevented completion. We have attempted to conjure his intellectual spirit in
this writing.
Introduction attention, facilitate memory, and guide decision

Emotions provide color and meaning to life. Major making (MacLeod, Mathews, & Tata, 1986; Cahill
events such as birth and death are typically book- & McGaugh, 1998; Rolls, 1999; Panksepp & Biven,
marked with intense emotional involvement. Even 2012; Damasio & Carvalho, 2013). From a mecha-
more mundane daily encounters—such as anger di- nistic perspective, the similarity and consistency of
rected at an inconsiderate driver, fear of the neigh- emotional expression across individuals and species,
bor’s dog, happiness at seeing one’s family after common neural activation patterns, and similarities
work—are common punctuations to daily experi- in contextual elicitors for a number of emotional ex-
ences. On a societal level, explorations of emotional periences suggest that many emotions are conserved
experiences are important components of art, litera- across evolution. Furthermore, these expressions
ture, and popular culture. All of these elements serve important roles in fostering life-preserving be-
demonstrate the important role emotion plays in haviors, promoting reproductive success, and com-
highlighting salient experiences of life. municating with conspecifics (Darwin, 1872/2009;
Although these features of emotion are clearly of Ekman & Davidson, 1994; Rolls, 1999; Panksepp &
existential importance, biological and psychological Biven, 2012; Damasio & Carvalho, 2013).
perspectives often ascribe a more functional role to We view emotion largely from this latter per-
emotion. Emotions serve to direct behavior, capture spective, and as such approach the topic of emotion
13
more from the standpoint of biological utility than tions and motivated behaviors evolved because they
experiential or constructivist perspectives (LeDoux, serve useful biological purposes. However, evolved
2012; Barrett, 2016). Core aspects of emotion can biological utility is not always adaptive across
be found in fundamental brain response patterns modern-day contexts, or for all individuals. Next,
(Hamann, 2012; Panksepp & Biven, 2012). In both we briefly discuss methodological approaches and
human and animal studies, emotional states such as current controversies, and close with important
desire and pleasure are associated consistently with challenges for future research in this area.
activity in mesolimbic brain regions, particularly
the ventral striatum and ventral prefrontal cortex Terms and Concepts
(Kuhn & Gallinat, 2012; Berridge & Kringelbach, Much of the terminology used herein refers to
2015). Recent neuroimaging research demonstrates common concepts in psychology and biology. Terms
that the distinctiveness of different emotional cate- such as motivation and emotion refer to “states”
gories is not as clear as once assumed (Hamann, that are generally understood but difficult to clearly
2012; Lindquist, Wager, Kober, Bliss-Moreau, & define. Though some general aspects of these con-
Barrett, 2012). However, we believe that on balance, cepts are shared in the field, important differences
evidence supports core neural constituents for spe- in conceptualization can lead to misunderstandings
cific emotions. Specifically, these emotions are dis- among researchers. Therefore, we offer some level of
tinguishable at the neurobiological systems level definitional detail and provide examples for key
(which include both anatomical and neurochemical concepts in the following sections.
components) and are shared across individuals and
species (Berridge & Kringelbach, 2013; Panksepp, Motivated Behavior
Lane, Solms, & Smith, 2017). However, we also Motivated behaviors are focused and goal-directed.
agree with perspectives put forth in traditional cog- Importantly, however, not all “goal directed” behav-
nitive neuroscience that the interaction between ior can be conceptualized as motivated behavior.
older brain regions and higher neocortical struc- Motivated behavior tends to be focused and highly
tures can generate complexities that are uniquely prioritized in terms of neuronal resources (Bradley
human (Panksepp et al., 2017). Additionally, we et al., 2003). Such behaviors typically involve move-
agree that emotional distinctions are not likely to ments that are rapid, are direct, and contain an ele-
emerge at the level of individual structures but ment of urgency (Beatty, Cranley, Carnaby, &
rather in interactions of several regions across inte- Janelle, 2016). For example, walking across the
grated circuits (Hamann, 2012). street is a behavior that is clearly goal oriented, but
In this chapter, we consider the confluence of it does not necessarily meet our definition. In con-
emotion and motivated behavior from a neurosci- trast, if this behavior was done rapidly to escape the
entific and biological perspective. Our overriding cold or to retrieve one’s crying toddler, it would be
framework is that, from the standpoint of behav- considered motivated. Given that motivated behav-
ioral expression, behaviors that arise from emotion ior contains an element of urgency, it may be per-
are motivated behavior (Beauchaine & Zisner, formed in favor of other potential behavioral lures
2017). Behavior that emerges from emotional ex- or influences (such as cross-traffic or encounters
perience is energized, directed, and focused by the with friends) in the environment.
emotional brain systems engaged: for instance,
withdrawal from threat is a behavior motivated by Emotion
fear, the compulsive search for sex or drugs is be- Emotion is a difficult and often contentious con-
havior motivated by pleasure, and prolonged cept to define clearly. Although terms such as fear
crying after losing a loved one is motivated by grief and anger are commonly used in the scientific lit-
and sadness. Thus, motivated behavior and emo- erature and offer convenient shorthand, interpreta-
tion are tightly coupled. However, they are not tions of such terms vary. Several theories have been
synonymous. There are important ways in which proposed to explain the experience of emotion
emotion can be dissociated from motivated behav- itself, referencing biological influences on physio-
ior, and some of these differences may be particu- logical arousal (Scherer, 2009), cognitive labeling
larly important for psychological health and psy- and contextual interpretation (Schacter & Singer,
chopathology. 1962; Reisenzein, 1983; Scherer, 2009; LeDoux,
We begin by defining key terms and concepts, 2014; Barrett, 2016), and social learning processes
then outline our theoretical perspective that emo- (Fogel et al., 1992), among others (Barrett, 2016).
14 Emotions as Regul ators of Motivated Behavior

Whether such emotional concepts emerge from c onsequence of past experience. Memory is stored
identical patterns of brain activation across individ- by novel patterns of brain activity and connections,
uals and species, require conscious experience, or which can elicit novel experiences that result from
are accompanied by universal expression are all im- that past experience.
portant matters of debate (Ekman & Cordaro, 2011;
Damasio & Carvalho, 2013; LeDoux, 2014; Barrett, Attention
2016; Panksepp et al., 2017). Working from a neu- Attention refers to active directing of sensory expe-
robiological perspective, we consider emotions to rience toward a specific domain, area, or sensory
be coordinated patterns of activity in central and expectation.
peripheral nervous systems, often accompanied by
neuroendocrine activity (Panksepp & Biven, 2012). Development
These coordinated patterns of physiological activity Development refers to regulated maturational
are accompanied by experiential states that, at changes in the brain, body, and behavior that occur
least among humans, are similar across individuals. between birth and adulthood. Notably, although
Neural substrates of emotion within the central maturational changes in the brain follow a prepro-
nervous system include both subcortical (deep and grammed timeline or ontogeny, environmental ex-
evolutionarily preserved across species) and neocor- perience and behavior play a critical role in guiding
tical (the outer layer of the brain that is the largest this process. One mechanistic example of this inter-
and most elaborated among primates and humans) active process is neuronal pruning, where intrinsic
regions. This activity is typically transitory—lasting signals guide exuberant initial synapse connection
seconds to minutes—and is often accompanied by and circuit formation, which is then refined by re-
some form of behavioral expression (Ekman & moval of connections that are underutilized (Stiles,
Davidson, 1994). There are three important points 2008).
to note about our conceptualization of emotion.
First, a critical feature is coordinated activity of sub- Social Behavior
cortical and cortical structures. This generates inter- Social behavior refers to behavior (both affiliative
nal states that are both multifaceted and organized. and/or agonistic) that is targeted toward or coordi-
Second, compilations of brain activity associated nated with a conspecific.
with specific emotions are recognizable patterns but
are not rigid. Just as the color red has many varia- Theoretical Perspective
tions that remain “red,” fear has many variations Panksepp’s Framework
from prototypical that still remain fear. Third, be- A basic premise of the Pankseppian model is that
havioral expression is a common but not necessary emotions are “kinds” in the universe. Emotions
feature of emotion, which is particularly important arise from distinctive patterns of brain activity, con-
for the subsequent discussion. served in their basic form across evolution, that
function to generate highly motivated and evolu-
Homeostasis tionarily adaptive behaviors. Because of their
Homeostasis is an important concept in physiology, adaptive value, these organized patterns became
and one that has historical roots in biological stud- embedded in the genome and standard architecture
ies of emotion and motivated behavior. Homeostasis of the nervous system (Panksepp & Biven, 2012).
is the active process of maintaining a steady state. Emotional kinds are brain systems organized prima-
For example, because maintaining constant levels of rily in subcortical structures in highly similar ways
osmolarity is critical for life, many systems—both across both individuals and species. Panksepp iden-
behavioral and physiological—function to maintain tified seven basic emotional systems that he believed
constant levels of fluidity and salinity within cells. were physiologically distinctive and form the basis
These processes may translate to human behavior: of all emotional experience: SEEKING, which gen-
for example, the imbalance of fluids may lead to a erates search and consummatory behavior; RAGE,
sensation of thirst, which motivates the search for which provokes aggressive responses against conspe-
liquids to ingest. cifics; FEAR, which is linked to withdrawal and
avoidance behaviors; LUST, which generates mating
Learning and Memory behavior; CARE, which leads to nurturant behav-
Learning refers to processes through which brain ior; PANIC-GRIEF, which is associated with social
activation patterns and/or behavior change as a
separation and loss; and PLAY, which is related to
Nelson, Morningstar, and Mat tson 15

affiliative exchange and promotes social cohesion tional experience, which can be construed as a
and social learning (Panksepp & Biven, 2012). Each meta-level of the primary process. This is frequently
of these emerges from distinctive patterns of activity the level at which cognitive neuroscientists deal
in subcortical brain systems and is present in similar with emotion. The tertiary level involves engage-
form in most mammals. Some of these patterns are ment of representations of primary process experi-
even evident to varying degrees in birds, amphibi- ences. According to Panksepp, secondary and ter-
ans, and reptiles (Maclean, 1990; Panksepp, 2011). tiary process emotions would not exist without
For example, the SEEKING system is a neural net- initial involvement of basic primary process states,
work that ascends from the ventral tegmental area but once they do appear they can function inde-
through the lateral hypothalamus and ventral stria- pendently of primary process states. Panksepp and
tum to the prefrontal cortex and consists primarily others argued that many psychiatric conditions are
of dopaminergic fibers. The SEEKING system is characterized by maladaptive emotional function-
associated with emotional states of wanting, excite- ing at the secondary and tertiary process levels, in
ment, and anticipation, and when engaged elicits addition to the primary core levels (Panksepp, 2010;
motivated searches for elements needed for survival LeDoux & Pine, 2016). This perspective is taken
and procreation (Panksepp & Biven, 2012). throughout this volume, and is a core aspect of the
An important feature of Panksepp’s model is that contemporary emotion dysregulation construct
emotions can be experienced at a variety of “levels.” (Beauchaine, 2015).
The most basic and hard-wired is the primary process In addition to the three levels of emotional expe-
level. At this level, basic emotional systems can be rience, another important aspect of the Pankseppian
most clearly differentiated and are most conserved model is bidirectional communication. By bidirec-
across evolution. Panksepp considered primary proc- tional communication, Panksepp referred to brain
ess the raw feelings of emotions and argued that responses that were both bottom-up (in which
many traditional animal-based affective neuroscien- primary process emotions influence behavior and
tists generally adopt this perspective in delineating cognitive activity) and top-down (in which tertiary
the neural basis of emotional experience (Cahill level emotional experience affects primary process
& McGaugh, 1998; Moriceau, Raineki, Holman, activity). Panksepp argued that activity in both di-
Holman, & Sullivan, 2009; Orsini & Maren, 2012; rections is stronger in humans than in other mam-
Berridge & Kringelbach, 2013; Vanderschuren & mals because so much more of the human brain is
Trezza, 2014; Panksepp et al., 2017). composed of neocortex. This results in a greater dis-
Although many brain-emotion researchers ac- sociation between behavior and primary process
knowledge a contribution of evolutionarily old emotions in humans. For example, neocortical ac-
subcortical systems to emotional experience, many tivity can inhibit and potentiate primary process
argue that true affective experiences that humans emotions, and also subvert or redirect (i.e., regulate)
consider “emotion” involve more complex cognitive behavioral outcomes following primary process en-
processing. Such processing includes concepts such gagement. In the present context, this is an impor-
as consciousness, linguistic labeling, and sense of tant observation because it indicates a greater degree
self (Rolls, 1999; LeDoux, 2012; Panksepp & Biven, of dissociation between emotional engagement and
2012; Damasio & Carvalho, 2013; LeDoux, 2014; behavior in humans than other animals. The ability
Barrett, 2016; Panksepp et al., 2017). Panksepp to control behavioral expression and regulate emo-
vehemently rejected this definition. However, he tional experience has become an important adaptive
did argue that emotions consist of more than just skill in the modern human environment.
core primary process states of intense activation. Although Panksepp’s model has been very influ-
Panksepp argued that primary states generated at ential, it has not been accepted universally. There
least two other levels of emotional experience. The are notable detractors and alternate interpretations
secondary process emerges from the primary process of the neurobiology of emotion (Rolls, 1999;
as a function of learning. Consistent association LeDoux, 2012; Damasio & Carvalho, 2013; Barrett,
of primary emotions with specific stimuli, classes of 2016; Panksepp et al., 2017). Indeed, aspects of the
stimuli, or contexts can elicit partial activation model, such as conscious experiential states of other
of primary process emotions, mixtures of primary species (Panksepp et al., 2017), are difficult to incor-
emotions, and even novel combinations of primary porate into standard scientific testing. However, be-
processes with novel brain activation patterns. cause the model clearly incorporates mechanisms,
Finally, Panksepp referred to a tertiary level of emo- brain function, and evolution into our discussion of

emotion more comprehensively than many other (Rolls, 1999; Izquierdo & Murray, 2010; Saez,
biological models, it is an important heuristic to Rigotti, Ostojic, Fusi, & Salzman, 2015; Saez, Saez,
which we appeal for the remainder of this chapter. Paton, Lau, & Salzman, 2017). Although directly rel-
evant for homeostatic regulation, Panksepp argued
Adaptive Nature of Emotions and that many functions associated with these neural
Motivated Behavior structures relate to secondary process emotions. In
When viewed from the perspective of biological contrast, primary process states are linked with envi-
utility, there are several specific roles for emotion in ronmental stimuli in an associative manner (Panksepp
promoting adaptive responses in fluctuating envi- & Biven, 2012). Much of the interindividual variance
ronments. Motivated behaviors are important inter- in emotional tendencies is evidenced at the secondary
mediaries for many of these functions. We highlight process level: unique fear responses by different indi-
some of these specific functions in this section. viduals following specific traumatic events are exam-
ples of secondary emotions being generated via asso-
Homeostasis ciational processes. These secondary emotional
Because life is only possible within relatively strict associations therefore play an important role in many
parameters, active adaptations to fluctuations— psychiatric conditions (Qin et al., 2014).
both internal and external to the organism—are Because environments vary widely between indi-
built into many aspects of physiology. Some of these viduals, the ability to flexibly apply basic emotional
operate at cellular and subcellular levels, but organism- activation patterns to unique environmental events
wide emotional behavior also plays an important is an important adaptive feature of motivational
role. For example, dehydration inevitably results in systems. Therefore, an important characteristic of
a motivated seeking response for water. One of the emotional and motivational systems is that they
simplest demonstrations that emotional responses capture attention and facilitate memory formation.
can index biological needs was demonstrated in a Affective neuroscience studies indicate that emotion
series of experiments on temperature hedonics. can capture attention by biasing limited neuronal
Cabanac (1971) found that warm water baths of ex- processing of sensory signals toward those associated
actly the same temperature were rated as pleasant by with the emotional stimulus (Schettino, Keil, Porcu,
those who were hypothermic but unpleasant by & Muller, 2016; Hammerschmidt, Sennhenn-Reulen,
those who were hyperthermic, whereas the opposite & Schacht, 2017) via feedback mechanisms from
was found for cool water baths. This simple experi- the amygdala and possibly other regions to primary
ment and many similar studies since demonstrated sensory areas (Pourtois, Schettino, & Vuilleumier,
the functional feature of emotional systems in guid- 2013). Thus, emotion may amplify relevant sensory
ing behavior toward adaptive outcomes (Cabanac, responses and filter irrelevant sensory responses via
1979; Ramirez & Cabanac, 2003). Adaptive re- associative regions including the amygdala and
sponding is also evident in experiments conducted striatum.
by Curt Richter in the 1930s in which he demon- Emotion also acts as a “bottom up” means of fa-
strated that plasma reductions in sodium induced cilitating acquisition of new behaviors and applying
by adrenalectomy induced a highly specific moti- established response patterns to novel stimuli.
vated appetite for salt in rats (Richter, 1976). More Emotional facilitation of learning is a well-established
recent examples include induction of panic attacks phenomenon that applies to both appetitive and
among individuals following carbon dioxide buildup aversive events and affects conditional, instrumen-
in the lungs (Pine et al., 1994), which presumably tal, and social learning (Reisberg & Hertl, 2004).
generates an energized search for consumable air. From the standpoint of biological adaptation, both
Panksepp viewed many of these homeostatic emo- the capturing of attention and learning are a means
tional responses as primary process behaviors, or of employing motivated behavior in a maximally
ones that do not require learning and are not flexible manner across a number of different stimuli
sculpted by environmental experiences. and contexts that may vary substantially across
individuals.
Attention, Learning, and Memory
Several more recent studies of reward valuation and Social Behavior
satiation in monkeys have focused on roles the In social interactions, basic emotions direct moti-
amygdala and orbitofrontal cortex play in assigning vated behavior in adaptive ways. For animals that
value to stimuli with homeostatic importance live in social groups, emotion modulation plays an

important role in guiding many aspects of behavior peaking shortly after puberty (Steinberg & Morris,
(Chang et al., 2013; Feldman, 2017). The PLAY, 2001; S. J. Blakemore & Mills, 2014).
NURTURE, and LUST systems all involve posi- From the standpoint of biological utility, devel-
tive, approach-related emotional motivation toward opmental shifts in patterns of emotional responding
conspecifics. The RAGE and PANIC emotional may direct motivated behavior toward features or
systems engage motivated behavior in agonistic en- stimulus categories that are most relevant for the
counters and in response to separation distress. specific phase of development the organism is in.
Although some specific behavioral patterns differ Development of the nervous system includes mech-
across mammalian species, there is considerable ho- anisms such as pruning, which is sensitive to envi-
mology in neurochemical and neuroanatomical ronmental input. Because emotional responding
controls over affective responses related to these mo- directs attention and learning toward developmen-
tivated behaviors. For example, there is a high tally relevant features in the environment, through
degree of concordance in the controls of maternal motivated behavior it may have potent effects on
behavior and sexual desire across mammals (Argiolas developmental outcomes.
& Melis, 2013; Love, 2014; Lonstein, Levy, &
Fleming, 2015). For humans and many nonhuman Maladaptive Emotional Responses
primates, the social world is of critical importance Despite the fact that emotions evolved because of
and also incredibly complex. Variables such as dom- their capacity to generate biologically adaptive mo-
inance, kinship, reciprocity, and alliance formation tivated behaviors, there are a number of ways in
factor into every encounter (de Waal, 1996; which motivated responses can be nonadaptive.
Cheney & Seyfarth, 2007; Dunbar & Shultz, 2017). Among humans, one factor that contributes to mal-
Emotionally mediated motivated behaviors play adaptive emotional experience and expression is the
important roles in guiding many aspects of social radical difference between environments that
behavior. Among humans, elaborate brain systems modern humans have constructed and our environ-
involved in perceptual and cognitive processing of ments of evolutionary adaptation (Pinker, 2002).
social information are interconnected strongly with This is particularly evident in motivated behaviors
brain regions related to motivated behavior and associated with the SEEKING emotional system.
emotion (Adolphs, 2009; Chang et al., 2013). This Obtaining hydration, calories, nutrients, and social
connectivity suggests that emotion and motivation contact with group members both is essential for
permeate virtually all aspects of social behavior. survival and depends on behavioral engagement.
Appetitive behavioral responses geared toward seek-
Development ing such essential features in the environment gen-
The role of motivation in development is often over- erate powerful reward responses upon consump-
looked, but is a vitally important adaptive feature. tion, which evolved in environments where
The stimuli and contexts that induce motivated be- sought-after stimuli such as high-calorie foods were
havior vary in a systematic fashion across develop- scarce. However, such items are readily available
ment (Nelson, Lau, & Jarcho, 2014; Nelson, Jarcho, now, making compulsory seeking and overcon-
& Guyer, 2016). This is perhaps most evident in sumption much more problematic than in our evo-
changes that take place in social motivation during lutionary history. The most obvious example of this
adolescence. However, regulated changes in affective is overconsumption of food, but recent changes in
sensitivity may apply in other domains and during the availability of constant social contact via social
other developmental periods as well (Forbes & Dahl, media provides another illustration of potentially
2010; Spear, 2011; Spielberg, Olino, Forbes, & Dahl, problematic overconsumption (Primack et al., 2017;
2014; Nelson et al., 2016). For example, caretaker Shensa et al., 2017). Furthermore, the ability to
separation induces a potent motivated response in cultivate and manufacture neurochemical agents
early development, but this is greatly attenuated with (opiates, cocaine, methamphetamine) that potently
age (Zhang et al., 2012). Similarly, physical play with activate the seeking/reward system independent of
peers demonstrates a classic inverted-U response that environmental experience has created a huge soci-
peaks in late childhood and declines into adolescence etal problem in which the functional utility of en-
and adulthood (Panksepp, Siviy, & Normansell, dogenous reward processes have, for some, been
1984; Vanderschuren & Trezza, 2014). Emotional re- usurped (Panksepp, Herman, Conner, Bishop, &
sponses to peer acceptance follow a similar trajectory, Scott, 1978).

A second factor that contributes to maladaptive e xcessive alcohol consumption or behavioral shut-
emotional responding in humans is the extent of down that accompanies depression (Sharp, 2017).
bidirectional communication between “top down” Although emotions evolved because of the
regulation and executive functions and “bottom up” adaptive value of motivated behavioral responses,
primary emotional systems. Humans have devel- resulting responses are not always optimal. This is
oped a strong capacity to willfully regulate behav- particularly relevant for modern humans, in part
ioral expression and override emotional/motiva- due to the highly flexible nature of human behavior
tional tendencies by engaging top-down inhibitory and executive functions, and in part the result of
mechanisms (Buhle et al., 2014). This is often an the relatively artificial environment humans have
adaptive response in certain environments/contexts created for themselves.
and can serve as an important means of managing
excessive emotional expression (Buhle et al., 2014). Current Methods and Findings
However, the ability to dissociate motivated behav- There are a number of ways to assess the effects of
ioral expression from the experience of emotion can emotions on brain and behavior. In human-based
eventuate in dysfunctional brain response patterns studies standard approaches include functional neu-
in the long term. Chronic stress associated with the roimaging, electroencephalography, and magneto-
repeated overriding of natural motivated behavior encephalography. More recent approaches include
tendencies predicts mood and anxiety disorders, functional near-infrared spectroscopy (Hoshi, 2016),
and compensatory drug and alcohol use (Mah, in which the blood oxygen level–dependent
Szabuniewicz, & Fiocco, 2016; Nusslock & Miller, (BOLD) signal is assessed through light sensors
2016; Sharp, 2017). Thus, there are both benefits placed on the skull, and transcranial electrical stim-
and potential drawbacks to using executive func- ulation, in which current is delivered to the brain
tions to override motivational tendencies. The mal- from scalp electrodes (Yavari, Jamil, Mosayebi
adaptive aspect of strong bilateral connections be- Samani, Vidor, & Nitsche, 2018). The typical ap-
tween primary emotions and executive functions is proach in all of these methods is to have partici-
also evident in reverse—hyperactivation of basic pants engage in a task (usually on a computer) that
emotional systems can generate long-term altera- manipulates emotionality with either standardized
tions in executive functions such as attention and (e.g., expressive faces or monetary gains/losses) or
memory, thereby reinforcing dysregulated emo- customized probes (Salimpoor, Zald, Zatorre,
tional expression (MacLeod et al., 1986; Rapee & Dagher, & McIntosh, 2015; Abrams et al., 2016).
Heimberg, 1997). Although most neuroimaging approaches still rely
Another way in which emotional/motivational on regression and parametric statistical compari-
activation and behavioral responses can differ mean- sons, a number of novel approaches have emerged
ingfully is in the duration of experience. Whereas recently. These include graph theory, causal model-
salient stimuli and events often occur transiently in ing, independent component analysis, and machine
the environment, emotional responses can linger learning approaches such as multivoxel pattern
from seconds to hours and generate even more analysis (Bullmore & Sporns, 2009; Marinazzo,
long-lasting emotional states (Heller et al., 2009, Liao, Chen, & Stramaglia, 2011; Saarimaki et al.,
2013, 2015). The persistence of emotional respond- 2016; Xie, Douglas, Wu, Brody, & Anderson, 2017).
ing in the absence of behavioral action can result A key problem with these approaches is that they
in long-term detrimental functioning (Teicher, impose strong limits on the degree to which behav-
Samson, Anderson, & Ohashi, 2016), although ior can be expressed. Brain measures typically re-
emotion may be amenable to conscious regulatory quire data acquisition in a highly controlled envi-
intervention in the absence of behavioral output ronment in which participants are not allowed to
(Denny, Inhoff, Zerubavel, Davachi, & Ochsner, move. However, some recent approaches have in-
2015). Finally, an important aspect of the relation- corporated measures of subtle differences in behav-
ship between emotion and behavior in humans is its ioral responses expressed inside the scanning envi-
equifinality: there is not always a unique behavioral ronment. These differences may provide important
expression for each experienced emotion. For in- insights into the relation between emotion and be-
stance, fear may generate drug seeking, compulsive havior. For example, researchers have begun to in-
hand-washing, or freezing. Anger may elicit agonis- vestigate brain differences in generating approach or
tic physical encounters, but it may also trigger withdrawal responses with joysticks (Radke et al.,

2015, 2017), by directing attention toward or away using pattern analysis techniques have detected
from a threatening stimulus (Price et al., 2014; emotion-specific patterns in neuroimaging studies
Ceravolo, Fruhholz, & Grandjean, 2016), and via (Hamann, 2012; Kragel et al., 2016; Saarimaki et al.,
grip strength elicited by aversive emotional stimuli 2016; Nummenmaa & Saarimaki, 2017—but see also
(R. L. Blakemore, Rieger, & Vuilleumier, 2016). Lindquist et al., 2012). Although emotion-specific
In some ways, animal studies are much more differences in brain activation are detectable in
flexible for inducing emotional states and measur- human neuroimaging studies, these differences tend
ing brain and behavioral responses. In addition to to be evident only at the network level and are not
standard pharmacological, electrophysiological, and reflected in one-to-one mapping of brain regions
targeted lesion methods, more recent advances in- with specific emotions. Although more specific as-
clude genetic knockouts (Crawley et al., 2007; sociations between individual brain regions or neu-
Araragi & Lesch, 2013) and in vivo regulation of rochemical systems is more evident in animal-based
brain function with optogenetics (Deng, Xiao, & emotion research than in human research, it is clear
Wang, 2016). Human analogs of some of these ap- that emotions are better characterized with networks
proaches include assessment of behavior among in- than by activity within unique and specific neural
dividuals following naturally occurring brain lesions structures (Floresco, 2015; Douglass et al., 2017).
(Damasio & Carvalho, 2013), or in rare cases inva-
sive measurement of brain function with intracra- Ongoing Controversies
nial recordings or deep brain stimulation, per- There continues to be a great deal of debate among
formed for clinical reasons (Pourtois, Spinelli, investigators who study the neurobiology of affect
Seeck, & Vuilleumier, 2010). regarding what exactly constitutes an emotion, to
A full accounting of findings from research on what extent different emotions represent “kinds” in
the intersection between emotion and motivated nature, how similar emotional experience is across
behavior in the brain is beyond the scope of this individuals, and how much homology exists in
chapter, but general observations can be made based emotional experience across species. Panksepp’s af-
on existing findings. First, engagement of emotional fective neuroscience model details unique signatures
and motivational states in humans and animals for seven basic emotional systems, each strongly tied
typically involves networks of brain regions includ- to a range of motivated behaviors (Panksepp &
ing both subcortical and neocortical structures Biven, 2012). In this model, different emotional sys-
(Hamann, 2012; Kragel, Knodt, Hariri, & LaBar, tems are unique “kinds” in the brain: they are fun-
2016; Nummenmaa & Saarimaki, 2017). Sub(neo) damentally shared across a number of species, typi-
cortical regions are more closely associated with cally contain specific behavioral outputs, and do not
what is typically considered to be the motivational require high-level cognitive activity to be experi-
(i.e., behavioral responsiveness) component of emo- enced. Although the details vary somewhat across
tion, even though associated behavior is restricted in investigators, this basic concept is largely shared by
most human-based studies. The most prominent many researchers who adopt a traditional behavioral
structures associated with motivation and emotion neuroscience and animal-based approach to emo-
include the insular and anterior cingulate cortices tion (Darwin, 1872/2009; Maclean, 1990; Ekman
(which are evolutionarily older cortical regions that & Davidson, 1994; Berridge & Kringelbach, 2013;
lie underneath the neocortex), the amygdala, stria- Perusini & Fanselow, 2015; Panksepp et al., 2017).
tum, and midbrain regions such as the ventral teg- On the other end of the spectrum are researchers
mental area and periaqueductal gray. Aberrant who argue against the notion that emotions are
activity in these regions is often associated with unique kinds in the brain, or that common experi-
emotion/motivation-based psychopathologies— ences can be assumed across individuals and partic-
such as anxiety, depression, addiction, and border- ularly across species (LeDoux, 2014; Barrett, 2016).
line personality (Drevets, Savitz, & Trimble, 2008; Investigators who adhere to this perspective believe
Filbey et al., 2016; Lichenstein, Verstynen, & that emotion is largely a high-level cognitive in-
Forbes, 2016; Rigoli, Ewbank, Dalgleish, & Calder, terpretation that emerges from a variety of inputs,
2016; Gola et al., 2017; Hein & Monk, 2017; Lago, including but not limited to physiological response
Davis, Grillon, & Ernst, 2017; Sharp, 2017). patterns. A variety of intermediary concepts lie along
Second, there is a tremendous amount of varia- this continuum, including dimensional approaches
bility in patterns of brain network activity engaged in which emotion is construed as elaborations along
across studies. However, several recent meta-analyses valence and arousal dimensions (Zachar & Ellis,

2012; Russell, 1980), and more truly hybrid ap- advances are being made, and careful use of defini-
proaches in which basic kinds exist but also interact tion and terminology may further facilitate progress
with cognitive schemas and interpretations (Izard, (Izard, 2007; Panksepp et al., 2017).
2007; Damasio & Carvalho, 2013). Another issue that has plagued emotion re-
Some of the controversy in this area relates to search—particularly at the intersection of animal
differences in semantics or fundamental inconsis- and human studies—is the role that conscious expe-
tencies in definitions and terminology (Izard, rience plays in emotional experience and expression
2007). However, real conceptual differences do exist (LeDoux, 2014; Panksepp et al., 2017). There is no
and have important effects on interpretation of the clear consensus on whether consciousness is neces-
intersection of motivation and emotion. Although sary for emotion, whether conscious experiences are
we certainly lean toward the Pankseppian model of comparable enough across species to make general-
basic kinds of emotion that are directly tied to izations, or even what the basic elements of con-
motivation and behavior, this is by no means a uni- sciousness are. These are issues at the forefront of
versally accepted approach (Barrett, 2016). neuroscience and philosophy—at present we have
Indeed, many of the initial neuroimaging studies no clear empirical resolution.
that have attempted to differentiate emotional expe-
riences based on functional brain activation have Theoretical Synthesis and Future Directions
not been supportive of many of the specific models. Our perspective is that emotion has strong and per-
Although functional neuroimaging has revealed vasive effects on behavioral expression, and that any
emotional activation of both cortical and subcorti- behavior that results from emotional induction is
cal structures (Pauli et al., 2015; R. L. Blakemore motivated behavior by definition. When compared
et al., 2016), there tends to be a great deal of overlap to behavior that does not result from emotion in-
between different emotions. Furthermore, contrary duction, motivated behavior is pervasive in that it
to Panksepp’s model, imaging studies of emotions involves a coordinated effort of cognitive, motor,
often do not demonstrate strong activation patterns neuroendocrine, and other physiological systems
within brain stem regions (Hamann, 2012; Lindquist all focused on a single stimulus, event, or goal.
et al., 2012). However, recent studies using more so- Behaviors that emerge from motivational states are
phisticated approaches to inducing and measuring usually directed toward adaptive outcomes, although
emotion have reported unique patterns of activation this is not always the case. Motivated behavior is
by emotional category, largely contained within the usually a highly effective means of obtaining desired
cortex (Hamann, 2012; Saarimaki et al., 2016). goals, but can be particularly difficult to manage or
An important caveat of all magnetic resonance suppress when those goals are not adaptive for the
imaging research is that, although it is the state of individual. Indeed, emotion induction does not
the art for noninvasively measuring neuronal activ- always generate behavior. The ability of an individ-
ity, it imposes several methodological constraints on ual to manage behavioral expression in spite of emo-
the elicitation of emotion. Neural “events” must be tional engagement, or the ability to manage the
generated while participants lie perfectly still inside degree of emotional engagement elicited by a stimu-
a huge metal tube, and because the BOLD signal is lus (emotion regulation), is an important skill that
relatively weak, experiences must be repeated many can also result in complex neuronal and psychologi-
times over the course of a single experimental cal states that may be linked to psychopathology.
session. The emotional experiences induced under There are several important directions for future
these circumstances are likely only a very weak re- research to address. First, from a practical stand-
semblance to those generated by the naturalistic and point, it is important to gain a better understanding
highly salient situations typically associated with of how to manage motivated behavior that is
emotion. The experiences measured in the scanner maladaptive for the individual. Two classic exam-
may be closer to what Panksepp has referred to as ples of maladaptive motivated behavior are compul-
secondary or tertiary emotional experiences derived sive drug use that occurs in addiction and excessive
from the more potent subcortically based primary avoidance behaviors that occur in anxiety. Probably
emotions (Panksepp & Biven, 2012; Panksepp et al., the most effective way of altering such maladaptive
2017). Controversies such as this have plagued motivation is through a combination of medication
emotion research since its inception (Izard, 2007; and/or top-down regulation to reduce the intensity
Barrett, 2016) and continue to be a barrier for truly of the motivational state and encourage behavior
integrative neuroscience research. However, some that is inconsistent with the maladaptive motivation.

Modern therapeutic approaches for humans, such as Adolphs, R. (2009). The social brain: Neural basis of social
cognitive-behavioral therapy, use these methods to knowledge. Annual Review of Psychology, 60, 693–716.
Araragi, N., & Lesch, K. P. (2013). Serotonin (5-HT) in the
promote effective management of maladaptive moti- regulation of depression-related emotionality: Insight from
vated behaviors. For these examples, therapeutic 5-HT transporter and tryptophan hydroxylase-2 knockout
goals might include reducing drug seeking or stop- mouse models. Current Drug Targets, 14, 549–570.
ping avoidance of feared stimuli. These changes in Argiolas, A., & Melis, M. R. (2013). Neuropeptides and central
behavior are extremely challenging to achieve, but control of sexual behaviour from the past to the present: A
review. Progress in Neurobiology, 108, 80–107.
repeated changes to the association between emotion Barrett, L. F. (2016). Navigating the science of emotion. In
and behavior can improve the likelihood of adaptive H. L. Meiselman (Ed.), Emotion measurement (pp. 31–63).
outcomes. Although effective methods have been New York, NY: Elsevier.
developed on these fronts, continued efforts to refine Beatty, G. F., Cranley, N. M., Carnaby, G., & Janelle, C. M.
and improve these approaches are needed. (2016). Emotions predictably modify response times in the
initiation of human motor actions: A meta-analytic review.
Second, at a more holistic level, motivational Emotion, 16, 237–251.
states can often be parsed into a pre-exposure period Beauchaine, T. P. (2015). Future directions in emotion
and a consummatory period. This is most com- dysregulation and youth psychopathology. Journal of Clinical
monly done for rewarding states (Berridge & Child and Adolescent Psychology, 44, 875–896.
Kringelbach, 2013; Luijten, Schellekens, Kuhn, Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion
regulation, and the latent structure of psychopathology:
Machielse, & Sescousse, 2017), but also may apply An integrative and convergent historical perspective.
to aversive situations where exposure to a poten- International Journal of Psychophysiology, 119, 108–118.
tially aversive condition is anticipated before it is Berridge, K. C., & Kringelbach, M. L. (2013). Neuroscience of
experienced (Grupe & Nitschke, 2013; Jarcho et al., affect: Rain mechanisms of pleasure and displeasure. Current
2015). In both appetitive and aversive conditions, Opinion in Neurobiology, 23, 294–303.
Berridge, K. C., & Kringelbach, M. L. (2015). Pleasure systems
the most powerful effects of motivation appear in in the brain. Neuron, 86, 646–664.
the period preceding exposure. This is also where the Blakemore, R. L., Rieger, S. W., & Vuilleumier, P. (2016). Negative
maladaptive behavioral aspects of motivated be- emotions facilitate isometric force through activation of
havior are most prevalent. The anticipatory and prefrontal cortex and periaqueductal gray. Neuroimage, 124,
consummatory components of a motivated experi- 627–640.
Blakemore, S. J., & Mills, K. L. (2014). Is adolescence a sensitive
ence are fundamentally different from each other at period for sociocultural processing? Annual Review of Psychology,
a neurobiological level, but they are also completely 65, 187–207.
interdependent. An important challenge for moti- Bradley, M. M., Sabatinelli, D., Lang, P. J., Fitzsimmons, J. R.,
vational research will be to gain a better understand- King, W., & Desai, P. (2003). Activation of the visual cortex in
ing of how consummatory and anticipatory compo- motivated attention. Behavioral Neuroscience, 117, 369–380.
Buhle, J. T., Silvers, J. A., Wager, T. D., Lopez, R., Onyemekwu, C.,
nents of a motivated experience are regulated and Kober, H., . . . Ochsner, K. N. (2014). Cognitive reappraisal of
how they vary across individuals. emotion: A meta-analysis of human neuroimaging studies.
Finally, a fundamental question for motivation re- Cerebral Cortex, 24, 2981–2990.
search is how novel motivational states become ac- Bullmore, E., & Sporns, O. (2009). Complex brain networks:
quired. Although some stimuli (e.g., required nutri- Graph theoretical analysis of structural and functional systems.
Nature Reviews Neuroscience, 10, 186–198.
ents, potential predators) are inherently motivational, Cabanac, M. (1971). Physiological role of pleasure. Science, 173,
for others the motivational states are acquired 1103–1107.
through learning (e.g., money) or development (e.g., Cabanac, M. (1979). Sensory pleasure. Quarterly Review of Biology,
sexual desire). Moreover, the motivational pull of 54, 1–29.
stimuli that were once highly appealing can fade over Cahill, L., & McGaugh, J. L. (1998). Mechanisms of emotional
arousal and lasting declarative memory. Trends in Neuroscience,
time. Understanding how these motivational states 21, 294–299.
change at the level of the brain and fluctuate with Ceravolo, L., Fruhholz, S., & Grandjean, D. (2016). Modulation
experience is an important feature of motivational of auditory spatial attention by angry prosody: An fMRI
learning that will be crucial to characterize further. auditory dot-probe study. Frontiers in Neuroscience, 10, 216.
Chang, S. W., Brent, L. J., Adams, G. K., Klein, J. T., Pearson,
J. M., Watson, K. K., & Platt, M. L. (2013). Neuroethology
References of primate social behavior. Proceedings of the National
Abrams, D. A., Chen, T., Odriozola, P., Cheng, K. M., Baker, Academy of Sciences, 110, S10387–S10394.
A. E., Padmanabhan, A., . . . Menon, V. (2016). Neural Cheney, D., & Seyfarth, R. (2007). Baboon metaphysics: The evolution
circuits underlying mother's voice perception predict social of a social mind. London, UK: University of Chicago Press.
communication abilities in children. Proceedings of the Crawley, J. N., Chen, T., Puri, A., Washburn, R., Sullivan, T. L.,
National Academy of Sciences, 113, 6295–6300. Hill, J. M., .
. .
Young, W. S. (2007). Social approach

behaviors in oxytocin knockout mice: Comparison of two Hammerschmidt, W., Sennhenn-Reulen, H., & Schacht, A.
independent lines tested in different laboratory environments. (2017). Associated motivational salience impacts early sensory
Neuropeptides, 41, 145–163. processing of human faces. Neuroimage, 156, 466–474.
Damasio, A., & Carvalho, G. B. (2013). The nature of feelings: Hein, T. C., & Monk, C. S. (2017). Research review: Neural
Evolutionary and neurobiological origins. Nature Reviews response to threat in children, adolescents, and adults after
Neuroscience, 14, 143–152. child maltreatment—a quantitative meta-analysis. Journal of
Darwin, C. (1872/2009). The expression of emotions in man and Child Psychology and Psychiatry, 58, 222–230.
animals (P. Ekman, Ed., 4th ed.). New York, NY: Oxford Heller, A. S., Fox, A. S., Wing, E. K., McQuisition, K. M., Vack,
University Press. N. J., & Davidson, R. J. (2015). The neurodynamics of affect
de Waal, F. (1996). Good natured: The origins of right and wrong in in the laboratory predicts persistence of real-world emotional
humans and other animals. New York, NY: Harvard University responses. Journal of Neuroscience, 35, 10503–10509.
Press. Heller, A. S., Johnstone, T., Peterson, M. J., Kolden, G. G.,
Deng, H., Xiao, X., & Wang, Z. (2016). Periaqueductal gray Kalin, N. H., & Davidson, R. J. (2013). Increased prefrontal
neuronal activities underlie different aspects of defensive cortex activity during negative emotion regulation as a
behaviors. Journal of Neuroscience, 36, 7580–7588. predictor of depression symptom severity trajectory over
Denny, B. T., Inhoff, M. C., Zerubavel, N., Davachi, L., & 6 months. JAMA Psychiatry, 70, 1181–1189.
Ochsner, K. N. (2015). Getting over it: Long-lasting effects Heller, A. S., Johnstone, T., Shackman, A. J., Light, S. N.,
of emotion regulation on amygdala response. Psychological Peterson, M. J., Kolden, G. G., . . . Davidson, R. J. (2009).
Science, 26, 1377–1388. Reduced capacity to sustain positive emotion in major
Douglass, A. M., Kucukdereli, H., Ponserre, M., Markovic, M., depression reflects diminished maintenance of fronto-striatal
Grundemann, J., Strobel, C., . . . Klein, R. (2017). Central brain activation. Proceedings of the National Academy of Sciences,
amygdala circuits modulate food consumption through 106, 22445–22450.
a positive-valence mechanism. Nature Neuroscience, 20, Hoshi, Y. (2016). Hemodynamic signals in fNIRS. Progress in
1384–1394. Brain Research, 225, 153–179.
Drevets, W. C., Savitz, J., & Trimble, M. (2008). The subgenual Izard, C. E. (2007). Basic emotions, natural kinds, emotion
anterior cingulate cortex in mood disorders. CNS Spectrums, schemas, and a new paradigm. Perspectives in Psychological
13, 663–681. Science, 2, 260–280.
Dunbar, R. I. M., & Shultz, S. (2017). Why are there so many Izquierdo, A., & Murray, E. A. (2010). Functional interaction of
explanations for primate brain evolution? Philosophical medial mediodorsal thalamic nucleus but not nucleus
Transactions of the Royal Society of London B Biological accumbens with amygdala and orbital prefrontal cortex is
Sciences, 372: 20160244; doi: 10.1098/rstb.2016.0244 essential for adaptive response selection after reinforcer
Ekman, P., & Cordaro, D. (2011). What is meant by calling devaluation. Journal of Neuroscience, 30, 661–669.
emotions basic. Emotion Review, 3, 364–370. Jarcho, J. M., Romer, A. L., Shechner, T., Galvan, A., Guyer,
Ekman, P., & Davidson, R. J. (1994). The nature of emotion: A. E., Leibenluft, E., . . . Nelson, E. E. (2015). Forgetting
Fundamental questions New York, NY: Oxford University Press. the best when predicting the worst: Preliminary observations
Feldman, R. (2017). The neurobiology of human attachments. on neural circuit function in adolescent social anxiety.
Trends in Cognitive Science, 21, 80–99. Developmental Cognitive Neuroscience, 13, 21–31.
Filbey, F. M., Dunlop, J., Ketcherside, A., Baine, J., Rhinehardt, Kragel, P. A., Knodt, A. R., Hariri, A. R., & LaBar, K. S. (2016).
T., Kuhn, B., . . . Alvi, T. (2016). fMRI study of neural Decoding spontaneous emotional states in the human brain.
sensitization to hedonic stimuli in long-term, daily cannabis PLoS Biology, 14, e2000106.
users. Human Brain Mapping, 37, 3431–3443. Kuhn, S., & Gallinat, J. (2012). The neural correlates of
Floresco, S. B. (2015). The nucleus accumbens: An interface subjective pleasantness. Neuroimage, 61, 289–294.
between cognition, emotion, and action. Annual Review of Lago, T., Davis, A., Grillon, C., & Ernst, M. (2017). Striatum on
Psychology, 66, 25–52. the anxiety map: Small detours into adolescence. Brain
Fogel, A., Nwokah, E., Dedo, J. Y., Messinger, D., Dickson, Research, 1654, 177–184.
K. L., Matusov, E., & Holt, S. A. (1992). Social process LeDoux, J. (2012). Rethinking the emotional brain. Neuron, 73,
theory of emotions: A dynamic systems approach. Social 653–676.
Development, 1, 123–142. LeDoux, J. E. (2014). Coming to terms with fear. Proceedings of
Forbes, E. E., & Dahl, R. E. (2010). Pubertal development and the National Academy of Sciences, 111, 2871–2878.
behavior: Hormonal activation of social and motivational LeDoux, J. E., & Pine, D. S. (2016). Using neuroscience to help
tendencies. Brain and Cognition, 72, 66–72. understand fear and anxiety: A two-system framework.
Gola, M., Wordecha, M., Sescousse, G., Lew-Starowicz, M., American Journal of Psychiatry, 173, 1083–1093.
Kossowski, B., Wypych, M., . . . Marchewka, A. (2017). Lichenstein, S. D., Verstynen, T., & Forbes, E. E. (2016).
Can pornography be addictive? An fMRI study of men Adolescent brain development and depression: A case for the
seeking treatment for problematic pornography use. importance of connectivity of the anterior cingulate cortex.
Neuropsychopharmacology, 42, 2021–2031. Neuroscience and Biobehavioral Reviews, 70, 271–287.
Grupe, D. W., & Nitschke, J. B. (2013). Uncertainty and Lindquist, K. A., Wager, T. D., Kober, H., Bliss-Moreau, E., &
anticipation in anxiety: An integrated neurobiological and Barrett, L. F. (2012). The brain basis of emotion: A meta-
psychological perspective. Nature Reviews Neuroscience, 14, analytic review. Behavioral and Brain Sciences, 35, 121–143.
488–501. Lonstein, J. S., Levy, F., & Fleming, A. S. (2015). Common and
Hamann, S. (2012). Mapping discrete and dimensional emotions divergent psychobiological mechanisms underlying maternal
onto the brain: Controversies and consensus. Trends in behaviors in non-human and human mammals. Hormones
Cognitive Science, 16, 458–466. and Behavior, 73, 156–185.

Love, T. M. (2014). Oxytocin, motivation and the role of Perusini, J. N., & Fanselow, M. S. (2015). Neurobehavioral
dopamine. Pharmacology Biochemistry and Behavior, 119, perspectives on the distinction between fear and anxiety.
49–60. Learning and Memory, 22, 417–425.
Luijten, M., Schellekens, A. F., Kuhn, S., Machielse, M. W., & Pine, D. S., Weese-Mayer, D. E., Silvestri, J. M., Davies, M.,
Sescousse, G. (2017). Disruption of reward processing in Whitaker, A. H., & Klein, D. F. (1994). Anxiety and
addiction: An image-based meta-analysis of functional congenital central hypoventilation syndrome. American
magnetic resonance imaging studies. JAMA Psychiatry, 74, Journal of Psychiatry, 151, 864–870.
387–398. Pinker, S. (2002). The blank slate. New York, NY: Penguin Books.
Maclean, P. (1990). The triune brain in evolution: Role in Pourtois, G., Schettino, A., & Vuilleumier, P. (2013). Brain
paleocerebral functions. New York, NY: Plenum Press. mechanisms for emotional influences on perception and
MacLeod, C., Mathews, A., & Tata, P. (1986). Attentional bias in attention: What is magic and what is not. Biological
emotional disorders. Journal of Abnormal Psychology, 95, 15–20. Psychology, 92, 492–512.
Mah, L., Szabuniewicz, C., & Fiocco, A. J. (2016). Can anxiety Pourtois, G., Spinelli, L., Seeck, M., & Vuilleumier, P. (2010).
damage the brain? Current Opinion in Psychiatry, 29, 56–63. Temporal precedence of emotion over attention modulations
Marinazzo, D., Liao, W., Chen, H., & Stramaglia, S. (2011). in the lateral amygdala: Intracranial ERP evidence from a
Nonlinear connectivity by Granger causality. Neuroimage, patient with temporal lobe epilepsy. Cognitive and Affect
58, 330–338. Behavioral Neuroscience, 10, 83–93.
Moriceau, S., Raineki, C., Holman, J. D., Holman, J. G., & Price, R. B., Siegle, G. J., Silk, J. S., Ladouceur, C. D., McFarland,
Sullivan, R. M. (2009). Enduring neurobehavioral effects of A., Dahl, R. E., & Ryan, N. D. (2014). Looking under the
early life trauma mediated through learning and corticosterone hood of the dot-probe task: An fMRI study in anxious youth.
suppression. Frontiers in Behavioral Neuroscience, 3, 22. Depression and Anxiety, 31, 178–187.
Nelson, E. E., Jarcho, J. M., & Guyer, A. E. (2016). Social re- Primack, B. A., Shensa, A., Sidani, J. E., Whaite, E. O., Lin,
orientation and brain development: An expanded and L. Y., Rosen, D., . . . Miller, E. (2017). Social media use and
updated view. Developmental Cognitive Neuroscience, 17, perceived social isolation among young adults in the U.S.
118–127. American Journal of Preventive Medicine, 53, 1–8.
Nelson, E. E., Lau, J. Y., & Jarcho, J. M. (2014). Growing pains Qin, S., Young, C. B., Duan, X., Chen, T., Supekar, K., &
and pleasures: How emotional learning guides development. Menon, V. (2014). Amygdala subregional structure and
Trends in Cognitive Sciences, 18, 99–108. intrinsic functional connectivity predicts individual differences
Nummenmaa, L., & Saarimaki, H. (2017). Emotions as discrete in anxiety during early childhood. Biological Psychiatry, 75,
patterns of systemic activity. Neuroscience Letters. Advance 892–900.
online publication. Radke, S., Volman, I., Kokal, I., Roelofs, K., de Bruijn,
Nusslock, R., & Miller, G. E. (2016). Early-life adversity and E. R. A., & Toni, I. (2017). Oxytocin reduces amygdala
physical and emotional health across the lifespan: A responses during threat approach. Psychoneuroendocrinology,
neuroimmune network hypothesis. Biological Psychiatry, 80, 79, 160–166.
23–32. Radke, S., Volman, I., Mehta, P., van Son, V., Enter, D., Sanfey,
Orsini, C. A., & Maren, S. (2012). Neural and cellular A., . . . Roelofs, K. (2015). Testosterone biases the amygdala
mechanisms of fear and extinction memory formation. toward social threat approach. Science Advances, 1, e1400074.
Neuroscience and Biobehavioral Reviews, 36, 1773–1802. Ramirez, J. M., & Cabanac, M. (2003). Pleasure, the common
Panksepp, J. (2010). Affective neuroscience of the emotional currency of emotions. Annals of the New York Academy of
BrainMind: Evolutionary perspectives and implications for Sciences, 1000, 293–295.
understanding depression. Dialogues in Clinical Neuroscience, Rapee, R. M., & Heimberg, R. G. (1997). A cognitive-behavioral
12, 533–545. model of anxiety in social phobia. Behavior Research and
Panksepp, J. (2011). The basic emotional circuits of mammalian Therapy, 35, 741–756.
brains: Do animals have affective lives? Neuroscience and Reisberg, D., & Hertl, P. (2004). Memory and emotion. New
Biobehavioral Reviews, 35, 1791–1804. York, NY: Oxford University Press.
Panksepp, J., & Biven, L. (2012). The archaeology of mind. Reisenzein, R. (1983). The Schachter theory of emotion: Two
New York, NY: Norton. decades later. Psychological Bulletin, 94, 239–264.
Panksepp, J., Herman, B., Conner, R., Bishop, P., & Scott, J. P. Richter, C. (1976). The psychobiology of Curt Richter (E. M. Blass,
(1978). The biology of social attachments: Opiates alleviate Ed.). Baltimore MD: York Press.
separation distress. Biological Psychiatry, 13, 607–618. Rigoli, F., Ewbank, M., Dalgleish, T., & Calder, A. (2016).
Panksepp, J., Lane, R. D., Solms, M., & Smith, R. (2017). Threat visibility modulates the defensive brain circuit
Reconciling cognitive and affective neuroscience perspectives underlying fear and anxiety. Neuroscience Letters, 612, 7–13.
on the brain basis of emotional experience. Neuroscience and Rolls, E. T. (1999). The brain and emotion. New York, NY:
Biobehavioral Reviews, 76, 187–215. Oxford University Press.
Panksepp, J., Siviy, S., & Normansell, L. (1984). The Russell, J. A. (1980). A circumplex model of emotion. Journal of
psychobiology of play: Theoretical and methodological Personality and Social Psychology, 39, 1161–1178.
perspectives. Neuroscience and Biobehavioral Reviews, 8, Saarimaki, H., Gotsopoulos, A., Jaaskelainen, I. P., Lampinen, J.,
465–492. Vuilleumier, P., Hari, R., . . . Nummenmaa, L. (2016).
Pauli, W. M., Larsen, T., Collette, S., Tyszka, J. M., Seymour, B., Discrete neural signatures of basic emotions. Cerebral Cortex,
& O’Doherty, J. P. (2015). Distinct contributions of 26, 2563–2573.
ventromedial and dorsolateral subregions of the human Saez, A., Rigotti, M., Ostojic, S., Fusi, S., & Salzman, C. D.
substantia nigra to appetitive and aversive learning. Journal of (2015). Abstract context representations in primate amygdala
Neuroscience, 35, 14220–14233. and prefrontal cortex. Neuron, 87, 869–881.

Saez, R. A., Saez, A., Paton, J. J., Lau, B., & Salzman, C. D. development alter threat processing? Developmental Cognitive
(2017). Distinct roles for the amygdala and orbitofrontal Neuroscience, 8, 86–95.
cortex in representing the relative amount of expected Steinberg, L., & Morris, A. S. (2001). Adolescent development.
reward. Neuron, 95, 70–77. Annual Review of Psychology, 52, 83–110.
Salimpoor, V. N., Zald, D. H., Zatorre, R. J., Dagher, A., & Stiles, J. (2008). The fundamentals of brain development:
McIntosh, A. R. (2015). Predictions and the brain: How integrating nature and nurture. Cambridge, MA: Harvard
musical sounds become rewarding. Trends in Cognitive University Press.
Sciences, 19, 86–91. Teicher, M. H., Samson, J. A., Anderson, C. M., & Ohashi, K.
Schacter, S., & Singer, J. E. (1962). Cognitive, social, and (2016). The effects of childhood maltreatment on brain
physiological determinants of emotional state. Psychological structure, function and connectivity. Nature Reviews
Review, 69, 379–399. Neuroscience, 17, 652–666.
Scherer, K. R. (2009). Emotions are emergent processes: They Vanderschuren, L. J., & Trezza, V. (2014). What the laboratory
require a dynamic computational architecture. Philosophical rat has taught us about social play behavior: Role in
Transactions of the Royal Society of London Series B Biological behavioral development and neural mechanisms. Current
Sciences, 364, 3459–3474. Topics in Behavioral Neuroscience, 16, 189–212.
Schettino, A., Keil, A., Porcu, E., & Muller, M. M. (2016). Xie, J., Douglas, P. K., Wu, Y. N., Brody, A. L., & Anderson,
Shedding light on emotional perception: Interaction of A. E. (2017). Decoding the encoding of functional brain
brightness and semantic content in extrastriate visual cortex. networks: An fMRI classification comparison of non-negative
Neuroimage, 133, 341–353. matrix factorization (NMF), independent component analysis
Sharp, B. (2017). Basolateral amygdala and stress-induced (ICA), and sparse coding algorithms. Journal of Neuroscientific
hyperexcitability affect motivated behaviors and addiction. Methods, 282, 81–94.
Translational Psychiatry, 7, 1–13. Yavari, F., Jamil, A., Mosayebi Samani, M., Vidor, L. P., &
Shensa, A., Escobar-Viera, C. G., Sidani, J. E., Bowman, N. D., Nitsche, M. A. (2018). Basic and functional effects of
Marshal, M. P., & Primack, B. A. (2017). Problematic social transcranial electrical stimulation (tES): An introduction.
media use and depressive symptoms among U.S. young Neuroscience and Biobehavioral Reviews, 85, 81–92.
adults: A nationally-representative study. Social Science and Zachar, P., & Ellis, R. (2012). Categorical versus dimensional
Medicine, 182, 150–157. models of affect: A seminar on the theories of Panksepp and
Spear, L. P. (2011). Rewards, aversions and affect in adolescence: Russell. Philadelphia, PA: John Benjamins.
Emerging convergences across laboratory animal and Zhang, B., Suarez-Jimenez, B., Hathaway, A., Waters, C.,
human data. Developmental Cognitive Neuroscience, 1, Vaughan, K., Noble, P. L., .
. .
Nelson, E. E. (2012).
392–400. Developmental changes of rhesus monkeys in response to
Spielberg, J. M., Olino, T. M., Forbes, E. E., & Dahl, R. E. separation from the mother. Developmental Psychobiology, 54,
(2014). Exciting fear in adolescence: Does pubertal 798–807.

CH A PTE R
Emotions as Regulators of
3 Social Behavior
Lane Beckes and Weston Layne Edwards
Abstract
This chapter provides an overview and novel theoretical synthesis of the literature on how and
why emotions regulate social behaviors. It outlines how theorists in this domain have long disagreed
on how to conceptualize the role of evolution and innateness in terms of functions of emotions.
Parsing theoretical and empirical traditions by level of domain specificity, the chapter argues for
a domain-relevant approach to emotion, which is more congruent with current understanding of
neurodevelopment and gene–environment interactions. It examines emotion as emergent information
about the motivational landscape and offers an alternative metaphorical approach to thinking about
evolution as it relates to socioemotional life based on river formation and change.
Keywords: emotion, social behavior, evolution, domain specific, construction, basic emotions,
attachment, emotion theory, emotion regulation, social baseline theory
Emotions, even though their hallmark is the internal state of the individual—the
viscera, the gut—are above all social phenomena. They are the basis of social
interaction, they are the products of social interaction, their origins, and their currency.
—Zajonc (1998, pp. 619–620)
Introduction ing emotion as emergent information about the

For humans, emotion emerges in social more than motivational landscape. Moreover, our motivations
nonsocial contexts (Reis, Collins, & Berscheid, and emotions are tied directly with our ability to
2000). Social connection is so critical that people predict and adapt to the environment through
are substantially more likely to die if they are so- learning and allostasis. Most of our basic needs are
cially isolated (Holt-Lunstad, Smith, & Layton, regulated through complex, highly variable systems
2010). Therefore, the manner in which emotions that develop with domain-relevant functions
shape social behavior, and vice versa, is of para- evolved to promote survival, growth, and reproduc-
mount importance to the study of emotion and its tion. Thinking of the brain as possessing many
(dys)regulation. There is wide disagreement regard- domain-specific mechanisms is incongruent with
ing the domain specificity of emotions and their evidence, and arguing that all mechanisms are
functions. Couched within this greater dispute are therefore domain general is oversimplifying.
various interpretations of the mechanisms and Here we introduce a new metaphor for these de-
nature of emotions. Resolving this debate is central velopmental processes, adding potentially useful
to the goal of understanding how emotions influ- language and heuristics for understanding how
ence social behavior. human sociality and emotionality are intimately
All perspectives might benefit from separating linked. This metaphor uses the language of geology
motivation and emotion more explicitly and defin- and fluvial systems to organize thinking about issues
27
related to nature and nurture, arguing that these phenomenon and developed a domain-general view
processes behave more like the development of river of emotion. That is, the brain does not produce
systems than the en vogue computer processing emotions via domain-specific neurobiological mecha-
metaphor can capture. This heuristic view of social- nisms, but rather via domain-general core systems
emotional development predicts specific types of (Barrett, 2014). The first is core affect, which is com-
hypotheses linking emotion and social behavior posed of both valence (determination of whether
through developmental processes. Finally, we argue something is positive or negative as it relates to the
that humans are adapted to a primarily social eco- organism) and some degree of peripheral nervous
logical niche that drives organization of neural sys- system arousal (Lindquist, 2013). The second ingre-
tems in a manner that is domain relevant. dient, conceptualization, is a process by which
In this chapter, we start with a discussion of the bodily sensations (core affect) and cues from outside
theoretical divisions regarding the domain specific- of the body are made meaningful, transforming
ity of emotion processes. Indeed, emotional influ- ambiguous core affect into a disambiguated discrete
ences on social behavior can only be understood by emotion.
taking a particular theoretical perspective. Because Critically, this view of emotion argues that each
of disagreements about most basic elements of what instance of an emotion may be highly variable, but
defines an emotion, the theoretical convictions of that through degeneracy the brain categorizes the
any given theorist are critical in interpreting evi- context and physiological state of the organism as a
dence and decoding relations between emotion and specific emotion (Barrett, 2017). Degeneracy refers
social behavior. to the fact that many different neurons will feed
into one, suggesting that many different patterns of
Theoretical Perspectives on the Nature and activity can result in the same categorization. Thus,
Mechanisms of Emotion and Its Functions many possible patterns across perceptual, motor,
Quarrels among emotion theorists emerged long and cognitive systems might produce any given
ago in philosophical debates between seminal phi- emotion. Conceptualization also functions primarily
losophers such as Plato and Aristotle (see Scherer, to assist allostasis (stability through change) or the
2000). The greatest dividing feature of these ap- maintenance of homeostatic systems through the
proaches is currently the degree of domain specific- procurement of resources, such as food from the en-
ity of emotions. Domain-specific mechanisms of vironment, and functions in a predictive rather than
emotion are most strongly associated with basic reactive manner.
emotion theories, which argue for natural kind We contend that Barrett’s (2017) view of emo-
types of emotion (c.f. Barrett, 2006). Domain- tion is likely more correct on several fronts than
specific approaches assert that mental mechanisms, most current emotion theories. Yet, there are some
often conceptualized as mental modules (see Fodor, potential problems with this view of emotion, rais-
1983), act to guide responses to recurring adaptive ing important questions. Is everything domain gen-
problems in human evolutionary history (Cosmides eral, and are there gradients of domain generality
& Tooby, 1994). These mechanisms are frequently and specificity? We all agree that certain outcomes
thought to act independently and automatically are necessary for survival, growth, and reproduc-
with the appropriate sensory or motivational input, tion, but where do they fit in the domain-general
leading to preprogrammed or prepared behavioral model of emotion? Behaviorists made a mistake
repertoires. For example, I may feel jealousy because decades ago when they assumed all learning was
I perceive a threat to my relationship from an inter- simply a function of our most basic needs (e.g.,
loper, and that emotional state produces behavioral food, water, etc.). Harlow (1958) disproved this po-
tendencies such as mate guarding or intrasexual sition, showing that infant monkeys preferred a soft
competition (Arnocky, Ribout, Mirza, & Knack, stimulus to a food stimulus. Given that we need
2014). Thus, emotion in such models predicts clear, various resources—hence the need for allostasis—
stereotyped elements within the emotion–social be- and that those resources are rewarding and preferred
havior relationship. Despite the heuristic benefits, it in a noncontingent manner, how does an entirely
is now widely believed that theories arguing for domain-general system self-organize in such an
domain-specific mechanisms in most areas of psy- adaptive manner? Furthermore, how does sexual
chology are largely untenable. behavior develop given that it is not a physiological
Lisa Feldman Barrett (2017) has taken early need? If the conceptual separation of the brain and
ideas about emotion as a psychologically constructed body is a mistake (c.f., Barrett, 2017), then how
28 Emotions as Regul ators of Social Behavior

does one contend with relatively domain-specific circuits or functions become domain dominant, but
endocrine functions such as the angiotensin system not domain specific. In this sense the human brain
and its regulation of fluid balance in a domain- is composed of many domain-relevant features, but
general account? Yes, variability in even these most few domain-specific features.
basic systems is both high and critically important The process of human brain development is
in understanding human emotion and motivation. largely competitive, through which various circuits
Yet does the domain-general argument risk ignoring and neurons compete to respond to environmental
that measures of dispersion are most useful in con- signals (Karmiloff-Smith, 1992, 1998). During this
junction with measures of central tendency? competition, synapses and neurons are pruned from
the system and specialization begins to emerge in
Evolution and Innateness circuits that have appropriate connections, neu-
Best estimates put average associations between rotransmitters, receptors, and other features that
genetic variants and complex behavioral phenotypes make a given circuit, region, or network effective at
a little under 50% (Polderman et al., 2015). Despite responding to a specific type of stimulus. A good
clear links between genes and behavior, develop- example of this process comes from the face process-
mental neuroscience approaches reveal clear probing literature, which provides strong evidence for
lems with the modularity hypothesis and domain- modularity within the fusiform face area (FFA;
specific theories more generally (Buller & Hardcastle, Kanwisher & Yovel, 2006). Kadosh and colleagues
2000; Karmiloff-Smith, 2015; Manuck & McCaffery, (Kadosh & Johnson, 2007; Kadosh, Johnson, Dick,
2014). Genetic studies indicate that any given be- Kadosh, & Blakemore, 2013) note that this process-
havioral phenotype is associated with numerous ing specialization only develops over time, and the
individual genes that only explain a small portion FFA only gradually becomes specialized during the
of variance in phenotypes (Manuck & McCaffery, first decade of life.
2014). Additionally, it is likely that very rare geno- Neuroconstructivism and domain-relevant think-
types, gene–environment interactions, epigenetics ing are wholly consistent with evidence regarding
(processes that modulate and modify gene expres- brain development, neural specialization, and innate
sion), and epistasis (gene–gene interaction) play im- input into human behavior. It is an elegant solution
portant roles in how genetic information gets trans- to the nature–nurture debate, and is consistent with
lated into phenotypic presentations. This complexity current understanding of gene–environment inter-
challenges the notion that massive modularity is the actions. We argue that any emotion theory that is
norm in brain development, but does not fully to stand the test of time will require this type of
dispel the position. In combination with evidence domain-relevant thinking.
regarding brain development, however, the case
for modularity falls apart rapidly. Unfortunately, Adaptive Basins as an Alternative
Barrett’s (2017) argument that degeneracy can ex- Model and Metaphor
plain all such findings is also wanting. Why does The massive modularity hypothesis conceptualizes
degeneracy seem to favor some types of outcomes the human mind as a set of diverse computational
more than others? Why does brain organization processes. This conceptualization comes from the
have tremendous normative properties if everything computer processing metaphor of the mind and
is simply degeneracy and all mechanisms are domain brain (Von Neumann, 1958/2012), and has been the
general? This position is close to correct, but missing dominant framework for decades in psychology.
critical subtlety as it relates to neurodevelopment. A recent surge in radical embodiment theories
Karmiloff-Smith (2006, 2009, 2015) takes the pushes back against the metaphor, arguing for a
neuroconstructivist position that biases in develop- more dynamic and organic perspective (Chemero,
ment lead to brain organization that is domain rel- 2009; Barrett, 2011, Wilson & Golonka, 2013).
evant, but not domain specific. This position is Here we present an alternative metaphor that better
wholly in line with decades of research on neurode- captures these dynamic and naturalistic features as
velopment and argues that complex interactions at related to innateness versus construction. For this,
multiple levels of the system (i.e., genes, epigenetics, we suggest the metaphor of a river.
molecular and cellular processes, network-level pro- River form is highly variable as a function of a
cesses, and environmental inputs) all interact and number of features of the environment and various
contribute to specialization and generalization of inputs into the river system (Charlton, 2007). River
various systems across the brain. Over time certain formation occurs because a region has more water
Beckes and Edwards 29

than the soil can absorb. Over time, large rivers Applying the Adaptive Basins Model
form with many tributaries acting as sources for the The adaptive basins model is congruent with
river. The form of the river is always changing, sub- Barrett’s (2017) view of what “a brain is for” in that
ject to morphological systems, such as those related to the primary function of the brain is to predict an
hill slopes and geological and biological features organism’s best actions given physiological needs.
of the channel, and cascading systems, which refer Allostasis, in conjunction with incentive processes
to the flow of water through the morphological (c.f., Berridge, 2007), determines current motiva-
system. These two systems interact to further shape tional demands. Emotions organize motivation by
a river. For a river, many morphological systems are providing feedback about success, failure, opportu-
substantially formed before a river matures. Thus, nity, risk, and problems with current predictions of
many aspects of the morphological system create outcomes. Thus, emotion acts as information about
structure upon which the river will form. Once motivation and goal pursuit.
sufficient water flow develops, cascades begin to
further carve the morphological system, cutting a Emotion as Information
deeper river basin. Researchers increasingly agree that emotions func-
Conceptualizing innate processes this way, tion to guide behavior, but not all researchers agree
evolved features of the mind start out as morpho- on the manner by which this occurs. Baumeister,
logical features defining the boundary conditions Vohs, De Wall, and Zhang (2007) argue for a dual-
for developing domain-relevant basins. Normative process model of affect in which emotions function
development requires appropriate inputs into the primarily as feedback that can be used to anticipate
system for competitive processes to unfold. Some future experiences and promote more functional be-
inputs, like tributaries, have their own morphologi- havior. In this way emotion is a learning signal.
cal features, some more rigid than others. The most This position is originally associated with Schwarz
rigid of these tributary processes include highly in- and Clore’s (1983; Clore & Huntsinger, 2007; Clore
stinctive or reflexive features of behavior. Classic & Storbeck, 2006; Clore, Wyer, Dienes, Gasper,
examples of such rigid morphologies include fight- Gohm, & Isbell, 2001) affect-as-information hypothe-
or-flight responses, which Ledoux (2012) refers to sis. According to this theory, affective phenomena,
as survival functions; reflexes, such as the grasping, including emotions, provide critical information re-
suckling, or rooting reflexes (Schott & Rossor, garding motivation. For example, sad music makes
2003); and homeostatic functions, like the angio- short hills look steeper (Riener, Stefanucci, Proffitt,
tensin systems in thirst (Fitzsimons, 1998). These & Clore, 2003). And specific emotion inductions
more rigid systems are exclusively evolved to solve modulate decision making in meaningful ways
adaptive problems related to homeostatic, repro- (Lerner, Small, & Lowenstein, 2004; Mackie, Devos,
ductive, and survival functions. & Smith, 2000; Schnall, Haidt, Clore, & Jordan,
Critically, abnormal development may occur if 2008).
cascade processes are missing. If too little energy is The affect-as-information hypothesis is highly
entering the system, it will fail to mature properly. congruent with neuroscience models of emotion
If tributary sources that are typical for develop- such as Damasio’s (1994) somatic marker hypothesis.
ment don’t receive enough input themselves, then This theory suggests that judgment and decision
an entire source of cascade energy is missing for making are influenced by somatic information, in-
larger downstream systems. For example, babies cluding heart rate, muscle movements, facial expres-
often show attentional biases to faces (e.g., Frank, sions, endocrine activity, respiration, and feedback
Vul, & Johnson, 2009), but infants classified as through the brainstem and thalamus into the so-
high risk for autism spectrum disorder (ASD) matosensory cortices, insula, and cingulate cortex.
attend less to faces and other social stimuli than This information is integrated with information re-
other infants (Chawarska, Macari, & Shic, 2013). garding motivation, long-term memory, and motor
Perturbations in tributaries to developing social- planning in the ventromedial prefrontal cortex
emotional systems may affect later development (vmPFC) to guide decision making. The vmPFC
in highly significant ways through impoverished creates somatic states through its top-down connec-
cascades. How does this model inform emotion tions with various structures such as the amygdala,
and social behavior, and what is emotion from allowing for simulations of possible scenarios, fur-
this perspective? ther aiding decision making. Numerous studies

indicate that damage to the vmPFC or any of the experience do these instincts become a goal-corrected
regions that provide affective information to the behavioral system. From our perspective one can
vmPFC impairs judgment in a variety of tasks reimagine this system as an adaptive basin whereby
(Bechara & Damasio, 2005). environmental feedback shapes these instincts in
Van Kleef (2009) takes the affect-as-information the service of a particular set of attachment-related
theory one step further by arguing that emotion not goals. Progress toward or away from desired end
only regulates individual behavior but also regulates states is signaled through emotion. In this light
the behavior of others in close proximity. The emotion is an emergent domain-relevant phenom-
emotion-as-social-information model outlines how enon that acts as a learning signal to organize behav-
perception of another person’s emotional expres- ioral and motivational components of the develop-
sions is perceived, processed, and taken into consid- ing system.
eration during behavioral decision making. This in- Myron Hofer’s (1984, 2006) research on social
sight is critical for understanding human behavior relationships as hidden regulators illustrates the
as it places emotions directly into a social context, adaptive-basins concept in action. Social isolation
which we argue is the primary ecological niche of in rat pups produces changes in adrenal endocrine
the human species. activity, heart rate, respiration, ultrasonic vocaliza-
tions (homologous to crying), and over long periods
Human Social Development, decreases in growth hormone release (Hofer, 1984,
Attachment, and Emotion Kuhn, Pauk, & Schanberg, 1990; Rosenfeld,
Attachment theory (Bowlby, 1969/1983) is not pri- Wetmore, & Levine, 1992; Shapiro & Salas, 1970;
marily a theory of emotion, but shares common fea- Stanton, Wallstrom, & Levine, 1987). Sensory stim-
tures, and serves as an excellent starting point when ulation mimicking the softness, warmth, and other
thinking about domain relevance and the adaptive features of the rat’s littermates and dam decreases
basins conceptualization in emotional and motiva- these homeostatic responses. Sensory features of
tional processes. Bowlby’s (1969/1983) seminal social contact serve as early tributary systems for
theory describes processes by which infants main- developing social attachments. Several homeostatic
tain physical proximity to caregivers. He hypothe- functions are regulated through social contact, in-
sized that an innate behavioral system evolved to cluding thermoregulation, energy regulation, and
keep vulnerable infants in close contact with attach- stress regulation (see Beckes, Ijzerman, & Tops,
ment figures (a primary caregiver with whom the 2015). These functions are in turn supported by
infant has a special bond). This system activates highly rigid tributary behavioral systems akin to in-
under stress, such as sickness, injury, and fear, or stincts, such as crying, huddling, clinging, and suck-
when the child is separated from the attachment ling. Over time these tributary functions provide
figure. The primary result of activating the attach- cascade energy into a developing attachment basin,
ment system is an emotional state called separation which serves to regulate attachment-related motiva-
distress, which motivates proximity-seeking behav- tions and promotes behaviors that support norma-
iors such as crying, following the attachment figure, tive development. Emotion acts to monitor and
and clinging to the attachment figure. Once prox- update attachment needs and motivations, provid-
imity is achieved, the child begins to experience felt ing feedback regarding whether and how attachment-
security, an emotional state associated with a sense related goals are being met. Separation distress often
of calm and comfort, at which point the child functions to indicate a need for change, whereas felt
begins exploratory activity again. security often serves as information that attachment
Two elements of attachment theory are impor- needs are being met.
tant for our purposes. First, the theory clearly de- The degree to which these systems receive appro-
scribes how social emotions drive social behaviors. priate environmental input is critical to the devel-
Second, Bowlby proposes an innate behavioral opment of the system. In rat pups, high-arched-
system, consistent with domain-relevant as opposed back nursing and licking and grooming behavior
to domain-specific theories. He argued that while increases the expression of hippocampal glucocorti-
certain elements of this system are hard-wired, the coid receptors (Liu et al., 1997), leading to less anx-
behavior system is shaped by experience. For exam- ious behavior in adulthood. This example shows
ple, clinging, suckling, crying, and other attach- how cascading inputs, licking and grooming, modify
ment behaviors are instinctive, but only through developing morphological systems, hippocampal

glucocorticoid receptor densities, in determining Social Baseline Theory and Our
emotional endophenotypes. These differences feed Social-Ecological Niche
back to future emotional episodes, creating a dy- Social baseline theory (SBT; Beckes & Coan,
namic recursive feedback process that further shapes 2011, 2012; Coan, Brown, & Beckes, 2014, Coan &
social-emotional development. Maresh, 2014; Coan & Sbarra, 2015) argues that
Severe social deprivation produces unusual emo- humans are adapted primarily for life in social
tional behavior in children, such as disorganized at- groups, and that placement within a network of
tachment, in which the child shows indiscriminate interdependent others is core to health and

friendliness and poor organization of attachment well-being. This theory posits two ways in which
behaviors (Bakermans-Kranenburg et al., 2011), social proximity is a baseline human condition.
which is frequently associated with extended time First, humans are not adapted to any particular
in institutional care. The adaptive-basins model terrestrial environment, achieving this flexibility

would argue that a lack of appropriate cascade primarily through social cooperation (Cohen &
system activity—in the form of stable relationship Janicki-Deverts, 2009; Holt-Lunstad et al., 2010).
interactions with a small number of caregivers— Second, physical contact with loved ones reduces
interacting with morphological features such as var- anxiety, stress responses, and threat reactivity (e.g.,
iations in the dopamine receptor D4 gene (Wazana Brown, Beckes, Allen, & Coan, 2017; Coan,
et al., 2015) is likely to lead to disorganization in Schaefer, & Davidson, 2006; Coan et al., 2017), but
the system. And greater risk accumulates over devel- researchers have not yet identified a clear neural
opmental time as systems go through pruning mechanism (e.g., vmPFC, ventral striatum) for this
(Bakermans-Kranenburg et al., 2011). effect. Beckes and Coan argue that there is a mis-
Extensions of Bowlby’s ideas suggest that attach- taken assumption that aloneness is a baseline con-
ment dynamics also emerge in adult relationships, dition for humans. For example, when looking at
whether sexual mates (e.g., Carter, Grippo, data in which social contact is manipulated, we tend
Pournajafi-Nazarloo, Ruscio, & Porges, 2008; to assume that being alone is the natural state.
Hazan & Diamond, 2000; Hazan & Shaver, 1987) Alternatively, if one assumes that togetherness is the
or a broader set of relationship partners (Beckes & natural state for humans, a hypothesis for which
Coan, 2011; Taylor, 2006). One of the key contro- there is now overwhelming evidence (see Berscheid,
versies surrounding such extensions is whether any 2003; Brewer & Caporael, 1990; Keltner, Haidt, &
of these relationships are truly attachment relation- Shiota, 2006), then being alone is a potentially
ships and, if so, how to verify their status as attach- anxiety-provoking situation for many people.
ment relationships (Fraley & Shaver, 2000). From SBT posits that through two primary mecha-
the adaptive-basins perspective, this question is nisms, risk distribution and load sharing, humans are
moot as there is no reason to imagine a categorical able to budget energy expenditure on various tasks
delineation of attachment status. Early features of in more efficient ways, including anticipatory anxi-
the developing brain may promote what is com- ety and vigilance for threat. Risk distribution refers
monly considered a true attachment, such as inter- to various processes through which vigilance and
actions in norepinephrine release and hippocampal- individual risk get distributed, such as when any
amygdala development (see Sullivan, 2003), but animal forms a group, there are more eyes and ears
differences are more likely emergent properties to detect predators (Krebs, Davies, & Parr, 1993).
of sensitive periods and the unique nature of the Load sharing refers to the fact that humans also
caregiver–child relationship. Patterns that develop form social networks characterized by interdepend-
early begin to form our general social behavior but ence and joint attention and goals, and can rely on
are subject to change with more input into the var- each other for aid and support more broadly.
ious tributaries and basins that feed into the more The net gain from social contact and proximity
general social basin. Relationships continue to is a reduction of risk and effort for the individual,
serve as regulators of homeostasis, but the manner altering perception and energy budgeting. Evidence
in which they do so varies by relationship, age of that energetic considerations alter the perceived
the individual, and other factors. The broadest difficulty of tasks is mounting (E. B. Gross &
sense in which social relationships regulate homeo- Proffitt, 2013; Proffitt, 2006). For example, wear-
stasis is described by social baseline theory (Beckes ing a heavy backpack increases the perceived slope
& Coan, 2011). of a hill, making the task appear more challenging

(Proffitt, Stefanucci, Banton, & Epstein, 2003; Given the premise that humans are primarily
Stefanucci, Proffitt, Banton, & Epstein, 2005). In a adapted to a social ecology rather than a particular
similar manner, close proximity to reliable and pre- physical ecology, it stands to reason that much of
dictable relationship partners modifies our percep- human emotional content will be social in nature.
tions and predictions regarding resource use, effort, Moreover, to the extent that domain-relevant sys-
and risk. If one assumes that affect and emotion act tems exist in the human mind, many of those sys-
as information about motivational features of the tems will be involved in managing the social envi-
situation, then the potential for risk distribution ronment. Traditional models of evolved emotional
and load sharing is included in the perception of mechanisms cannot capture the complexity of such
the individual’s affective state, and outcome predic- systems, which are not modular. Rather, thinking of
tions. In a bottom-up manner, this information emotion as emergent information about motivation
changes the perceived difficulty of the environ- that is largely rooted in the dynamic development
ment, anticipatory anxiety, and the individual’s of domain-relevant, distributed systems likely cap-
energy budget. tures this subtlety and complexity.
As a thought experiment, one can think of many
times in which one had to walk in an unfamiliar Synthesis
place late at night. This is potentially risky, and it is From these frameworks, we propose a definition of
normative for people to experience increased vigi- emotion as emergent information about the moti-
lance and anxiety. However, with a group, one au- vational landscape. We think this conclusion serves
tomatically perceives the potential for load sharing two purposes. First, it fits data indicating that emo-
and risk distribution, reducing anxiety. Thus, in- tions are not natural kinds, and are therefore emer-
formation about our social resources is embedded gent phenomena, but are often domain relevant and
in the information that emerges as an emotional have functions derived from both evolution and
experience. sociocultural processes. Second, defining emotion
The manner in which any individual perceives as information about motivational concerns helps
those social resources is influenced by the develop- clarify that emotion is a dynamically recursive
ment of cascading and morphological systems (e.g., process that is composed of many components, but
Gonzalez, Beckes, Chango, Allen, & Coan, 2015; its main function is to provide information about
Maresh, Beckes, & Coan, 2013). A more challeng- motivationally relevant aspects of life, such as ho-
ing history in cascade systems, such as unreliable meostatic function.
relationship partners or poor neighborhood quality, A good starting place is to follow J. J. Gross’s
and certain morphological features, such as de- (2015) definition of emotion. He notes that affect is
creased hippocampal glucocorticoid receptor ex- an overarching term for emotion-related elements.
pression or allele variations of the oxytocin receptor Affect is a state of valuation and includes moods,
gene rs237915 (Gonzalez, Puglia, Morris, & emotions, and stress. Notably, he distinguishes
Connelly, 2017), interact to change the likelihood moods and stress from emotion, indicating that
that one will perceive risk and the potential benefit moods are kind of like the climate, long term and
of social resources. These cascading and morpho- less variable, whereas emotions are brief pertur-
logical features of the individual and his or her envi- bances or variations like weather. Moreover, one
ronment serve as features that form domain-relevant may have activation of the autonomic nervous
social systems (see Figure 3.1). From this organiza- system without an emotion, but such activation is
tion, individuals develop differences in their percep- often considered a necessary component of emo-
tion of risk, energy, and social resources, modifying tion. Emotions from this view are loosely coupled
how affective information emerges and guides be- changes in emotional components (subjective expe-
havior. In a very real sense, domain relevance is an rience, physiological arousal, and behavior).
important feature of these systems, emotion serves For such a phenomenon to be nonemergent,
as information about domain-relevant situations, basic, or latent, there would need to be a central
and the type of emotion conceptualization one ex- mechanism that triggered these loosely coupled re-
periences is linked through learning to domains in a sponses. Yet, there is little evidence for such central
probabilistic, not causal, manner. For example, lust mechanisms, and emotions are better characterized
is more likely to emerge due to activity in a domain- as emergent processes than as superordinate basic
relevant sex basin than not. mechanisms. Moreover, given that stress without an

Figure 3.1 A conceptual model of the adaptive-basins approach to thinking about domain-relevant motivational systems. The model
shows how certain tributary systems related to instinctive behaviors such as suckling, crying, and clinging feed into basins that
regulate homeostasis in energy, thermal, and stress systems through social interaction organizing a broader domain-relevant basin of
attachment behavior. That basin then feeds into more general social behaviors that develop over time. Notably, the attachment basin is
not the sole feed into the general social basin. Moreover, one failing of this metaphor is that in neural systems information flow is
multidirectional, unlike water systems. While imperfect, the metaphor provides heuristic language that clarifies certain features of
domain-relevant systems, such as tributaries, morphological systems (represented as elevation and slope in this figure), cascading
systems, and the general idea of a flexible but clearly structured basin upon which neural systems become domain relevant.
Map is modified and based on map data from Google ©2017.
emotion is widely recognized by emotion research- but are not clearly definable only from the external
ers, it is clearly the case that arousal of the sympa- world. In a sense, emotional episodes can be thought
thetic nervous system can occur before an emotion. of as having mobilizing and perceptual features that
If this is true, it creates a conundrum for defining dynamically and recursively feed back to each other.
emotion. Arousal typically occurs in response to a Emotion as a concept is better characterized as the
change in the motivational landscape. It frequently perceptual part of the cycle and motivation as the
entails the detection of something surprising or mobilization part of the cycle.
of motivational relevance such as an opportunity In addition, we argue that many human emo-
or risk, which leads to the body’s preparation for tions will be social in nature. As information, those
action. If this is not an emotion, then more compo- emotions feed into our ability to form opinions and
nents are needed for emotion to occur. judgments or to decide on actions, and ultimately
We think a separation between the mobilization are critical in determining many of our social behav-
and perceptual phases of emotions clarifies this dis- iors. Many of those emotions are domain relevant
tinction. If we consider the mobilization element as because they tap into flexible behavioral systems
more closely related to changes in the motivational that act as adaptive basins for human behavior.
landscape and emotion as part of the perception of Those basins include attachment behavior—including
that change, then it might be better to clarify that separation distress and felt security—and sexual be-
motivation is more associated with the mobilization havior, for which lust and passionate love may pro-
phase and emotion is more associated with the per- vide information about our goals, whether we can
ceptual phase. Further, this definition comports achieve them, and, if so, how.
well with the idea that emotion serves as informa-
tion. Notably, we are not arguing that this separa- Future Directions
tion is always clear in practice, or that one can truly We recommend several directions for future re-
separate these two constructs. Both constructs are search. First, researchers should pay close attention
conceptual ideas that have correlations with reality to developmental processes. Any understanding of

emotion from our perspective needs to attend to References
how emotional responses affect and are affected by Arnocky, S., Ribout, A., Mizra, R. S., & Knack, J. M. (2014).
social context in development. Further, understand- Perceived mate availability influences intrasexual competition,
jealousy, and mate-guadring behavior. Journal of Evolutionary
ing how emotion becomes dysregulated must be Psychology, 12, 45–64.
sensitive to developmental processes and attuned to Bakermans-Kranenburg, M. J., Steele, H., Zeanah, C. H.,
whether the social and emotional environment is Muhamedrahimov, R. J., Vorria, P., Dobrova-Krol, N. A., . . .
supplying stimulation. Gunnar, M. R. (2011). Attachment and emotional development
Second, researchers who study human develop- in institutional care: Characteristics and catch up. Monographs
of the Society for Research in Child Development, 76, 62–91.
ment should attempt to determine the degree to Barrett, L. (2011). Beyond the brain: How the body and environment
which likely innate behaviors, such as fight or shape cognition. New Jersey: Princeton University Press.
flight, crying, suckling, following, and so forth, Barrett, L. F. (2006). Are emotions natural kinds? Perspectives on
provide a foundation for later behavior. In partic- Psychological Science, 1, 28–58.
ular, studying the neurodevelopment of other sys- Barrett, L. F. (2014). The conceptual act theory: A précis. Emotion
Review, 6, 292–297.
tems as they relate to survival circuits and simple Barrett, L. F. (2017). The theory of constructed emotion: An
social and emotional behaviors may illuminate active inference account of interoception and categorization.
how psychological adaptations emerge within de- Social Cognitive and Affective Neuroscience, 12, 1–23.
velopment and guide the formation of better Baumeister, R. F., Vohs, K. D., DeWall, N. C., & Zhang, L. (2007).
models of social and affective disorders. In addi- How emotion shapes behavior: Feedback, anticipation, and
reflection, rather than direct causation. Personality and Social
tion, efforts should be made to make clear connec- Psychology Review, 11, 167–203.
tions between emotion theory and theories of mo- Bechara, A., & Damasio, A. R. (2005). The somatic marker
tivation and social behavior. Many such theories hypothesis: A neural theory of economic decision. Games and
have amassed tremendous evidence that is directly Economic Behavior, 52, 336–372.
relevant to emotion theory. Beckes, L., & Coan, J. A. (2011). Social baseline theory: The role
of social proximity in emotion and economy of action. Social
Third, social context must be considered when and Personality Psychology Compass, 5, 976–988.
understanding emotion and its (dys)regulation. Beckes, L., & Coan, J. A. (2012). Social baseline theory and the
Social connection is foundational for human life, social regulation of emotion. In The science of the couple: The
and inattention to social networks will lead to a fail- Ontario Symposium (Vol. 12, pp. 81–93).
ure to fully understand any given individual’s emo- Beckes, L., Ijzerman, H., & Tops, M. (2015). Toward a radically
embodied neuroscience of attachment and relationships.
tional and psychological situation. Often emotion Frontiers in Human Neuroscience, 9, 266.
dysregulation is not simply an intrapersonal phe- Berridge, K. C. (2007). The debate over dopamine’s role in
nomenon, but an interpersonal problem, and it reward: The case for incentive salience. Psychopharmacology,
should be recognized as such. 191, 391–431.
Berscheid, E. (2003). The human’s greatest strength: Other
humans. In L. G. Aspinwall & U. M. Staudinger (Eds.),
Conclusion A psychology of human strengths: Fundamental questions and
The emotion field has been rife with dichotomous future directions for a positive psychology (pp. 37–47). San
thinking about the nature of emotion. While de- Francisco, CA: Berrett-Koehler.
bates have frequently been fruitful, accurate models Bowlby, J. (1969/1982). Attachment (Vol. 1). New York, NY:
will need to contend with both variability between Basic Books.
Brewer, M. B., & Caporael, L. R. (1990). Selfish genes vs. selfish
people and normative tendencies across the species. people: Sociobiology as origin myth. Motivation and Emotion,
We suggest that thinking of emotion as emergent 14, 237–243.
information about motivation helps to bridge this Brown, C. L., Beckes, L., Allen, J. P., & Coan, J. A. (2017).
divide. It clearly defines emotion as the perceptual Subjective general health and the social regulation of
side of a motivated process, frequently related to hypothalamic activity. Psychosomatic Medicine, 79, 670–673.
Buller, D. J., & Hardcastle, V. (2000). Evolutionary psychology,
domain-relevant behavioral systems that emerge meet developmental neurobiology: Against promiscuous
through complex developmental processes, many of modularity. Brain and Mind, 1, 307–325.
which are likely social in nature. Those domain- Carter, C. S., Grippo, A. J., Pournajafi-Nazarloo, H., Ruscio,
relevant processes are not innate per se, but are the M. G., & Porges, S. W. (2008). Oxytocin, vasopressin and
result of gene–environment interactions across de- sociality. Progress in Brain Research, 170, 331–336.
Charlton, R. (2007). Fundamentals of fluvial geomorphology.
velopment. Some processes, usually very simple New York, NY: Routledge.
ones, may be relatively more rigid and modular Chawarska, K., Macari, S., & Shic, F. (2013). Decreased
than others, but most will be large, dynamic systems spontaneous attention to social scenes in 6-month-old
that work in a domain-relevant rather than a infants later diagnosed with autism spectrum disorders.
domain-specific manner. Biological Psychiatry, 74, 195–203.

Chemero, A. (2009). Radical embodied cognitive science. Cambridge, Gross, J. J. (2015). Emotion regulation: Current status and future
MA: MIT Press. prospects. Psychological Inquiry, 26, 1–26.
Clore, G. L., & Huntsinger, J. R. (2007). How emotions inform Harlow, H. F. (1958). The nature of love. American Psychologist,
judgment and regulate thought. Trends in Cognitive Sciences, 13, 673–685.
11, 393–399. Hazan, C., & Diamond, L. M. (2000). The place of attachment
Clore, G. L., & Storbeck, J. (2006). Affect as information about in human mating. Review of General Psychology, 4, 186–204.
liking, efficacy, and importance. In J. P. Forgas (Ed.), Affect Hazan, C., & Shaver, P. (1987). Romantic love conceptualized
in social thinking and behavior (pp. 123–141). New York, NY: as an attachment process. Journal of Personality and Social
Psychology Press. Psychology, 52, 511–524.
Clore, G. L., Wyer, R. S., Dienes, B., Gasper, K., Gohm, C., Hofer, M. A. (1984). Relationships as regulators: A psychobiologic
& Isbell, L. (2001). Affective feelings as feedback: Some perspective on bereavement. Psychosomatic Medicine, 46,
cognitive consequences. In L. L. Martin & G. L. Clore 183–197.
(Eds.), Theories of mood and cognition: A user’s guidebook Hofer, M. A. (2006). Psychobiological roots of early attachment.
(pp. 27–62). Mahwah, NJ: Erlbaum. Current Directions in Psychological Science, 15, 84–88.
Coan, J. A., Beckes, L., Gonzalez, M. Z., Maresh, E. L., Brown, Holt-Lunstad, J., Smith, T. B., & Layton, J. B. (2010). Social
C. L., & Hasselmo, K. (2017). Relationship status and perceived relationships and mortality risk: A meta-analytic review.
support in the social regulation of neural responses to threat. PLoS Medicine, 7, e1000316.
Social Cognitive and Affective Neuroscience, 10, 1574–1583. Kadosh, K. C., & Johnson, M. H. (2007). Developing a cortex
Coan, J. A., Brown, C., & Beckes, L. (2014). Our social baseline: specialized for face perception. Trends in Cognitive Sciences,
The role of social proximity in economy of action. In 11, 367–369.
M. Mikulincer & P. R. Shaver (Eds.), Nature and formation Kadosh, K. C., Johnson, M. H., Dick, F., Kadosh, R. C., &
of social connections: From brain to group (pp. 89–104). Blakemore, S. J. (2013). Effects of age, task performance,
Washington, DC: American Psychological Association Press. and structural brain development on face processing. Cerebral
Coan, J. A., & Maresh, E. L. (2014). Social baseline theory and Cortex, 7, 1630–1642.
the social regulation of emotion. Handbook of Emotion Kanwisher, N., & Yovel, G. (2006). The fusiform face area:
Regulation, 2, 221–236. A cortical region specialized for the perception of faces.
Coan, J. A., Schaefer, H. S., & Davidson, R. J. (2006). Lending Philosophical Transactions of the Royal Society of London B:
a hand: Social regulation of the neural response to threat. Biological Sciences, 361, 2109–2128.
Psychological Science, 17, 1032–1039. Karmiloff-Smith, A. (1992). Nature, nurture and PDP:
Coan, J. A., & Sbarra, D. A. (2015). Social baseline theory: The Preposterous developmental postulates? Connection Science,
social regulation of risk and effort. Current Opinion in 4, 253–269.
Psychology, 1, 87–91. Karmiloff-Smith, A. (1998). Development itself is the key to
Cohen, S., & Janicki-Deverts, D. (2009). Can we improve our understanding developmental disorders. Trends in Cognitive
physical health by altering our social networks? Perspectives Sciences, 2, 389–398.
on Psychological Science, 4, 375–378. Karmiloff-Smith, A. (2006). The tortuous route from genes
Cosmides, L., & Tooby, J. (1994). Beyond intuition and instinct to behavior: A neuroconstructivist approach. Cognitive,
blindness: Toward an evolutionarily rigorous cognitive Affective, and Behavioral Neuroscience, 6, 9–17.
science. Cognition, 50, 41–77. Karmiloff-Smith, A. (2009). Nativism versus neuroconstructivism:
Damasio, A. R. (1994). Testing the somatic marker hypothesis. Rethinking the study of developmental disorders.
In A. R. Damasio (Ed.), Descartes’ error: Emotion, reason, and Developmental Psychology, 45, 56–63.
the human brain (pp. 205–222). New York, NY: Penguin. Karmiloff-Smith, A. (2015). An alternative to domain-general or
Fitzsimons, J. T. (1998). Angiotensin, thirst, and sodium domain-specific frameworks for theorizing about human
appetite. Physiological Reviews, 78, 583–686. evolution and ontogenesis. AIMS Neuroscience, 2, 91–104.
Fodor, J. A. (1983). The modularity of mind: An essay on faculty Keltner, D., Haidt, J., & Shiota, M. N. (2006). Social
psychology. Cambridge, MA: MIT Press. functionalism and the evolution of emotions. In M. Schaller,
Fraley, R. C., & Shaver, P. R. (2000). Adult romantic attachment: J. A. Simpson, & D. T. Kenrick (Eds.), Evolution and social
Theoretical developments, emerging controversies, and psychology (pp. 115–142). New York, NY: Psychology Press.
unanswered questions. Review of General Psychology, 4, Krebs, J. R., Davies, N. B., & Parr, J. (1993). An introduction to
132–154. behavioural ecology. Cambridge, MA: Blackwell Scientific
Frank, M. C., Vul, E., & Johnson, S. P. (2009). Development of Publications.
infants’ attention to faces during the first year. Cognition, 110, Kuhn, C. M., Pauk, J., & Schanberg, S. M. (1990). Endocrine
160–170. responses to mother-infant separation in developing rats.
Gonzalez, M. Z., Beckes, L., Chango, J., Allen, J. P., & Coan, Developmental Psychobiology, 23, 395–410.
J. A. (2015). Adolescent neighborhood quality predicts adult LeDoux, J. (2012). Rethinking the emotional brain. Neuron, 73,
neural response to social exclusion. Social Cognitive and 653–676.
Affective Neuroscience, 10, 921–928. Lerner, J., Small, D., & Lowenstein, G. (2004). Heart strings
Gonzalez, M. Z., Puglia, M. H., Morris, J. P., & Connelly, J. J. and purse strings: Carryover effects of emotions on economic
(2017). Oxytocin receptor genotype and economic privilege decisions. Psychological Science, 15, 337–341.
reverses ventral striatum-social anxiety association. Social Lindquist, K. A. (2013). Emotions emerge from more basic
Neuroscience, 17, 1–13. psychological ingredients: A modern psychological
Gross, E. B., & Proffitt, D. R. (2013). The economy of social constructionist model. Emotion Review, 5, 356–368.
resources and its influence on spatial perception. Frontiers in Liu, D., Diorio, J., Tannenbaum, B., Caldji, C., Francis, D.,
Human Neuroscience, 7, 772. Freedman, A., . . . Meaney, M. J. (1997). Maternal care,

hippocampal glucocorticoid receptor gene expression and Schott, J. M., & Rossor, M. N. (2003). The grasp and other
hypothalamic-pituitary-adrenal responses to stress. Science, primitive reflexes. Journal of Neurology, Neurosurgery and
277, 1659–1662. Psychiatry, 74, 558–560.
Mackie, D. M., Devos, T., & Smith, E. R. (2000). Intergroup Schwarz, N., & Clore, G. L. (1983). Mood, misattribution, and
emotions: Explaining offensive action tendencies in an judgments of well-being: Informative and directive functions
intergroup context. Journal of Personality and Social of affective states. Journal of Personality and Social Psychology,
Psychology, 79, 602–616. 45, 513–523.
Manuck, S. B., & McCaffery, J. M. (2014). Gene-environment Shapiro, S., & Salas, M. (1970). Behavioral responses of infant
interaction. Annual Review of Psychology, 65, 41–70. rats to maternal odor. Physiology and Behavior, 5, 815–817.
Maresh, E. L., Beckes, L., & Coan, J. A. (2013). The social Stanton, M. E., Wallstrom, J., & Levine, S. (1987). Maternal
regulation of attentional disengagement in highly anxious contact inhibits pituitary-adrenal stress responses in
individuals. Frontiers in Human Neuroscience, 7, 515. preweanling rats. Developmental Psychobiology, 20, 131–145.
Polderman, T. J., Benyamin, B., De Leeuw, C. A., Sullivan, P. F., Stefanucci, J. K., Proffitt, D. R., Banton, T., & Epstein, W.
Van Bochoven, A., Visscher, P. M., & Posthuma, D. (2015). (2005). Distances appear different on hills. Perception and
Meta-analysis of the heritability of human traits based on Psychophysics, 67, 1052–1060.
fifty years of twin studies. Nature Genetics, 47, 702–709. Sullivan, R. M. (2003). Developing a sense of safety: The
Proffitt, D. R. (2006). Embodied perception and the economy of neurobiology of neonatal attachment. Annals of the New York
action. Perspectives in Psychological Science, 1, 110–122. Academy of Sciences, 1008, 122–131.
Proffitt, D. R., Stefanucci, J., Banton, T., & Epstein, W. (2003). Taylor, S. E. (2006). Tend and befriend: Biobehavioral bases of
The role of effort in perceiving distance. Psychological Science, affiliation under stress. Current Directions in Psychological
14, 106–112. Science, 15, 273–277.
Reis, H. T., Collins, W. A., & Berscheid, E. (2000). The Van Kleef, G. A. (2009). How emotions regulate social life: The
relationship context of human behavior and development. emotions as social information (EASI) model. Current
Psychological Bulletin, 126, 844–872. Directions in Psychological Science, 18, 184–188.
Riener, C., Stefanucci, J. K., Proffitt, D., & Clore, G. L. (2003). Von Neumann, J. (1958/2012). The computer and the brain. New
Mood and the perception of spatial layout. Poster presented Haven, CT: Yale University Press.
at the 44th Annual Meeting of the Psychonomic Society, Wazana, A., Moss, E., Jolicoeur-Martineau, A., Graffi, J., Tsabari,
Vancouver, BC, Canada. G., Lecompte, V., . . . Meaney, M. J. (2015). The interplay
Rosenfeld, P., Wetmore, J. B., & Levine, S. (1992). Effects of of birth weight, dopamine receptor D4 gene (DRD4),
repeated maternal separations of the adrenocortical response and early maternal care in the prediction of disorganized
to stress of preweanling rats. Physiology and Behavior, 52, attachment at 36 months of age. Developmental Psychopathology,
787–791. 27, 1145–1161.
Scherer, K. R. (2000). Psychological models of emotion. Wilson, A. D., & Golonka, S. (2013). Embodied cognition is not
Neuropsychology of Emotion, 137, 137–162. what you think it is. Frontiers in Psychology, 4, 58.
Schnall, S., Haidt, J., Clore, G., & Jordan, A. H. (2008). Disgust Zajonc, R. B. (1998). Emotions. In D. T. Gilbert, S. T. Fiske, &
as embodied moral judgment. Personality and Social G. Lindzey (Eds.), The handbook of social psychology (4th ed.,
Psychology Bulletin, 34, 1096–1109. Vol. 2, pp. 591–632). Boston, MA: McGraw-Hill.

CH A PT E R
Cognition and Emotion in
4 Emotion Dysregulation
Kateri McRae and Paree Zarolia
Abstract
Emotion dysregulation often implies that high levels of (frequently negative) emotion are simply not
regulated by cognition. However, emotion dysregulation can refer to positive feedback loops that
are created and maintained both by a lack of effective cognitive processes that regulate emotion,
and by strong effects of emotion on cognition. This chapter first discusses the effect of cognition on
emotion, with an emphasis on the effects of attention and cognitive control (e.g., emotion regulation)
processes upon emotions. Then, it discusses the effect of emotion on cognition, with an emphasis on
attention, memory, decision making, and cognitive control. Finally, it examines the implications of both
types of emotion–cognition interactions by discussing the positive-feedback cycles that can produce
dysregulated emotion.
Keywords: cognition, emotion, cognitive control, emotion regulation, decision making, memory,
attention
Introduction being regulated, while cognitive neural systems are

Emotion dysregulation is often defined by patterns thought of as performing regulation (Buhle et al.,
of emotional experience and expression that inter- 2013). However, to understand dysregulated emo-
fere with adaptive, goal-directed behavior (Thompson, tion, it is more appropriate to think of emotion
1994). By this definition, emotion dysregulation is and cognition as parts of a complex system, having
observed in many forms of psychopathology (see bidirectional influences on one another (Todd,
Beauchaine, 2015). Despite a common focus on the Cunningham, Anderson, & Thompson, 2012).
emotional outcome (the magnitude or amount of The goal of the present chapter is to review liter-
emotion present), emotion dysregulation more spe- ature outlining interactions between emotion and
cifically implicates not merely that emotions are at several types of cognition: attention, memory, deci-
unwanted levels, but that the high levels of emotion sion making, and cognitive control. In light of the
have not been effectively diminished or kept in complex, bidirectional relationships between emo-
check by emotion regulation. tion and cognition, we divide this chapter into two
It is common to think of regulation as brakes parts: how cognition affects emotion and how emo-
or checks on a system, or the ability to reduce un- tion affects cognition. We will focus our review on
wanted emotions. However, regulation can refer to dysregulation of negative emotion because of its
any change to the frequency, rate, or extent of another clinical relevance; however, many of the effects of
process. More important, regulation is often the prod- emotion on cognition have been attributed to emo-
uct of complex, interdependent systems, in which the tional arousal more generally, which characterizes
same processes both are regulated and perform regula- both negative and positive emotion. We will discuss
tion. In the case of emotion regulation, emotional key differences between negative and positive emo-
neural systems and responses are often thought of as tion when relevant.
39
How Cognition Affects Emotion et al., 2003; Habel et al., 2007; Winston, O’Doherty,
There is a large literature focused on the effects of & Dolan, 2003), and some scholars argue that con-
cognition on emotion. Specifically, one prolific re- scious awareness is not required, much less focused
search tradition defines emotion regulation as a va- attention (Jessen & Grossmann, 2015; Morris &
riety of processes by which someone can influence Dolan, 2001; Whalen et al., 2004; but see Pessoa,
his or her own emotional trajectory in terms of the 2005).
onset, offset, magnitude, duration, or quality of an Another set of studies explores a closely related
emotional response (Gross, 2015; Gross & question: whether restricting attentional resources
Thompson, 2007). This research was born of the affects the magnitude of brain and bodily emotional
coping literature, but in its current instantiation, it responses. These studies examine restricted atten-
largely references the process model of emotion tion by presenting emotional and nonemotional
regulation, which outlines five points during emo- stimuli together, with instructions to respond to
tion generation in which regulation processes might nonemotional stimuli, or by presenting a dual task
occur (Gross, 1998b). These include situation selec- along with emotional stimuli. These researchers find
tion (avoidance or engagement with situations that that emotional responding diminishes as concur-
have potential to cause unwanted emotion), situa- rent attentional demands increase (Pessoa, Padmala,
tion modification (utilizing agency to change prop- & Morland, 2005; Silvert et al., 2007). In other
erties of situations that may cause unwanted emo- words, emotional responses to stimuli can be di-
tion), attentional modification (directing attention minished significantly under more impoverished at-
toward and away from aspects of situations that tentional conditions (Habel et al., 2007). So, while
may cause unwanted emotion), cognitive change complete attention does not seem to be required for
(changing the cognitions, evaluations, and apprais- the production of brain and/or bodily emotional
als that lead to emotion), and expressive suppression responses, these responses do decrease when atten-
(directly influencing emotional responses, including tional resources are more limited.
bodily responses and facial expressions of emotion). Examining distraction as an explicit emotion
Attentional modification and cognitive change are regulation strategy is one way that emotion re-
most relevant to this review because they refer to searchers have examined influences of attention on
well-specified cognitive processes. It is possible to use emotion (Gross, 1998b; Salovey, Mayer, Goldman,
attentional modulation and cognitive change to either Turvey, & Palfai, 1995). In an everyday context, dis-
diminish or enhance emotional responding. traction from a negative event, such as a breakup of
a romantic relationship, might involve a purpose-
How Attention Influences Emotion fully overstuffed social calendar; an increased focus
How attention can diminish emotion on other priorities, such as work; or engagement
Most theories of emotion imply that some atten- with unrelated narratives, such as those in books or
tional resources must be devoted to an emotional films. In a laboratory context, distraction from neg-
event to elicit a response (Gross, 1998b). If emotion ative stimuli can be implemented either broadly,
is a downstream consequence of attention, it follows with an instruction such as “think of something else
naturally that changes in attention can have strong so that you do not feel as negative,” or quite specifi-
effects on subsequent emotion. More recently, re- cally, by giving the participant a secondary task to
searchers have examined whether emotional stimuli complete while processing emotional stimuli. Both
require focused attention (or even conscious aware- types of distraction are effective, in that when im-
ness; Jessen & Grossmann, 2015; Pessoa, 2005) to plemented, they reduce self-reported negative emo-
be processed preferentially in the brain compared to tion (Joorman, Siemer, & Gotlib, 2007; Sheppes &
neutral stimuli (Anderson, Christoff, Panitz, De Meiran, 2008), along with other brain and bodily
Rosa, & Gabrieli, 2003). These studies use labora- emotional responses (Kanske, Heissler, Schönfelder,
tory manipulations that severely limit or prevent Bongers, & Wessa, 2011; McRae et al., 2010; Shafir,
conscious processing of emotional stimuli, and ex- Schwartz, Blechert, & Sheppes, 2015). One benefit
amine whether a stimulus still elicits an emotional of distraction is that it can be used even when there
(> neutral) brain and/or bodily response. Using is limited time for emotion regulation (Sheppes &
amygdala activation and physiological responses as Gross, 2011; Sheppes & Meiran, 2008). In addition,
indices of emotion, there is considerable evidence it can be used to effectively reduce emotional re-
that directed attention is not necessary for the brain sponding even in response to relatively intense emo-
and body to respond to certain stimuli (Anderson tional stimuli. However, there is some evidence that
40 Cognition and Emotion in Emotion Dysregul ation

the effectiveness of distraction is not long-lasting, in goals, consciously or not, before an emotional re-
that it does not generalize beyond the encounter sponse can occur (Gross, 1998a). Reappraisal, then,
during which distraction is used (Thiruchselvam, refers to any attempts to change an interpretation
Blechert, Sheppes, Rydstrom, & Gross, 2011). or evaluation of an emotional stimulus or an event
When distraction is used as an emotion regulation in order to change its meaning and, therefore, the
strategy and the same stimulus is encountered at a emotion that follows (Giuliani & Gross, 2009).
later time, the emotional response unfolds as though For example, a public case of mistaken identity
no emotion regulation has ever taken place. might be later reappraised as a comedic goldmine
Finally, it is possible that emotion regulation for future stories, transforming embarrassment into
occurs when one changes attentional biases, albeit delight. Studies of individual differences indicate
with some amount of practice. A relatively recent that frequent use of reappraisal to regulate emo-
literature has examined the role of attention train- tions is largely adaptive, in that it is associated with
ing paradigms on biases toward (and away from) lower depressive symptoms and negative emotion,
emotional stimuli. These training paradigms and higher positive emotion (Aldao, Nolen-
emerged from a broader literature on attention and Hoeksema, & Schweizer, 2010; Gross & John,
findings that some anxiety disorders are associated 2003; Potthoff et al., 2016). Increases in use of
with vigilance for threatening stimuli and negative reappraisal are associated with better treatment

emotion (Yiend, 2010). In these studies, attention response and recovery from psychopathology

biases become a target of an intervention in which (McRae, Rekshan, Williams, Cooper, & Gross,
focus is directed away from negative emotion by di- 2014; Smits, Julian, Rosenfield, & Powers, 2012).
recting participants to engage in hundreds of atten- Frequency of reappraisal use is less heritable than
tion modifying dot-probe trials (Amir, Beard, either neuroticism, a personality variable character-
Burns, & Bomyea, 2009; Heeren, Reese, McNally, ized by negative emotion, or suppression, another
& Philippot, 2012). Several studies have demon- emotion regulation strategy (McRae et al., 2017).
strated that by the end of the training session, atten- By contrast, reappraisal is relatively more influ-
tion can be directed away from emotional stimuli, enced by environmental variables not shared with
which produces concomitant changes in anxiety siblings, which could reflect educational, social,
symptoms (Bar-Haim, 2010). and career contexts, as well as efforts to change
emotion regulation over the course of psychother-
How attention can enhance emotion apy. In a therapeutic context, reappraisal is often
Despite an emphasis in the literature on the use of referred to as “cognitive reframing” and is a corner-
attention to diminish affective responding, atten- stone of cognitive and cognitive-behavioral thera-
tion can also be used to enhance emotion. Directing pies (Beck & Dozois, 2011).
attention toward an emotional cue increases cogni- Over the past several decades, researchers have
tive processing of that stimulus (Pessoa et al., 2005; found that cognitive reappraisal, when deployed
Silvert et al., 2007). Rumination refers to the in the laboratory, can reduce negative emotional
process of redirecting attention to causes and conse- responding, including self-reported negative affect
quences of a negative emotional response (Koster, (Gross, 1998a), expression of negative emotion
De Lissnyder, Derakshan, & De Raedt, 2011), (Goldin, McRae, Ramel, & Gross, 2008; Jackson,
which often has the effect of prolonging or main- Malmstadt, Larson, & Davidson, 2000; Ray,
taining the emotion (Young & Nolen-Hoeksema, McRae, Ochsner, & Gross, 2010; Webb, Miles, &
2001). Individual differences in rumination are as- Sheeran, 2012), psychophysiological responding
sociated with depressive symptoms and negative (McRae, Ciesielski, & Gross, 2012), and recruit-
affect (Nolen-Hoeksema, 2000). ment of amygdala resources (Ochsner, Bunge,
Gross, & Gabrieli, 2002), which likely modulates
How Cognitive Change Affects Emotion: some of these bodily changes. Furthermore,
Cognitive Reappraisal changes due to reappraisal are relatively long-lasting.
How reappraisal diminishes emotion Upon re-exposure to a stimulus that you’ve previ-
Cognitive reappraisal is perhaps the most com- ously reappraised, there is some savings of that
monly studied form of emotion regulation. previous effort, reflected in lower levels of emo-
Consistent with appraisal theory, the modal model tional responding (Denny, Inhoff, Zerubavel,
of emotion suggests that a person must evaluate an Davachi, & Ochsner, 2015; Thiruchselvam, Blechert,
event as consistent or inconsistent with his or her Sheppes, Rydstrom, & Gross, 2011). Therefore,
M c Rae and Zarolia 41

reappraisal is viewed as a relatively effective emo- Derntl, & Heekeren, 2017). Neuroimaging evi-
tion regulation strategy. dence has indicated that reappraisal recruits largely
overlapping regions with other forms of cognitive
How reappraisal enhances emotion control, such as distraction, although most regions
Although reappraisal is often used to diminish nega- that support both reappraisal and distraction are re-
tive emotional responding, reappraisal can also be cruited by reappraisal to a greater degree (McRae et
used to increase positive or negative emotion (Giuliani, al., 2010). Individual differences in reappraisal are
McRae, & Gross, 2008; Kim & Hamann, 2007). For also related to cognitive control and executive func-
example, amygdala activation can be both enhanced tioning (Lantrip, Isquith, Koven, Welsh, & Roth,
and decreased by reappraisal (Ochsner et al., 2004), 2016; McRae, Jacobs, Ray, John, & Gross, 2012;
with both directions of reappraisal recruiting largely Schmeichel, Volokhov, & Demaree, 2008). In addi-
overlapping regions in prefrontal and parietal cortices. tion, reappraisal and several other forms of cogni-
In addition, reappraisal can be used to create negative tive control improve throughout adolescence,
emotion in response to a neutral stimulus, as evi- which coincides with prefrontal cortex develop-
denced by enhanced amygdala activation to neutral ment (McRae, Gross, et al., 2012; Silvers et al.,
stimuli when paired with self-generated (Ochsner et 2012). Studies of transcranial magnetic stimulation
al., 2009) or other-generated (Otto et al., 2014) nega- indicate that reappraisal use can be facilitated by
tive narratives. Finally, reappraisal can be used to en- stimulation of the dorsolateral prefrontal cortex
hance positive emotion, even in response to a negative (Feeser, Prehn, Kazzer, Mungee, & Bajbouj, 2014;
stimulus (McRae, Ciesielski, & Gross, 2012; Shiota & Lantrip, Gunning, Flashman, Roth, & Holtzheimer,
Levenson, 2012; Waugh et al., 2016). 2017). Therefore, it is likely that reappraisal will be
less effective in individuals whose prefrontal cortex
Limitations of reappraisal is not fully developed, degenerating with age, or
Although reappraisal is generally adaptive, there compromised by injury or disease. Similarly, there
are several situations in which reappraisal is not as are other conditions that lead to suboptimal pre-
effective or even unhelpful. Studies have shown that frontal engagement, potentially mediated by poor
reappraisal may be less preferred, less effective prefrontal functioning, such as high stress (Troy,
(Shafir et al., 2015), and more effortful (Silvers, Wilhelm, Shallcross, & Mauss, 2010) or poor sleep
Weber, Wager, & Ochsner, 2015) when used on in- quality (Mauss, Troy, & LeBourgeois, 2012).
tense negative emotions, and it is not as effective Taken together, these findings reveal that many
when the time available to reappraise is severely lim- types of cognition can enhance, diminish, and
ited (e.g., in the context of reappraising a negative change emotional responses in a variety of contexts.
picture, < 4 seconds; Sheppes & Meiran, 2008). Exerting cognitive control over emotional respond-
Reappraisal may also be counterproductive when ing can be a powerful tool, leading to emotional
the situation leading to the emotional response is lives that are more in line with our emotional goals.
controllable—the most adaptive response to nega- However, the influence of cognition on emotion is
tive job performance feedback from a trusted super- not unidirectional, and emotion can also affect cog-
visor, for example, may be a change in behavior nitive control, including what we attend to, remem-
rather than a change in thinking (Troy, Shallcross, ber, and decide.
& Mauss, 2013). Furthermore, there is preliminary
evidence that the way an emotion is generated How Emotion Affects Cognition
might affect how it is regulated. Specifically, emo- Effects of Emotion on Attention and Memory
tions generated perceptually, by encounters with How emotion enhances attention
negative stimuli, may be less effectively regulated by and memory
cognitive reappraisal than emotions generated cog- Emotions have a powerful effect on attention. More
nitively, by imagined or invented current or future specifically, the presence of emotional stimuli is
situations (McRae, Misra, Prasad, Pereira, & Gross, known to capture attention, sustain attention, and
2011; Nelson, Fitzgerald, Klumpp, Shankman, & make it harder to disengage with the stimulus
Phan, 2015). (Öhman, Flykt, & Esteves, 2001), especially if
Cognitive reappraisal recruits medial and lateral it signals threat (Koster, Crombez, Van Damme,
prefrontal cortices, including regions that are Verschuere, & De Houwer, 2004). For example, a
thought to subserve cognitive control more broadly snake might be more quickly identified than a rock
(Ochsner, Silvers, & Buhle, 2012; Morawetz, Bode, when hiking, or the sound of a baby’s cry might

seem to cut through a noisy house more than the Mood-congruent memory, which refers to
sound of household electronics. The preference for increased availability of memories that are consist-
emotion in attentional capture is supported by find- ent with a current mood state, is another way in
ings that emotional items (especially faces) are more which emotion influences memory (Bower, 1981;
quickly identified in a search task (Vuilleumier, Riskind, 1989). People feeling sad, for example, can
2005) and that emotional, especially negative, stim- bring to mind more sad events from their past than
uli draw early eye movements, perhaps to facilitate people feeling neutral or happy (Berntsen, 2002;
collection of relevant information (Huang, Chang, Mayer, McCormick, & Strong, 1995). Positive
& Chen, 2011). Emotional stimuli can even con- states also make positively-valenced items more
tinue to capture attention when they are no longer accessible for memory retrieval (Isen, Shalker, Clark,
present (Hajcak & Olvet, 2008), as evidenced by & Karp, 1978).
poorer performance following emotional stimuli in
an attentional blink task (Ogawa & Suzuki, 2004). How emotion diminishes attention
Finally, emotional stimuli are more difficult to dis- and memory
engage from than neutral stimuli, meaning they sus- The effects of emotion on attention and memory
tain our attention longer. Unrelated, or background may not always be desirable. For example, negative
emotional states can also influence attention. mood states result in a narrowed attentional focus,
Attentional biases toward emotional information where the central object of our attention receives
are strengthened when in a congruent mood state, prioritized processing compared with peripheral
such as faster reaction times to positive words details (Berntsen, 2002; Fenske & Eastwood, 2003;
among individuals reporting high levels of state Fredrickson & Branigan, 2005). (This narrowing
positive emotion (Strauss & Allen, 2006). quality of attention may be specific to highly arous-
Another way in which emotion affects cognition ing negative emotions (Gable & Harmon-Jones,
is through memory. Emotion-enhanced memory 2010; Kensinger et al., 2007; Mather et al., 2006;
refers to the preferential treatment of emotion Talarico, Berntsen, & Rubin, 2009).) By the same
memories in encoding and storage (Phelps, 2004). token, mood-congruent memory occurs at the ex-
Previously neutral stimuli that are paired with pense of mood-incongruent memory, which can
highly emotional events are remembered better, and lead to decreased accuracy in mood mismatch con-
can later elicit emotional responses consistent with ditions. This may be especially true among those
the emotional stimulus, a variant of classical condi- with a history of major depression (Joormann &
tioning known as fear conditioning. In addition, Siemer, 2004). Mood-incongruent memory, al-
highly arousing stimuli (whether positive or nega- though requiring more effort, may be one avenue
tive) are remembered better than neutral stimuli for emotion regulation—for example, the effortful
(Buchanan, Etzel, Adolphs, & Tranel, 2006; Cahill recall of positive memories can counteract a nega-
& McGaugh, 1995). This enhanced memory usu- tive emotional state (Rusting & DeHart, 2000).
ally reflects increased memory for central (rather Finally, highly arousing events tend to result in an
than peripheral) aspects of emotional events or increase in subjective confidence in memories, re-
scenes (Kensinger, Garoff-Eaton, & Schacter, 2007; sulting in the perception of highly accurate “flash-
Mather et al., 2006), especially in the case of nega- bulb” memories. However, it is likely that these
tive information (Touryan, Marian, & Shimamura, effects are more likely to reflect perception than re-
2007). In that sense, emotionally enhanced memory ality. Studies demonstrate that the effect of emotion
might be considered a consequence of enhanced on subjective confidence is seen despite marked in-
(and narrowed) attention for emotional stimuli consistency in memories over time (Talarico &
rather than neutral stimuli. Fear conditioning is Rubin, 2003).
thought to be mediated by amygdala circuits (LaBar, One important ramification of these relation-
Gatenby, Gore, LeDoux, & Phelps, 1998), as pa- ships between emotion, attention and memory is
tients with amygdala damage are unable to encode that together, they can create self-sustaining feed-
or retrieve new associations with fearful stimuli. back loops. For example, if the central object of at-
Emotionally enhanced memories are thought to tention contains negative information, it is likely to
arise from arousal-based amygdala influences on the capture and sustain attention, this sustained atten-
hippocampus (Cahill et al., 1996; Hamann, 2001), tion may cause an increase in negative mood, lead-
making the amygdala a central brain region in the ing to mood-congruent memory. This increased
effect of emotion on memory. accessibility of negative memories may prolong


negative mood even more, which may bias attention Prospect theory describes biases as primarily det-
toward incoming negative information, further sus- rimental and tangential to decision making. The
taining negative mood. Therefore, emotional effects risk-as-feeling hypothesis extends prospect theory
on attention and memory can compound, contrib- by stating that feelings are a source of information
uting to a “downward spiral” of emotion and cogni- as central to decision making as other cognition,
tion (Garland et al., 2010). but maintains that these feelings are often detri-
mental to optimal decision making. In fact, when
Effects of Emotions on Decision Making emotional responses and other cognitions diverge,
How emotions hurt decision making feelings often dictate behavioral outcomes
It is a common assumption that decisions should be (Loewenstein, Weber, Hsee, & Welch, 2001). The
made from a dispassionate, purely reason-based per- risk-as-feeling model posits that responses to risky
spective. Research findings are often consistent with situations are a composite of both direct emotional
this assumption, with studies demonstrating that influences and cognitive evaluations. The theory
emotion can bias our choices away from optimiza- states that direct—or anticipatory—emotion is gen-
tion. One such theory in decision-science prospect erated from the stimulus itself, a direct reaction to a
theory revolutionized economics by demonstrating feature of one’s decision (e.g., a reaction to the color,
that emotional responses to choices—defined price, or size of something), and is independent of
broadly as rapid positive or negative responses—can cognitive evaluations (Floresco & Ghods-Sharifi,
cause systematic biases in decision making. These 2007; Slovic, Finucane, Peters, & MacGregor,
biases may lead individuals to make decisions that 2004; Slovic & Peters, 2006; Song & Schwarz,
may not be in their best interest (Kahneman & 2009). Furthermore, subsequent research reveals
Tversky, 1979; Tversky & Kahneman, 1991). For that direct neural projections from sensory regions
example, loss aversion refers to people’s tendency to can bypass cognitive regions to influence behavior
overweight a loss as compared to the same monetary directly (Öngür & Price, 2000; Zald, 2003). Thus,
gain; loss aversion produces a pattern of decision emotional responding appears to be central to deci-
making that suggests that individuals do not simply sion making, rather than a supplemental influence
assess the overall objective value of each option on cognitive inferences.
(which is equal for losses and gains) but also the
emotional value, or a summary value based on how How emotions help decision making
one feels toward the option. While some research appears to support colloquial
Subsequent research has extended early findings, beliefs that emotions impair decision making, some
demonstrating that emotional influences in decision research demonstrates that this might not be the
making often lead to suboptimal choices as measured case. The affect-as-information hypothesis (Schwarz
by financial gain in investment paradigms. For exam- & Clore, 1983) is one such line of research. It states
ple, when participants are asked to make an invest- that individuals use emotion, or affect more broadly,
ment under conditions of risk, they often underin- experienced at the moment of the decision as a reac-
vest even though investing regardless of the risk tion to what is being judged, to guide behavior. This
would ultimately leave them with more money (Shiv, phenomenon has been illustrated in myriad do-
Loewenstein, Bechara, Damasio, & Damasio, 2005). mains as disparate as consumer products (Adaval,
In these tasks, emotional biasing (i.e., an emotional 2013) to life satisfaction (Schwarz & Clore, 1983).
influence on decision making) is thought to prevent In the latter example, participants reported greater life
risk taking even when that risk would lead to better satisfaction on sunny days compared to rainy, dem-
outcomes. Healthy participants and patients with onstrating that they inferred that their “sunny” dispo-
cognitive deficits (but not emotional deficits) did not sition was due to their overall satisfaction with life
make the most optimal choice (i.e., always investing), (Schwarz & Clore, 1983). The affect-as-information
though patients with emotional deficits consistently hypothesis explains such behavioral patterns as the
chose to invest, leading to more optimal decision result of individuals using their current emotional
making (Shiv et al., 2005). This pattern indicates that state to determine the value of choice options. The
the ability to “rationally” choose the riskier option is affect-as-information hypothesis further posits that
improved by a lack of emotion, suggesting that emo- in addition to incidental emotional evaluations,
tional responding, rather than cognitive processing, emotional responses can also be generated by the
leads to loss (and risk) aversion. decision options. This occurs when we have rapid,

valid, informative emotional responses to choices examines how we enact top-down control to main-
that indicate whether we like or dislike them. tain, inhibit, and shift between different types of
Importantly, these evaluations are often adaptive information. Studies of instructed emotion regula-
and can provide critical decision-relevant information, such as those that direct participants to use
tion about possible outcomes. These decision- reappraisal and/or distraction, are helpful for identi-
relevant, emotional evaluations can be generated in fying many separable executive functions (Ochsner
response to any sort of option or option feature, & Gross, 2005). Much of the literature to date has
whether they are similar (e.g., the price of each focused on establishing a meaningful taxonomy of
option) or dissimilar (e.g., the style of option 1 and cognitive control in a neutral context (Miyake &
the status of option 2). Emotion, or affect more Friedman, 2012). However, some researchers have
broadly, therefore may serve as a common currency examined the effects of cognitive control on emo-
through which individuals can compare distinct option by examining the degree to which cognitive
tions that are not readily comparable through cog- control can also operate on emotional, rather than
nitive evaluation alone (Clore & Huntsinger, 2007). neutral, stimuli (Zelazo, Qu, & Kesek, 2010). Other
This model solidifies that emotion plays a critical researchers have induced emotions in the laboratory
role in decision making and proposes that this role and then asked participants to engage in neutral
is a helpful one. cognitive control tasks, therefore examining the
The somatic marker hypothesis further extends effects of induced emotional contexts on cognitive
the role of emotion from complementary to neces- control.
sary in the decision-making process. Not only are
somatic markers an essential part of decision-making How emotion hurts cognitive control
processes, but also cognitive evaluation may even be Most studies report impaired performance when
superfluous (Bechara & Damasio, 2005; Bechara, cognitive tasks are performed on emotional (rather
Damasio, Tranel, & Damasio, 2005; Dunn, than neutral) stimuli. These studies conclude that
Dalgleish, & Lawrence, 2006). The central premise emotion (positive or negative) can impair perfor-
of the somatic marker hypothesis is that emotional mance in cognitive control domains, including con-
responses conveyed through bio-regulatory mecha- flict adaptation (Padmala, Bauer, & Pessoa, 2011),
nisms (e.g., changes in electrodermal activity, endo- working memory (Schweizer & Dalgleish, 2016),
crine release, heart rate, smooth muscle contraction, and switch costs (Zhou et al., 2011). One explana-
posture, facial expression, etc.) are necessary for tion for these findings is that emotional stimuli cap-
adaptive decision making (Bechara & Damasio, ture attention (i.e., are distracting), which leaves
2005; Dunn, Dalgleish, & Lawrence, 2006; fewer resources for initiating and executing cogni-
Reimann & Bechara, 2010). Thus, there are two key tive control processes (Blair et al., 2007). There is
elements of this hypothesis: (1) bio-regulatory mech- some evidence that the presence of emotional stim-
anisms convey emotional information that is rele- uli can reduce engagement of prefrontal regions
vant to the decision at hand, and (2) use of this emo- typically associated with cognitive control during
tional information during decision making is in fact these tasks (Dolcos & McCarthy, 2006; Hur et al.,
adaptive. These are significant additions to previous 2015). Additionally, these decreases in prefrontal
theories, which identified potential benefits of emo- engagement are paired with increases in other
tions on decision making but did not view them as cortical regions and/or limbic regions, which is
essential to adaptive choices (Schwarz & Clore, consistent with a distraction effect (Dolcos &
1983; Clore & Huntsinger, 2007; Loewenstein et al., McCarthy, 2006).
2001; Kahneman & Tversky, 1979). Trait and state negative affect may also have
detrimental effects on cognitive control. Studies of
Effects of Emotion on Cognitive Control trait anxiety indicate that anxiety impedes cogni-
Many processes affect our ability to engage in cognitive control processes such as working memory
tive control, which allows us to make and imple- (Hayes, Hirsch, & Mathews, 2008) and switching
ment long-term, multistep cognitive plans; strategi- (Derakshan, Smyth, & Eysenck, 2009). In addi-
cally direct attention; inhibit prepotent responses; tion, there is a large literature indicating deficits in
and hold multiple pieces of information in mind— cognitive control more broadly among individuals
often referred to as executive functioning (Miyake with depression (Holmes & Pizzagalli, 2007;
et al., 2000). The executive functioning literature Joormann & Siemer, 2011; Snyder, 2013).

How emotions enhance Implications of Emotion–Cognition
cognitive control Interactions
However, in a few cases, emotion can enhance cog- We have summarized multiple ways in which emo-
nitive control. There is some evidence that even neg- tion can affect attention, memory, cognitive con-
ative emotion can improve conflict resolution trol, and decision making, as well as ways in which
(Kanske & Kotz, 2011; Schuch, Zweerings, Hirsch, these cognitive processes in turn can affect emotion.
& Koch, 2017) and can enhance conflict adaptation Because of these bidirectional relationships, the pos-
in a Flanker task (Zeng et al., 2017) and working sibility exists for unchecked feedback, either in the
memory (Levens & Phelps, 2008; Xie & Zhang, direction of more emotion (typically thought to be
2016). Positive emotion seems to have a more undesirable in the case of negative emotion) or in
consistent facilitation effect on cognitive control. the direction of less emotion (typically thought to
Positive emotion has long been thought to facilitate be desirable in the case of negative emotion).
creative thinking, and state positive affect has been Previous scholars have referred to these unchecked
shown to improve performance on tasks like remote feedback loops as downward and upward spirals, re-
associates (Isen, Daubman, & Nowicki, 1987), and spectively (Burns et al., 2008; Fredrickson & Joiner,
may also make people more likely to focus on simi- 2002). One common downward spiral, for exam-
larities and therefore group things together (Isen & ple, might involve the quick capture of a negative
Daubman, 1984). It is possible that positive emotion stimulus into attention, resulting in enhanced pro-
enhances cognitive flexibility (switching) and cessing of that stimulus, leading to increases in neg-
broader (global) thinking at the expense of more ative mood and increased accessibility of negative
narrow attentional focus, which can lead to greater memories, and then prolonging negative mood,
working memory maintenance and stability (Dreisbach which disturbs sleep. Prolonged negative mood and
& Goschke, 2004; Storbeck & Maswood, 2016). sleep disruption may further affect cognitive con-
When participants can earn a reward for their per- trol, making the use of cognition to curtail emotion
formance on a task, cognitive control ability is en- less effective. In this example, the feedback between
hanced (Krebs, Boehler, & Woldorff, 2010; Savine, cognitive and emotional systems continues to en-
Beck, Edwards, Chiew, & Braver, 2010). Much of hance negativity.
the literature lumps emotion and motivation to- Conversely, an upward spiral might occur when
gether—that is, positive emotion (pleasant subjec- someone is able to successfully engage in emotion
tive feeling) is often expected to have the same effect regulation and curtail a negative emotion, dimin-
on cognitive control as reward contexts (tasks in ishing the possibility that more negative emotions
which performance is positively reinforced). Both will be cued in autobiographical memory, making
positive emotion and reward might improve cogni- sleep disturbances less likely, and preserving cogni-
tive processes such as task switching, and lower tive control resources to handle future encounters
switch costs (Wang & Guo, 2008). The benefits of with negative stimuli or situations. Therefore, inter-
reward contexts extend to enhanced go–no-go per- rupting downward spirals might be effective as one
formance under reinforcement conditions, but di- type of intervention. Even more potent might be
minished control under threat conditions (Cohen the elicitation of positive emotion, given that some
et al., 2016). Reward contexts seem to enhance en- cognitive effects of positive emotion might be op-
gagement in the prefrontal cortex during cognitive posite to those of negative emotion. Therefore, pos-
control (Locke & Braver, 2008). Work connecting itive emotion not only slows or halts the downward
positive emotion and reward to tonic and phasic spiral process but also might reverse it. Generating
dopaminergic activity, respectively, makes strong positive emotion may be one way to begin an
predictions about the more specific effects of positive upward spiral, as noted in the positive psychology
emotion versus reward on cognitive control (Chiew literature (Fredrickson, 2001).
& Braver, 2014). For example, experimental work One important implication of these spirals is
demonstrates that a reward context might bias cog- that there are multiple points of entry to enact
nitive control toward proactive control rather than change. Cognitive reappraisal is a commonly used
reactive control (Chiew & Braver, 2011). One possi- tool in cognitive-behavioral therapy because it is
ble neural mechanism for this shift might be in- one way to interrupt a downward spiral (Mansell,
creased activation in cognitive control regions under Harvey, Watkins, & Shafran, 2008). Interventions
conditions of reward (Jimura, Locke, Braver, & such as cognitive-behavioral therapy and/or an in-
Smith, 2010). tervention that might improve sleep and therefore

improve regulatory functioning could be powerful offers multiple targets for intervention, which is a
ways to slow the spiral. However, it is possible that cause for hope that many individuals will be able to
any disruption of a negative emotion, such as using find a point in the emotion–cognition interaction
distraction, might result in a short-term reprieve spiral to make meaningful change.
from negative emotion, which could be a first step
to reducing a downward spiral. Psychoactive medi- References
cation, for example, antidepressant medication, Adaval, R. (2013). The utility of an information processing
typically has as its primary target the blunting of approach for behavioral price research. Academy of Marketing
negative emotion. Although these neurotransmit- Science Review, 3, 130–134.
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
ters are likely to act upon emotion generation and
Emotion-regulation strategies across psychopathology: A
emotion regulation neural circuitry alike, it is meta-analytic review. Clinical Psychology Review, 30, 217–237.
thought that this initial effect can be capitalized Amir, N., Beard, C., Burns, M., & Bomyea, J. (2009). Attention
upon if then paired with a cognitive intervention, modification program in individuals with generalized anxiety
such as cognitive-behavioral therapy (Cuijpers, Van disorder. Journal of Abnormal Psychology, 118, 28.
Anderson, A. K., Christoff, K., Panitz, D., De Rosa, E., &
Straten, Hollon, & Andersson, 2010). Individuals
Gabrieli, J. D. E. (2003). Neural correlates of the automatic
who benefit most from antidepressant medication processing of threat facial signals. Journal of Neuroscience, 23,
are those who increase their frequency of reap- 5627–5633.
praisal, even when not undergoing formal psycho- Bar-Haim, Y. (2010). Research review: Attention bias
social treatment (McRae et al., 2014). modification (ABM): A novel treatment for anxiety disorders.
The interactions between emotion and cognition Journal of Child Psychology and Psychiatry, 51, 859–870.
Baumeister, R. F., Heatherton, T. F., & Tice, D. M. (1994).
outlined here support a potential distinction be- Losing control: How and why people fail at self-regulation. San
tween two types of emotion dysregulation Diego: CA: Academic Press.
(Baumeister, Heatherton, & Tice, 1994; Campbell- Beauchaine, T. P. (2015). Future directions in emotion
Sills & Barlow, 2007; Carver & Scheier, 1981). dysregulation and youth psychopathology. Journal of Clinical
Some dysregulated affect may be the result of under- Child and Adolescent Psychology, 44, 875–896.
Bechara, A., & Damasio, A. R. (2005). The somatic marker
utilization of effective regulatory mechanisms, a hypothesis: A neural theory of economic decision. Games
spiral in which strong negative emotion is going and Economic Behavior, 52(2), 336–372. doi:10.1016/j.
largely unchecked by cognitive processes. However, geb.2004.06.010
other dysregulation might be due to use of mal- Bechara, A. A., Damasio, H. H., Tranel, D. D., & Damasio, A. R.
(2005). The Iowa Gambling Task and the somatic marker
adaptive emotion regulation strategies, which has
hypothesis: Some questions and answers. Trends in Cognitive
been termed misregulation of emotion (Campbell- Sciences, 9(4), 159–162. doi:10.1016/j.tics.2005.02.002
Sills & Barlow, 2007). Misregulation of emotion Beck, A. T., & Dozois, D. J. (2011). Cognitive therapy: Current
might paradoxically result in up-regulation (rather status and future directions. Annual Review of Medicine, 62,
than down-regulation) of negative emotion. 397–409.
Berntsen, D. (2002). Tunnel memories for autobiographical
Rumination is one example of misregulation of
events: Central details are remembered more frequently
affect (Nolen-Hoeksema, 2000). Individuals whose from shocking than from happy experiences. Memory and
negative emotion is unchecked due to underuti- Cognition, 30, 1010–1020.
lization of regulation might benefit from interven- Blair, K. S., Smith, B. W., Mitchell, D. G. V., Morton, J.,
tions targeted at emotion regulation frequency. Vythilingam, M., Pessoa, L., .
.
.
Blair, R. J. R. (2007).
Modulation of emotion by cognition and cognition by
However, those who are misregulating emotions
emotion. NeuroImage, 35, 430–440.
might benefit from interventions that instead target Bower, G. H. (1981). Mood and memory. American Psychologist,
the success, or efficacy, of those emotion regulation 36, 129.
strategies (McRae, 2013). Buchanan, T. W., Etzel, J. A., Adolphs, R., & Tranel, D. (2006).
Emotion dysregulation is a hallmark of many The influence of autonomic arousal and semantic relatedness
on memory for emotional words. International Journal of
mood and anxiety disorders (Aldao et al., 2010;
Psychophysiology, 61, 26–33.
Gross & John, 2003; Kring & Werner, 2004), but it Buhle, J. T., Silvers, J. A., Wager, T. D., Lopez, R., Onyemekwu,
is the result of any number of interactions between C., Kober, H., .
.
.
Ochsner, K. N. (2013). Cognitive
emotion and attention, memory, decision making, reappraisal of emotion: A meta-analysis of human
emotion regulation, or cognitive control processes. neuroimaging studies. Cerebral Cortex, 24.
Burns, A. B., Brown, J. S., Sachs-Ericsson, N., Plant, E. A.,
The heterogeneity of mechanisms that can produce
Curtis, J. T., Fredrickson, B. L., & Joiner, T. E. (2008).
emotion dysregulation may be frustrating for Upward spirals of positive emotion and coping: Replication,
anyone trying to simply understand the causes of extension, and initial exploration of neurochemical substrates.
his or her distress. However, this heterogeneity also Personality and Individual Differences, 44, 360–370.

Cahill, L., Haier, R., Fallon, J., Akire, M., Tang, C., Keator, making. Cerebral Cortex, 17(2), 251–260. doi:10.1093/
D., . . . McGaugh, J. (1996). Amygdala activity at encoding cercor/bhj143
correlated with long-term, free recall of emotional Fredrickson, B. L. (2001). The role of positive emotions in
information. Proceedings of the National Academy of Sciences, positive psychology: The broaden-and-build theory of
93, 8016–8321. positive emotions. American Psychologist, 56, 218–226.
Cahill, L., & McGaugh, J. L. (1995). A novel demonstration of Fredrickson, B. L., & Branigan, C. (2005). Positive emotions
enhanced memory associated with emotional arousal. broaden the scope of attention and thought-action
Consciousness and Cognition, 4, 410–421. repertoires. Cognition and Emotion, 19, 313–332.
Campbell-Sills, L., & Barlow, D. H. (2007). Incorporating Fredrickson, B. L., & Joiner, T. (2002). Positive emotions trigger
emotion regulation into conceptualizations and treatments upward spirals toward emotional well-being. Psychological
of anxiety and mood disorders. In J. J. Gross (Ed.), Handbook Science, 13, 172–175.
of emotion regulation (pp. 542–559). New York, NY: Guilford. Gable, P., & Harmon-Jones, E. (2010). The blues broaden, but
Carver, C. S., & Scheier, M. F. (1981). Absence of regulation, and the nasty narrows. Psychological Science, 21, 211–215.
misregulation. In C. S. Carver & M. F. Scheier (Eds.), Garland, E. L., Fredrickson, B., Kring, A. M., Johnson, D. P.,
Attention and self-regulation: A control-theory approach to Meyer, P. S., & Penn, D. L. (2010). Upward spirals of positive
human behavior (pp. 167–182). New York, NY: Springer. emotions counter downward spirals of negativity: Insights
Chiew, K. S., & Braver, T. S. (2011). Positive affect versus reward: from the broaden-and-build theory and affective neuroscience
Emotional and motivational influences on cognitive control. on the treatment of emotion dysfunctions and deficits in
Frontiers in Psychology, 2, 279. psychopathology. Clinical Psychology Review, 30, 849–864.
Chiew, K. S., & Braver, T. S. (2014). Dissociable influences of Giuliani, N. R., & Gross, J. J. (2009). Reappraisal. In D. Sander
reward motivation and positive emotion on cognitive & K. R. Scherer (Eds.), Oxford companion to the affective
control. Cognitive, Affective, and Behavioral Neuroscience, 14, sciences (pp. 329–330). New York, NY: Oxford University
509–529. Press.
Clore, G. L., & Huntsinger, J. R. (2007). How emotions inform Giuliani, N. R., McRae, K., & Gross, J. J. (2008). The up- and
judgment and regulate thought. Trends in Cognitive Sciences, down-regulation of amusement: Experiential, behavioral,
11(9), 393–399. doi:10.1016/j.tics.2007.08.005 and autonomic consequences. Emotion, 8, 714–719.
Cohen, A. O., Dellarco, D. V., Breiner, K., Helion, C., Heller, Goldin, P. R., McRae, K., Ramel, W., & Gross, J. J. (2008).
A. S., Rahdar, A., . . . Galvan, A. (2016). The impact of The neural bases of emotion regulation: Reappraisal and
emotional states on cognitive control circuitry and function. suppression of negative emotion. Biological Psychiatry, 63,
Journal of Cognitive Neuroscience, 28, 446–459. 577–586.
Cuijpers, P., Van Straten, A., Hollon, S. D., & Andersson, G. Gross, J. J. (1998a). Antecedent- and response-focused emotion
(2010). The contribution of active medication to combined regulation: Divergent consequences for experience, expression,
treatments of psychotherapy and pharmacotherapy for adult and physiology. Journal of Personality and Social Psychology,
depression: A meta-analysis. Acta Psychiatrica Scandinavica, 74, 224–237.
121(6), 415–423. Gross, J. J. (1998b). The emerging field of emotion regulation: An
Denny, B. T., Inhoff, M. C., Zerubavel, N., Davachi, L., & integrative review. Review of General Psychology, 2, 271–299.
Ochsner, K. N. (2015). Getting over it: Long-lasting effects Gross, J. J. (2015). Emotion regulation: Current status and future
of emotion regulation on amygdala response. Psychological prospects. Psychological Inquiry, 26, 1–26.
Science, 26, 1377–1388. Gross, J. J., & John, O. P. (2003). Individual differences in
Derakshan, N., Smyth, S., & Eysenck, M. W. (2009). Effects two emotion regulation processes: implications for affect,
of state anxiety on performance using a task-switching relationships, and well-being. Journal of Personality and Social
paradigm: An investigation of attentional control theory. Psychology, 85, 348–362.
Psychonomic Bulletin and Review, 16, 1112–1117. Gross, J. J., & Thompson, R. A. (2007). Emotion regulation:
Dolcos, F., & McCarthy, G. (2006). Brain systems mediating Conceptual foundations. In J. J. Gross (Ed.), Handbook of
cognitive interference by emotional distraction. Journal of emotion regulation (pp. 3–24). New York, NY: Guilford Press.
Neuroscience, 26, 2072–2079. Habel, U., Windischberger, C., Derntl, B., Robinson, S.,
Dreisbach, G., & Goschke, T. (2004). How positive affect Kryspin-Exner, I., Gur, R. C., & Moser, E. (2007).
modulates cognitive control: Reduced perseveration at the Amygdala activation and facial expressions: Explicit
cost of increased distractibility. Journal of Experimental emotion discrimination versus implicit emotion processing.
Psychology-Learning Memory and Cognition, 30, 343–352. Neuropsychologia, 45, 2369–2377.
Dunn, B. D., Dalgleish, T., & Lawrence, A. D. (2006). The Hajcak, G., & Olvet, D. M. (2008). The persistence of
somatic marker hypothesis: A critical evaluation. Neuroscience attention to emotion: Brain potentials during and after
and Biobehavioral Reviews, 30(2), 239–271. doi:10.1016/j. picture presentation. Emotion, 8, 250–255.
neubiorev.2005.07.001 Hamann, S. (2001). Cognitive and neural mechanisms of
Feeser, M., Prehn, K., Kazzer, P., Mungee, A., & Bajbouj, M. emotional memory. Trends in Cognitive Sciences, 5, 394–400.
(2014). Transcranial direct current stimulation enhances Hayes, S., Hirsch, C., & Mathews, A. (2008). Restriction of
cognitive control during emotion regulation. Brain working memory capacity during worry. Journal of Abnormal
Stimulation, 7, 105–112. Psychology, 117, 712–717.
Fenske, M. J., & Eastwood, J. D. (2003). Modulation of focused Heeren, A., Reese, H. E., McNally, R. J., & Philippot, P. (2012).
attention by faces expressing emotion: Evidence from flanker Attention training toward and away from threat in social
tasks. Emotion, 3, 327–343. phobia: Effects on subjective, behavioral, and physiological
Floresco, S. B., & Ghods-Sharifi, S. (2007). Amygdala- measures of anxiety. Behaviour Research and Therapy, 50,
prefrontal cortical circuitry regulates effort-based decision- 30–39.

Holmes, A. J., & Pizzagalli, D. A. (2007). Task feedback effects Koster, E. H., De Lissnyder, E., Derakshan, N., & De Raedt, R.
on conflict monitoring and executive control: Relationship (2011). Understanding depressive rumination from a cognitive
to subclinical measures of depression. Emotion, 7, 68–76. science perspective: The impaired disengagement hypothesis.
Huang, S.-L., Chang, Y.-C., & Chen, Y.-J. (2011). Task-irrelevant Clinical Psychology Review, 31, 138–145.
angry faces capture attention in visual search while modulated Krebs, R. M., Boehler, C. N., & Woldorff, M. G. (2010). The
by resources. Emotion, 11, 544–552. influence of reward associations on conflict processing in the
Hur, J., Miller, G. A., McDavitt, J. R. B., Spielberg, J. M., Stroop task. Cognition, 117, 341–347.
Crocker, L. D., Infantolino, Z. P., . . . Heller, W. (2015). Kring, A. M., & Werner, K. H. (2004). Emotion regulation and
Interactive effects of trait and state affect on top-down psychopathology. In P. Philippot & R. S. Feldman (Eds.),
control of attention. Social Cognitive and Affective Neuroscience, The regulation of emotion (pp. 359–385). Mahwah, NJ:
10, 1128–1136. Lawrence Erlbaum Associates.
Isen, A. M., & Daubman, K. A. (1984). The influence of affect LaBar, K. S., Gatenby, J. C., Gore, J. C., LeDoux, J. E., &
on categorization. Journal of Personality and Social Psychology, Phelps, E. A. (1998). Human amygdala activation during
47, 1206–1217. conditioned fear acquisition and extinction: A mixed-trial
Isen, A. M., Daubman, K. A., & Nowicki, G. P. (1987). Positive fMRI study. Neuron, 20, 937–945.
affect facilitates creative problem solving. Journal of Lantrip, C., Gunning, F. M., Flashman, L., Roth, R. M., &
Personality and Social Psychology, 52, 1122–1131. Holtzheimer, P. E. (2017). Effects of transcranial magnetic
Isen, A. M., Shalker, T. E., Clark, M., & Karp, L. (1978). Affect, stimulation on the cognitive control of emotion: Potential
accessibility of material in memory, and behavior: A cognitive antidepressant mechanisms. Journal of ECT, 33, 73–80.
loop? Journal of Personality and Social Psychology, 36, 1–12. Lantrip, C., Isquith, P. K., Koven, N. S., Welsh, K., & Roth,
Jackson, D. C., Malmstadt, J. R., Larson, C. L., & Davidson, R. J. R. M. (2016). Executive function and emotion regulation
(2000). Suppression and enhancement of emotional responses strategy use in adolescents. Applied Neuropsychology: Child, 5,
to unpleasant pictures. Psychophysiology, 37, 515–522. 50–55.
Jessen, S., & Grossmann, T. (2015). Neural signatures of conscious Levens, S. M., & Phelps, E. A. (2008). Emotion processing
and unconscious emotional face processing in human infants. effects on interference resolution in working memory.
Cortex, 64, 260–270. Emotion, 8, 267–280.
Jimura, K., Locke, H. S., Braver, T. S., & Smith, E. E. (2010). Locke, H. S., & Braver, T. S. (2008). Motivational influences on
Prefrontal cortex mediation of cognitive enhancement in cognitive control: Behavior, brain activation, and individual
rewarding motivational contexts. Proceedings of the National differences. Cognitive, Affective, and Behavioral Neuroscience,
Academy of Sciences of the United States of America, 107, 8, 99–112.
8871–8876. Loewenstein, G. F., Weber, E. U., Hsee, C. K., & Welch, N.
Joormann, J., & Siemer, M. (2004). Memory accessibility, mood (2001). Risk as feelings. Psychological Bulletin, 127(2), 267.
regulation, and dysphoria: Difficulties in repairing sad mood doi: 10.1037/0033-2909.127.2.267
with happy memories? Journal of Abnormal Psychology, 113, Mansell, W., Harvey, A., Watkins, E. R., & Shafran, R. (2008).
179–188. Cognitive behavioral processes across psychological disorders:
Joormann, J., & Siemer, M. (2011). Affective processing and A review of the utility and validity of the transdiagnostic
emotion regulation in dysphoria and depression: Cognitive approach. International Journal of Cognitive Therapy, 1, 181–191.
biases and deficits in cognitive control. Social and Personality Mather, M., Mitchell, K. J., Raye, C. L., Novak, D. L., Greene,
Psychology Compass, 5, 13–28. E. J., & Johnson, M. K. (2006). Emotional arousal can
Joorman, J., Siemer, M., & Gotlib, I. H. (2007). Mood impair feature binding in working memory. Journal of
regulation in depression: Differential effects of distraction Cognitive Neuroscience, 18, 614–625.
and recall of happy memories on sad mood. Journal of Mauss, I. B., Troy, A. S., & LeBourgeois, M. K. (2012). Poorer
Abnormal Psychology, 116, 484–490. sleep quality is associated with lower emotion-regulation
Kanske, P., Heissler, J., Schönfelder, S., Bongers, A., & Wessa, ability in a laboratory paradigm. Cognition and Emotion, 27,
M. (2011). How to regulate emotion? Neural networks for 567–576.
reappraisal and distraction. Cerebral Cortex, 21, 1379–1388. Mayer, J. D., McCormick, L. J., & Strong, S. E. (1995). Mood-
Kanske, P., & Kotz, S. A. (2011). Emotion triggers executive congruent memory and natural mood: New evidence.
attention: Anterior cingulate cortex and amygdala responses Personality and Social Psychology Bulletin, 21, 736–746.
to emotional words in a conflict task. Human Brain Mapping, McRae, K. (2013). Emotion regulation frequency and success:
32, 198–208. Separating constructs from methods and time scale. Social
Kensinger, E. A., Garoff-Eaton, R. J., & Schacter, D. L. (2007). and Personality Psychology Compass, 7, 289–302.
Effects of emotion on memory specificity: Memory trade- McRae, K., Ciesielski, B., & Gross, J. J. (2012). Unpacking
offs elicited by negative visually arousing stimuli. Journal of cognitive reappraisal: Goals, tactics, and outcomes. Emotion,
Memory and Language, 56, 575–591. 12, 250–255.
Kim, S. H., & Hamann, S. (2007). Neural correlates of positive McRae, K., Gross, J. J., Weber, J., Robertson, E. R., Sokol-
and negative emotion regulation. Journal of Cognitive Hessner, P., Ray, R. D., . . . Ochsner, K. N. (2012). The
Neuroscience, 19, 776–798. development of emotion regulation: An fMRI study of
Kahneman, D., & Tversky, A. (1979). Prospect theory: An cognitive reappraisal in children, adolescents and young
analysis of decision under risk. Econometrica: Journal of the adults. Social Cognitive and Affective Neuroscience, 7, 11–22.
Econometric Society, 263–291. doi: 10.2307/1914185 McRae, K., Hughes, B., Chopra, S., Gabrieli, J. D. E., Gross,
Koster, E. H., Crombez, G., Van Damme, S., Verschuere, B., & J. J., & Ochsner, K. N. (2010). The neural bases of
De Houwer, J. (2004). Does imminent threat capture and distraction and reappraisal. Journal of Cognitive Neuroscience,
hold attention? Emotion, 4, 312–317. 22, 248–262.

McRae, K., Jacobs, S. E., Ray, R. D., John, O. P., & Gross, J. J. Ogawa, T., & Suzuki, N. (2004). On the saliency of negative
(2012). Individual differences in reappraisal ability: Links stimuli: Evidence from attentional blink. Japanese Psychological
to reappraisal frequency, well-being, and cognitive control. Research, 46, 20–30.
Journal of Research in Personality, 46, 2–7. Öhman, A., Flykt, A., & Esteves, F. (2001). Emotion drives
McRae, K., Misra, S., Prasad, A. K., Pereira, S. C., & Gross, J. J. attention: Detecting the snake in the grass. Journal of
(2011). Bottom-up and top-down emotion generation: Experimental Psychology, 130, 466–478.
Implications for emotion regulation. Social Cognitive and Öngür, D., & Price, J. L. (2000). The organization of networks
Affective Neuroscience, 7, 253–262. within the orbital and medial prefrontal cortex of rats,
McRae, K., Rekshan, W., Williams, L. M., Cooper, N., & Gross, monkeys and humans. Cerebral Cortex, 10(3), 206–219. doi:
J. J. (2014). Effects of antidepressant medication on emotion 10.1093/cercor/10.3.206
regulation in depressed patients: An iSPOT-D report. Journal Otto, B., Misra, S., Prasad, A., & McRae, K. (2014). Functional
of Affective Disorders, 159, 127–132. overlap of top-down emotion regulation and generation: An
McRae, K., Rhee, S., Gatt, J., Godinez, D., Williams, L., & fMRI study identifying common neural substrates between
Gross, J. J. (2017). Genetic and environmental influences cognitive reappraisal and cognitively generated emotions.
on emotion regulation: A twin study of cognitive reappraisal Cognitive, Affective, & Behavioral Neuroscience, 14(3), 923–938.
and expressive suppression. Emotion, 17, 772–777. Padmala, S., Bauer, A., & Pessoa, L. (2011). Negative emotion
Miyake, A., & Friedman, N. P. (2012). The nature and impairs conflict-driven executive control. Frontiers in
organization of individual differences in executive functions: Psychology, 2, 192.
Four general conclusions. Current Directions in Psychological Pessoa, L. (2005). To what extent are emotional visual stimuli
Science, 21(1), 8–14. processed without attention and awareness? Current Opinion
Miyake, A., Friedman, N. P., Emerson, M. J., Witzki, A. H., in Neurobiology, 15, 188–196.
Howerter, A., & Wager, T. D. (2000). The unity and diversity Pessoa, L., Padmala, S., & Morland, T. (2005). Fate of unattended
of executive functions and their contributions to complex fearful faces in the amygdala is determined by both
“frontal lobe” tasks: A latent variable analysis. Cognitive attentional resources and cognitive modulation. NeuroImage,
Psychology, 41(1), 49–100. 28, 249–255.
Morawetz, C., Bode, S., Derntl, B., & Heekeren, H. R. (2017). Phelps, E. A. (2004). Human emotion and memory: Interactions
The effect of strategies, goals and stimulus material on the of the amygdala and hippocampal complex. Current Opinion
neural mechanisms of emotion regulation: a meta-analysis in Neurobiology, 14, 198–202.
of fMRI studies. Neuroscience & Biobehavioral Reviews, 72, Potthoff, S., Garnefski, N., Miklósi, M., Ubbiali, A., Domínguez-
111–128. Sánchez, F. J., Martins, E. C., . . . Kraaij, V. (2016). Cognitive
Morris, J., & Dolan, R. (2001). The amygdala and unconscious emotion regulation and psychopathology across cultures: A
fear processing. In B. De Gelder & E. H. F. De Haan (Eds.), comparison between six European countries. Personality and
Out of mind: Varieties of unconscious processes (pp. 185–204). Individual Differences, 98, 218–224.
London, UK: Oxford University Press. Ray, R. D., McRae, K., Ochsner, K. N., & Gross, J. J. (2010).
Nelson, B. D., Fitzgerald, D. A., Klumpp, H., Shankman, S. A., Cognitive reappraisal of negative affect: Converging evidence
& Phan, K. L. (2015). Prefrontal engagement by cognitive from EMG and self-report. Emotion, 10, 587–592.
reappraisal of negative faces. Behavioural Brain Research, 279, Reimann, M., & Bechara, A. (2010). The somatic marker
218–225. framework as a neurological theory of decision-making:
Nolen-Hoeksema, S. (2000). The role of rumination in Review, conceptual comparisons, and future neuroeconomics
depressive disorders and mixed anxiety/depressive symptoms. research. Journal of Economic Psychology, 31(5), 767–776. doi:
Journal of Abnormal Psychology, 109, 504–511. 10.1016/j.joep.2010.03.002
Ochsner, K. N., Bunge, S. A., Gross, J. J., & Gabrieli, J. D. E. Riskind, J. H. (1989). The mediating mechanisms in mood and
(2002). Rethinking feelings: An fMRI study of the cognitive memory: A cognitive-priming formulation. Journal of Social
regulation of emotion. Journal of Cognitive Neuroscience, 14, Behavior and Personality, 4, 173–184.
1215–1229. Rusting, C. L., & DeHart, T. (2000). Retrieving positive
Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of memories to regulate negative mood: Consequences for
emotion. Trends in Cognitive Sciences, 9, 242–249. mood-congruent memory. Journal of Personality and Social
Ochsner, K. N., Ray, R. D., Cooper, J. C., Robertson, E. R., Psychology, 78, 737–752.
Chopra, S., Gabrieli, J. D., & Gross, J. J. (2004). For better Salovey, P., Mayer, J. D., Goldman, S. L., Turvey, C., & Palfai,
or for worse: neural systems supporting the cognitive down- T. P. (1995). Emotional attention, clarity, and repair:
and up-regulation of negative emotion. Neuroimage, 23(2), Exploring emotional intelligence using the Trait Meta-Mood
483–499. Scale. In J. W. Pennebaker (Ed.), Emotion, disclosure, and
Ochsner, K. N., Ray, R. R., Hughes, B., McRae, K., Cooper, health (pp. 125–154). Washington DC: American Psychological
J. C., Weber, J., . . . Gross, J. J. (2009). Bottom-up and t op- Association.
down processes in emotion generation: Common and Savine, A. C., Beck, S. M., Edwards, B. G., Chiew, K. S., &
distinct neural mechanisms. Psychological Science, 20, Braver, T. S. (2010). Enhancement of cognitive control by
1322–1331. approach and avoidance motivational states. Cognition and
Ochsner, K. N., Silvers, J. A., & Buhle, J. T. (2012). Functional Emotion, 24, 338–356.
imaging studies of emotion regulation: A synthetic Schmeichel, B. J., Volokhov, R. N., & Demaree, H. A. (2008).
review and evolving model of the cognitive control of Working memory capacity and the self-regulation of
emotion. Annals of the New York Academy of Sciences, emotional expression and experience. Journal of Personality
1251, E1–E24. and Social Psychology, 95, 1526–1540.

Schuch, S., Zweerings, J., Hirsch, P., & Koch, I. (2017). Conflict not: Emotion, working memory and executive control.
adaptation in positive and negative mood: Applying a Cognition and Emotion, 30, 925–938.
success-failure manipulation. Acta Psychologica, 176, 11–22. Strauss, G. P., & Allen, D. N. (2006). The experience of positive
Schwarz, N., & Clore, G. L. (1983). Mood, misattribution, and emotion is associated with the automatic processing of
judgments of well-being: Informative and directive functions positive emotional words. Journal of Positive Psychology, 1,
of affective states. Journal of Personality and Social Psychology, 150–159.
45(3), 513. doi: 10.1037/0022-3514.45.3.513 Talarico, J. M., Berntsen, D., & Rubin, D. C. (2009). Positive
Schweizer, S., & Dalgleish, T. (2016). The impact of affective emotions enhance recall of peripheral details. Cognition and
contexts on working memory capacity in healthy populations Emotion, 23, 380–398.
and in individuals with PTSD. Emotion, 16, 16–23. Talarico, J. M., & Rubin, D. C. (2003). Confidence, not
Shafir, R., Schwartz, N., Blechert, J., & Sheppes, G. (2015). consistency, characterizes flashbulb memories. Psychological
Emotional intensity influences pre-implementation and Science, 14, 455–461.
implementation of distraction and reappraisal. Social Thiruchselvam, R., Blechert, J., Sheppes, G., Rydstrom, A., &
Cognitive and Affective Neuroscience, 10, 1329–1337. Gross, J. J. (2011). The temporal dynamics of emotion
Sheppes, G., & Gross, J. J. (2011). Is timing everything? Temporal regulation: An EEG study of distraction and reappraisal.
considerations in emotion regulation. Personality and Social Biological Psychology, 87, 84–92.
Psychology Review, 15, 319–331. Thompson, R. A. (1994). Emotion regulation: A theme in search
Sheppes, G., & Meiran, N. (2008). Divergent cognitive costs of definition. Monographs of the Society for Research in Child
for online forms of reappraisal and distraction. Emotion, 8, Development, 59, 25–52.
870–874. Todd, R. M., Cunningham, W. A., Anderson, A. K., &
Shiota, M. N., & Levenson, R. W. (2012). Turn down the Thompson, E. (2012). Affect-biased attention as emotion
volume or change the channel? Emotional effects of detached regulation. Trends in Cognitive Sciences, 16, 365–372.
versus positive reappraisal. Journal of Personality and Social Touryan, S. R., Marian, D. E., & Shimamura, A. P. (2007).
Psychology, 103, 416–429. Effect of negative emotional pictures on associative memory
Shiv, B., Loewenstein, G., Bechara, A., Damasio, H., & for peripheral information. Memory, 15, 154–166.
Damasio, A. R. (2005). Investment behavior and the Troy, A. S., Shallcross, A. J., & Mauss, I. B. (2013). A person-by-
negative side of emotion. Psychological Science, 16(6), situation approach to emotion regulation: Cognitive
435–439. doi: 10.1111/j.0956-7976.2005.01553.x reappraisal can either help or hurt, depending on the context.
Silvers, J. A., McRae, K., Gabrieli, J. D. E., Gross, J. J., Remy, Psychological Science, 24, 2505–2514.
K. A., & Ochsner, K. N. (2012). Age-related differences in Troy, A. S., Wilhelm, F. H., Shallcross, A. J., & Mauss, I. B.
emotional reactivity, regulation, and rejection sensitivity in (2010). Seeing the silver lining: Cognitive reappraisal ability
adolescence. Emotion, 12, 1235–1247. moderates the relationship between stress and depression.
Silvers, J. A., Weber, J., Wager, T. D., & Ochsner, K. N. (2015). Emotion, 10, 783–795.
Bad and worse: Neural systems underlying reappraisal of Tversky, A., & Kahneman, D. (1991). Loss aversion in riskless
high- and low-intensity negative emotions. Social Cognitive choice: A reference—dependent model. The Quarterly
and Affective Neuroscience, 10, 172–179. Journal of Economics, 106(4), 1039–1061. doi: 10.2307/
Silvert, L., Lepsien, J., Fragopanagos, N., Goolsby, B., Kiss, M., 2937956
Taylor, J. G., . . . Nobre, A. C. (2007). Influence of attentional Vuilleumier, P. (2005). How brains beware: Neural mechanisms
demands on the processing of emotional facial expressions in of emotional attention. Trends in Cognitive Sciences, 9,
the amygdala. Neuroimage, 38, 357–366. 585–594.
Slovic, P., Finucane, M. L., Peters, E., & MacGregor, D. G. Wang, Y., & Guo, D. (2008). The effects of positive emotions on
(2004). Risk as analysis and risk as feelings: Some thoughts task switching. Acta Psychologica Sinica, 40, 301–306.
about affect, reason, risk, and rationality. Risk Analysis, 24(2), Waugh, C. E., Zarolia, P., Mauss, I. B., Lumian, D., Ford, B.,
311–322. doi:?10.1111/j.0272-4332.2004.00433 Davis, T., . . .
McRae, K. (2016). Emotion regulation
Slovic, P., & Peters, E. (2006). Risk perception and affect. changes the duration of the BOLD response to emotional
Current Directions in Psychological Science, 15(6), 322–325. stimuli. Social Cognitive and Affective Neuroscience, 11,
doi: 10.1111/j.1467-8721.2006.00461.x 1550–1559.
Song, H., & Schwarz, N. (2009). If it’s difficult to pronounce, Webb, T. L., Miles, E., & Sheeran, P. (2012). Dealing with
it must be risky fluency, familiarity, and risk perception. feeling: A meta-analysis of the effectiveness of strategies
Psychological Science, 20(2), 135–138. doi: 10.1111/j.1467-9280. derived from the process model of emotion regulation.
2009.02267.x Psychological Bulletin, 138, 775–808.
Smits, J. A. J., Julian, K., Rosenfield, D., & Powers, M. B. Whalen, P. J., Kagan, J., Cook, R. G., Davis, F. C., Kim, H.,
(2012). Threat reappraisal as a mediator of symptom change Polis, S., . . . Johnstone, T. (2004). Human amygdala
in cognitive-behavioral treatment of anxiety disorders: responsivity to masked fearful eye whites. Science,
A systematic review. Journal of Consulting and Clinical 306, 2061.
Psychology, 80, 624–635. Winston, J. S., O'Doherty, J., & Dolan, R. J. (2003).
Snyder, H. R. (2013). Major depressive disorder is associated Common and distinct neural responses during direct and
with broad impairments on neuropsychological measures of incidental processing of multiple facial emotions.
executive function: A meta-analysis and review. Psychological NeuroImage, 20, 84–97.
Bulletin, 139, 81–132. Xie, W., & Zhang, W. (2016). Negative emotion boosts quality
Storbeck, J., & Maswood, R. (2016). Happiness increases verbal of visual working memory representation. Emotion, 16,
and spatial working memory capacity where sadness does 760–774.

Yiend, J. (2010). The effects of emotion on attention: A review of Zeng, Q., Qi, S., Li, M., Yao, S., Ding, C., & Yang, D. (2017).
attentional processing of emotional information. Cognition Enhanced conflict-driven cognitive control by emotional
and Emotion, 24, 3–47. arousal, not by valence. Cognition and Emotion, 31,
Young, E. A., & Nolen-Hoeksema, S. (2001). Effects of 1083–1096.
ruminations on the saliva cortisol response to a social stressor. Zhou, J., Gao, T., Zhang, Y., Liang, J., Shui, R., & Shen, M.
Psychoneuroendocrinology, 26, 319–329. (2011). Losing control in front of a fearful face: the
Zald, D. H. (2003). The human amygdala and the emotional effect of emotional information on cognitive control.
evaluation of sensory stimuli. Brain Research Reviews, 41(1), Quarterly Journal of Experimental Psychology, 64(6),
88–123. doi: 10.1016/S0165-0173(02)00248-5 1187–1199.

CH A PT E R
What Emotion Dysregulation
5 Looks Like
Inferences from Behavioral Observations
K. Ashana Ramsook, Pamela M. Cole, and Margaret A. Fields-Olivieri
Abstract
Recent conceptualizations of emotion dysregulation define it as a process that unfolds over multiple
time scales and that leads to short- or long-term impairments. This chapter discusses the advantages
of observational methods for measuring emotion dysregulation as a process, focusing on three
patterns and associated evidence of them from observational studies. First, the chapter discusses
context-inappropriate emotion, the absence of an expected emotional reaction or an atypical reaction
for the situational context. Second, it discusses atypical emotion dynamics, specifically emotional
expressions that change abruptly, including but not limited to emotional lability. Third, it discusses
ways in which emotions endure and are difficult to modify, pointing to ineffective strategy use as a
mechanism. It concludes by discussing new directions for observational research, including creative
study design and analytic methods that can capture emotion dysregulation.
Keywords: emotions, emotion dysregulation, observational methods, behavioral observations,

context-inappropriate emotion, atypical emotion dynamics, emotional lability, observational research,
emotional behavior
Introduction In recent years, a vast amount of research has

Mental health professionals—including both scien- emerged on emotion dysregulation as a possible
tists and practitioners—often use the term “emo- mechanism in psychiatric disorders (e.g., Aldao,
tion dysregulation” to refer to emotional behavior Nolen-Hoeksema, & Schweizer, 2010; Joormann
that appears to compromise individuals’ adaptive & Gotlib, 2010; Kring & Moran, 2008; Mennin,
function (Beauchaine, 2015; Thompson, 1990; Heimberg, Turk, & Fresco, 2002). In fact, emotion
Chapter 8, this volume). This may include emo- dysregulation has been offered as an explanation for
tional reactions that are unusual in or insensitive to symptoms such as affective lability, mania, blunted
the context in which they occur. For example, an affect, prolonged irritability, callousness, and other
adolescent might unemotionally describe witness- symptoms involving emotions (e.g., Blair, 2010;
ing his father’s violent attack on his mother, or a McMillan, Williams, & Bryant, 2003; Reich,
child may be frightened by a birthday party game Zanarini, & Fitzmaurice, 2012). Emotion dysregu-
that other children enjoy. Other examples include lation is so pervasive among mental health problems
unpredictable emotional changes (i.e., lability), that emotion-related constructs were included in
such as a parent laughing about a child’s misbehav- the National Institute of Mental Health Research
ior in one moment and then exhibiting hostility Domain Criteria (RDoC; Fernandez, Jazaieri, &
toward the child the next moment. Emotional reac- Gross, 2016; Insel et al., 2010). RDoC is a transdi-
tions may also endure despite one’s coping efforts. agnostic framework intended, among other diverse
These and other observations fuel intense interest in objectives, to guide and advance mental health re-
emotion regulation and dysregulation. search by focusing on how functional psychological
53
processes, such as those involved in healthy emo- functional perspective on emotional development
tional functions, deviate from normal and become (K. C. Barrett & Campos, 1987; Campos, Mumme,
dysfunctional. The RDoC matrix comprises five Kermoian, & Campos, 1994), as well as dynamic
domains, including positive, negative, cognitive, systems principles (Fogel et al., 1992; M. D. Lewis
social, and arousal/regulatory systems—which col- & Granic, 2002). According to these perspectives,
lectively capture aspects of emotional functioning emotions are relational, dynamic, and continuous
involving threat, frustration, loss, reward, and affili- psychological processes rather than events. These
ation. Taken together, clinical observations, clinical perspectives inform how we approach the concept
research, and the efforts such as RDoC underscore of emotion regulation and how we distinguish regu-
the need to understand the role of emotion in im- latory patterns that are normal and effective from
paired psychological function. The study of emo- those that are atypical and dysfunctional.
tion dysregulation is one approach to understand- The functionalist perspective views emotions as
ing the nature and development of these problems relational processes. That is, emotions are defined
and ultimately treating or preventing them (e.g., by how we relate to situations, both actual and per-
Beauchaine & Zisner, 2017). ceived, as they bear on our short- and long-term
In this chapter, we discuss how observations of goals for well-being (K. C. Barrett & Campos, 1987;
emotional behavior can be translated into meaning- Campos et al., 1994). In this view, emotions are not
ful research on emotion dysregulation. We offer discrete events; they are not things. Rather, emo-
definitions of emotion, emotion regulation, and tions are continuous, interactive processes through
emotion dysregulation, acknowledging the lack of which we relate to changing environments in ways
consensus, and exploring whether emotion regula- that promote our own well-being, while simultane-
tion can be differentiated from emotion. We then ously preparing us to act to achieve those goals (see
illustrate three clinical patterns of emotion dysregu- Cole, 2016 for further discussion). What we inter-
lation that can be studied using behavioral observa- pret as a discrete emotion—a feeling or an emo-
tions (Cole, Hall, & Hajal, 2017). Next, we review tional expression—is the product of (1) continuous
available evidence for these patterns, discuss limita- appraisal of the significance of ongoing circum-
tions of existing research, and suggest future direc- stances for well-being and (2) continuous changes
tions that can contribute to meaningful observa- in readiness to act in particular ways (e.g., approach
tional research on emotion dysregulation. with force, yield, escape) to regain, preserve, attain,
or maintain our goals (Arnold, 1960; Frijda, 1986).
Theoretical Perspectives and Definitions This informs how we conceptualize emotion dys-
Defining emotion dysregulation offers several chal- regulation.
lenges. For example, there is no consensus regarding Prior to the 1980s, the term “emotion dysregula-
whether humans are biologically prepared to experi- tion” appeared only sporadically in empirical papers
ence and express a core set of universal emotions, in psychology. During a resurgence of scientific in-
whether emotions are constructions of our percep- terest in emotion in the 1980s, the term appeared in
tions and interpretations of physiological arousal, or titles of a special issue of Developmental Psychology
both (see, e.g., Tracy & Randles, 2011). Discrete (Dodge, 1989) and an edited volume (Dodge &
emotion theories posit that emotions such as joy, Garber, 1991). These publications did not define
anger, fear, sadness, and disgust are biologically pre- emotion dysregulation but used the term to imply
pared and observed across cultures and even species dysfunctional patterns of emotion regulation. The
(Ekman, 1992; Izard, 2007; Tomkins, 1962, 1963; emphasis on regulation is important. It acknowl-
Panksepp, 1992, 2017; Sauter, Eisner, Ekman, & edges that emotions are never out of control; what
Scott, 2010; Chapter 2, this volume). In contrast, appears out of control to the average person is a pat-
according to core affect theory, humans’ physiologi- tern of emotion that is problematic by some crite-
cal experiences vary in valence and arousal, and our rion (Cole, Michel, & Teti, 1994). Even sustained or
interpretations of these experiences yield cognitive intense emotion is not inherently dysfunctional;
constructions that we experience as emotion over millennia, the capacity for strong, enduring
(L. F. Barrett, 2011; James, 1884; Russell, 2003; emotions has been conserved because this capacity
Widen & Russell, 2008). enables us to protect and achieve our goals for well-
We see value in understanding both the funda- being, helping us communicate our needs and act
mental function of emotion and different functions on our own behalves (Cole, 2016; Cole, Martin, &
of discrete emotions. To this end, we draw from the Dennis, 2004).
54 What Emotion Dysregul ation Looks Like

As outlined earlier, the functionalist perspective e xpression that interfere with a person’s immediate
defines emotions as continuous processes. Application (e.g., problem solving or a social interaction) or
of dynamic systems theory to emotion provides a way long-term developmental goals (e.g., socioemo-
to conceptualize and study these processes. Both ap- tional competence or mental health). We emphasize
proaches view emotions as dynamic, inherently regu- that certain patterns of emotion regulation can be
latory processes (Campos et al., 2004; Hollenstein & both functional and dysfunctional, depending on
Lanteigne, in press; Witherington & Crichton, 2007). context (Cole et al., 1994). Consider dissociation,
Notably, however, if emotion is conceptualized as the experience of psychological disconnection from
self-organizing, it may not be possible to differentiate ongoing circumstances, which often occurs among
emotion regulation from emotion (Campos et al., young children who experience incest (Cole &
2004; Hollenstein & Lanteigne, in press). Dynamic Putnam, 1992). In the immediate situation, disso-
systems theory draws on evidence from diverse human ciation protects these children from overwhelming,
biological functions, such as motor development and confusing circumstances and associated physiologi-
self-organization of the nervous system (e.g., Kelso, cal stress. It is protective for young children who
1994; Ochsner et al., 2009; Thelen, 2002). often have few alternatives for preventing or ending
Behavioral observations, however, involve a dif- the abuse. However, for some survivors, dissociation
ferent level of analysis, as intrinsic biological dy- becomes a routine regulatory process that is dys-
namics are not observable. Observational studies functional. Overreliance on dissociation interferes
often conceptualize emotion regulation as applica- with coping and may lead to interpersonal problems
tion of intra- and interpersonal strategies to shape and relationship failures in the long term. Thus,
and constrain emotional experience and expression spontaneous cognitive processes that interrupt emo-
(e.g., Sheppes et al., 2014). This conceptualization tional experience can be adaptive in reducing psy-
entails regulatory influences that are not defined by chological and physiological stress, but establish a
emotion and yet have the capacity to regulate emo- pattern of emotion dysregulation when it later in-
tion. In fact, to infer emotion dysregulation from terferes with healthy functioning. It is thus critical
observations, the distinction between regulatory in- to understand emotion regulation across multiple
fluences (e.g., strategies) and emotions is necessary. time scales (Cole & Hollenstein, 2018; Granic,
To integrate these viewpoints and levels of analy- 2005), to understand how moment-to-moment be-
sis, we conceptualize emotion regulation as a change haviors and expressions, which may serve immedi-
in a changing process (Cole et al., 2004). We appre- ate goals, become repeated experiences that develop
ciate the dynamic, continuous, changing physical into maladaptive, dysregulated patterns.
nature of emotions as we encounter and navigate the
ever-changing circumstances of life. We assert that Inferring Emotion Dysregulation
one form of emotion regulation, sometimes referred Through Observation
to as top-down regulation, involves recruitment of Why focus on behavioral observations when there
one set of processes—executive processes—that are less time-consuming ways, such as self-report, to
can modulate intrinsic dynamics of self-organizing conduct emotion dysregulation research? Our view
emotion systems (e.g., Beauchaine & Zisner, 2017). of emotion dysregulation as a dysfunctional dy-
We find this approach to be not only essential for namic pattern unfolding on quick time scales in
use of behavioral observations but also clinically situational context necessitates behavioral observa-
useful as interventions often rely on teaching indi- tions (Cole et al., 1994; Cole et al., 2004). Other
viduals strategies to modulate emotional experience. methods have advantages but are limited in captur-
In this chapter, we focus on observations of patterns ing emotion dysregulation as a set of processes. In
of emotion that are atypical and often dysfunc- addition, behavioral observations provide an alter-
tional, and involve the absence of or ineffective use native when participants are unable to report or
of strategies to alter the intrinsic dynamics of emo- have difficulty reporting accurately on their emo-
tions. Specifically, observed emotion dysregulation tional experiences and strategy use. In this section,
can be conceptualized and measured in terms of we discuss advantages of behavioral observations
atypical intrinsic emotion dynamics, which may and describe three patterns of dysregulation that we
often involve ineffective strategic efforts to modu- observe clinically.
late emotion dynamics. Self-reports of emotional experience, reports
As outlined earlier, emotion dysregulation in- from others close to an individual, and perceptions
volves patterns of emotional experience and/or of professional observers are primary methods
Ramsook, Cole, and Fields-Olivieri 55

through which we evaluate and study emotion (dys) of internal states (see Durbin, 2010; A. R. Lewis,
regulation (Aldao et al., 2010; Cole et al., 2004; Zinbarg, & Durbin, 2010; Zeman, Klimes-Dougan,
Rothbart & Bates, 2006). Often, we administer Cassano, & Adrian, 2007). Although we include
questionnaires to one or more informants (e.g., par- parent and/or teacher reports, these adults may not
ents, teachers). Advantages of this method include always observe more subtle aspects of children’s
its convenience in terms of cost and time, the fact emotion regulation. Indeed, young children may
that informants often have extensive experience engage in self-regulation more readily when caregiv-
with the client, and, in the case of self-reports, the ers are not present. For example, in our research on
access yielded to subjective experiences. Commonly young children’s masking of disappointment (e.g.,
used questionnaires for studying emotion dysregu- Cole et al., 1994), parents often express concern
lation in children are the Emotion Regulation about how their children behave and are surprised
Checklist (Shields & Cicchetti, 1997) and the to learn that typically developing children manage
Emotion Management Scales (Zeman & Garber, to smile when a research assistant gives them a
1996; Zeman, Cassano, Suveg, & Shipman, 2010). “prize” that they clearly do not want. Moreover, in
For adults, the Difficulties with Emotion Regulation some risk conditions, there is heightened likelihood
Scale (Gratz & Roemer, 2004) is most commonly of bias in adult reports (e.g., Boyle & Pickles, 1997;
used, and other instruments include the Toronto Chilcoat & Breslau, 1997; Najman et al., 2001);
Alexithymia Scale (Bagby, Parker, & Taylor, 1994), parents with their own psychological problems may
the Affective Control Scale (Williams, Chambless, be overly negative or minimize regulatory behaviors
& Ahrens, 1997), and the Affect Regulation and of their children. Thus, observations are essential
Experiences Questionnaire (Westen, Muderrisoglu, when studying emotion dysregulation dynamics,
Fowler, Shedler, & Koren, 1997). especially in children.
Questionnaires and rating scales focus on trait- In sum, if we conceptualize emotion dysregula-
like characteristics of the individual but are limited tion as a set of dynamic, moment-to-moment pro-
in detecting changes in emotion dysregulation processes, we cannot capture it through static ap-
cesses in context (Diaz & Eisenberg, 2015). proaches that summarize perceptions of behavior.
Conceptualizing emotion dysregulation in terms of In contrast, we can use behavioral observations to
fast time scale changes situated in the ecology of a infer regulatory processes, to discriminate regula-
person’s circumstances requires a less static approach. tory attempts that occur on a moment-to-moment
Experience sampling methods (Csikszentmihalyi & basis, to link these to evidence of current or subse-
Larson, 2014), such as daily diaries and ecological quent impairments in psychological functioning,
momentary assessment (Stone & Shiffman, 1994), and, ultimately, to investigate heterogeneity of pat-
can evaluate emotion dysregulation in situational terns that characterize normative and pathological
context. They too are self-report methods, but carry functioning (Aldao & Nolen-Hoeksema, 2010;
the advantage of situating self-report in both time Cole et al., 1994). By studying emotion dysregula-
and circumstance, often repeated over hours or days. tion as a set of processes, we can conduct observa-
They permit temporal analyses, including anteced- tions that are clinically relevant, a crucial step for
ent conditions of emotional reactions, sequences of full understanding of the development of psychopa-
emotions and strategies, and their consequences. thology, and for using evidence to improve the
However, they also share some limitations of self- design of preventive or therapeutic interventions
reports. In particular, some participants are not able (Wakschlag et al., 2005). We illustrate three pat-
to report on their experiences, such as young chil- terns of observable behavior indicative of emotion
dren and individuals with conditions that impair dysregulation (Cole, Hall, & Hajal, 2017):
their self-report ability or accuracy (Denham, Wyatt,
1. Emotions that are context inappropriate
Bassett, Echeverria, & Knox, 2009).
2. Emotions that change too abruptly
Our interest in children’s emotion regulation,
3. Emotions that endure because strategies are
and how it deviates from normal development and
ineffective
contributes to emerging psychopathology, moti-
vates our use of behavioral observations. Such ob- In the next section, we provide illustrations of
servations are critical because of the limitations of these patterns and highlight observational evidence
accurate self-report with young children, who are for each. As we show, there is a dearth of rich obser-
developing other crucial cognitive and emotional vational studies of emotion dysregulation. Therefore,
capacities that facilitate awareness and description after our review, we provide an additional section

discussing future directions that can enrich our ability 2003). Preschool- and school-age children from
to understand the nature and development of emo- families in which a parent is abusive or has depres-
tion dysregulation using observational methods. sion also display positive emotion, in addition to
hostility, while observing simulated angry conflicts
Emotions That Are Context Inappropriate between two adults (Maughan & Cicchetti, 2002;
Maria, a 13-year-old, was admitted to a psychiatric Maughan, Cicchetti, Toth, & Rogosch, 2007).
unit by her adoptive parents because they could not con- Context-inappropriate positive emotion in response
trol her defiance, truancy, and running away. Although to neutral or negative stimuli is also observed in
they were concerned about her well-being, they stated adults and differentiates those with bipolar disorder
they could no longer care for her and had begun pro- from healthy controls (Gruber, 2011). Thus, expres-
ceedings to relinquish custody. In group therapy sessions, sions of joy or happiness, although generally re-
individual therapy sessions, and interactions with nurs- garded as healthy, are associated with externalizing
ing staff, Maria laughed and dismissed staff attempts to behaviors when present in situations that normally
help her deal with her situation. Her emotions, al- elicit negative or neutral emotions.
though on the one hand positive, interfered not only There is less research on context-inappropriate
with her therapy but also with progress of other youth in negative emotion, but the available evidence links it
the group. After eight weeks of intensive inpatient inter- with anxiety. In novel and uncertain situations,
vention, Maria succumbed to deep depression. She ex- most toddlers display some degree of hesitation or
pressed hopelessness that any parent could love her. She fear, but children who are especially fearful are at
also came to understand that her laughing and joking greater risk for developing social anxiety disorders
masked her painful sadness. Slowly, she came to terms (Schwartz, Snidman, & Kagan, 1999). Moreover,
with her circumstances and began to manage her sad- toddlers who are fearful in novel but low-threat sit-
ness and cope with her situation. uations that most toddlers enjoy (e.g., a puppet
Maria’s presentation of positive emotion in the show) show more symptoms of social anxiety and
context of staff efforts to help her deal with the re- more wariness in social interactions by the time
alities of her situation was not consistent with the they reach kindergarten (Buss et al., 2013). Thus,
seriousness of her circumstances. Laughing and context-inappropriate fear is a risk factor for devel-
joking served to avoid the overwhelming sadness opment of anxiety symptoms (Buss, 2011). Although
of her impending loss and its meaning. Maria’s fear is a desirable response to circumstances that
context-inappropriate emotional presentation is but may pose a threat to well-being, displaying fearful
one way that emotional reactions may deviate from behavior in low-threat situations is context inappro-
normative responses. Moreover, context-inappropriate priate and predicts development of later impair-
emotions often impair a person’s interpersonal ment.
function or problem solving. Another form of context-inappropriate emotion
Evidence that context-inappropriate positive is the absence of typical or expected emotional re-
emotion represents one form of emotion dysregula- sponses. In fact, access to a full range of emotions is
tion comes from studies linking it to a variety of a hallmark of emotional competence and mental
childhood problems. For example, some children health (e.g., Saarni, 1999). Kindergartners with ex-
(ages 4 to 14 years) express happiness while viewing ternalizing behavior problems display less fear and
fear-eliciting film clips, whereas most children dis- sadness in response to parental anger, but similar
play fear. Children who express happiness are rated levels of anger, relative to nonproblem children
by their parents as callous and unemotional (Dadds (Stoolmiller & Snyder, 2006). Moreover, exposure
et al., 2016). Context-inappropriate positive emo- to certain forms of anger or maltreatment can lead
tion is also observed in dyadic interactions between to the absence or blunting of emotional responding
mothers and preschoolers who exhibit externalizing in situations that typically elicit strong emotion.
behavior problems (Cole, Teti, & Zahn-Waxler, Some four- to six-year-olds who are exposed to mal-
2003; Lunkenheimer, Kemp, Lucas-Thompson, treatment, domestic violence, or maternal depres-
Cole, & Albrecht, 2017). In one of these studies, sion do not appear distressed during anger simula-
analysis of parent–child and child–parent contin- tions, as typically developing children do, which is
gent emotions reveals that, in dyads with clinically interpreted as emotional overcontrol (Cummings,
elevated externalizing symptoms, both partners 1987; Maughan & Cicchetti, 2002; Maughan et al.,
express positive emotion when the other is angry, 2007). This pattern also extends to positive emotion
often laughing at the partner’s anger (Cole et al., expression. In parent-child interactions, one- to

four-year-olds who experienced maltreatment dis- ages 24 and 36 months (Cole et al., 2011). Thus,
played less intense positive affect than their peers short latency to react emotionally may indicate
who were not maltreated (Robinson et al., 2009). emotion dysregulation.
In sum, there is observational evidence that Emotional lability, defined by quick rise time to
context-inappropriate emotion is a form of emotion peak intensity and frequent changes in emotion
dysregulation. This evidence links indicators of psy- types, may be a more sensitive index of emotion
chopathology with either context-inappropriate dysregulation than simple latency. Indeed, emo-
positive emotion or a lack of observable emotion. tional lability is one of the two scales of the oft-used
Very few studies address context-inappropriate neg- Emotion Regulation Checklist (Shields & Cicchetti,
ative emotion. Context-inappropriate emotion can 1997). Using experience sampling methods, greater
also reflect an effort to control or avoid emotions, as reports of emotional lability are related to elevated
with Maria’s avoidance of sadness. symptoms of depression in adolescents (Silk,
Steinberg, & Morris, 2003) and higher levels of be-
Emotions That Change Too Abruptly havior problems in children with attention-deficit/
Mateo, a 15-year-old boy, is on a psychiatric inpatient hyperactivity disorder (Rosen, Walerius, Fogleman,
unit because of an overdose of an over-the-counter & Factor, 2015). Individuals with borderline per-
medication. He has been working with the staff to earn sonality disorder, relative to healthy controls, also
a weekend pass. He appears happy at the outset of a report more emotion changes while passively view-
family session where he will tell his parents that he has ing emotion-eliciting video clips (Schoenleber et al.,
earned the pass. However, without warning, he be- 2016).
comes very angry, cursing at his father, surprising his We could not find observational studies of intra-
parents and therapist. He is inexplicably enraged and personal emotional lability, although emotional la-
efforts to calm him do not help. The nursing staff come bility is attributed to children with disorders such as
and escort Mateo to an isolation room where he is autism spectrum disorder (Ashburner, Ziviani, &
asked to reflect on his behavior. He starts laughing, but Rodger, 2010; Scarpa & Reyes, 2011) and attention-
staff insist he remain in the isolation room and prepare deficit/hyperactivity disorder (Biederman et al.,
to discuss his behavior calmly. When the nurse comes to 2012; Surman et al., 2011). However, several observa-
process events with him, he is at first pleasant and tional studies capture emotional lability in interper-
polite but suddenly becomes enraged again. sonal contexts. For example, during a challenging
Mateo’s anger is intense but it also occurs ab- construction task between preschool-aged children
ruptly and without staff or his parents being able to and their mothers, children in dyads that exhibit
predict his outbursts. Therefore, it is difficult for more frequent, unpredictable emotional shifts have
adults to find ways to help him understand his feel- higher levels of mother-rated externalizing problems
ings and manage his reactions to make them less by kindergarten (Lunkenheimer, Olson, Hollenstein,
abrupt. Thompson (1990, 1994) suggests that tem- Sameroff, & Winter, 2011). Dyads with aggressive
poral dynamics of emotion expressions—latency, preschoolers also show more transitions between es-
duration, rise time to peak intensity, and recovery calating and de-escalating aversive behaviors during
from peak intensity—index emotion regulation. a conflict (Snyder, Edwards, McGraw, Kilgore, &
These may also serve as observable indices of dys- Holton, 1994). Greater emotional lability, defined
regulation. Indeed, latency to the onset of an emo- by wider range of emotions and less predictable
tion and rise time to peak intensity may distinguish emotions, is also observed during planning and
individuals with and without symptoms of various problem-solving interactions of parents and their
forms of psychopathology. Kindergarteners with be- depressed adolescent relative to nondepressed adoles-
havior problems are quicker to express anger com- cents (Hollenstein, Allen, & Sheeber, 2016). In addi-
pared to kindergarteners without behavior prob- tion, mothers and self-injuring adolescents are more
lems (Stoolmiller & Snyder, 2006, 2013). Moreover, likely to escalate conflicts, as measured by the inten-
one-year-olds who are quicker to express anger in sity of their moment-to-moment aversive behaviors
challenging situations have more serious behavior (Crowell et al., 2013). Emotional lability is also as-
problems by age five than one-year-olds who anger sociated with callous-unemotional characteristics.
more slowly (Halligan et al., 2013). Longitudinally, Across three observations of parents and their ado-
typically developing children become increasingly lescents, adolescents rated as higher in callous-
slower to express anger in frustrating situations be- unemotional traits displayed more within-person
tween ages 18 and 48 months, particularly between variability in anger or irritability compared to

adolescents without callous-unemotional traits Enduring emotions have been studied in several
(O’Connor, Humayun, Briskman, & Scott, 2016). ways. Perhaps most well documented is the observa-
These quasi-naturalistic observational procedures tion that emotions endure longer in at-risk and
are designed to mimic typical situations in families’ clinical populations. This pattern of longer dura-
lives, strengthening their ecological validity. Moreover, tions of negative emotion has been documented in
the paradigms and analyses used in this dyadic re- young children who were maltreated or whose
search could easily be applied to the study of emo- mothers are depressed (Cummings, 1987; Maughan
tions or behaviors within an individual (Hollenstein, & Cicchetti, 2002; Maughan et al., 2007), pre-
2007). schoolers with elevated externalizing and internal-
In sum, emotions that change too abruptly make izing symptoms (Cole et al., 1994), and 4- to
up another relevant pattern of emotion dysregula- 12-year-olds admitted to psychiatric hospitals
tion. Several studies document links between be- (Potegal, Carlson, Margulies, Gutkovitch, & Wall,
havioral impairment and shorter than typical onset 2009; Potegal & Davidson, 2003). More advanced
of emotional expression—particularly anger. Less is analytic approaches reveal more nuance to this dys-
known about temporal factors related to other dis- regulated pattern in observational work, capturing
crete emotional displays (e.g., latency to exhibiting not just one temporal indicator, but overall patterns
happiness, sadness, or fear). In addition, an exten- across tasks that suggest enduring emotions. For
sive literature documents the importance of emo- example, preschool-age girls with hostile mothers
tional lability to various forms of psychopathology. show increasingly longer duration of negative emo-
Although this work has focused largely on self-reports tion as their negative emotions accumulate (Dagne
of emotion in adults, observations with parent–child & Snyder, 2011). Thus, not only can children’s emo-
dyads provide support for this pattern being linked tions endure longer than expected, but also accu-
to child psychopathology as well, and offer the ad- mulation of these emotions can lead to even longer
vantage of measuring lability in an ecologically valid durations as observations progress. Moreover, emo-
context. This work can be extended to examine tional rigidity—the tendency to “get stuck” in emo-
emotional lability in other social contexts or when tional states—is a hallmark of psychopathology
an individual is alone. (Cole, 2016). It is observed in parent–child dyads in
which children have internalizing and externalizing
Emotions That Endure Because problems (Coburn, Crnic, & Ross, 2015;
Strategies Are Ineffective Hollenstein, Granic, Stoolmiller, & Snyder, 2004).
Lena, a nine-year-old girl, is invited to a friend’s birth- In dyadic observations, emotional rigidity is charac-
day party. However, Lena suffers from social anxiety. terized by a limited range of emotional states, infre-
Lena is a polite, cooperative child and when her par- quent transitions between states, and long durations
ents reason with her she nods and agrees—she will within states (Hollenstein et al., 2004). Although it
enjoy the party. She also does breathing exercises they has not been studied in an intrapersonal context,
encourage. Lena decides to go to the party. However, methods used to study emotional rigidity could
with each step she takes, her anxiety builds. She starts easily be applied in this way (Hollenstein, 2007).
perspiring and says she cannot go. Her parents continue What these studies do not tell us is why emo-
to coach her, and she cooperates with their suggested tional responses endure or resist change. There may
strategies, but she is overwhelmed and begins to cry. be a number of reasons, but in many studies of
Lena misses the party. adolescent and adult emotion regulation the focus is
Lena’s anxiety is not lessened or resolved by rea- on strategy use, that is, engagement of strategies
sonable strategies her parents offer. She tries their that should modulate emotion (e.g., Aldao et al.,
suggestions but the anxiety increases. Their sugges- 2010; Gross & Thompson, 2007). In Gross’s model
tions involve commonly prescribed strategies, such (1998), for example, there are particular times when
as countering negative thoughts and breathing more different strategies to modulate emotions can be en-
deeply. Yet, when she does these things, her at- gaged and certain strategies should be more effective
tempts seem to exacerbate her anxiety. Emotions than others. Reappraisal and distraction are consid-
that resist change, or do not easily resolve, also indi- ered to be the most effective strategies—a claim
cate dysregulation, particularly when they interfere supported by studies using experimental paradigms
with an individual’s functioning and well-being. in which participants are instructed to use particular
Lena’s example points out that strategies, even those strategies while they view emotion-eliciting images
that should work, are not always effective. (Augustine & Hemenover, 2009). This method is

limited, however, as it does not evaluate spontane- Synthesis and Future Directions
ous strategy use and images may lack personal rele- Emotional symptoms are common in many forms
vance/ecological validity vis-à-vis everyday experience. of psychopathology, and emotion dysregulation
When using behavioral observations to infer may be a central mechanism in their development
emotion regulation in young children, a few stud- and maintenance (e.g., Aldao et al., 2010). There is
ies assess spontaneous strategy use and emotion no commonly accepted definition of emotion dys-
expression (e.g., Calkins, Gill, Johnson, & Smith, regulation; however, there is growing consensus that
1999; Cole et al., 2011; Gilliom, Shaw, Beck, emotion dysregulation should be conceptualized as
Schonberg, & Lukon, 2002, Stansbury & Sigman, a process. The functional perspective on emotional
2000). Measuring both observed emotions and development informs our definition of emotion
strategy use enables assessment of the degree to regulation and dysregulation as a set of psychologi-
which strategies successfully regulate emotions cal and physiological processes through which one
(Cole et al., 2004), although few studies actually relates to the environment, and dynamic systems
test direct effects of strategies on emotion change. principles inform how one set of processes (e.g.,
However, some evidence suggests that emotions strategy use) influences emotion dynamics. From
endure when strategies are ineffective. At-risk pre- this perspective, emotion regulation unfolds over the
school boys use strategies that should enhance course of situations (moment-to-moment changes),
frustration tolerance—specifically, distracting one- and changes with age (longer time scale) (Cole &
self with an activity or passively waiting. However, Hollenstein, 2018; Granic, 2005). We regard emo-
although these strategies are expected to minimize tion dysregulation as those patterns of emotion reg-
frustration, their use is not associated with less anger ulation that compromise an individual’s short- or
(Gilliom et al., 2002). The method used did not long-term developmental goals, even if they serve
reveal whether there were momentary decreases in some useful immediate function.
anger after those boys’ strategy use; however, an- We illustrated three examples of emotion
other study used advanced modeling of time-series dysregulation—context-inappropriate emotion, ab-
data to examine temporal dynamics in the same ruptly changing emotion, and enduring emotion
type of waiting task ( Cole, Bendezú, Ram, & that is not responsive to strategy attempts—that we
Chow, 2017). For children described by their moth- observe clinically and can study using observational
ers as higher in temperamental negative affectivity, methods. For each pattern, there is research sup-
strategy use amplified their desire for the restricted port, however limited. As we will discuss, there are
item and frustration about waiting. Thus, although innovative observational approaches that will enrich
these children used putative regulatory strategies, our understanding of these and other patterns of
their strategies exacerbated their difficulty tolerating emotion dysregulation. These involve new features
the wait. There are similar patterns observed in of design and analysis. First, we discuss the need to
adults with bipolar disorder (Gruber, Harvey, & consider the length and number of observations
Gross, 2012). Although these individuals report en- required to observe patterns of emotion dysregula-
gaging in appropriate spontaneous strategy use after tion, including the length of a single observation
watching emotional video clips, observations reveal and the use of multiple observational periods across
that reported strategies are less effective at reducing development. Next, we describe task considerations
their emotional responses. that can strengthen inferences drawn from observa-
In sum, prolonged emotions are observed in at- tions, including careful consideration of task con-
risk and clinical populations. Conceptual models of texts and the measurement of stimuli to which
emotion regulation suggest particular strategies that individuals are exposed. Finally, we review analytic
should decrease the duration of negative emotions. approaches that capitalize on the rich, complex
Studies capitalizing on time-series analytic ap- nature of observational data and allow researchers
proaches of observational data are few, but these can to test hypotheses about dynamics of emotion
reveal that even when individuals spontaneously use dysregulation.
a strategy, its use may not account for change in
emotion. Understanding when strategies fail to Length and Number of Observations
shorten the duration of an emotion and under- Although some patterns of emotion dysregulation
standing when (and for whom) they succeed are may be observed during a short observational
important areas for future research. period, others may occur infrequently or emerge

slowly, and may therefore be captured best through autonomic nervous system arousal during postchal-
more extended observations. Many published ob- lenge recovery periods are linked to children’s be-
servational studies of emotion regulation or dysreg- havior (Santucci et al., 2008) and adolescents’ exter-
ulation use single, relatively short (e.g., 10 minutes nalizing symptoms (Heleniak, McLaughlin, Ormel,
or less) tasks (e.g., Cole et al., 2011; Lunkenheimer & Riese, 2016; Sijtsema, Van Roon, Groot, & Riese,
et al., 2017). Others examine overall emotion patterns 2015).
(often dyadic) across longer periods (e.g., hours), Finally, longitudinal designs that incorporate
sometimes across multiple types of tasks (e.g., Dagne multiple observations across development will also
& Snyder, 2011; Hollenstein et al., 2004). help researchers distinguish normative from dys-
The length of an observation that is sufficient to regulated patterns of emotion. There are longitudi-
detect emotion dysregulation processes is an open nal studies suggesting trait-like continuities in
question in research (Aldao, 2013). Thus, it is im- emotion regulation across developmental periods
portant to consider carefully the dynamics of a par- (Blandon, Calkins, Keane, & O’Brien, 2008;
ticular pattern, or set of patterns, of emotion dys- Feldman, 2015; Halligan et al., 2013; Gullone,
regulation and to design observations sufficient in Hughes, King, & Tonge, 2010; Raffaelli, Crockett,
length or number to capture that dysregulated & Shen, 2005). However, observational designs
process. For example, a researcher interested in
provide a unique opportunity to describe normal
studying emotions that endure or change slowly development of emotion regulation dynamics and
may need to consider that children’s immediate and deviations that are linked to later psychopathology
delayed emotional responses may be meaningfully or impairments in functioning (Granic, 2005). For
different. Researchers interested in this pattern may example, as early as 36 months, children rated as
need to design observational paradigms that are higher on externalizing problems show a regulatory
longer than a few minutes, and continue to observe process of emotional and behavioral responses that
the participant during recovery periods after an dampened their use of effective regulatory strategies
evocative or challenging task. (Cole, Bendezú et al., 2017). Observational research
Importantly, manipulating task length or fre- that examines dynamics longitudinally may expand
quency may influence emotion dysregulation. In on this work by identifying normative changes in
studies of adult self-regulation that focus on re- patterns of emotion and behavior, deviations from
source depletion, increased task length or number normative processes, and their implications for
of observations appears to tax regulatory capacity longer term functioning and psychopathology.
(Baumeister & Heatherton, 1996; Baumeister,
Muraven, & Tice, 2000). To our knowledge, no Task Considerations
studies have tested whether the length or order of Another design consideration is careful selection of
tasks influences our ability to observe emotion the type and variety of observations needed to ob-
dysregulation. Studies with children frequently use serve particular patterns of emotion dysregulation.
a series of challenging tasks interleaved with non- One issue to consider is whether tasks are designed
challenging tasks that serve as recovery periods. to tap inter- or intrapersonal dysregulation processes.
Psychophysiological studies document changes in Another is to consider whether multiple types of
baseline reactivity across multiple tasks (Beauchaine, tasks, or strategic changes in task demands, are re-
Hong, & Marsh, 2008; Beauchaine, Katkin, quired to capture patterns of dysregulation.
Strassberg, & Snarr, 2001), indicating cumulative Importantly, much of the observational research
physiological effects of undergoing a series of chal- evidence on emotion dysregulation has focused on
lenges, even with brief opportunities for recovery. In regulation processes within interpersonal context.
addition, one observational study shows changes in Evocative relationships are likely key to observing
the speed at which individuals are able to downreg- emotion dysregulation and have the advantage of
ulate negative emotions as negative emotion experi- being personally relevant to individuals. In the case
ences accumulate over the course of a one-hour ob- of young children, the family context is crucial for
servation (Dagne & Snyder, 2011). More research is emotion socialization processes (e.g., Morris, Silk,
needed to understand how the length or order of Steinberg, Myers, & Robinson, 2007), so it is not
observational tasks influences regulatory patterns, surprising that parent–child interactions are oppor-
and whether that depends on characteristics of the tune for researchers to elicit emotional response
individual. For example, individual differences in patterns. In the available research, evocative contexts

are often used to test hypotheses about an individu- symptoms (see section on emotions that are context
al’s emotional reactions or regulation during or after inappropriate; Buss, 2011; Buss et al., 2013).
interactions with significant others (Cummings,
1987; Maughan et al., 2007; Stoolmiller & Snyder, Analytic Approach
2006). This approach was used to test hypotheses If emotion dysregulation is appreciated as a dy-
related to different patterns of emotion dysregula- namic process, then we must understand its tempo-
tion, including context-inappropriate emotion and ral features, changes in emotion and regulatory ef-
emotions changing too abruptly and changing too forts as task time unfolds. Too often researchers
slowly or enduring. Yet it is also important to conduct observations that are video-recorded and
consider emotion dysregulation as an intrapersonal later painstakingly coded, often using brief time in-
process, for example, examining the influence of tervals; however, they then sum or aggregate the
strategies on emotion (Cole, Bendezú, et al., 2017). data across the entire observation. Rather than con-
If emotions indicate an individual’s appraisal of sider emotion dysregulation as the total amount of
his or her environment, knowing what aspects of negative or positive emotion expressions or regula-
the environment are eliciting emotions is a critical tory attempts, a dynamic systems perspective sug-
next step in research. Dynamic systems approaches gests that we model time, the moment-to-moment
involve systematically manipulating aspects of the changes in emotion and how they are changed by
environment—causing perturbations to a system— regulatory attempts (Cole et al., 2004; Hollenstein
and observing subsequent changes in emotional and & Lanteigne, in press). To quantify emotions in this
behavioral patterns (Granic, Hollenstein, & dynamic way, observational researchers have capi-
Lichtwarck-Aschoff, 2016). Thus, it can be useful to talized on several analytic approaches.
use tasks with multiple phases designed to challenge First, examining patterns of emotion dysregu-
an individual’s emotion regulation. For example, lation requires researchers to have independent
during a parent–child problem-solving task, pat- examinations of emotions and behavior, and to estab-
terns of mutual hostility emerge only after the level lish their temporal order (Cole et al., 2004). As dis-
of challenge is increased (dyads are told to “wrap cussed previously, emotion expressions and behav-
up”), and only for children with comorbid external- iors are often treated the same, but evidence reveals
izing and internalizing symptoms (Granic & Lamey, that they operate differently (Hubbard, 2001; Strayer
2002). Measuring a person’s emotional responses & Roberts, 2004). The degree to which emotions
subsequent to these changes in a task can help influence inappropriate behavior and, conversely,
strengthen inferences that an environmental factor behaviors such as regulatory strategies influence
altered an emotional response. In intrapersonal par- emotions also requires researchers to establish
adigms, researchers can consider measuring aspects temporal precedence. Sequence analyses are a rela-
of stimuli, such as marking important events or tively simple method that several researchers have
characters in films. These types of clear events and capitalized on to address questions about the unidi-
changes in stimuli can help researchers tap dynam- rectional influence of behaviors on concurrent and
ics of change in an emotional or behavioral re- subsequent emotional responses (Buss & Goldsmith,
sponse, consistent with dynamics systems ap- 1998; Gilliom et al., 2002; Stifter & Braungart,
proaches. 1995). More advanced time-series analyses such as
Finally, adaptive or maladaptive patterns may be ordinal differential equation modeling allow re-
detected not only within tasks but also across tasks. searchers to test bidirectional associations between
For example, a study using self-reports to assess emotions and behaviors over time (Cole, Bendezú,
emotion found that individuals who were depressed et al., 2017).
reported feeling sad while viewing multiple films, Temporality is also important for capturing pat-
each intended to elicit a variety of emotions; this terns of emotions enduring or changing too
was interpreted as depression involving context- abruptly. Capturing this by measuring the latency
insensitive emotion (Rottenberg, Gross, & Gotlib, to emotional or behavioral displays, and average du-
2005). Other studies examine emotional reactions ration of these displays, is most common in the
in situations designed to elicit varying intensities of work we have reviewed (e.g., Cole et al., 2011,
an emotion. For example, fear dysregulation, de- Potegal et al., 2009). However, other approaches
fined as displaying fearfulness in low-threat situa- may provide unique information. For example, in
tions, is a risk factor for development of anxiety the experience-sampling literature, mean squared

successive difference (MSSD) scores (Woyshville, behavior or the absence of an expected behavior. For
Lackamp, Eisengart, & Gilliland, 1999) have been example, when using emotional suppression strate-
used to capture emotional lability or instability. gies, adults display greater sympathetic nervous
MSSD includes information about variability in system arousal despite having reduced facial expres-
emotions in terms of amplitude, frequency, and sions of negative emotion (Egloff, Schmukle, Burns,
temporal order (see Ebner-Priemer, Eid, Kleindienst, & Schwerdtfeger, 2006; Gross & Levenson, 1993).
Stabenow, & Trull, 2009 for review). Greater MSSD Moreover, recent work suggests that desynchrony
of suicidal ideation in adults uniquely predicts between facial expressions and autonomic reactivity
suicide attempts (Witte, Fitzpatrick, Joiner, &
predicts severity of boys’ externalizing symptoms
Schmidt, 2005). This method can be applied to ob- (Marsh, Beauchaine, & Williams, 2008) and dis-
servational work, which similarly contains complex cordant patterns of these measures predict girls’ in-
time-series data that have temporal dependencies. ternalizing symptoms (Lanteigne, Flynn,
State-space grids have also been used to capture sta- Eastabrook, & Hollenstein, 2014). Increasingly, re-
bility or instability of emotional patterns in dyads, searchers employ both behavioral observations and
and this work could be applied to intrapersonal physiological measures, a pairing that lends itself
paradigms, such as examining changes in emotional well to temporal analyses of emotion dysregulation
responses across meaningful events or perturbations dynamics (Beauchaine & Gatzke-Kopp, 2012;
(Hollenstein, 2007). In addition to measuring over- Brooker & Buss, 2010). It is noteworthy that the use
all emotional (in)stability in observations, time- of multiple levels of analysis also presents challenges
series approaches can be applied to test how quick- that are beyond the scope of this chapter (but see
ness and slowness of emotional responses change Fox & Calkins, 1999; Calkins & Fox, 2002).
within an observation. Survival analysis and
Bayesian approaches can be used to examine changes Conclusions
in emotional or behavioral responses as a function Emotion dysregulation has long been of clinical in-
of recurring events or perturbations (Dagne, Brown, terest and is a core feature of many forms of psycho-
& Howe, 2003; Stoolmiller & Snyder, 2006). An pathology (Aldao et al., 2010; Dodge, 1989). In this
especially new approach, multistate convergence chapter, we present three clinically relevant patterns
cross-mapping, allows researchers to estimate bidi- of emotion dysregulation: context-inappropriate
rectional, nonlinear associations in time-series data emotion, emotions that change too abruptly, and
when evaluating emotional responding in dyadic emotions that endure because regulatory attempts
interactions (Crowell, et al., 2017). are ineffective (Cole, Hall, & Hajal, 2017). These
patterns were used to illustrate the advantages of ob-
Limitations to Observational Work servational methods for enriching our understand-
Although research benefits from observational ing of patterns of emotion dysregulation. Finally, we
methods, which can enhance assessment of emotion reviewed several future directions for observational
dysregulation as a process, there are limitations to methods, including considerations related to study
observational approaches. First, single or even a design and analytic approaches. We emphasize that
few observations of an individual’s behavior may methods that capture patterns of behaviors unfold-
not be representative of that person’s behavior in ing across a carefully designed task and over devel-
daily life. For example, there is evidence that chil- opmental time are critical next steps in this research.
dren’s behaviors differ across contexts, and that
when multi-informant reports differ in ratings of Acknowledgments
behavior, this captures meaningful information The research reported here was supported in part by a training
grant from the Institute of Education Sciences (R305B090007),
(De Los Reyes, Henry, Tolan, & Wakschlag, 2009;
awarded to the first author. Opinions expressed are those of
Hourigan, Goodman, & Southam-Gerow, 2011). the authors and do not necessarily represent the granting
This additionally highlights the value of using mul- agencies.
tiple observations in research. This work was supported by a grant from the Eunice
Second, not all patterns of emotion dysregulation Kennedy Shriver National Institute of Child Health and Human
Development, HD076994, awarded to the second author.
are observable. We may not see an emotional reac-
This material is based on work supported by the
tion (masked anger) or a regulatory strategy (cogni- National Science Foundation Graduate Research Fellowship
tive reappraisal). Physiological methods are often (DGE1255832), awarded to the third author. Any opinion, find-
used to strengthen inferences about the meaning of ings, and conclusions or recommendations expressed in this

material are those of the authors and do not necessarily reflect and pediatric attention deficit hyperactivity disorder: A
the views of the National Science Foundation. family risk analysis. Psychological Medicine, 42, 639–646.
Blair, C. (2010). Stress and the development of self-regulation in
context. Child Development Perspectives, 4, 181–188.
References Blandon, A. Y., Calkins, S. D., Keane, S. P., & O’Brien, M.
Aldao, A. (2013). The future of emotion regulation research: (2008). Individual differences in trajectories of emotion
Capturing context. Perspectives on Psychological Science, 8, regulation processes: The effects of maternal depressive
155–172. symptomatology and children's physiological regulation.
Aldao, A., & Nolen-Hoeksema, S. (2010). Specificity of cognitive Developmental Psychology, 44, 1110.
emotion regulation strategies: A transdiagnostic examination. Boyle, M. H., & Pickles, A. R. (1997). Influence of maternal
Behaviour Research and Therapy, 48, 974–983. depressive symptoms on ratings of childhood behavior.
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Journal of Abnormal Child Psychology, 25, 399–412.
Emotion-regulation strategies across psychopathology: A Brooker, R. J., & Buss, K. A. (2010). Dynamic measures of RSA
meta-analytic review. Clinical Psychology Review, 30, 217–237. predict distress and regulation in toddlers. Developmental
Arnold, M. B. (1960). Emotion and personality. New York, NY: Psychobiology, 52, 372–382.
Columbia University Press. Buss, K. A. (2011). Which fearful toddlers should we worry
Ashburner, J., Ziviani, J., & Rodger, S. (2010). Surviving in the about? Context, fear regulation, and anxiety risk. Developmental
mainstream: Capacity of children with autism spectrum Psychology, 47, 804–819.
disorders to perform academically and regulate their Buss, K. A., Davis, E. L., Kiel, E. J., Brooker, R. J., Beekman, C.,
emotions and behavior at school. Research in Autism Spectrum & Early, M. C. (2013). Dysregulated fear predicts social
Disorders, 4, 18–27. wariness and social anxiety symptoms during kindergarten.
Augustine, A. A., & Hemenover, S. H. (2009). On the relative Journal of Clinical Child and Adolescent Psychology, 42,
effectiveness of affect regulation strategies: A meta-analysis. 603–616.
Cognition and Emotion, 23, 1181–1220. Buss, K. A., & Goldsmith, H. H. (1998). Fear and anger
Bagby, R. M., Parker, J. D., & Taylor, G. J. (1994). The twenty- regulation in infancy: Effects on the temporal dynamics of
item Toronto Alexithymia Scale—I. Item selection and cross- affective expression. Child Development, 69, 359–374.
validation of the factor structure. Journal of Psychosomatic Calkins, S. D., & Fox, N. A. (2002). Self-regulatory processes in
Research, 38, 23–32. early personality development: A multilevel approach to the
Barrett, K. C., & Campos, J. J. (1987). Perspectives on emotional study of childhood social withdrawal and aggression.
development II: A functionalist approach to emotions. In Development and Psychopathology, 14, 477–498.
J. D. Osofsky (Ed.), Handbook of infant development (2nd Calkins, S. D., Gill, K., Johnson, M. C., & Smith, C. (1999).
ed., pp. 555–578). New York, NY: Wiley. Emotional reactivity and emotion regulation strategies as
Barrett, L. F. (2011). Was Darwin wrong about emotional predictors of social behavior with peers during toddlerhood.
expressions? Current Directions in Psychological Science, 20, Social Development, 8, 310–341.
400–406. Campos, J. J., Frankel, C. B., & Camras, L. (2004). On the
Baumeister, R. F., & Heatherton, T. F. (1996). Self-regulation nature of emotion regulation. Child Development, 75,
failure: An overview. Psychological Inquiry, 7, 1–15. 377–394.
Baumeister, R. F., Muraven, M., & Tice, D. M. (2000). Ego Campos, J. J., Mumme, D. L., Kermoian, R., & Campos, R. G.
depletion: A resource model of volition, self-regulation, and (1994). A functionalist perspective on the nature of emotion.
controlled processing. Social Cognition, 18, 130–150. Monographs of Society for Research in Child Development, 59,
Beauchaine, T. P. (2015). Future directions in emotion 284–303.
dysregulation and youth psychopathology. Journal of Clinical Chilcoat, H. D., & Breslau, N. (1997). Does psychiatric history
Child and Adolescent Psychology, 44, 875–896. bias mothers’ reports? An application of a new analytic
Beauchaine, T. P., & Gatzke-Kopp, L. M. (2012). Instantiating approach. Journal of the American Academy of Child and
the multiple levels of analysis perspective in a program of Adolescent Psychiatry, 36, 971–979.
study on externalizing behavior. Development and Coburn, S. S., Crnic, K. A., & Ross, E. K. (2015). Mother–infant
Psychopathology, 24, 1003–1018. dyadic state behaviour: Dynamic systems in the context of
Beauchaine, T. P., Hong, J., & Marsh, P. (2008). Sex differences risk. Infant and Child Development, 24, 274–297.
in autonomic correlates of conduct problems and aggression. Cole, P. M. (2016). Emotion and the development of
Journal of the American Academy of Child and Adolescent psychopathology. In D. Cicchetti (Ed.), Developmental
Psychiatry, 47, 788–796. psychopathology: Theory and method (Vol. 1, 3rd ed.,
Beauchaine, T. P., Katkin, E. S., Strassberg, Z., & Snarr, J. pp. 265–324). Hoboken, NJ: Wiley.
(2001). Disinhibitory psychopathology in male adolescents: Cole, P. M., Bendezú, J. J., Ram, N., & Chow, S. M. (2017).
Discriminating conduct disorder from attention-deficit/ Dynamical systems modeling of early childhood self-
hyperactivity disorder through concurrent assessment of regulation. Emotion, 17, 684–699.
multiple autonomic states. Journal of Abnormal Psychology, Cole, P. M., Hall, S. E., & Hajal, N. J. (2017). Emotion
110, 610–624. dysregulation as a vulnerability to psychopathology. In
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent
regulation, and the latent structure of psychopathology: psychopathology (pp. 346–386). Hoboken, NJ: Wiley.
An integrative and convergent historical perspective. Cole, P. M., & Hollenstein, T. (Eds.). (2018). Emotion regulation:
International Journal of Psychophysiology, 119, 108–118. A matter of time. New York, NY: Routledge.
Biederman, J., Spencer, T., Lomedico, A., Day, H., Petty, C. R., Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion
& Faraone, S. V. (2012). Deficient emotional self-regulation regulation as a scientific construct: Methodological

challenges and directions for child development research. Dodge, K. A. (1989). Coordinating responses to aversive stimuli:
Child Development, 75, 317–333. Introduction to a special section on the development of
Cole, P. M., Michel, M. K., & Teti, L. O. D. (1994). The emotion regulation. Developmental Psychology, 25, 339–342.
development of emotion regulation and dysregulation: A Dodge, K. A., & Garber, J. (1991). Domains of emotion
clinical perspective. Monographs of the Society for Research in regulation. In J. Garber & K. A. Dodge (Eds.), The
Child Development, 59, 73–102. development of emotion regulation and dysregulation (pp. 3–11).
Cole, P. M., & Putnam, F. W. (1992). Effect of incest on self Cambridge, UK: Cambridge University Press.
and social functioning: A developmental psychopathology Durbin, C. E. (2010). Validity of young children’s self-reports of
perspective. Journal of Consulting and Clinical Psychology, 60, their emotion in response to structured laboratory tasks.
174–184. Emotion, 10, 519.
Cole, P. M., Tan, P. Z., Hall, S. E., Zhang, Y., Crnic, K. A., Ebner-Priemer, U. W., Eid, M., Kleindienst, N., Stabenow, S., &
Blair, C. B., & Li, R. (2011). Developmental changes in Trull, T. J. (2009). Journal of Abnormal Psychology, 118, 195–202.
anger expression and attention focus: Learning to wait. Egloff, B., Schmukle, S. C., Burns, L. R., & Schwerdtfeger, A.
Developmental Psychology, 47, 1078–1089. (2006). Spontaneous emotion regulation during evaluated
Cole, P. M., Teti, L. O., & Zahn-Waxler, C. (2003). Mutual speaking tasks: Associations with negative affect, anxiety
emotion regulation and the stability of conduct problems expression, memory, and physiological responding. Emotion,
between preschool and early school age. Development and 6, 356–366.
Psychopathology, 15, 1–18. Ekman, P. (1992). An argument for basic emotions. Cognition
Crowell, S. E., Baucom, B. R., McCauley, E., Potapova, N. V., and Emotion, 6, 169–200.
Fitelson, M., Barth, H., . . . Beauchaine, T. P. (2013). Feldman, R. (2015). Mutual influences between child emotion
Mechanisms of contextual risk for adolescent self-injury: regulation and parent–child reciprocity support development
Invalidation and conflict escalation in mother–child across the first 10 years of life: Implications for developmental
interactions. Journal of Clinical Child & Adolescent Psychology, psychopathology. Development and Psychopathology, 27,
42, 467–480. 1007–1023.
Crowell, S. E., Butner, J., Wiltshire, T. J., Munion, A. K., Fernandez, K. C., Jazaieri, H., & Gross, J. J. (2016). Emotion
Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating regulation: A transdiagnostic perspective on a new RDoC
emotional and biological sensitivity to maternal domain. Cognitive Therapy and Research, 40, 426–440.
behavior among depressed and self-injuring adolescent girls Fogel, A., Nwokah, E., Dedo, J. Y., Messinger, D., Dickson,
using nonlinear dynamics. Clinical Psychological Science, 5, K. L., Matusov, E., & Holt, S. A. (1992). Social process
272–285. theory of emotion: A dynamic systems approach. Social
Csikszentmihalyi, M., & Larson, R. (2014). Validity and Development, 1, 122–142.
reliability of the experience-sampling method. In Fox, N. A., & Calkins, S. D. (1999). Multiple measure
M. Csikszentmihalyi (Ed.), Flow and the foundations of approaches to the study of infant emotion. In M. Lewis &
positive psychology (pp. 35–54). Dordrecht, The Netherlands: J. Haviland (Eds.), Temperament: Individual differences at the
Springer. interface of biology and behavior (pp. 167–184). Washington,
Cummings, E. M. (1987). Coping with background anger in DC: American Psychological Association.
early childhood. Child Development, 58, 976–984. Frijda, N. H. (1986). The emotions: Studies in emotion and social
Dadds, M. R., Gale, N., Godbee, M., Moul, C., Pasalich, D. S., interaction. Cambridge, UK: Cambridge University Press.
Fink, E., & Hawes, D. J. (2016). Expression and regulation Gilliom, M., Shaw, D. S., Beck, J. E., Schonberg, M. A., &
of attachment-related emotions in children with conduct Lukon, J. L. (2002). Anger regulation in disadvantaged
problems and callous–unemotional traits. Child Psychiatry preschool boys: Strategies, antecedents, and the development
and Human Development, 47, 647–656. of self-control. Developmental Psychology, 38, 222–235.
Dagne, G. A., Brown, C. H., & Howe, G. W. (2003). Bayesian Granic, I. (2005). Timing is everything: Developmental
hierarchical modeling of heterogeneity in multiple psychopathology from a dynamic systems perspective.
contingency tables: An application to behavioral observation Developmental Review, 25, 386–407.
data. Journal of Educational and Behavioral Statistics, 28, Granic, I., Hollenstein, T., & Lichtwarck-Aschoff, A. (2016).
339–352. A survey of dynamic systems methods for developmental
Dagne, G. A., & Snyder, J. (2011). Relationship of maternal psychopathology. In D. Cicchetti (Ed.), Developmental
negative moods to child emotion regulation during psychopathology: Theory and method (Vol. 1, 3rd ed.,
family interaction. Development and Psychopathology, 23, pp. 717–759). Hoboken, NJ: Wiley.
211–223. Granic, I., & Lamey, A. V. (2002). Combining dynamic systems
De Los Reyes, A., Henry, D. B., Tolan, P. H., & Wakschlag, L. S. and multivariate analyses to compare the mother–child
(2009). Linking informant discrepancies to observed variations interactions of externalizing subtypes. Journal of Abnormal
in young children’s disruptive behavior. Journal of Abnormal Child Psychology, 30, 265–283.
Child Psychology, 37, 637–652. Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment
Denham, S. A., Wyatt, T. M., Bassett, H. H., Echeverria, D., & of emotion regulation and dysregulation: Development,
Knox, S. S. (2009). Assessing social-emotional development factor structure, and initial validation of the difficulties in
in children from a longitudinal perspective. Journal of emotion regulation scale. Journal of psychopathology and
Epidemiology and Community Health, 63, i37–i52. behavioral assessment, 26, 41–54.
Diaz, A., & Eisenberg, N. (2015). The process of emotion Gross, J. J. (1998). Antecedent- and response-focused emotion
regulation is different from individual differences in emotion regulation: Divergent consequences for experience, expression,
regulation: Conceptual arguments and a focus on individual and physiology. Journal of Personality and Social Psychology,
differences. Psychological Inquiry, 26, 37–47. 74, 224–237.

Gross, J. J., & Levenson, R. W. (1993). Emotional suppression: Kring, A. M., & Moran, E. K. (2008). Emotional response
Physiology, self-report, and expressive behavior. Journal of deficits in schizophrenia: Insights from affective science.
Personality and Social Psychology, 64, 970–986. Schizophrenia Bulletin, 34, 819–834.
Gross, J. J., & Thompson, R. A. (2007). Emotion regulation: Lanteigne, D. M., Flynn, J. J., Eastabrook, J. M., & Hollenstein,
Conceptual foundations. In J. J. Gross (Ed.), Handbook T. (2014). Discordant patterns among emotional experience,
of emotion regulation (2nd ed., pp. 3–24). New York, NY: arousal, and expression in adolescence: Relations with
Guilford. emotion regulation and internalizing problems. Canadian
Gruber, J. (2011). Can feeling too good be bad? Positive emotion Journal of Behavioural Science, 46, 29–39.
persistence (PEP) in bipolar disorder. Current Directions in Lewis, A. R., Zinbarg, R. E., & Durbin, C. E. (2010). Advances,
Psychological Science, 20, 217–221. problems, and challenges in the study of emotion regulation:
Gruber, J., Harvey, A. G., & Gross, J. J. (2012). When trying is A commentary. Journal of Psychopathology and Behavioral
not enough: Emotion regulation and the effort–success gap Assessment, 32, 83–91.
in bipolar disorder. Emotion, 12, 997–1003. Lewis, M. D., & Granic, I. (Eds.). (2002). Emotion, development,
Gullone, E., Hughes, E. K., King, N. J., & Tonge, B. (2010). The and self-organization: Dynamic systems approaches to emotional
normative development of emotion regulation strategy use in development. Cambridge, UK: Cambridge University Press.
children and adolescents: A 2-year follow-up study. Journal of Lunkenheimer, E., Kemp, C. J., Lucas-Thompson, R. G., Cole,
Child Psychology and Psychiatry, 51, 567–574. P. M., & Albrecht, E. C. (2017). Assessing biobehavioural
Halligan, S. L., Cooper, P. J., Fearon, P., Wheeler, S. L., Crosby, self-regulation and coregulation in early childhood: The
M., & Murray, L. (2013). The longitudinal development parent-child challenge task. Infant and Child Development,
of emotion regulation capacities in children at risk for 26, e1965.
externalizing disorders. Development and Psychopathology, Lunkenheimer, E. S., Olson, S. L., Hollenstein, T., Sameroff,
25, 391–406. A. J., & Winter, C. (2011). Dyadic flexibility and positive
Heleniak, C., McLaughlin, K. A., Ormel, J., & Riese, H. (2016). affect in parent–child coregulation and the development of
Cardiovascular reactivity as a mechanism linking child child behavior problems. Development and Psychopathology,
trauma to adolescent psychopathology. Biological Psychology, 23, 577–591.
120, 108–119. Marsh, P., Beauchaine, T. P., & Williams, B. (2008). Dissociation
Hollenstein, T. (2007). State space grids: Analyzing dynamics of sad facial expressions and autonomic nervous system
across development. International Journal of Behavioral responding in boys with disruptive behavior disorders.
Development, 31, 384–396. Psychophysiology, 45, 100–110.
Hollenstein, T., Allen, N. B., & Sheeber, L. (2016). Affective Maughan, A., & Cicchetti, D. (2002). Impact of child
patterns in triadic family interactions: Associations with maltreatment and interadult violence on children’s emotion
adolescent depression. Development and Psychopathology, regulation abilities and socioemotional adjustment. Child
28, 85–96. Development, 73, 1525–1542.
Hollenstein, T., Granic, I., Stoolmiller, M., & Snyder, J. (2004). Maughan, A., Cicchetti, D., Toth, S. L., & Rogosch, F. A.
Rigidity in parent-child interactions and the development of (2007). Early-occurring maternal depression and maternal
externalizing and internalizing behavior in early childhood. negativity in predicting young children’s emotion regulation
Journal of Abnormal Child Psychology, 32, 595–607. and socioemotional difficulties. Journal of Abnormal Child
Hollenstein, T., & Lanteigne, D. M. (2018). Emotion regulation Psychology, 35, 685–703.
dynamics in adolescence. In P. M. Cole & T. Hollenstein McMillan, T. M., Williams, W. H., & Bryant, R. (2003). Post-
(Eds.), Emotion regulation: A matter of time. New York, NY: traumatic stress disorder and traumatic brain injury: A
Routledge. review of causal mechanisms, assessment, and treatment.
Hourigan, S. E., Goodman, K. L., & Southam-Gerow, M. A. Neuropsychological Rehabilitation, 13, 149–164.
(2011). Discrepancies in parents’ and children’s reports of Mennin, D. S., Heimberg, R. G., Turk, C. L., & Fresco, D. M.
child emotion regulation. Journal of Experimental Child (2002). Applying an emotion regulation framework to
Psychology, 110, 198–212. integrative approaches to generalized anxiety disorder.
Hubbard, J. A. (2001). Emotion expression processes in children’s Clinical Psychology: Science and Practice, 9, 85–90.
peer interaction: The role of peer rejection, aggression, and Morris, A. S., Silk, J. S., Steinberg, L., Myers, S. S., & Robinson,
gender. Child Development, 72, 1426–1438. L. R. (2007). The role of the family context in the
Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D. S., development of emotion regulation. Social Development, 16,
Quinn, K., .
.
.
Wang, P. (2010). Research domain criteria 361–388.
(RDoC): Toward a new classification framework for research on Najman, J. M., Williams, G. M., Nikles, J., Spence, S., Bor, W.,
mental disorders. American Journal of Psychiatry, 167, 748–751. O’Callaghan, M., . . . Shuttlewood, G. J. (2001). Bias
Izard, C. E. (2007). Basic emotions, natural kinds, emotion influencing maternal reports of child behaviour and
schemas, and a new paradigm. Perspectives on Psychological emotional state. Social Psychiatry and Psychiatric Epidemiology,
Science, 2, 260–280. 36, 186–194.
James, W. (1884). What is an emotion? Mind, 9, 188–205. Ochsner, K. N., Ray, R. R., Hughes, B., McRae, K., Cooper,
Joormann, J., & Gotlib, I. H. (2010). Emotion regulation in J. C., Weber, J., . . . Gross, J. J. (2009). Bottom-up and top-
depression: Relation to cognitive inhibition. Cognition and down processes in emotion generation: Common and
Emotion, 24, 281–298. distinct neural mechanisms. Psychological Science, 20,
Kelso, J. A. S. (1994). The informational character of self- 1322–1331.
organized coordination dynamics. Human Movement Science, O’Connor, T. G., Humayun, S., Briskman, J. A., & Scott, S.
13, 393–413. (2016). Sensitivity to parenting in adolescents with callous/

unemotional traits: Observational and experimental findings. disorder. Personality Disorders: Theory, Research, and
Journal of Abnormal Psychology, 125, 502–513. Treatment, 7, 211–220.
Panksepp, J. (1992). A critical role for “affective neuroscience” in Schwartz, C. E., Snidman, N., & Kagan, J. (1999). Adolescent
resolving what is basic about basic emotions. Psychological social anxiety as an outcome of inhibited temperament in
Review, 99, 554–560. childhood. Journal of the American Academy of Child and
Panksepp, J. (2017). The psycho-neurology of cross-species Adolescent Psychiatry, 38, 1008–1015.
affective/social neuroscience: Understanding animal affective Sheppes, G., Scheibe, S., Suri, G., Radu, P., Blechert, J., &
states as a guide to development of novel psychiatric Gross, J. J. (2014). Emotion regulation choice: A conceptual
treatments. Current Topics in Behavioral Neuroscience, 30, framework and supporting evidence. Journal of Experimental
109–125. Psychology: General, 143, 163–181.
Potegal, M., Carlson, G., Margulies, D., Gutkovitch, Z., & Wall, Shields, A., & Cicchetti, D. (1997). Emotion regulation among
M. (2009). Rages or temper tantrums? The behavioral school-age children: The development and validation of a new
organization, temporal characteristics, and clinical criterion Q-sort scale. Developmental Psychology, 33, 906–916.
significance of angry-agitated outbursts in child psychiatry Sijtsema, J. J., Van Roon, A. M., Groot, P. F. C., & Riese, H.
inpatients. Child Psychiatry and Human Development, 40, (2015). Early life adversities and adolescent antisocial
621–636. behavior: The role of cardiac autonomic nervous system
Potegal, M., & Davidson, R. J. (2003). Temper tantrums in reactivity in the TRAILS study. Biological Psychology, 110,
young children: 1. Behavioral composition. Journal of 24–33.
Developmental and Behavioral Pediatrics, 24, 140–147. Silk, J. S., Steinberg, L., & Morris, A. S. (2003). Adolescents’
Raffaelli, M., Crockett, L. J., & Shen, Y. L. (2005). emotion regulation in daily life: Links to depressive
Developmental stability and change in self-regulation from symptoms and problem behavior. Child Development, 74,
childhood to adolescence. Journal of Genetic Psychology, 166, 1869–1880.
54–76. Snyder, J., Edwards, P., McGraw, K., Kilgore, K., & Holton, A.
Reich, D. B., Zanarini, M. C., & Fitzmaurice, G. (2012). (1994). Escalation and reinforcement in mother-child
Affective lability in bipolar disorder and borderline conflict: Social processes associated with the development of
personality disorder. Comprehensive Psychiatry, 53, 230–237. physical aggression. Development and Psychopathology, 6,
Robinson, L. R., Morris, A. S., Heller, S. S., Scheeringa, M. S., 305–321.
Boris, N. W., & Smyke, A. T. (2009). Relations between Stansbury, K., & Sigman, M. (2000). Responses of preschoolers
emotion regulation, parenting, and psychopathology in in two frustrating episodes: Emergence of complex strategies
young maltreated children in out of home care. Journal of for emotion regulation. Journal of Genetic Psychology, 161,
Child and Family Studies, 18, 421–434. 182–202.
Rosen, P. J., Walerius, D. M., Fogleman, N. D., & Factor, P. I. Stifter, C. A., & Braungart, J. M. (1995). The regulation of
(2015). The association of emotional lability and emotional negative reactivity in infancy: Function and development.
and behavioral difficulties among children with and without Developmental Psychology, 31, 448–455.
ADHD. Attention Deficit and Hyperactivity Disorders, 7, Stone, A. A., & Shiffman, S. (1994). Ecological momentary
281–294. assessment (EMA) in behavioral medicine. Annals of
Rothbart, M. K., & Bates, J. E. (2006). Temperament. In Behavioral Medicine, 16, 199–202.
W. Damon, R. Lerner, & N. Eisenberg (Eds.), Handbook of Stoolmiller, M., & Snyder, J. (2006). Modeling heterogeneity in
child psychology. Social, emotional, and personality development social interaction processes using multilevel survival analysis.
(Vol. 3, pp. 99–166). New York, NY: Wiley. Psychological Methods, 11, 164–177.
Rottenberg, J., Gross, J. J., & Gotlib, I. H. (2005). Emotion Stoolmiller, M., & Snyder, J. (2013). Embedding multilevel
context insensitivity in major depressive disorder. Journal of survival analysis of dyadic social interaction in structural
Abnormal Psychology, 114, 627–639. equation models: Hazard rates as both outcomes and
Russell, J. A. (2003). Core affect and the psychological predictors. Journal of Pediatric Psychology, 39, 222–232.
construction of emotion. Psychological Review, 110, 145–172. Strayer, J., & Roberts, W. (2004). Empathy and observed anger
Saarni, C. (1999). The development of emotional competence. and aggression in five-year-olds. Social Development, 13, 1–13.
New York, NY: Guilford Press. Surman, C. B., Biederman, J., Spencer, T., Yorks, D., Miller,
Santucci, A. K., Silk, J. S., Shaw, D. S., Gentzler, A., Fox, N. A., C. A., Petty, C. R., & Faraone, S. V. (2011). Deficient
& Kovacs, M. (2008). Vagal tone and temperament as emotional self-regulation and adult attention deficit
predictors of emotion regulation strategies in young children. hyperactivity disorder: A family risk analysis. American
Developmental Psychobiology, 50, 205–216. Journal of Psychiatry, 168, 617–623.
Sauter, D. A., Eisner, F., Ekman, P., & Scott, S. K. (2010). Cross- Thelen, E. (2002). Self-organization in developmental processes:
cultural recognition of basic emotions through nonverbal Can systems approaches work. In M. H. Johnson, Y. Munakata,
emotional vocalizations. Proceedings of the National Academy & R. O. Gilmore (Eds.), Brain development and cognition: A
of Sciences, 107, 2408–2412. reader (pp. 555–591). Hoboken, NJ: Blackwell.
Scarpa, A., & Reyes, N. M. (2011). Improving emotion regulation Thompson, R. A. (1990). Emotion and self-regulation. In
with CBT in young children with high functioning autism R. A. Thompson (Ed.), Nebraska Symposium on Motivation:
spectrum disorders: A pilot study. Behavioural and Cognitive Socioemotional development (Vol. 36, pp. 383–483). Lincoln,
Psychotherapy, 39, 495–500. NE: University of Nebraska Press.
Schoenleber, M., Berghoff, C. R., Tull, M. T., DiLillo, D., Thompson, R. A. (1994). Emotion regulation: A theme in search
Messman-Moore, T., & Gratz, K. L. (2016). Emotional of definition. Monographs of the Society for Research in Child
lability and affective synchrony in borderline personality Development, 59, 25–52.

Tomkins, S. S. (1962). Affect imagery consciousness: The positive Witherington, D. C., & Crichton, J. A. (2007). Frameworks
affect. New York, NY: Springer. for understanding emotions and their development:
Tomkins, S. S. (1963). Affect imagery consciousness: The negative Functionalist and dynamic systems approaches. Emotion,
affects. New York, NY: Springer. 7, 628–637.
Tracy, J. L., & Randles, D. (2011). Four models of basic emotions: Witte, T. K., Fitzpatrick, K. K., Joiner, T. E., & Schmidt, N. B.
A review of Ekman and Cordaro, Izard, Levenson, and (2005). Variability in suicidal ideation: A better predictor of
Panksepp and Watt. Emotion Review, 3, 397–405. suicide attempts than intensity or duration of ideation?
Wakschlag, L. S., Leventhal, B. L., Briggs-Gowan, M. J., Danis, Journal of Affective Disorders, 88, 131–136.
B., Keenan, K., Hill, C., . . . Carter, A. S. (2005). Defining Woyshville, M. J., Lackamp, J. M., Eisengart, J. A., & Gilliland,
the “disruptive” in preschool behavior: What diagnostic J. A. (1999). On the meaning and measurement of affective
observation can teach us. Clinical Child and Family Psychology instability: Clues from chaos theory. Biological Psychiatry, 45,
Review, 8, 183–201. 261–269.
Westen, D., Muderrisoglu, S., Fowler, C., Shedler, J., & Zeman, J. L., Cassano, M., Suveg, C., & Shipman, K. (2010).
Koren, D. (1997). Affect regulation and affective experience: Initial validation of the children’s worry management scale.
Individual differences, group differences, and measurement Journal of Child and Family Studies, 19, 381–392.
using a Q-sort procedure. Journal of Consulting and Clinical Zeman, J., & Garber, J. (1996). Display rules for anger, sadness,
Psychology, 65, 429–439. and pain: It depends on who is watching. Child Development,
Widen, S. C., & Russell, J. A. (2008). Children acquire emotion 67, 957–973.
categories gradually. Cognitive Development, 23, 291–312. Zeman, J., Klimes-Dougan, B., Cassano, M., & Adrian, M.
Williams, K. E., Chambless, D. L., & Ahrens, A. (1997). Are (2007). Measurement issues in emotion research with
emotions frightening? An extension of the fear of fear children and adolescents. Clinical Psychology: Science and
construct. Behaviour Research and Therapy, 35, 239–248. Practice, 14, 377–401.

CH A PTE R
6 Emotion Dysregulation and Aging
Patrick Whitmoyer and Ruchika Shaurya Prakash
Abstract
This chapter presents an overview of literature relevant to understanding relations between aging
and emotion dysregulation. Although a number of studies suggest that aging leads to shifts in emotion
regulation and emotional well-being, the extent to which aging affects emotion dysregulation is less
clear. To clarify the effects of aging on emotion dysregulation, this chapter begins by examining shifts
in effectiveness of emotion regulation that occur with age, considering pertinent theories, and then
expands on these findings by examining more specifically how context appropriateness of emotions,
consequences of emotions on behavior, duration of emotions, and etiology and presentation of
psychopathology are altered by aging processes. Finally, this chapter concludes by identifying gaps in the
literature and recommendations for future empirical endeavors to advance our current understanding
of effects of aging on emotion dysregulation.
Keywords: aging, emotion dysregulation, strategy use, context, cognitive control, behavior
Introduction related shifts in the experience of emotions or

Aging is characterized by notable declines in physical changes in the emotion regulation process.
and cognitive function. Despite these declines, One proposed explanation is that shifts in the
an abundant literature suggests that emotional processes that underlie the experience and expres-
well-being—referring to a state of good mental health sion of emotion account for age-related shifts in
and adaptive experience of both positive and nega- emotional well-being. Emotions themselves are
tive affect—remains stable and may even improve inherently regulatory (Campos, Mumme, Kermoian,
with age. Both cross-sectional studies and longitu- & Campos, 1994; Cole, Hall, & Hajal, 2017). The
dinal follow-up studies, which help rule out cohort experience of emotions of varying valences and
effects, provide evidence for continued stability and intensities often begins or is closely followed by
enhancement of hedonic well-being in late adult- appraisal or evaluation of the current situation,
hood (Carstensen, Pasupathi, Mayr, & Nesselroade, which elicits a regulatory action—either adaptive or
2000; Charles, Reynolds, & Gatz, 2001; Hasin, maladaptive—to current circumstances. One of the
Goodwin, Stinson, & Grant, 2005; E.M. Kessler & prominent theories, the aging brain model, proposed
Staudinger, 2009; Kunzmann, Little, & Smith, by Cacioppo, Bernston, Bechara, Tranel, and Hawkley
2000; Mroczek & Kolarz, 1998; Reynolds, Pietrzak, (2011), posits that the experience of emotions shifts
El-Gabalawy, Mackenzie, & Sareen, 2015). This as a function of age-related declines in the structural
paradoxical finding of maintained emotional health integrity of the amygdala, a subcortical brain region
despite declining physical and cognitive function that is critical to generating various emotions
is at center stage in the aging literature, much of (among other functions). According to Cacioppo
which is devoted to understanding the extent to et al., reduced integrity of the amygdala alters emo-
which such age-related shifts represent general age- tional processing (i.e., evaluation/appraisal) and
69
reactivity (i.e., emotion generation and behavioral emotions (Carstensen et al., 1999; Lang & Carstensen,
responsivity to emotion), which leads to reduced 2002), and a critical role of cognitive control in
sensitivity to negative, but not positive, stimuli, successful emotion regulation among older adults
thus explaining age-related shifts in well-being. (Mather & Knight, 2005; Opitz, Lee, Gross, &
However, contrary to this model, there is significant Urry, 2014). However, there is inconsistent evidence
neuroimaging evidence for structural and functional for limited future time perspective as an underlying
preservation of the amygdala with increasing age mechanism of positive emotional function in late
relative to other brain regions (Allen, Bruss, Brown, & adulthood (Charles & Carstensen, 2008; Lang &
Damasio, 2005; Nashiro, Sakaki, & Mather, 2012). Carstensen, 2002). Rather, numerous studies in-
Postmortem studies indicate no volumetric decline dicate that limited future time perspective is asso-
in the amygdala with age (Brabec et al., 2010), and ciated with worse negative emotional outcomes
functional studies suggest preserved amygdala reac- (Allemand, Hill, Ghaemmaghami, & Martin, 2012;
tivity in older adults (Jacques, Dolcos, & Cabeza, Gruhn et al., 2015; E.M. Kessler & Staudinger,
2010; Wright et al., 2008). 2009; Ramsey & Gentzler, 2014). Thus, there may
Thus, there is currently little support for the in fact be an increasing emphasis on emotion regu-
theory that age-related shifts in general emotional lation with advancing age, but shrinking future ho-
reactivity are responsible for age differences in emo- rizons may not mediate effects of age on enhanced
tional well-being. In contrast, emerging evidence well-being.
from behavioral and neuroimaging investigations The selection, optimization, and compensation
suggests that emotion regulation goals and strategies with emotion regulation framework (SOC-ER; Urry
play a critical role in explaining age-related shifts in & Gross, 2010), an application of Baltes and Baltes’s
emotional well-being (for a review see Nashiro et al., (1990) selection, optimization, and compensation
2012). As a result, emotion regulation—referring theory (SOC), offers a different explanation for how
here to volitional (explicit) and avolitional (implicit) age-related shifts in emotion regulation lead to
processes involved in modulation of initial emotional enhanced well-being. The SOC-ER framework sug-
responses (Cole et al., 2017; Gross, 1998, 2015)—is gests that older adults use alternative methods of
a dominant topic of study in the aging and well-being emotion regulation that rely more heavily on re-
literature. Several recent theories propose that sources that improve or are relatively preserved with
emotion regulation goals and the manner in which age (e.g., social networking, predicting feelings of
such goals are implemented shift with age, and that arousal) to compensate for losses of other resources
these shifts help to account for shifts in well-being. (e.g., cognitive control). Support for this framework
Socioemotional selectivity theory (SST; Carstensen, comes from findings indicating that in the wake of
Fung, & Charles, 2003), for example, proposes that significant cognitive decline, older adults exhibit
as temporal horizons shrink with increasing age, greater preference for and are more effective at
emotion regulation goals become more salient. As a implementing emotion regulation strategies that
result, older adults are more motivated to allocate rely less on cognitive control processes than young
greater resources to emotion regulation and use adults (Allard & Kensinger, 2014b; Isaacowitz,
more effective strategies to regulate, leading to en- Toner, Goren, & Wilson, 2008; Scheibe, Sheppes,
hanced emotional well-being. The cognitive control & Staudinger, 2015). Combining aspects of the SST
hypothesis subsumed within SST accounts for age- and SOC frameworks, strength and vulnerability
related cognitive decline, positing that older adults integration theory (SAVI; Charles & Piazza, 2009)
still require cognitive control for successful emotion specifies several age-related strengths and weak-
regulation and thus older adults with preserved nesses that appear to account for instances in which
cognitive control should exhibit greater emotional age confers affective benefits. Strengths identified
well-being than those with lower cognitive control include increased motivation to regulate emotions
capacities (Mather & Carstensen, 2005). and shrinking perception of time left with age,
Consistent with predictions from SST, there is whereas weaknesses include ability to regulate emo-
reliable evidence supporting age-related shifts in tions in response to prolonged stressors that elicit
strategies used to regulate emotions (for a review see high levels of arousal. SAVI extends upon tenets of
Mather, 2016), age-related decreases in future time SST and SOC by proposing that daily contexts in
perspective (Carstensen, Isaacowitz, & Charles, 1999; which emotions are experienced and regulated are
Gruhn, Sharifan, & Chu, 2016; Lang & Carstensen, integral to developing a complete understanding of
2002), age-related increases in motivation to regulate age-related shifts in emotional well-being. Together,
70 Emotion Dysregul ation and Aging

SST, SOC-ER, and SAVI posit that aging should be e xpression, in this chapter we start with a discussion
associated with more effective emotion regulation of age-related shifts in emotion regulation processes,
contingent upon the availability of sufficient re- and how these shifts relate to immediate regulation
sources. These theories propose several age-related goals and emotional outcomes. Understanding emo-
shifts in emotion regulation likely to play an inte- tion regulation processes requires that we specify
gral part in contributing to emotional well-being in how resources used to regulate emotions shift with
late adulthood (e.g., strategy shifts, cognitive decline). age, and how preferences for particular emotion
In contrast to emotion regulation, emotion dysregulation strategies shift with age. In the remainder
regulation—defined broadly within this volume as of this chapter we therefore focus on clinically
any pattern of emotional experience and/or expres- meaningful outcomes to more thoroughly identify
sion that interferes with appropriate goal-directed and distinguish emotion dysregulation from com-
behavior and therefore disrupts and compromises petent regulation. We pay particular attention to
adaptive life outcomes (Beauchaine, 2015)—has re- (1) contexts in which emotions are regulated,
ceived little direct attention in the aging literature. (2) effects of emotions on behavioral function, and
Emotions can be considered dysregulated when (3) durations of emotions in response to regulation
they are functionally maladaptive in terms of either efforts. Given that development of psychopathology
their short-term or long-term consequences, be- is often accompanied by problems with emotion
ginning with their immediate, context-dependent dysregulation, our review concludes by examining
effects. However, even if immediately effective, how the etiology and presentation of psychopathol-
patterns of emotion expression can be dysfunctional ogy shift with age. Finally, we offer a synthesis of
if their long-term costs outweigh their short-term current findings, highlight gaps in the literature,
benefits (Cole et al., 2017; Cole, Michel, & Teti, and offer suggestions for future research.
1994). It is also important to consider that emotions
are usually characterized as dysregulated only when Aging and Emotion Regulatory Processes
repetitive patterns of emotional responding are Understanding how emotion regulatory processes
maladaptive—not by a single instance in which a change with age is an important starting point for
maladaptive response occurs. understanding relations between age and emotion
Considering symptoms of psychopathology can dysregulation. The extent to which age changes are
help to distinguish emotion dysregulation from observed in immediate emotion regulation efforts
competent emotion regulation. For instance, in the provides some initial insight into how aging affects
Diagnostic and Statistical Manual of Mental Disorders, emotion dysregulation. General age-related shifts in
5th edition (DSM-5; American Psychiatric Association, emotion regulation are also tied strongly to appro-
2013), emotional symptoms typically meet diagnostic priateness of emotional responses across contexts,
criteria for various forms of psychopathology when effects of emotions on behavior, and the extent to
they are disproportionate/excessive in the context in which emotions resist change. To understand effects
which they occur and endure for a prolonged period of aging on emotion regulation, we must first un-
of time, thereby causing significant distress and im- derstand how the resources required for emotion
pairing function across a number of life domains. regulation and emotion regulation strategy use shift
Similarly, emotion dysregulation is characterized by with age.
emotional responses that endure despite regulation
attempts, are context inappropriate, interfere signif- Age Differences in Cognitive Control
icantly with behavioral function, and change too During Emotion Regulation
quickly or slowly in response to regulation efforts A primary resource needed for successful emotion
(Cole et al., 2017; Thompson, 1990). It is imperative regulation at most any age—including late
to evaluate further the extent to which shifts in emo- adulthood—
is cognitive control (Mather &
tion regulation reflect emotion dysregulation to better Carstensen, 2005; Mather & Knight, 2005; Urry &
understand their meaning and clinical relevance. Gross, 2010). This notion may seem paradoxical given
Increasing focus on emotion dysregulation vis-à-vis that age-related cognitive decline is well documented;
clinically meaningful criteria should help produce a older adults exhibit declines across a number of cog-
more objective, comprehensive view of aging effects nitive domains (Verhaeghen, 2011; Verhaeghen &
on emotion regulation and emotional well-being. Salthouse, 1997), as well as structural declines in
Given that emotion dysregulation refers to brain regions critical to implementing cognitive
maladaptive patterns of emotional experience and control processes associated with successful emotion
Whitmoyer and Prakash 71

regulation (Fjell et al., 2009; Kryla-Lighthall & are usually asked to either upregulate or downregulate
Mather, 2009; Ochsner & Gross, 2005). Nevertheless, emotional responses to emotional stimuli such as
several sources of evidence suggest that successful pictures or film clips. Emotion regulation success in
emotion regulation among older adults depends on these tasks is typically defined by one’s ability to in-
the availability of cognitive resources and active use crease or decrease emotional responses over a short
of cognitive control strategies (Kryla-Lighthall & time interval, consistent with instructions (e.g., if
Mather, 2009). First, older adults with better cogni- instructed to decrease negative emotions in response
tive abilities are more effective at regulating their to pictures, emotions during instructed regulation
emotions. Greater executive function is associated periods are less intense than emotions during passive
with enhanced positivity during processing of observation of pictures). Emotional responses are
emotional memories (Mather & Knight, 2005), in- typically assessed via self-report (e.g., “How strongly
creased resistance to declines in mood (Isaacowitz, did you experience negative emotion?”) but may also
Toner, & Neupert, 2009), and greater emotion be assessed via physiological measures such as skin
regulation success (Opitz et al., 2014). Emotion conductance, heart rate, or neural activity (most
dysregulation is also more common among older commonly measured using electroencephalography
adults with compromised cognitive capacities—such [EEG] or functional magnetic resonance imaging
as those with mild cognitive impairment (MCI) and [fMRI]) during emotion regulation.
Alzheimer’s disease (AD)—than among healthy Recent reviews identify several brain regions,
older adults (Geda et al., 2008; Goodkind, Gyurak, particularly in the prefrontal cortex (PFC), that play
McCarthy, Miller, & Levenson, 2010; Sturm et al., key roles in implementing cognitive control over
2013). Additionally, how older adults process emo- emotion (Mather, 2016; Ochsner, Silvers, & Buhle,
tional information appears to depend on cognitive 2012). Four subregions of the PFC that are critical
processing constraints. A bias toward positive emo- for cognitive control are most commonly implicated
tional information is only observed when sufficient in both emotion regulation and its decline with age.
resources are available for goal-directed processing These include the ventromedial prefrontal cortex
(Mather & Knight, 2005). Of note, older adults (vmPFC), orbitofrontal cortex (OFC), anterior
exhibit a bias toward negatively valenced emotional cingulate cortex (ACC), and dorsolateral prefrontal
stimuli when cognitive resources are limited (Knight cortex (dlPFC; see Beauchaine & Zisner, 2017;
et al., 2007). Mather, 2016). Some studies show that older adults
The role of cognitive control in emotion regula- recruit the lateral PFC less than young adults, and
tion is typically assessed by examining correlations that reduced recruitment is associated with less suc-
between cognitive measures and either self-reports cessful downregulation of negative emotions (Opitz
or behavioral measures of emotion regulation, or et al., 2012; Winecoff, LaBar, Madden, Cabeza, &
by directly manipulating cognitive control during Huettel, 2011). In addition, less successful down-
emotion regulation tasks. In such studies, compu- regulation of amygdala activity is associated with
terized or pencil-and-paper neuropsychological tests, poorer performance on cognitive measures (Winecoff
such as the Flanker task (Scheibe et al., 2015) and et al., 2011). Such findings suggest that cognitive
the Attentional Network test (Mather & Knight, control plays an important role in emotion regula-
2005), are commonly used to index cognitive tion among younger and older adults alike, but that
function. Direct manipulation of cognitive control older adults may be less successful at exerting cogni-
occurs via placing constraints on cognitive resources tive control to regulate emotions than younger adults.
such as attentional processing during emotion regu- This latter notion seems to conflict with findings of
lation (Knight et al., 2007). Self-report measures enhanced emotional well-being in late adulthood.
of emotion regulation typically assess more stable More recent investigations offer some explanation
characteristics of emotional function, whereas be- for these seemingly discrepant findings.
havioral tasks can be used to provide information In a recent series of analyses, Allard and Kensinger
about functional relations between stimuli and elic- (2014a, 2014b) examined age differences in timing
ited emotional responses under controlled conditions and neural recruitment during downregulation of
(Wilhelm & Grossman, 2010). Likely due to the negative emotions in response to emotional film
increased level of control they permit, behavioral tasks clips, focusing on average activation throughout the
are more commonly used to evaluate effects of cogni- entirety of film clips, as well as activation during
tive control on emotion regulation success. During specific emotional clips. In contrast to initial find-
behavioral emotion regulation tasks, participants ings indicating that older adults are less successful at

recruiting PFC regions to regulate emotions, these deployment), by modifying perception of a situation
analyses revealed that older adults are as successful (cognitive change), and by modifying emotional
as young adults at recruiting the PFC to down- reactions, such as thought suppression or expressive
regulate negative emotions, but that specific regions suppression (response modulation). Thus, various
recruited vary by age. Older adults recruited more regulation strategies may be implemented either
medial PFC regions, including the vmPFC and before (antecedent) or after (response focused) an
OFC, which are less susceptible to age-related de- emotion is generated. Among these, age-related dif-
cline than lateral PFC regions (Fjell et al., 2009). In ferences have been examined in use of (1) cognitive
contrast, young adults recruited more from lateral reappraisal (i.e., a cognitive change strategy that
PFC regions. The timing of PFC recruitment also involves reinterpreting perceptions of emotional
differed by age groups, such that older adults re- stimuli), (2) thought/experiential suppression (i.e.,
cruited from PFC regions only during emotional a response modulation strategy in which thoughts
peaks of film clips, whereas young adults recruited and/or feelings are pushed down), (3) expressive
from the PFC throughout the entirety of film clips. suppression (i.e., a response modulation strategy in
Thus, older adults may exert cognitive control more which outward expression of emotions is restrained),
selectively than younger adults for purposes of emo- (4) attention deployment strategies such as distrac-
tion regulation and rely more on medial cognitive tion or selective attention (i.e., viewing only partic-
control regions as opposed to lateral regions that ular aspects of emotional stimuli), and (5) situation
are more susceptible to age-related decline. These selection (sometimes referred to as avoidance; Gross
findings suggest that general declines in cognitive & John, 2003; Mather, 2012; Prakash, Whitmoyer,
resources might not necessarily lead to difficulties Aldao, & Schirda, 2015; Scheibe et al., 2015; Schirda,
in implementing emotion regulation, so long as Valentine, Aldao, & Prakash, 2016).
compensatory mechanisms are intact. However, such One overarching theme in the aging literature
age differences in PFC recruitment do imply that is that older adults prefer passive strategies that do
older adults engage differential strategies to regulate not involve direct confrontation with emotion-
their emotions. generating stimuli, such that use of proactive strate-
gies involving direct confrontation of negative emo-
Shifting Emotion Regulation tions declines with age (Blanchard-Fields, Stein, &
Strategies With Age Watson, 2004; Etxeberria, Etxebarria, Urdaneta, &
Consistent with findings of differential PFC re- Yanguas, 2016; Lipovcan, Prizmic, & Franc, 2009;
cruitment during emotion regulation among older Scheibe et al., 2015; Yeung, Fung, & Kam, 2012).
adults, strategies used to regulate emotions also shift Given that the ability to effectively use proactive
with age. Since strategy choices have ramifications strategies declines in late adulthood, adopting use
for emotion regulation success, understanding age- of passive strategies may compensate for shifts in
related shifts in preferred strategies and their effec- available cognitive resources (Heckhausen, 2006;
tiveness is important for understanding whether Urry & Gross, 2010). In support of this notion,
shifts in emotion regulation patterns are adaptive or disengagement from negative stimuli to selectively
maladaptive (i.e., whether emotions are regulated or attend to positive emotional information appears to
dysregulated). Although emotions may be regulated entail selective deployment of attentional resources.
through either volitional or avolitional processes This is suggested by increased vmPFC and ACC ac-
(Gyurak, Gross, & Etkin, 2011), very few behavioral tivity among older adults who show increased posi-
studies examine the mechanisms of avolitional tivity biases during passive viewing tasks (Brassen,
emotion regulation, most likely due to the difficulty Gamer, & Buechel, 2011; Jacques et al., 2010; Leclerc
of directly measuring such processes (Mauss, Bunge, & Kensinger, 2011). These are the same PFC regions
& Gross, 2007). Thus, the aging literature has pre- that older adults rely on more often than younger
dominantly focused on the different ways in which adults during emotion regulation tasks (Allard &
emotions are volitionally regulated. According to Kensinger, 2014a, 2014b). Also, passive strategies
Gross (2015), there are five families of strategies are less demanding than more active strategies.
through which emotion generation may be volition- Preliminary evidence suggests that (1) older adults
ally regulated: by changing situations experienced exhibit less lateral PFC recruitment when using pas-
(situation selection), by changing features of a sit- sive strategies than when using more active strategies
uation (situation modification), by shifting atten- (Allard & Kensinger, 2014b) and (2) preference for
tion to different features of a situation (attention distraction is associated negatively with cognitive

resources (Scheibe et al., 2015). Although passive cognitive control since it requires ignoring emotions,
regulation strategies are typically regarded as less whereas positive reappraisal requires sustaining
effective than proactive strategies, they may never- focus on emotions (Shiota & Levenson, 2009).
theless be more optimal for older adults who are Consistent with this view, initial evidence suggests
motivated to limit negative experiences (Carstensen that detached reappraisal is associated more strongly
et al., 1999). with cognitive control—specifically mental set-
Consistent with this notion, older adults appear shifting—than positive reappraisal (Liang, Huo,
to be more effective than younger adults at using Kennison, & Zhou, 2017). Also consistent with
passive strategies such as avoidance (Birditt, 2013) this view are findings that detached reappraisal is
and attention deployment (Lohani & Isaacowitz, used less frequently (Scheibe et al., 2015; Shiota &
2014). Among young adults, these strategies tend to Levenson, 2009) and is less effective (Scheibe et al.,
be maladaptive, yet older adults’ tendency to imple- 2015; Smoski, LaBar, & Steffens, 2014) among
ment attention deployment strategies is associated older adults, whereas most studies indicate that use
with reports of higher well-being and more positive and effectiveness of positive reappraisal increase
mood (Isaacowitz et al., 2008; Scheibe et al., 2015). with age (Garnefski & Kraaij, 2006; Lohani &
Additionally, some evidence suggests that age-related Isaacowitz, 2014; Shiota & Levenson, 2009, but
increases in more passive, repressive strategies to also see Schirda et al., 2016 and Nolen-Hoeksema
regulate emotions may be linked to reduced rates & Aldao, 2011).
of psychopathology observed in late adulthood Despite difficulties with detached reappraisal
(Erskine, Kvavilashvili, Conway, & Myers, 2007). among older adults, positive reappraisal appears to
That older adults are able to regulate emotions using be a more effective strategy to regulate negative
passive cognitive strategies suggests that such strate- emotions than suppression or attention deployment
gies may be a particularly efficient way of allocating (Lohani & Isaacowitz, 2014) and is associated
available cognitive resources. with wide-ranging benefits including better mental
Although there is fairly consistent evidence for health and overall well-being (Kraaij, Pruymboom,
increased use and effectiveness of disengagement & Garnefski, 2002; Nowlan, Wuthrich, & Rapee,
strategies with age, evidence for reappraisal is 2015, 2016). Together, these findings indicate that
more mixed, with some studies reporting increases aging is associated with increased reliance on pos-
with age (John & Gross, 2004; Peng, Tian, Jex, & itive reappraisal to regulate emotions, and that
Chen, 2017), others finding decreased use (Erskine increased reliance on positive reappraisal may be
et al., 2007), and others finding no age differences an adaptive compensatory mechanism. Associations
(Brummer, Stopa, & Bucks, 2014; Schirda et al., between positive reappraisal and emotional benefits
2016). Part of this discrepancy appears to be attrib- among older adults suggest that its more frequent
utable to different ways in which emotional stimuli use may contribute to less emotion dysregulation
can be reinterpreted via reappraisal. Two distinct among older adults. However, further investigation
reappraisal strategies have been identified and ex- of positive reappraisal in daily life, and its relation to
hibit differential relations to aging: detached reap- more long-term emotional goals, is required to sub-
praisal (reinterpreting situations from an unemotional stantiate this claim.
and distanced perspective) and positive reappraisal As with reappraisal, the extent to which older
(reinterpreting a situation to emphasize positive adults prefer and are able to use different suppression
outcomes). Notably, several self-report measures, strategies varies (Nolen-Hoeksema & Aldao, 2011;
such as the Emotion Regulation Questionnaire Peng et al., 2017; Schirda et al., 2016). Suppression
(Gross & John, 2003), fail to distinguish between refers to either pushing thoughts/feelings out of
these different means of reappraisal, and instead one’s mind (thought/experiential suppression) or
combine them into one general “cognitive reap- hiding outward expression of emotion (expressive
praisal” strategy. At the same time, laboratory studies suppression). Although older adults are able to im-
of emotion regulation often fail to distinguish among plement expressive suppression (Brummer et al.,
particular types of reappraisal that participants are 2014; Magai, Consedine, Krivoshekova, Kudadjie-
asked to use. Gyamfi, & McPherson, 2006; Peng et al., 2017;
When focusing on studies in which positive and Phillips, Henry, Hosie, & Milne, 2008; Shiota &
detached reappraisal strategies are distinguished, a Levenson, 2009), thought suppression requires
clearer picture of age differences in reappraisal greater inhibitory control, and ability to implement
emerges. Detached reappraisal may rely more on this strategy appears to decline with age (Anderson,

Reinholz, Kuhl, & Mayr, 2011; Beadel, Green, et al., 2017). Although there is solid evidence for
Hosseinbor, & Teachman, 2013; Magee & Teachman, age-related shifts in emotion regulation strategies,
2012). Of note, preference for each suppression strat- many studies neglect context. This is a significant
egy appears to depend on its effectiveness. Whereas oversight given that substantial shifts in context
frequency of expressive suppression increases with typically occur with age (e.g., retirement, reduced
age (Brummer et al., 2014; Hofer, Burkhard, & physical activity), along with physical declines that
Allemand, 2015; Peng et al., 2017), adults tend to may be related to emotional functioning. Thus, the
use thought suppression less frequently as they age extent to which emotion regulation and particular
(Erskine et al., 2007; Prakash et al., 2015). However, emotion regulation strategies are adaptive or mal-
despite fairly consistent behavioral evidence for adaptive across various contexts is poorly under-
preservation of expressive suppression ability with stood in the aging literature (Aldao, 2013).
age (Hofer et al., 2015; Magai et al., 2006; Shiota & One context in which age differences in emotion
Levenson, 2009; Lohani & Isaacowitz, 2014), regulation have been well studied is the context of
self-report findings are more equivocal, and indicate stress and arousal. Studies that assess moderating ef-
that expressive suppression may be related to in- fects of arousal on relations between emotion regu-
creased depressive symptoms and poorer well-being lation and aging typically involve instructions to
(Orgeta, 2011a; Gross & John, 2003) or, paradox- modify emotions while viewing emotional stimuli
ically, to increased affective well-being (Brummer of varying arousal levels. In these studies, age-related
et al., 2014; Peng et al., 2017). These contradictory improvements in emotion regulation appear to be
findings may indicate that expressive suppression is greater for low-arousal stimuli than for high-
effective initially for regulating emotions but has arousal stimuli (Dolcos, Katsumi, & Dixon, 2014;
negative ramifications in the long run. However, E.M. Kessler & Staudinger, 2009), as indicated by
further investigations into long-term consequences self-report (E.M. Kessler & Staudinger, 2009) and
of expressive suppression are required to under- reduced amygdala reactivity as corroborated by
stand implications of increased use with age. In self-report (Dolcos et al., 2014). Additionally, rela-
contrast, thought suppression is implicated consist- tive to younger adults, older adults show a greater
ently as a maladaptive emotion regulation strategy, bias toward neutral and low-arousing stimuli and
and its effectiveness appears to decline with age. away from high-arousal stimuli (Sands & Isaacowitz,
Thus, reduced reliance on this strategy seems to 2017; Scheibe et al., 2015). This suggests that older
be an adaptive approach to emotion regulation in adults may possess some awareness of their limited
late adulthood. resources and use avoidance strategies to compen-
sate. However, when unable to avoid such stimuli,
Understanding Emotion Dysregulation older adults may be less effective at regulating their
in Aging emotions. Still, emotion regulation is more difficult
The literature reviewed previously indicates clear for higher arousal stimuli, regardless of age (Sheppes,
age-related shifts in volitional processes associated 2014). Thus, it is difficult to determine from avail-
with emotion regulation. As regulation strategy pref- able data the extent to which emotion regulation
erences shift to compensate for declining cognitive difficulties are age related.
resources, engaged strategies nevertheless yield suc- When assessing whether emotional responses
cessful regulation of emotional responses. Although during stress and arousal are context appropriate or
understanding emotion regulation offers an impor- atypical, it is also important to consider how the
tant starting point for specifying emotion dysreg- experience of stressors in daily life shifts with age.
ulation, we must also consider affect modulation Older adults experience fewer daily stressors than
in terms of (1) contexts within which emotional young adults (Brose, Scheibe, & Schmiedek, 2013;
responses occur, (2) functional ramifications of reg- Neupert, Almeida, & Charles, 2007; Piazza,
ulated responses, and (3) the duration of emotional Charles, & Almeida, 2007) and exhibit less variabil-
responses. In the next section, we provide an over- ity in the types of stressors they experience (Brose
view of these modulating factors. et al., 2013). Older adults may also exhibit less
emotional reactivity to stressors (Brose et al., 2013;
The Role of Context in Emotion Neupert et al., 2007; Piazza et al., 2007), particu-
Dysregulation larly in response to interpersonal stressors (Birditt,
Adaptive emotion regulation requires appropriate Fingerman, & Almeida, 2005). Age-related increases
responses to varying contextual demands (see Cole in affective well-being and reductions in daily stressors

are linked to older adults’ reliance on avoidance of strategies in our sample. We uncovered three
strategies (see earlier), at least in contexts of inter- main factors: cognitive strategies (e.g., reappraisal,
personal stress (Charles & Carstensen, 2008; Charles, problem solving), maladaptive strategies (e.g.,
Piazza, Luong, & Almeida, 2009). Thus, older adults’ experiential suppression, expressive suppression,
reduced stress and stress reactivity may help to self-criticism, thought avoidance, worry/rumination),
explain their increases in emotional well-being. and acceptance (i.e., allowing or accepting feelings)
However, age differences in reactivity to stress have as its own unique factor.
not yet been linked directly to more global or long- The results of our study provided support for
term measures of emotional well-being. Additionally, the critical role of context in explaining age-related
similar to laboratory findings that older adults are differences in strategy use. Compared to young
less able to regulate emotions in response to higher adults, older adults reported greater use of accept-
levels of arousal (Dolcos et al., 2014; E.M. Kessler & ance strategies in situations of moderate intensity
Staudinger, 2009), older adults exhibit greater and in situations that evoked anxiety and sadness.
affective reactivity in response to more intense In contrast, there were no age differences in use
stressors than young adults (Mroczek & Almeida, of cognitive strategies. In addition, use of mala-
2004; Sliwinski, Almeida, Smyth, & Stawski, 2009; daptive strategies declined with age in high- and
Wrzus, Mueller, Wagner, Lindenberger, & Riediger, moderate-intensity situations and in situations evok-
2013). Taken together, these findings suggest that ing anxiety and sadness. Older adults’ reduced use
relations between aging and emotion dysregulation of maladaptive strategies and increased use of ac-
may depend on both the frequency and intensity ceptance strategies may suggest that aging is asso-
of stressors. Aging may be associated with adapt- ciated with more effective emotion regulation in
ive emotion regulation patterns in response to less response to situations eliciting moderate-intensity
chronic and less intense/complex stress, but less anxiety and sadness. However, maladaptive strate-
adaptive emotion regulation in response to pro- gies were identified merely based on factor analysis
longed, intense stress. and reference to previous literature, and no other
Although several studies have investigated age measures of emotion regulation success or emotion
differences in emotion regulation in certain con- dysregulation were collected. Given some evidence
texts, there is not a clear picture of how aging affects for age-related shifts in strategy effectiveness (e.g.,
whether adaptive or maladaptive emotion regula- Brummer et al., 2014; Lohani & Isaacowitz, 2014),
tion strategies are used across various contexts clear links between aging and strategy effectiveness
(i.e., the extent to which effective strategies across across various contexts cannot be inferred until
contexts differ with age). To our knowledge, only results are replicated using more direct measures of
one study to date has examined this question. Using emotion regulation.
an idiographic contextual emotion regulation as-
sessment (Aldao & Nolen-Hoeksema, 2012), we re- Effects of Emotions on Behavior
cently examined age differences in the use of several To classify patterns of emotion regulation as func-
strategies across various emotion-eliciting contexts tionally adaptive or maladaptive, aside from identi-
(emotion elicited, intensity of emotion, and situa- fying whether they are context appropriate, it is
tion type [social vs. achievement]; Schirda et al., important to specify behavioral consequences of
2016). Participants generated 24 personal situations emotional responses. As outlined previously, emo-
that occurred over the preceding two weeks in a tion dysregulation is often defined by any pattern of
3 × 2 × 4 matrix consisting of the levels of different emotional experience and/or expression that interferes
contexts: intensity (low, moderate, high), emotions with appropriate goal-directed behavior (Beauchaine,
elicited (anxiety, anger, sadness, happiness), and 2015). Patterns of either positive or negative emo-
situation type (social, achievement). Then, eight of tion can therefore be dysregulated if they lead to
these situations (selected quasi-randomly from the violations of social norms or compromise goals
24 situations generated) were presented back to (Cole et al., 2017). Consistent with this conceptual-
participants that elicited each of the four types ization, relations between aging and effects of emo-
of emotions at two of the intensities (moderate, tions on behavior can be assessed by examining
high), and participants were asked to recall the emotion–behavior sequences, by studying how typ-
emotion regulation strategies used in each of these ical behavior under intense emotion differs across
situations. We then conducted factor analyses the lifespan, or by investigating how reactions to an
across the reported strategies to identify clusters initial emotional response lead to inappropriate be-

havior (see Cole et al., 2004). Some recent studies In contrast to limiting effects of older adults’
(e.g., Orgeta, 2009; Prakash et al., 2015) have emotion regulation goals on decision making, in-
examined age-related shifts in behavioral conse- creased motivation to regulate emotions appears to
quences of emotional responses via self-report. benefit older adults’ behavior in social settings.
These studies reveal age-related declines in effects on Biases toward more positive aspects of close rela-
goal-directed behavior when individuals are upset. tionships in late adulthood lead to a selective nar-
Both studies used the Difficulties in Emotion rowing of social networks (English & Carstensen,
Regulation Scale (DERS; Gratz & Roemer, 2004), 2014). Older adults report deciding to actively dis-
which assesses characteristic reactions during the continue social relationships primarily as a function
experience of intense emotions. To date however, as- of reduced interest in these relationships (Lang,
sessment of relations between emotions and behav- 2001), and emotion plays an increasingly central
ior among older adults has predominantly examined role in determining the relationships that receive
effects of emotion on more specific behaviors such continual investment in later life (Lang, Wagner,
as decision making, cognitive task performance, and Wrzus, & Neyer, 2013). This selective pruning proc-
responding to interpersonal conflict. ess appears to serve as an antecedent form of emo-
Although older adults’ tendency to increase tion regulation as longitudinal evidence indicates
engagement with positive emotional material and that social network reductions are primarily ob-
disengage from negative material (see earlier) seems served in the number of peripheral members, and
to serve adaptive purposes in terms of immediate cross-sectionally, older adults report that social net-
mood regulation, there is some concern that such work members elicit less negative and more positive
strategies could interfere with decision making. For emotion, which in turn predicts more positive
example, such strategies may lead to overweighting daily emotional experience (Carstensen, Gross, &
positive information and underweighting nega- Fung, 1997; English & Carstensen, 2014). Such
tive information, producing suboptimal choices. selectivity—along with age-related increases in mo-
Decision-making biases have most commonly been tivation to regulate emotions—may also enable older
explored in contexts of health outcomes, as such de- adults to exhibit more adaptive behavior in social
cisions become especially important in light of in- contexts even amid conflict. Preliminary evidence
creased chronic illnesses in older age. A bias toward seems to support this notion. When attempting to
positive information could limit health-related in- resolve interpersonal problems, older adults use a
formation seeking in older adults (Löckenhoff & more diverse repertoire of strategies that are more
Carstensen, 2004). Consistent with this hypothesis, closely tailored to problem-solving contexts at hand,
when reviewing health-related information without including the domain of the problem and the types
specific instructions, older adults review and recall of emotions elicited (Blanchard-Fields et al., 2004;
more positive than negative information about skin Hoppmann & Blanchard-Fields, 2010). In contrast,
cancer, physicians, and health care plans (Isaacowitz younger adults prefer active problem-solving strat-
& Choi, 2012; Löckenhoff & Carstensen, 2007). egies (Blanchard-Fields, Chen, & Norris, 1997).
However, these age differences are eliminated when When solving emotionally salient interpersonal
both older and younger adults are given instructions problems, older adults use more passive emotion
that elicit information-gathering goals (Isaacowitz regulation strategies and experience less anger
& Choi, 2012; Löckenhoff & Carstensen, 2007). (Blanchard-Fields et al., 2004; Blanchard-Fields &
Additionally, when given instructions to review in- Coats, 2008), consistent with findings of reduced
formation with the goal of managing emotions, older affective and physiological reactivity to negative social
adults typically look less at negative content, more interactions with increasing age (Luong & Charles,
rapidly regulate their moods, and when making deci- 2014). Older adults also more effectively employ
sions are less affected than young adults (Isaacowitz & strategies, particularly when responding to interper-
Choi, 2012). This suggests that age-related shifts sonal problems (Blanchard-Fields, 2009; Blanchard-
that are considered to be beneficial for emotional Fields, Mienaltowski, & Seay, 2007). Thus, it seems
well-being may limit health-related information that older adults’ increased consideration of emotional
seeking and influence attention, memory, and deci- context when resolving interpersonal problems may
sion making. However, effects on information seeking help them respond more effectively. However, it is
and decision making seem to be attributable largely possible that age-related reductions in the intensity
to age-related goals, and can be eliminated by simple of emotions produced by these negative social interac-
motivational manipulations. tions could be confounding results given that older

adults report less anger (a high-arousal emotion). more rapidly regulate their reactions than younger
Replication using more salient mood inductions adults (Larcom & Isaacowitz, 2009). Among older
may be required to rule out this possibility. adults, more rapid emotion regulation was associ-
One common way to investigate effects of emo- ated with lower trait anxiety and fewer depressive
tions on behavior is to evaluate emotion regulation symptoms, and older adults who rapidly regulated
during performance of neuropsychological tasks that their emotions reported increases in positive affect
assess cognitive constructs such as working memory that persisted 20 minutes later. No such effect was
and processing speed (see earlier). Such investigations found for younger adults. These findings suggest
reveal that cognitive performance is less affected that among older adults, emotion regulation may
by emotion regulation efforts among older versus be more rapid and enduring than among young
younger adults. When instructed to downregulate adults. In seeming contrast to these findings, a
feelings of disgust following mood induction, older third study found that when placed in a rumina-
adults exhibit increased working memory perfor- tion condition, older adults did not exhibit more
mance, whereas young adults exhibit decreased rapid emotion recovery than younger adults, and
performance (Scheibe & Blanchard-Fields, 2009). even exhibited delayed blood pressure recovery
Similarly, engaging in expressive suppression during (Robinette & Charles, 2016). Findings from this
a memory task led to reduced memory for emotional study highlight the important role that regulation
stimuli only in young adults (Emery & Hess, 2011). strategies play in age differences in emotion dys-
Healthy older adults’ performance on cognitive tasks regulation and suggest there may be age-specific
also appears to be less affected by anger and regret vulnerabilities related to particular types of emotion
(Brassen, Gamer, Peters, Gluth, & Büchel, 2012). regulation strategies. Taken together, these studies
In this study, age-related decreases in responsivity offer preliminary evidence for older adults’ ability to
to regret were paralleled by increases in ACC activ- more rapidly regulate emotions than younger adults,
ity and more reward-specific striatal activation, sug- and for possible age-specific benefits to such rapid
gesting adaptive shifts in emotion regulation with regulation. However, the strategies and biological
age. Nevertheless, laboratory investigations require processes underlying these age differences in regula-
replication across a broader array of cognitive do- tion and recovery, as well as the broader effects of
mains and emotionally salient contexts. such age-related shifts on functioning, are currently
poorly understood.
Duration of Emotions
Given that effective emotion regulation depends Aging and Psychopathology
on modulating emotional responses in the service of A final way of estimating effects of aging on emo-
long-term and short-term goals, another important tion dysregulation is to examine age differences in
consideration for distinguishing shifts in emotion the etiology and presentation of psychopathology.
dysregulation is the duration of emotions during As noted previously, emotion dysregulation is a
and following regulation efforts. Emotions may prominent characteristic of most psychiatric dis-
change too slowly in response to modification efforts, orders (Beauchaine & Zisner, 2017; Kring & Sloan,
indicating poor emotional recovery, or too abruptly, 2009). In most epidemiological studies, rates of
indicating lability. Emotions become dysregulated psychiatric disorders decrease with age, particularly
when they resist change to the point of impairing anxiety, mood, and substance use disorders (Hasin
function (Cole et al., 2017; Thompson, 1990). et al., 2005; R. C. Kessler et al., 2005; Reynolds
Unfortunately, there is a dearth of research examining et al., 2015), with the lowest 12-month and lifetime
the extent to which temporal dynamics of emotion prevalence rates for mood and anxiety disorders
are affected by aging. Only a few studies have exam- seen among those above age 65 (Hasin et al., 2005).
ined such temporal processes, all within contexts of Among older adults specifically, increased anxiety
relatively brief mood inductions in laboratory set- (Orgeta, 2011a) and depressive (Orgeta, 2011b)
tings. Following a 10-minute anger induction and a symptoms are associated with greater self-reported
10-minute sadness induction, young adults reported difficulties regulating emotional responses. Thus,
longer durations of shame, contempt, and joy than although older adults generally exhibit lower rates
older adults (Magai et al., 2006). Older adults were of psychopathology than younger adults, aging may
also better at suppressing emotions during an inhi- lead to changes in the experience and causes of
bition condition than younger adults. Similarly, certain psychiatric disorders, particularly depression
following negative emotion induction, older adults and anxiety.

Late-life depression is one clinical issue that has younger adults (Diefenbach, Stanley, & Beck, 2001).
received particular attention in the aging literature. Additionally, much like depression, anxiety in older
Depression presents differently among older adults adults more often manifests as somatic symptoms
than younger adults, and may be more detrimental. and is associated with several medical conditions
Older adults often endorse fewer affective symptoms (Alwahhabi, 2003; Turnbull, 1989). Unfortunately,
and are more likely to report cognitive changes, much of this evidence for age differences in the
somatic symptoms, and loss of interest (Fiske, experience of anxiety is inferred via comparing
Wetherell, & Gatz, 2009). Late-life depression is symptom rates across studies, and there is a dearth
also associated with more self-neglect, as well as of empirical evidence directly comparing older
higher rates of suicidal ideation, attempts, and adults to younger adults within the same study
completion relative to depression in younger adults (Wolitzky-Taylor, Castriotta, Lenze, Stanley, &
(Blazer, 2003). Also of note, the majority of de- Craske, 2010).
pressed older adults have their first episode after age
60 (Brodaty et al., 2001; Bruce et al., 2002; Fiske Synthesis
et al., 2009), which suggests that age-specific vul- The aging literature paints a fairly positive picture of
nerabilities and risk factors contribute. For example, emotional well-being in late adulthood. For the most
both aging and depression are associated with neu- part, aging is associated with more adaptive patterns
roendocrine dysregulation such as hypersecretion of emotion regulation. However, there are some
of corticotropin-releasing factor (CRF) and lower moderating variables and exceptions. The extent to
testosterone levels (Alexopoulos, 2005; Blazer & which aging is related to emotion dysregulation
Hybels, 2005). Age-related neuroendocrine dysreg- appears to depend on availability of resources and
ulation may compromise the integrity of frontos- contexts in which regulation efforts occur. Aging
triatal brain networks, increasing vulnerability to brings about physical and neurocognitive declines
depression. In addition, reduced white matter in- that may lead to difficulty regulating emotions in
tegrity, greater declines in hippocampal volume, response to prolonged, highly arousing stressors,
and Lewy bodies are more common among patients and that may impair one’s ability to use cognitively
with late-life versus early-life depression (Fiske demanding strategies that are adaptive among
et al., 2009; Krishnan, 2002; Sachs-Ericsson et al., young adults. Although somewhat speculative, such
2013; Tsopelas et al., 2011). Vascular damage, more declines may contribute to development of anxiety
commonly seen in late life, can also influence neural and depressive disorders in late adulthood—even
connectivity in frontostriatal and frontolimbic path- though such disorders are generally less common
ways that are involved in emotion regulation and among older adults. These declines are consistent
may contribute to depressive symptoms (Taylor, with predictions about emotion regulation success
Aizenstein, & Alexopoulos, 2013). Still, further re- depending on the availability of resources made by
search is necessary to link such declines to disrup- SST, the SOC-ER, and the SAVI model. However,
tion in emotion regulation and establish temporal also consistent with SAVI and SST, aging is related
precedence of age-related declines in their relation- to increased prioritization of emotional goals;
ship to symptoms. increased ability to regulate emotions over short
Although they have received less attention, anxi- intervals of time in response to acute, low-arousal
ety disorders are the most common form of psycho- stressors and interpersonal stressors; and increased
pathology experienced by older adults (R. C. Kessler ability to engage in several goal-directed behaviors
et al., 2005). Anxiety commonly co-occurs with under intense emotions. Age-related shifts in strate-
depression and predicts both incident and recurrent gies used to regulate emotions are also observed,
depressive symptoms in older adults (Potvin et al., such that older adults rely more on less cognitively
2013). Among older adults, anxiety is tied to in- demanding strategies and selectively limit their
creased use of maladaptive active emotion regula- exposure to intense negative stimuli. Thus, con-
tion strategies (Orgeta & Orrell, 2014) and reduced sistent with the SOC-ER framework, older adults
use of adaptive emotion regulation strategies such as appear to rely on more preserved processes to
positive reappraisal (Nowlan et al., 2016). Although compensate for reduced cognitive resources and
presentation of anxiety is similar across the lifespan, in turn optimize emotion regulation processes.
there are a few notable shifts with age. Older adults However, motivations to disengage from negative
with anxiety disorders worry more about health and stimuli may have some negative implications for
disability and less about work and finances than decision making.

Although the majority of the aging literature to the temporal precedence of contextual factors
date has focused on adaptive rather than maladap- related to emotion regulation. For instance, despite
tive emotion regulation processes, age-related shifts reported associations between age-related physical
in the effectiveness of emotion regulation have and neurocognitive declines and various metrics of
clear implications for emotion dysregulation. With emotion dysregulation such as increased psychopa-
regard to context, older adults appear to exhibit more thology and increased use of maladaptive emotion
adaptive emotional responses to acute, low-arousal regulation strategies, almost no longitudinal data
emotional stimuli than young adults (particularly address age-related declines as causes of emotion
when allowed to use preferred strategies). However, dysregulation. It is conceivable that emotion dys-
in contexts of prolonged, high-arousal stressors and regulation precedes physical declines, especially given
contexts in which constraints are placed on cogni- findings that emotional processes mediate health
tive resources, older adults may be less effective at behavior effects on physical function late in life
regulating their emotional responses. With regard (Depp, Vahia, & Jeste, 2010). Second, long-term
to the effects of emotion on behavior, older adults implications of short-term emotion regulation suc-
seem to exhibit more adaptive behavioral responses cess remain unclear. Although adaptive in the short
in social settings and on cognitive performance term, it is possible that passive and avoidant strat-
tasks during the experience of intense emotions egies preferred by older adults have detrimental
than younger adults. However, increased motiva- long-term effects on behavior or emotion. To im-
tion to regulate emotions among older adults also prove our understanding of such effects, future
appears to interfere with decision making. Finally, work should incorporate longitudinal designs that
when considering durations of emotion, there is permit assessment of directionality in relations be-
preliminary evidence that older adults are able to tween emotion dysregulation and factors hypoth-
more rapidly regulate than younger adults, and that esized to underlie age-related shifts in emotion
among older adults specifically, more rapid emotion dysregulation, such as changes in emotional goals,
regulation is related to better long-term emotional strategy use, and neurocognitive function. Studies
well-being. of such relations should be conducted at multiple
levels of analysis (self-report, behavioral, and physi-
Future Directions ological) to corroborate findings and rule out
Despite numerous theoretical frameworks that help potential confounds.
to account for age differences in emotion regula- Finally, despite numerous examinations of how
tion, there is still much to be understood about the volitional (explicit) emotion regulation processes
effects of aging on emotion dysregulation. Although shift with age, the extent to which aging affects avo-
studies suggest that context moderates the effective- litional (implicit) emotion regulation is unknown
ness of emotion regulation efforts, emotion regula- and warrants direct investigation in future studies.
tion has been explored in a limited number of con- Overall, these gaps indicate that there is still much
texts. As a result, there is poor understanding of the to learn about how aging affects processes through
extent to which aging influences the appropriate- which emotions become dysregulated. Given the
ness of emotions and regulation ability across central role of emotion dysregulation in psychopa-
daily life contexts outside of social settings, or how thology, clarifying such processes may help to iden-
specific age-related shifts in emotion dysregulation tify more accurate, relevant targets for treating psy-
relate to clinically relevant shifts in behavioral func- chiatric disorders across the lifespan. Thus, it will be
tion. To address these gaps, future studies should important for future studies to more thoroughly
assess emotion regulation shifts across a broader evaluate long-term functions of emotions and their
variety of relevant contexts (e.g., work/achievement, modulation across the lifespan to better understand
family life, and various health contexts), and should how specific aging processes may ameliorate or lead
more thoroughly examine effects of emotion regula- to dysfunctional patterns of emotion dysregulation.
tion on relevant measures of functional consequences
(e.g., ability to complete independent activities of References
daily living) and clinically significant changes in Aldao, A. (2013). The future of emotion regulation research:
psychopathology. Capturing context. Perspectives on Psychological Science, 8,
155–172.
Another gap in the literature concerns the extent Aldao, A., & Nolen-Hoeksema, S. (2012). The influence of context
to which temporal processes of emotion regulation on the implementation of adaptive emotion regulation
shift with age. First, there is poor understanding of strategies. Behaviour Research and Therapy, 50, 493–501.

Alexopoulos, G. S. (2005). Depression in the elderly. Lancet, problems. Journals of Gerontology. Series B, Psychological
365, 1961–1970. Sciences and Social Sciences, 62, P61–P64.
Allard, E. S., & Kensinger, E. A. (2014a). Age-related differences in Blanchard-Fields, F., Stein, R., & Watson, T. L. (2004). Age
functional connectivity during cognitive emotion regulation. differences in emotion-regulation strategies in handling
Journals of Gerontology. Series B, Psychological Sciences and everyday problems. Journals of Gerontology. Series B, 59,
Social Sciences, 69, 852–860. P261–P269.
Allard, E. S., & Kensinger, E. A. (2014b). Age-related differences Blazer, D. G. (2003). Depression in late life: Review and
in neural recruitment during the use of cognitive reappraisal commentary. Journals of Gerontology. Series A, Biological
and selective attention as emotion regulation strategies. Sciences and Medical Sciences, 58, 249–265.
Frontiers in Psychology, 5: 296. Blazer, D. G., & Hybels, C. F. (2005). Origins of depression in
Allemand, M., Hill, P. L., Ghaemmaghami, P., & Martin, M. later life. Psychological Medicine, 35(9), 1241–1252.
(2012). Forgivingness and subjective well-being in adulthood: Brabec, J., Rulseh, A., Hoyt, B., Vizek, M., Horinek, D.,
The moderating role of future time perspective. Journal of Hort, J., & Petrovicky, P. (2010). Volumetry of the human
Research in Personality, 46, 32–39. amygdala—an anatomical study. Psychiatry Research, 182,
Allen, J. S., Bruss, J., Brown, C. K., & Damasio, H. (2005). 67–72.
Normal neuroanatomical variation due to age: The major Brassen, S., Gamer, M., & Buechel, C. (2011). Anterior cingulate
lobes and a parcellation of the temporal region. Neurobiology activation is related to a positivity bias and emotional stability
of Aging, 26, 1279–1282. in successful aging. Biological Psychiatry, 70, 131–137.
Alwahhabi, F. (2003). Anxiety symptoms and generalized anxiety Brassen, S., Gamer, M., Peters, J., Gluth, S., & Büchel, C. (2012).
disorder in the elderly: A review. Harvard Review of Psychiatry, Don’t look back in anger! Responsiveness to missed chances in
11, 180–193. successful and nonsuccessful aging. Science, 336, 612–614.
American Psychiatric Association. (2013). Diagnostic and Brodaty, H., Luscombe, G., Parker, G., Wilhelm, K., Hickie, I.,
statistical manual of mental disorders (5th ed.). Arlington, VA: Austin, M. P., & Mitchell, P. (2001). Early and late onset
American Psychiatric Publishing depression in old age: Different aetiologies, same
Anderson, M. C., Reinholz, J., Kuhl, B. A., & Mayr, U. (2011). phenomenology. Journal of Affective Disorders, 66, 225–236.
Intentional suppression of unwanted memories grows more Brose, A., Scheibe, S., & Schmiedek, F. (2013). Life contexts
difficult as we age. Psychology and Aging, 26, 397–405. make a difference: Emotional stability in younger and older
Baltes, P. B., & Baltes, M. M. (1990). Psychological perspectives Adults. Psychology and Aging, 28, 148–159.
on successful aging: The model of selective optimization with Bruce, M. L., McAvay, G. J., Raue, P. J., Brown, E. L., Meyers,
compensation. In Successful aging:Â Perspectives from the B. S., Keohane, D. J., . . . Weber, C. (2002). Major depression
behavioral sciences (pp. 1–34). New York, NY, US: Cambridge in elderly home health care patients. American Journal of
University Press. Psychiatry, 159, 1367–1374.
Beadel, J. R., Green, J. S., Hosseinbor, S., & Teachman, B. A. Brummer, L., Stopa, L., & Bucks, R. (2014). The influence of age
(2013). Influence of age, thought content, and anxiety on on emotion regulation strategies and psychological distress.
suppression of intrusive thoughts. Journal of Anxiety Disorders, Behavioural and Cognitive Psychotherapy, 42, 668–681.
27, 598–607. Cacioppo, J., Bernston, G., Bechara, A., Tranel, D., & Hawkley, L.
Beauchaine, T. P. (2015). Future directions in emotion (2011). Could an aging brain contribute to subjective well-
dysregulation and youth psychopathology. Journal of Clinical being? The value added by a social neuroscience perspective. In
Child and Adolescent Psychology, 44, 875–896. A. Todorov, S. Fiske, & D. Prentice (Eds.), Social neuroscience:
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion Toward understanding the underpinnings of the social mind (pp.
regulation, and the latent structure of psychopathology: An 249–262). New York, NY: Oxford University Press.
integrative and convergent historical perspective. International Campos, J. J., Mumme, D. L., Kermoian, R., & Campos, R. G.
Journal of Psychophysiology. 119, 108–118. (1994). A functionalist perspective on the nature of emotion.
Birditt, K. S. (2013). Age differences in emotional reactions to Monographs of the Society for Research in Child Development,
daily negative social encounters. Journals of Gerontology. Series 59, 284–303.
B, Psychological Sciences and Social Sciences, 69, 557–566. Carstensen, L. L., Fung, H. H., & Charles, S. T. (2003).
Birditt, K. S., Fingerman, K. L., & Almeida, D. M. (2005). Age Socioemotional selectivity theory and the regulation of
differences in exposure and reactions to interpersonal tensions: emotion in the second half of life. Motivation and Emotion,
A daily diary study. Psychology and Aging, 20, 330–340. 27, 103–123.
Blanchard-Fields, F. (2009). Flexible and adaptive socio-emotional Carstensen, L. L., Gross, J., & Fung, H. (1997). The social
problem solving in adult development and aging. Restorative context of emotional experience. In M. P. Lawton &
Neurology and Neuroscience, 27, 539–550. K. W. Schaie (Eds.), Annual review of geriatrics and gerontology
Blanchard-Fields, F., Chen, Y., & Norris, L. (1997). Everyday (pp. 325–352). New York, NY: Springer.
problem solving across the adult life span: Influence of Carstensen, L. L., Isaacowitz, D. M., & Charles, S. T. (1999).
domain specificity and cognitive appraisal. Psychology and Taking time seriously: A theory of socioemotional selectivity.
Aging, 12, 684–693. American Psychologist, 54, 165–181.
Blanchard-Fields, F., & Coats, A. H. (2008). The experience Carstensen, L. L., Pasupathi, M., Mayr, U., & Nesselroade, J. R.
of anger and sadness in everyday problems impacts age (2000). Emotional experience in everyday life across the
differences in emotion regulation. Developmental Psychology, adult life span. Journal of Personality and Social Psychology,
44, 1547–1556. 79, 644–655.
Blanchard-Fields, F., Mienaltowski, A., & Seay, R. B. (2007). Charles, S. T., & Carstensen, L. L. (2008). Unpleasant situations
Age differences in everyday problem-solving effectiveness: elicit different emotional responses in younger and older
Older adults select more effective strategies for interpersonal adults. Psychology and Aging, 23, 495–504.

Charles, S. T., & Piazza, J. R. (2009). Age differences in affective Emotion Regulation Scale. Journal of Psychopathology and
well-being: Context matters. Social and Personality Psychology Behavioral Assessment, 26, 41–54.
Compass, 3, 711–724. Gross, J. J. (1998). Antecedent- and response-focused emotion
Charles, S. T., Piazza, J. R., Luong, G., & Almeida, D. A. (2009). regulation: Divergent consequences for experience, expression,
Now you see it, now you don’t: Age differences in affective and physiology. Journal of Personality and Social Psychology,
reactivity to social tensions. Psychology and Aging, 24, 645–653. 74, 224–237.
Cole, P. M., Hall, S. E., & Hajal, N. J. (2017). Emotion Gross, J. J. (2015). The extended process model of emotion
dysregulation as a vulnerability to psychopathology. In regulation: Elaborations, applications, and future directions.
T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent Psychological Inquiry, 26, 130–137.
psychopathology (3rd ed., pp. 346–386). Hoboken, NJ: Wiley. Gross, J. J., & John, O. P. (2003). Individual differences in
Cole, P. M., Michel, M. K., & Teti, L. O. (1994). The two emotion regulation processes: Implications for affect,
development of emotion regulation and dysregulation: relationships, and well-being. Journal of Personality and Social
A clinical perspective. Monographs of the Society for Research Psychology, 85, 348–362.
in Child Development, 59, 73–100. Grühn, D., Sharifian, N., & Chu, Q. (2016). The limits of a
Charles, S. T., Reynolds, C. A., & Gatz, M. (2001). Age-related limited future time perspective in explaining age differences
differences and change in positive and negative affect over in emotional functioning. Psychology and Aging, 31(6),
23 years. Journal of Personality and Social Psychology, 80, 583–593.
136–151. Gyurak, A., Gross, J. J., & Etkin, A. (2011). Explicit and implicit
Depp, C., Vahia, I. V., & Jeste, D. (2010). Successful aging: emotion regulation: A dual-process framework. Cognition
Focus on cognitive and emotional health. Annual Review of and Emotion, 25(3), 400–412.
Clinical Psychology, 6, 527–550. Hasin, D. S., Goodwin, R. D., Stinson, F. S., & Grant, B. F.
Diefenbach, G. J., Stanley, M. A., & Beck, J. G. (2001). Worry (2005). Epidemiology of major depressive disorder: Results
content reported by older adults with and without generalized from the National Epidemiologic Survey on Alcoholism
anxiety disorder. Aging and Mental Health, 5, 269–274. and Related Conditions. Archives of General Psychiatry, 62,
Dolcos, S., Katsumi, Y., & Dixon, R. A. (2014). The role of 1097–1106.
arousal in the spontaneous regulation of emotions in healthy Heckhausen, J. (2006). Developmental regulation in adulthood:
aging: A fMRI investigation. Frontiers in Psychology, 5, 681. Age-normative and socio-structural constraints as adaptive
Emery, L., & Hess, T. M. (2011). Cognitive consequences of challenges. New York, NY: Cambridge University Press.
expressive regulation in older adults. Psychology and Aging, Hofer, M., Burkhard, L., & Allemand, M. (2015). Age differences
26, 388–396. in emotion regulation during a distressing film scene. Journal
English, T., & Carstensen, L. L. (2014). Selective narrowing of of Media Psychology, 27, 47–52.
social networks across adulthood is associated with improved Hoppmann, C. A., & Blanchard-Fields, F. (2010). Goals and
emotional experience in daily life. International Journal of everyday problem solving: Manipulating goal preferences
Behavioral Development, 38, 195–202. in young and older adults. Developmental Psychology, 46,
Erskine, J. A. K., Kvavilashvili, L., Conway, M. A., & Myers, L. 1433–1443.
(2007). The effects of age on psychopathology, well-being and Isaacowitz, D. M., & Choi, Y. (2012). Looking, feeling, and
repressive coping. Aging and Mental Health, 11, 394–404. doing: Are there age differences in attention, mood, and
Etxeberria, I., Etxebarria, I., Urdaneta, E., & Javier Yanguas, J. behavioral responses to skin cancer information? Health
(2016). Age differences among older adults in the use of Psychology, 31, 650–659.
emotion regulation strategies. What happens among over 85s Isaacowitz, D. M., Toner, K., Goren, D., & Wilson, H. R.
and centenarians? Aging and Mental Health, 20, 974–980. (2008). Looking while unhappy mood-congruent gaze in
Fiske, A., Wetherell, J. L., & Gatz, M. (2009). Depression in young adults, positive gaze in older adults. Psychological
older adults. Annual Review of Clinical Psychology, 5, 363–389. Science, 19, 848–853.
Fjell, A. M., Westlye, L. T., Amlien, I., Espeseth, T., Reinvang, I., Isaacowitz, D. M., Toner, K., & Neupert, S. D. (2009). Use of
Raz, N., . . . Walhovd, K. B. (2009). High consistency of gaze for real-time mood regulation: Effects of age and
regional cortical thinning in aging across multiple samples. attentional functioning. Psychology and Aging, 24, 989–994.
Cerebral Cortex, 19, 2001–2012. Jacques, P. S., Dolcos, F., & Cabeza, R. (2010). Effects of aging
Garnefski, N., & Kraaij, V. (2006). Relationships between on functional connectivity of the amygdala during negative
cognitive emotion regulation strategies and depressive evaluation: A network analysis of fMRI data. Neurobiology of
symptoms: A comparative study of five specific samples. Aging, 31, 315–327.
Personality and Individual Differences, 40, 1659–1669. John, O. P., & Gross, J. J. (2004). Healthy and unhealthy emotion
Geda, Y. E., Roberts, R. O., Knopman, D. S., Petersen, R. C., regulation: Personality processes, individual differences, and
Christianson, T. J. H., Pankratz, V. S., . . . Rocca, W. A. (2008). life span development. Journal of Personality, 72, 1301–1334.
Prevalence of neuropsychiatric symptoms in mild cognitive Kessler, E.M., & Staudinger, U. M. (2009). Affective experience
impairment and normal cognitive aging: Population-based in adulthood and old age: The role of affective arousal and
study. Archives of General Psychiatry, 65, 1193–1198. perceived affect regulation. Psychology and Aging, 24, 349–362.
Goodkind, M. S., Gyurak, A., McCarthy, M., Miller, B. L., & Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas,
Levenson, R. W. (2010). Emotion regulation deficits in K. R., & Walters, E. E. (2005). Lifetime prevalence and age-
frontotemporal lobar degeneration and Alzheimer’s disease. of-onset distributions of DSM-IV disorders in the National
Psychology and Aging, 25, 30–37. Comorbidity Survey replication. Archives of General Psychiatry,
Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment 62, 593–602.
of emotion regulation and dysregulation: Development, Knight, M., Seymour, T. L., Gaunt, J. T., Baker, C., Nesmith, K.,
factor structure, and initial validation of the Difficulties in & Mather, M. (2007). Aging and goal-directed emotional

attention: Distraction reverses emotional biases. Emotion, 7, Magee, J. C., & Teachman, B. A. (2012). Distress and recurrence
705–714. of intrusive thoughts in younger and older adults. Psychology
Kraaij, V., Pruymboom, E., & Garnefski, N. (2002). Cognitive and Aging, 27, 199–210.
coping and depressive symptoms in the elderly: A longitudinal Mather, M. (2012). The emotion paradox in the aging
study. Aging & Mental Health, 6, 275–281. brain. Annals of the New York Academy of Sciences, 1251,
Kring, A. M., & Sloan, D. M. (Eds.). (2009). Emotion regulation 33–49.
and psychopathology: A transdiagnostic approach to etiology and Mather, M. (2016). The affective neuroscience of aging. Annual
treatment. New York, NY: Guilford. Review of Psychology, 67, 213–238.
Krishnan, K. R. R. (2002). Biological risk factors in late life Mather, M., & Carstensen, L. L. (2005). Aging and motivated
depression. Biological Psychiatry, 52, 185–192. cognition: The positivity effect in attention and memory.
Kryla-Lighthall, N., & Mather, M. (2009). The role of cognitive Trends in Cognitive Sciences, 9, 496–502.
control in older adults’ emotional well-being. In Mather, M., & Knight, M. (2005). Goal-directed memory: The
V. L. Bengston, D. Gans, N. M. Pulney, & M. Silverstein role of cognitive control in older adults’ emotional memory.
(Eds.), Handbook of theories of aging (pp. 323–344). New York, Psychology and Aging, 20, 554–570.
NY: Springer. Mauss, I. B., Bunge, S. A., & Gross, J. J. (2007). Automatic
Kunzmann, U., Little, T. D., & Smith, J. (2000). Is age-related emotion regulation. Social and Personality Psychology Compass,
stability of subjective well-being a paradox? Cross-sectional 1(1), 146–167.
and longitudinal evidence from the Berlin Aging Study. Mroczek, D. K., & Almeida, D. M. (2004). The effect of daily
Psychology and Aging, 15, 511–526. stress, personality, and age on daily negative affect. Journal of
Lang, F. R. (2001). Regulation of social relationships in Personality, 72, 355–378.
later adulthood. Journals of Gerontology. Series B, 56(6), Mroczek, D. K., & Kolarz, C. M. (1998). The effect of age on
P321–P326. positive and negative affect: A developmental perspective on
Lang, F. R., & Carstensen, L. L. (2002). Time counts: Future happiness. Journal of Personality and Social Psychology, 75,
time perspective, goals, and social relationships. Psychology 1333–1349.
and Aging, 17, 125–139. Nashiro, K., Sakaki, M., & Mather, M. (2012). Age differences in
Lang, F. R., Wagner, J., Wrzus, C., & Neyer, F. J. (2013). Personal brain activity during emotion processing: Reflections of age-
effort in social relationships across adulthood. Psychology and related decline or increased emotion regulation? Gerontology,
Aging, 28(2), 529–539. 58, 156–163.
Larcom, M. J., & Isaacowitz, D. M. (2009). Rapid emotion Neupert, S. D., Almeida, D. M., & Charles, S. T. (2007). Age
regulation after mood induction: Age and individual differences in reactivity to daily stressors: The role of personal
differences. Journals of Gerontology. Series B, 64B, 733–741. control. Journals of Gerontology. Series B, Psychological Sciences
Leclerc, C. M., & Kensinger, E. A. (2011). Neural processing and Social Sciences, 62, P216–P225.
of emotional pictures and words: A comparison of young Nolen-Hoeksema, S., & Aldao, A. (2011). Gender and age
and older adults. Developmental Neuropsychology, 36, differences in emotion regulation strategies and their
519–538. relationship to depressive symptoms. Personality and
Liang, Y., Huo, M., Kennison, R., & Zhou, R. (2017). The role Individual Differences, 51, 704–708.
of cognitive control in older adult cognitive reappraisal: Nowlan, J. S., Wuthrich, V. M., & Rapee, R. M. (2015). Positive
Detached and positive reappraisal. Frontiers in Behavioral reappraisal in older adults: A systematic literature review.
Neuroscience, 11, 27. Aging and Mental Health, 19, 475–484.
Lipovcan, L. K., Prizmic, Z., & Franc, R. (2009). Age and Nowlan, J. S., Wuthrich, V. M., & Rapee, R. M. (2016). The
gender differences in affect regulation strategies. Drustvena impact of positive reappraisal on positive (and negative)
Istrazivanja, 18, 1075–1088. emotion among older adults. International Psychogeriatrics,
Löckenhoff, C. E., & Carstensen, L. L. (2004). Socioemotional 28, 681–693.
selectivity theory, aging, and health: The increasingly delicate Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of
balance between regulating emotions and making tough emotion. Trends in Cognitive Sciences, 9, 242–249.
choices. Journal of Personality, 72, 1395–1424. Ochsner, K. N., Silvers, J. A., & Buhle, J. T. (2012). Functional
Löckenhoff, C. E., & Carstensen, L. L. (2007). Aging, emotion, imaging studies of emotion regulation: A synthetic review
and health-related decision strategies: Motivational and evolving model of the cognitive control of emotion.
manipulations can reduce age differences. Psychology and Annals of the New York Academy of Sciences, 1251, E1–E24.
Aging, 22, 134–146. Opitz, P. C., Lee, I. A., Gross, J. J., & Urry, H. L. (2014). Fluid
Lohani, M., & Isaacowitz, D. M. (2014). Age differences in cognitive ability is a resource for successful emotion
managing response to sadness elicitors using attentional regulation in older and younger adults. Frontiers in Psychology,
deployment, positive reappraisal and suppression. Cognition 5, 609.
and Emotion, 28, 678–697. Opitz, P. C., Rauch, L. C., Terry, D. P., & Urry, H. L. (2012).
Luong, G., & Charles, S. T. (2014). Age differences in affective Prefrontal mediation of age differences in cognitive reappraisal.
and cardiovascular responses to a negative social interaction: Neurobiology of Aging, 33, 645–655.
The role of goals, appraisals, and emotion regulation. Orgeta, V. (2009). Specificity of age differences in emotion
Developmental Psychology, 50, 1919–1930. regulation. Aging and Mental Health, 13, 818–826.
Magai, C., Consedine, N. S., Krivoshekova, Y. S., Kudadjie- Orgeta, V. (2011a). Emotion dysregulation and anxiety in late
Gyamfi, E., & McPherson, R. (2006). Emotion experience adulthood. Journal of Anxiety Disorders, 25, 1019–1023.
and expression across the adult life span: Insights from a Orgeta, V. (2011b). Regulation of affect in late adulthood: Effects
multimodal assessment study. Psychology and Aging, 21, of mild depressive symptoms. Aging & Mental Health, 15,
303–317. 866–872.

Orgeta, V., & Orrell, M. (2014). Coping styles for anxiety and processes: Findings from two measurement-burst diary
depressive symptoms in community-dwelling older adults. studies. Psychology and Aging, 24, 828–840.
Clinical Gerontologist, 37, 406–417. Smoski, M. J., LaBar, K. S., & Steffens, D. C. (2014). Relative
Peng, Y., Tian, B., Jex, S. M., & Chen, Y. (2017). Employees’ age effectiveness of reappraisal and distraction in regulating
moderates relationships of emotional suppression with emotion in late-life depression. American Journal of Geriatric
health and well-being. Work Aging and Retirement, 3, 89–101. Psychiatry, 22, 898–907.
Phillips, L. H., Henry, J. D., Hosie, J. A., & Milne, A. B. (2008). Sturm, V. E., Yokoyama, J. S., Seeley, W. W., Kramer, J. H.,
Effective regulation of the experience and expression of Miller, B. L., & Rankin, K. P. (2013). Heightened emotional
negative affect in old age. Journals of Gerontology. Series B, contagion in mild cognitive impairment and Alzheimer’s
Psychological Sciences and Social Sciences, 63, P138–P145. disease is associated with temporal lobe degeneration.
Piazza, J. R., Charles, S. T., & Almeida, D. M. (2007). Living Proceedings of the National Academy of Sciences, 110,
with chronic health conditions: Age differences in affective 9944–9949.
well-being. Journals of Gerontology. Series B, 62, P313–P321. Taylor, W. D., Aizenstein, H. J., & Alexopoulos, G. S. (2013).
Potvin, O., Bergua, V., Swendsen, J., Meillon, C., Tzourio, C., The vascular depression hypothesis: Mechanisms linking
Ritchie, K., . . . Amieva, H. (2013). Anxiety and 10-year risk vascular disease with depression. Molecular Psychiatry, 18,
of incident and recurrent depressive symptomatology in 963–974.
older adults. Depression and Anxiety, 30, 554–563. Thompson, R. A. (1990). Emotion and self-regulation. In
Prakash, R. S., Whitmoyer, P., Aldao, A., & Schirda, B. (2015). R. A. Thompson (Ed.), Nebraska Symposium on Motivation:
Mindfulness and emotion regulation in older and young Vol. 36. Socioemotional development (pp. 383–483). Lincoln,
adults. Aging and Mental Health, 21, 77–87. NE: University of Nebraska Press.
Ramsey, M. A., & Gentzler, A. L. (2014). Age differences in Tsopelas, C., Stewart, R., Savva, G. M., Brayne, C., Ince, P.,
subjective well-being across adulthood: The roles of savoring Thomas, A., . . . Medical Research Council Cognitive Function
and future time perspective. International Journal of Aging and Ageing Study. (2011). Neuropathological correlates of
and Human Development, 78, 3–22. late-life depression in older people. British Journal of Psychiatry,
Reynolds, K., Pietrzak, R. H., El-Gabalawy, R., Mackenzie, 198, 109–114.
C. S., & Sareen, J. (2015). Prevalence of psychiatric disorders Turnbull, J. M. (1989). Anxiety and physical illness in the elderly.
in U.S. older adults: Findings from a nationally representative Journal of Clinical Psychiatry, 50, S40–S45.
survey. World Psychiatry, 14, 74–81. Urry, H. L., & Gross, J. J. (2010). Emotion regulation in
Robinette, J. W., & Charles, S. T. (2016). Age, rumination, and older age. Current Directions in Psychological Science, 19,
emotional recovery from a psychosocial stressor. Journals of 352–357.
Gerontology. Series B, Psychological Sciences and Social Sciences, Verhaeghen, P. (2011). Aging and executive control: Reports of a
71, 265–274. demise greatly exaggerated. Current Directions in Psychological
Sachs-Ericsson, N., Corsentino, E., Moxley, J., Hames, J. L., Science, 20, 174–180.
Rushing, N. C., Sawyer, K., . . . Steffens, D. C. (2013). Verhaeghen, P., & Salthouse, T. A. (1997). Meta-analyses of
A longitudinal study of differences in late- and early-onset age-cognition relations in adulthood: Estimates of linear
geriatric depression: Depressive symptoms and psychosocial, and nonlinear age effects and structural models. Psychological
cognitive, and neurological functioning. Aging and Mental Bulletin, 122, 231–249.
Health, 17, 1–11. Wilhelm, F. H., & Grossman, P. (2010). Emotions beyond the
Sands, M., & Isaacowitz, D. M. (2017). Situation selection across laboratory: Theoretical fundaments, study design, and
adulthood: The role of arousal. Cognition and Emotion, 31, analytic strategies for advanced ambulatory assessment.
791–798. Biological Psychology, 84, 552–569.
Scheibe, S., & Blanchard-Fields, F. (2009). Effects of regulating Winecoff, A., LaBar, K. S., Madden, D. J., Cabeza, R., &
emotions on cognitive performance: What is costly for young Huettel, S. A. (2011). Cognitive and neural contributors to
adults is not so costly for older adults. Psychology and Aging, emotion regulation in aging. Social Cognitive and Affective
24, 217–223. Neuroscience, 6, 165–176.
Scheibe, S., Sheppes, G., & Staudinger, U. M. (2015). Distract Wolitzky-Taylor, K. B., Castriotta, N., Lenze, E. J., Stanley,
or reappraise? Age-related differences in emotion-regulation M. A., & Craske, M. G. (2010). Anxiety disorders in older
choice. Emotion, 15, 677–681. adults: A comprehensive review. Depression and Anxiety, 27,
Schirda, B., Valentine, T. R., Aldao, A., & Prakash, R. S. (2016). 190–211.
Age-related differences in emotion regulation strategies: Wright, C. I., Negreira, A., Gold, A. L., Britton, J. C., Williams,
Examining the role of contextual factors. Developmental D., & Barrett, L. F. (2008). Neural correlates of novelty and
Psychology, 52, 1370–1380. face-age effects in young and elderly adults. NeuroImage, 42,
Sheppes, G. (2014). Emotion regulation choice: Theory and 956–968.
findings. In J. J. Gross (Ed.), Handbook of emotion regulation Wrzus, C., Mueller, V., Wagner, G. G., Lindenberger, U., &
(2nd ed., pp. 126–139). New York, NY: Guilford. Riediger, M. (2013). Affective and cardiovascular responding
Shiota, M. N., & Levenson, R. W. (2009). Effects of aging on to unpleasant events from adolescence to old age: Complexity
experimentally instructed detached reappraisal, positive of events matters. Developmental Psychology, 49, 384–397.
reappraisal, and emotional behavior suppression. Psychology Yeung, D. Y., Fung, H. H., & Kam, C. (2012). Age differences
and Aging, 24, 890–900. in problem solving strategies: The mediating role of future
Sliwinski, M. J., Almeida, D. M., Smyth, J., & Stawski, R. S. time perspective. Personality and Individual Differences, 53,
(2009). Intraindividual change and variability in daily stress 38–43.

CH A PT E R
Emotion Generation, Regulation,
7 and Dysregulation as Multilevel
Transdiagnostic Constructs
Sheila E. Crowell, Robert D. Vlisides-Henry, and Parisa R. Kaliush
Abstract
Emotion generation, regulation, and dysregulation are complex constructs that are challenging to
define and measure. This chapter reviews prevailing definitions and theories of these constructs
and examines the literature across multiple levels of analysis. It adopts a developmental perspective,
which guides interpretation of the literature and helps clarify discrepant points of view. The extent
to which emotion generation and regulation are separable represents a significant controversy in the
field. When viewed as cognitive constructs, it is virtually impossible to disentangle emotion generation
and regulation. However, at the biological level, there are important differences in neural structures
involved in bottom-up emotion generation processes versus those associated with top-down regulation
of emotions. From a developmental perspective, emotions and emotion dysregulation emerge early
in life, whereas emotion regulation strategies develop more gradually as a function of maturation
and socialization. Future research should continue to reconcile different perspectives on emotion
generation, regulation, and dysregulation.
Keywords: emotion dysregulation, transdiagnostic, development, emotions, multiple levels of analysis
Introduction when emotional processes become dysregulated,

Philosophers, psychologists, and laypeople have consequences can be costly.
long sought to understand and define emotions. Not Emotional development begins in utero, with
surprisingly, this has led to many divergent perspec- facial expressions of distress becoming increasingly
tives on emotions—their universality, evolutionary complex and frequent across the third trimester
functions, underlying neural mechanisms, physio- (Reissland, Francis, & Mason, 2013). Thus, expres-
logical and behavioral signatures, and interactions sions of pain and discomfort begin before birth and
with motivation and cognition. Most definitions of therefore likely confer significant adaptive benefit
emotion and related processes have limitations, for all infants. Individual differences in emotional
leading to debate in the field. This has yielded a rich expression also emerge early in development.
and complex literature on emotion, which is among Variation in intensity, duration, and soothability of
the most researched topics in psychology. Emotion negative emotion may be one index of early tem-
regulation and dysregulation can also be challenging perament (e.g., Johnson, Posner, & Rothbart, 1991).
to define and measure. As a result, emotion regula- Several interacting and independent factors affect
tion researchers have developed creative paradigms these temperamental differences. For example, spe-
to capture what happens when we attempt to con- cific genetic variants underlie aspects of early tem-
trol or suppress emotions, reappraise or re-evaluate perament, contributing to heritable differences in
their meaning, amplify them, or simply let them trait impulsivity and trait anxiety (Beauchaine,
run their natural course. Importantly, emotions Zisner, & Sauder, 2017; Sallis, Davey Smith, &
are such an integral part of human experience that Munafò, 2018). Researchers have also begun to
85
examine epigenetic effects as mechanisms of early to inform the literature today—many scholars still
temperament (Conradt, Adkins, Crowell, Monk, & view emotional processes as emerging from interac-
Kobor, 2018). Epigenetics, defined by alterations to tions between physiology and cognitions (see, e.g.,
gene expression rather than gene structure, repre- Gross, 2015). Importantly, however, Schachter and
sent one type of Gene × Environment interaction Singer’s conceptualization does not account fully for
that contribute to early emerging individual differ- individual differences in emotion generation and
ences in emotional processes (see Chapter 16, this expression early in life, that is, prior to developing
volume). By birth, postnatal environments begin to cognitive schemas needed to label and categorize
shape emotional expression through Temperament × emotional reactions.
Caregiving interactions, which lay a foundation More recently, distinctions between emotion
for emotion regulation and dysregulation. Thus, generation and regulation have become a source of
emotion generation, regulation, and dysregulation ongoing debate in the field. According to one per-
are developmental processes that result from com- spective, emotion generation is affected by apprais-
plex transactions across multiple levels of analysis als, or the extent to which an emotional stimulus
beginning at conception. (1) captures a person’s attention and (2) is given mean-
In this chapter, we review emotion and related ing (Gross, 2015). In other words, for an emotion to
constructs from a developmental perspective. This emerge, a person must attend to and appraise a
helps clarify discrepant empirical findings and theo- stimulus in some manner, even if that process occurs
ries that emerge when researchers investigate emo- automatically and outside of conscious awareness.
tional processes cross-sectionally or within relatively This “situation–attention–appraisal–response” per-
narrow developmental windows (e.g., adolescence). spective has been articulated in many foundational
Indeed, when environments are constrained, such theoretical papers (Gross, 1998, 2015; Gross &
as in early development, there are fewer influences Feldman Barrett, 2011; McRae, Misra, Prasad, Pereira,
on emotional processes and, consequently, biologi- & Gross, 2011; Gross, Sheppes, & Urry, 2011;
cal predispositions take precedence. Over time, so- Ochsner et al., 2009; see Chapter 10, this volume).
cialization, family and peer dynamics, cultural fac- This perspective offers an advantage of identifying
tors, exposure to interventions, and many other distinct and separable elements of the emotion
forces interact to affect emotion-related processes. generation process, each of which could be amena-
Consistent with the developmental psychopathol- ble to regulation.
ogy perspective (Beauchaine, Constantino, & In an alternate theoretical perspective, Panksepp
Hayden, 2018; Cicchetti, 1984, 1993), taking a lifes- and colleagues define emotion generation as a bio-
pan approach helps elucidate continuities and dis- logically driven process that emerges from coordi-
continuities in risk/resilience trajectories and poten- nated interactions between subcortical and neocor-
tial points for intervention. tical regions (Panksepp, 1982, 1998; Panksepp &
Watt, 2011; see Chapter 2, this volume). According
Terms and Concepts to this theory, primary emotions originate within
Emotion Generation subcortical structures, which have been preserved
For the past half century of psychological research, evolutionarily across species (see also Beauchaine,
scholars have typically conceptualized emotions as a 2015a). These primary emotions are not shaped by
multilevel process, emerging from rapid feedback environmental inputs, prior learning, or appraisals.
between physiological and cognitive systems. For Rather, their principal function is to stimulate mo-
example, Schachter and Singer (1962) described tivated behaviors, such as those that allow an organ-
emotion generation in two steps: First, physiologi- ism to acquire new skills, maintain homeostasis,
cal arousal occurs; then, a person evaluates whether survive, and reproduce (Panksepp & Watt, 2011).
that arousal is consistent with observable stimuli. If Consequently, neural structures involved in primary
a person perceives a match, he or she can label that emotion generation are essentially indistinguishable
experience in terms of readily available cognitions from circuits involved in movement, approach-
(e.g., my heart is racing and I am about to receive a or avoidance-related motivation, and reward
shock; therefore, I am anxious). However, if there is (Beauchaine et al., 2017). Across development,
dissonance between arousal and perception, the primary emotions become associated with specific
person may need to search for alternate explana- contexts, stimuli, or patterns of stimuli. This leads to
tions to describe an experience appropriately (e.g., secondary emotion processes, which are characterized
too much caffeine). This two-step model continues by learned associations between primary emotions
86 Multilevel Transdiagnostic Constructs

and life experiences. Because environments vary & Zisner, 2017; Felix-Ortiz, Burgos-Robles, Bhagat,
widely, secondary emotional processes are necessar- Leppla, & Tye, 2016; Monk et al., 2008). Perhaps
ily more complex and variegated. Finally, tertiary unsurprisingly, trait anxious individuals are at
emotions reflect dynamic interactions between elevated risk for internalizing psychopathology,

neural systems involved in (1) primary and second- including depressive and anxiety disorders (e.g.,

ary emotions and (2) higher order processes, such as Beauchaine & Thayer, 2015; Weems et al., 2007).
language, consciousness, and self/identity (Panksepp, In contrast, trait impulsivity, or extreme
1998). Secondary and tertiary emotions rely on ne- approach motivation and trait exuberance (e.g.,

ocortical systems and structures—the top layer of Dollar, Stifter, & Buss, 2017), is linked to risk for
the cerebral hemisphere that is involved in higher externalizing disorders (Beauchaine, 2015a).
order functions—which are largest and most fully Impulsive individuals show less functional connec-
developed in primates. According to this perspec- tivity between mesolimbic structures and the PFC
tive, emotion regulation is believed to reflect effective (e.g., Beauchaine & Zisner, 2017; Trost et al., 2014).
secondary and tertiary processes, whereas dysregula- Trait impulsivity is associated with concurrent and
tion is believed to reflect ineffective secondary and prospective risk for attention deficit hyperactivity
tertiary processes (see Chapter 2 for a more thor- disorder (ADHD), conduct disorder, and criminal
ough review). activity (e.g., Beauchaine et al., 2017; Blonigen,
More recently, Beauchaine and Zisner (2017) ar- Hicks, Krueger, Patrick, & Iacono, 2005; Swann,
ticulated an integrated theory of motivation, emo- Bjork, Moeller, & Dougherty, 2002). Similar to
tion regulation, and psychopathology that incorpo- Panksepp, Beauchaine attributes emotion genera-
rates key elements of Gross’s (cognitive neuroscience) tion processes to subcortical structures. However,
and Panksepp’s (basic neuroscience) perspectives as by incorporating motivational theories and, specifi-
well as several independent lines of psychological cally, individual differences in behavioral approach
and biological research. In this review and others, and avoidance, Beauchaine’s theory bridges basic
Beauchaine has extended neuroscientific findings neuroscience research on emotion with develop-
to the broader developmental psychopathology mental psychopathology theories. Importantly, and
literature, placing greater emphasis on longitudi- similar to both Panksepp and Gross, Beauchaine
nal transactions between basic motivational tenden- acknowledges that emotion regulation involves
cies and potentiating environmental experiences “top-down emotion regulation systems,” which are
(Beauchaine, 2001, 2012, 2015a; Beauchaine & cortically mediated.
Zisner, 2017; Beauchaine et al., 2017). According
to this perspective, individual differences in basic Emotion Regulation
motivational tendencies are driven by “bottom-up To date, researchers have used a range of definitions
emotion generation systems,” which are largely sub- of emotion regulation, and there is ongoing debate
cortical. A primary function of emotion generation in the field. Some view emotion regulation as largely
systems is to activate appropriate behavior in re- distinct from emotion generation (e.g., Beauchaine
sponse to motivationally salient cues. Specifically, & Zisner, 2017), whereas others contend that the
these neural response patterns function to motivate two cannot be disentangled (e.g., Gross, 1998).
approach (wanting/liking) or avoidance (anxiety) Nonetheless, across these disparate perspectives lies
behaviors and to resolve basic approach–avoidance, an overarching, mostly agreed-upon definition:
approach–approach, or avoidance–avoidance con- Emotion regulation reflects processes through which
flicts (see also Corr, 2013). Biologically mediated people use top-down cortical mechanisms to iden-
individual differences in approach and avoidance tify, select, implement, and monitor how emotions are
motivation form a basis for temperament, and may experienced and/or expressed in relation to personal
give rise to psychopathology at their extremes (e.g., goals (Beauchaine, 2015a; Beauchaine & Zisner,
Sutton & Davidson, 1997). 2017; Gross, 1998; Thompson, 1993). Steps involved
Trait anxiety, an extreme manifestation of in emotion regulation have been articulated in
avoidance motivation or behavioral inhibition (e.g., several theoretical and empirical papers by Gross
Kagan, 2017), involves apprehensiveness about and colleagues (e.g., Gross, 1998, 2015; Gross &
approaching stimuli. High behavioral inhibition is Feldman Barrett, 2011; McRae et al., 2011), who
associated with altered connectivity between the propose that emotion regulation strategies can be
amygdala and regions of the prefrontal cortex (PFC) identified at distinct points along a timeline of an
and anterior cingulate cortex (ACC; e.g., Beauchaine unfolding emotional response. Regulation can occur
Crowell, Vlisides-Henry, and Kaliush 87

before an emotion begins (antecedent focused) or can happen within a person (intrapersonally) or
once it has become activated (response focused). b etween people (interpersonally; Sheppes, Suri, &
Response-focused regulation involves several steps, Gross, 2015). Although some emotion regulation
beginning with emotion identification. strategies emerge early in development (e.g., thumb
In brief, identification has two substeps: recog- sucking; Eisenberg, Spinrad, & Eggum, 2010), most
nizing a generated emotion and deciding whether are shaped through coregulation and socialization—
or not to regulate it. If one decides to regulate, selec- becoming increasingly sophisticated, cognitively
tion follows. Selection involves choosing an emo- mediated, and independent across development
tion regulation strategy based on context and (Vohs & Baumeister, 2016). Thus, early signs of
personal goals. That is, different situations warrant emotion dysregulation (e.g., expressions of emotion
different regulation strategies. For instance, emo- that are more intense than typical, age-normative
tion regulation in anticipation of a job interview distress) likely emerge earlier in development than
likely differs from regulation in response to en- emotion regulation.
countering a dangerous animal in the woods. From a developmental perspective, emotion dys-
Implementation entails translating a chosen emo- regulation is likely tied closely to emotion genera-
tion regulation strategy into specific tactics. Finally, tion, especially early in life. Accordingly, individual
monitoring involves ongoing evaluation of regula- differences in neural functions of motivational
tion, where a person decides whether to maintain, systems that subserve generation of approach and
change, or stop an emotion entirely. Gross (2015) avoidance emotions may heighten risk for emotion
describes monitoring as an ongoing process that dysregulation in two ways: (1) directly, due to tem-
is constantly acting upon emotion generation pro- peramental differences in emotional intensity or
cesses. For more details on these emotion regulation duration, and/or (2) indirectly, as when distress re-
steps, see Jazaieri, Uusberg, Uusberg, and Gross mains unchanged despite attempts at self-regulation.
(Chapter 10 of this volume). Emotion regulation is, Under typical developmental circumstances, emo-
by nature, difficult to measure because it is often tion regulation skills and strategies improve as the
conceptualized as the absence of emotional prob- PFC develops. However, neuromaturational devel-
lems (Cole, Martin, & Dennis, 2004). Therefore, opment of the PFC and acquisition of emotion
researchers rely on complex paradigms or self-report regulation strategies can be disrupted, especially in
measures to determine (1) whether a person experi- family environments characterized by neglect,
enced an emotion and (2) whether the emotion abuse, invalidation, or coercive conflict escalation
was regulated (Beauchaine, 2015a; Cole, Hall, & (Beauchaine, Hinshaw, & Bridge, 2019; Crowell
Hajal, 2017). et al., 2013, 2014, 2017; Crowell, Puzia, &
Yaptangco, 2015). By adulthood, associations be-
Emotion Dysregulation tween emotion generation and emotion dysregula-
Emotion dysregulation, in contrast, is often easier tion may be more difficult to disentangle because
to observe and measure (see Beauchaine, 2015a). In effects of intervening contextual forces on neural
this Handbook, we define emotion dysregulation as mechanisms of emotion regulation and self-control
patterns of emotional experience and expression that accrue across the lifespan in high-risk environments
are too intense, labile, rigid, or prolonged or that in- (see, e.g., Beauchaine et al., 2017).
terfere with appropriate goal-directed or interper- In sum, emotion generation, regulation, and
sonal behavior (Beauchaine, 2015a; Cole et al., dysregulation are distinct but related constructs.
2004; Gratz & Roemer, 2004). As noted earlier, Most existing definitions do not attend to develop-
emotional expressions and sensations emerge early mental processes, which may contribute to discrep-
in development—beginning prenatally (Kurjak, ant views in the field. At the simplest level, emotion
Azumendi, Andonotopo, & Salihagic-Kadic, 2007)— dysregulation could be defined as abnormal emo-
and serve adaptive communicative and survival function regulation (i.e., “dys-” is of Greek origin and
tions at birth (Abe & Izard, 1999). Therefore, emer- means “bad,” “abnormal,” or “difficult”). However,
gent signs of emotion dysregulation may also have it may be more accurate to conceptualize dysregula-
origins prior to birth. Importantly, emotion dysregu- tion as a foundational human tendency (indeed, all
lation is not merely the opposite or absence of regula- infants show some degree of dysregulation) that is
tion (Cole et al., 2004, 2017). As noted previously, gradually altered across development. As a result,
emotion regulation involves conscious or automatic there is a wide phenotypic spectrum of adult emo-
activation of a goal to influence emotions, which tion regulation abilities, which are shaped through

longitudinal interactions between a child’s motiva- able children (i.e., high trait anxious and/or impul-
tional tendencies and potentiating environmental sive), risk for emotion dysregulation and psychopa-
experiences. thology is highest within the context of adverse
childrearing environments, such as those character-
Developmental Theory ized by maltreatment, neglect, and/or invalidation
There is an extensive empirical and theoretical lit- (see Beauchaine, Hinshaw, et al., 2019). Furthermore,
erature describing emotion generation, regulation, maltreatment rarely occurs in the absence of other
and dysregulation from a developmental perspective significant forms of familial dysfunction, including
(e.g., Beauchaine, Hinshaw, et al., 2019; Crowell et al., harsh parenting, corporal punishment, inconsistent
2013, 2017; Herts, McLaughlin, & Hatzenbuehler, discipline, low warmth, and coercive parenting
2012). Briefly, individual differences in emotion strategies that inadvertently socialize emotion dys-
generation are highly heritable (e.g., Blonigen regulation through negative reinforcement pro-
et al., 2005), arising from subcortical structures and cesses (e.g., Crowell, Yaptangco, & Turner, 2016;
networks that are established early in development Skowron, & Reinemann, 2005; Wilson, Rack, Shi,
(Beauchaine & Zisner, 2017). Dopamine (DA) neu- & Norris, 2008). Thus, from a developmental per-
rons, for example, form during the first trimester spective, emotion dysregulation emerges from herit-
(around 5 weeks postconception), and factors such able individual differences in emotion generation
as maternal nutrition, substance use, and immune systems, which interact with potentiating environ-
functioning can affect development and function of mental experiences across development to shape
DA neurons, producing lasting variation in infant emotional lability and reactivity, ultimately increas-
phenotypes (Gatzke-Kopp, 2011; Luan, Hammond, ing risk for many distinct forms of psychopathology.
Vuillermot, Meyer, & Eyles, 2018). These functional
differences in neural responding provide a basis for Current Methods and Findings
temperament, which can be defined as “constitu- Given difficulties in observing and defining emo-
tionally based individual differences in reactivity tion generation, regulation, and dysregulation, it
and self-regulation, with the term constitutional re- follows that measuring these constructs is equally
ferring to the person’s relatively enduring biological complex. We argue from a developmental perspec-
makeup” (Rothbart, Ahadi, & Hershey, 1994, p. 22). tive that these constructs can—and should—be
There are multiple theories of temperament, measured across multiple levels of analysis (see also
each with different labels and conceptualizations Cole et al., 2004). Indeed, it is misguided to assume
(e.g., Rothbart, 1986; Solmeyer & Feinberg, 2011). that human emotions (and associated cognitions
Although most existing models are based on obser- and behaviors) can be explained by one-dimensional
vations of healthy infants and ordinary variation in measurement. Rather, multiple neurobiological sys-
infant disposition, they can be extended to better tems interact with interpersonal and cultural factors
understand the extreme ends of continuously dis- to shape emotion generation, regulation, and dysregu-
tributed traits. Examining these extremes is essential lation (e.g., Ashkanasy, 2003; Cicchetti, Ackerman,
for understanding emotion dysregulation as a trans- & Izard, 1995; Robinson, 2014; Rogers, Schröder,
diagnostic vulnerability factor for later psychopa- & von Scheve, 2014; Strauman, 2017). We explore
thology (e.g., Beauchaine et al., 2017). In other some of those interacting systems next.
words, understanding the etiology of psychopa-
thology requires consideration of more extreme Intrapersonal Levels of Emotion
trait vulnerabilities, significant environmental risks, Genetics
and Biology × Environment interactions across Identifying genetic effects (e.g., single nucleotide
development. polymorphisms, epigenetic alterations in gene func-
Behavioral inhibition and trait anxiety, which tion) is one important avenue for elucidating bio-
are characterized by excessive fear, worry, and/or logical underpinnings of individual differences in
dysphoria, predispose to later internalizing disor- affective behavior (Drabant et al., 2006; Strauman,
ders, such as separation anxiety disorder and gener- 2017; for a review of molecular genetics and
alized anxiety disorder (e.g., Kagan, 2017; Kagan & emotion regulatory processes, see Chapter 15, this
Snidman, 1999). In contrast, trait impulsivity con- volume). This area of research aligns with Beauchaine
fers risk for externalizing disorders, including op- and Zisner’s (2017) emphasis on longitudinal trans-
positional defiant disorder, conduct disorder, and actions between heritable emotion generation sys-
substance use (Beauchaine et al., 2017). For vulner- tems and potentiating environmental contexts in

shaping emotion dysregulation and risk for polymorphisms within the serotonin system often
psychopathology. For instance, the mesolimbic
interact with environmental exposures to potentiate
DA system—and related dopaminergic subsystem risk for emotion dysregulation and related psycho-
genes—is a primary neural substrate of affective pathology.
states (e.g., wanting, liking) related to approach mo- In considering Gene × Environment interac-
tivation (Beauchaine, 2015a; Beauchaine & Zisner, tions, Kim and colleagues (2011) explored how
2017). When individuals experience heritable defi- genes interact with culture to influence emotion
ciencies in DA responding, they may exhibit exces- generation, regulation, and dysregulation. The oxy-
sive approach behaviors and be at increased risk for tocin receptor polymorphism (OXTR) rs53576 is a
externalizing disorders in the context of adverse genetic variant that has been associated with socio-
childrearing environments (Beauchaine, 2015a; emotional sensitivity among European Americans
Beauchaine et al., 2017). Accordingly, genes in- (Kim et al., 2011). Those high in socioemotional
volved in DA neurotransmission have been a focus sensitivity are more responsive to social feedback re-
of research on externalizing behavior (e.g., Gizer, garding appropriate behavioral expression (Butler,
Otto, & Ellingson, 2016). 2012). Kim and colleagues (2011) found that emo-
The enzyme catechol-O-methyltransferase tion regulation tendencies among European and
(COMT) metabolizes DA and therefore plays a key Korean Americans were associated significantly
role in shaping human cognitions, behaviors, and with the OXTR rs53576 GG genotype. Whereas
emotion generation (Bearden et al., 2005). Drabant Korean Americans with this genotype exhibited
and colleagues (2006) explored the influence of a more emotional suppression, European Americans
polymorphism (i.e., a compositional variation) in exhibited less emotional suppression. These mani-
the COMT gene on corticolimbic activity during a festations of emotion regulation were consistent
face-matching paradigm. Individuals with the MET with participants’ respective cultural norms and,
allele exhibit increases in hippocampal and ventro- notably, could appear dysregulated outside of a spe-
lateral prefrontal cortex activation when viewing cific cultural context. Findings highlight the impor-
faces with negative expressions (e.g., fear, anger) and tance of considering interactions among heritable
show other neurological indices of temperamental emotion generation systems, cortically mediated
inflexibility. The researchers concluded that those emotion regulation processes, and environmental
with heritable variations in DA neurotransmission, contexts when investigating the development of
associated with the MET allele of the COMT poly- emotion dysregulation.
morphism, may demonstrate rigid affective process-
ing that could lead to emotion dysregulation and Neurological Level
related psychological disorders. Given the inordinate complexity of the brain,
Decades of research have implicated genetic vari- emotion generation, regulation, and dysregulation
ants in the serotonin system in the pathophysiology are challenging to delineate (see Chapter 1, this
of depression and other internalizing disorders volume). One line of research stems from Gray’s
(Owens & Nemeroff, 1994). More recently, re- early work on anxiety and impulsivity. According
searchers have extended these findings to studies of to J. A. Gray (e.g., 1982), the septo-hippocampal
emotion regulatory processes involved in those dis- system—including projections from the amygdala—
orders. Specifically, the serotonin transporter-linked subserves trait anxiety and passive avoidance of
polymorphism (5-HTTLPR) has been associated threat (see J. A. Gray & McNaughton, 2000). In
with physiological reactivity to emotional stimuli contrast, the midbrain DA system—including pro-
(Plieger et al., 2017), attachment and emotion regu- jections from the ventral tegmental area to the nu-
latory capacities among young children (Viddal, cleus accumbens—subserves pleasurable affective
Berg-Nielsen, Belsky, & Wichstrøm, 2017), poor states and approach (see, e.g., Schultz, 2002).
distress tolerance among emotionally abused youth These projections and adjacent interconnected
(Amstadter et al., 2012), and nonsuicidal self-injury neural structures make up the ventral striatum
and suicidal behaviors among adults (Mann, Brent, (VS; see Beauchaine, 2012, 2015a). DA neurons
& Arango, 2001). In addition, our lab found that in the VS are less responsive to reinforcers among
peripheral serotonergic function among self-injuring impulsive individuals (see Plichta & Scheres, 2014).
adolescents interacted with their negativity and In turn, low DA responding is experienced psy-
parental conflict to explain 64% of the variance in chologically as an aversive, irritable mood state
self-injuring behaviors (Crowell et al., 2008). Thus, (Laakso et al., 2003). Consequently, impulsive

individuals often engage in excessive reward-seeking In addition, deficient connectivity between the
behaviors to upregulate their aversive mood (see amygdala and PFC is associated with increased
Beauchaine, 2012). behavioral inhibition, emotion dysregulation, and
Several researchers extended Gray’s work to risk for internalizing psychopathology (Beauchaine
further delineate neurological underpinnings of
& Zisner, 2017; Monk et al., 2008). Less bilateral
emotions and approach/avoidance behaviors (e.g., insular cortex volume has been associated with vio-
Beauchaine & Zisner, 2017; Casey, Giedd, & lent and impulsive behaviors among adolescents
Thomas, 2000; Davidson, 2000). Their work aligns with early presentations of borderline personality
closely with that of Panksepp (1982, 1998) by dif- disorder (BPD; Takahashi et al., 2009) as well as
ferentiating emotion generation from regulation. self-injuring adolescent girls who are at risk for de-
Whereas emotion generation derives from early- veloping BPD (Beauchaine, Sauder, et al., in press).
maturing subcortical, limbic brain regions (e.g., These discoveries of extended neuromaturational
nucleus accumbens, amygdala, hippocampus, and time courses associated with transdiagnostic risk
ventral tegmental area), emotion regulation origi- factors, like emotion dysregulation, self-injury, and
nates from later maturing cortical structures, in- impulsivity, offer a promising direction for preven-
cluding the PFC, ACC, lateral orbitofrontal cortex tion and early intervention programs involving
(OFC), insular cortex, and inferior frontal gyrus emotion regulation strategies (Beauchaine, Sauder,
(IFG). Neuroimaging studies—particularly those et al., in press; Goldin, McRae, Ramel, & Gross,
implementing functional magnetic resonance imag- 2008).
ing (fMRI)—have advanced our understanding of
the development and functions of these brain Psychophysiology
structures (Casey, Jones, & Hare, 2008). For in- Respiratory sinus arrhythmia (RSA) is a measure of
stance, it is now well established that the PFC parasympathetic influences on beat-to-beat variabil-
is one of the last brain regions to mature, and its ity in heart rate. Low resting RSA and, to a lesser
top-down regulatory functions become more fine- extent, excessive decreases in RSA in response to
tuned across development (Casey et al., 2000; emotionally evocative tasks are consistent biomark-
Casey, Tottenham, Liston, & Durston, 2005). This ers of emotion dysregulation (Beauchaine, 2015b;
formulation aligns with observed normative de- Beauchaine & Thayer, 2015). For instance, whereas
clines in impulsive behaviors and improvements in adolescents with high resting RSA demonstrate re-
self-regulation through adolescence and into adult- silience in the face of adversity and are buffered
hood (Casey et al., 2008). Similarly, it informs cur- from internalizing and externalizing pathology,
rent understanding of nonlinear developmental those with low resting RSA demonstrate more de-
trajectories of impulsive versus risk-taking behav- pressive symptoms and aggression when raised in
iors (Casey et al., 2008). Whereas impulsive behav- contexts of unsupportive parenting (Beauchaine,
iors tend to decline across development due to 2015b; Gordis, Feres, Olezeski, Rabkin, & Trickett,
steadily maturing cortical brain regions, risk-taking 2010). Research on associations between RSA de-
behaviors appear to increase during adolescence creases and psychopathology are more mixed. On
relative to childhood, likely due to an imbalance the one hand, some research demonstrates a protec-
between mature emotion generation systems and tive effect of RSA withdrawal against development
immature regulatory control (Casey et al., 2008). of internalizing psychopathology among maltreated
By adulthood, both generation and regulation sys- youth (see, e.g., McLaughlin, Alves, & Sheridan,
tems are more fully developed, which accounts for 2014). On the other hand, large decreases in RSA
reduced impulsivity and risk taking. are associated with emotion dysregulation and
Cortical volumetric and functional abnormali- self-harm among teens (Crowell et al., 2005). A
ties confer neural vulnerabilities to emotion dysregu- common interpretation is that modest decreases in
lation and related psychopathology (Beauchaine, RSA—as seen during attention deployment (e.g.,
Sauder, Derbidge, & Uyeji, in press; Beauchaine Suess, Porges, & Plude, 1994)—reflect effective reg-
et al., 2017). For instance, adolescents with conduct ulatory strategies, whereas excessive decreases indi-
disorder and impulsive tendencies exhibit signifi- cate emotion dysregulation (Beauchaine, 2015a,
cantly less gray matter pruning in frontal brain 2015b; S. A. O. Gray, Jones, Theall, Glackin, &
structures as they mature (De Brito et al., 2009)—a Drury, 2017; Mezulis, Crystal, Ahles, & Crowell,
likely neural underpinning of their difficulties with 2015; Price & Crowell, 2016; Yaptangco, Crowell,
emotion regulation (Beauchaine & Zisner, 2017). Baucom, Bride, & Hansen, 2015).

Biological Sex reinforce gender-based stereotypic emotion expres-
Most theorists agree that emergence of sex differ- sion by using a greater variety of emotion-related
ences in emotion generation, regulation, and dys- words with their daughters and more anger-related
regulation are developmental processes involving words with their sons (Cervantes & Callanan, 1998;
biological and social components. In infancy, boys Chaplin, Cole, & Zahn-Waxler, 2005). In addition,
typically demonstrate higher arousal and approach parents are less tolerant of atypical gendered behav-
behaviors, lower language abilities, and less effortful ior among their children (Kim, Arnold, Fisher, &
control than girls (Brody, 1999; Martel, 2013). In Zeljo, 2005). For example, parents practice more
contrast, girls often demonstrate high negative emo- overreactive disciplinary actions when their sons
tionality and effortful control and low approach be- and daughters exhibit internalizing and externaliz-
haviors (Crowell & Kaufman, 2016; Martel, 2013). ing behaviors, respectively (Kim et al., 2005). Finally,
These early sex differences are often attributed to peer groups can reinforce sex-specific emotional
gene expression and influences of sex hormones in processes, as boys tend to engage in more physical
utero (Zahn-Waxler, Shirtcliff, & Marceau, 2008). activities with larger groups of children and girls
Furthermore, they contribute to differing rates of typically disclose more feelings to smaller groups of
externalizing and internalizing disorders among friends (Rose & Rudolph, 2006). In sum, sex and
boys and girls: Whereas boys are at heightened risk gender effects offer important bridges between in-
for externalizing psychopathology such as conduct trapersonal and interpersonal Biology × Environment
disorder and oppositional defiance, girls are at interactions in emotion generation, regulation, and
heightened risk for internalizing psychopathology dysregulation.
such as anxiety and depression (Crowell & Kaufman,
2016; Eme, 2015). These sex-typical trajectories are Interpersonal Levels of Emotion
implicated in the disproportionate diagnostic rates Emotions often occur in interpersonal contexts, and
of antisocial and borderline personality disorders individuals may even regulate each other’s emo-
among males and females, respectively (Beauchaine, tions, be it purposefully or automatically, for proso-
Klein, Crowell, Derbidge, & Gatzke-Kopp, 2009; cial or selfish reasons (Butler, 2015). Emotional
Crowell & Kaufman, 2016). Notably, a growing processes are influenced by cultural standards that
body of literature suggests that externalizing psy- dictate which emotions are warranted under various
chopathology is associated prospectively with bord- circumstances (Butler, Lee, & Gross, 2007). Thus,
erline personality pathology among both girls and although literature on interpersonal levels of emo-
boys (Burke & Stepp, 2012; Swanson et al., 2014). tion rarely intersects with that of intrapersonal, they
As well, some boys may develop borderline person- are of equal importance in understanding emotion
ality pathology via a more traditionally internalizing regulation and dysregulation.
trajectory (Crowell & Kaufman, 2016). Thus, despite
the common occurrence of sex-specific trajectories Dyadic Interactions
to emotion dysregulation and psychopathology, People often seek assistance from trusted friends
there are also important multifinal outcomes that and family when struggling with overwhelming
are likely driven by biology–environment interac- emotions. Butler (2015) outlined a clear picture of
tions (Beauchaine et al., 2009). how dynamic interpersonal emotions stem from
Sex-specific socialization practices interact with three interdependent processes, including (1) con-
biologically based emotion generation systems to vergence of individuals’ emotional responses to ex-
predict differences in emotion dysregulation (Crowell ternal stimuli, (2) individuals’ emotional reactions
& Kaufman, 2016; Hughes, Crowell, Uyeji, & Coan, to each other, and (3) interpersonal emotion regula-
2012). Through various social contexts (e.g., media, tion. For example, we can imagine two partners, P1
interactions with adults and peers), children inter- and P2, rock climbing together. At the base of the
nalize messages associated with their own identified climb, P1 expresses apprehension, first nonverbally,
sex (male or female) and proceed to practice emo- then verbally, and P2 picks up on P1’s anxiety (i.e.,
tion expression that aligns with their chosen sex convergence of emotional responses to the external
schema (Chaplin, 2015). For example, a young boy world). Initially, P2 may feel angry in response to
may internalize the message that boys are tough and P1’s expressed anxiety (i.e., emotional reaction to
do not cry and consequently overregulate emotions social partner) but is able to regulate that anger as
that evoke tears, such as sadness and guilt, which well as P1’s emotions by making reassuring state-
are more accepted among women. Parents often ments (i.e., interpersonal emotion regulation).

Diamond and Aspinwall (2003) consider these displayed heightened emotional reactivity—measured
dyadic regulatory interactions as optimal develop- physiologically and behaviorally—in response to
mental outcomes within relationships. When in watching a sad film. Thus, they concluded that
dyadic contexts, the goal of emotion regulation is cultural norms can play an influential role in shap-
not affective homeostasis; rather, it is emotional ing emotion expression.
flexibility and the capacity to pursue and prioritize Individuals’ capacities for emotion regulation
different context-specific goals. These kinds of and dysregulation are also linked to the social con-
dyadic emotional interactions can be difficult to dis- texts in which they live, as if they are “culturally
entangle, however, because they emerge from non- trained” for adaptive emotional control (Heatherton,
linear relations and are embedded within multilevel 2011; Murata, Moser, & Kitayama, 2012; Strauman,
feedback loops (Butler, 2017). 2017). Oftentimes, individuals’ desires for group in-
In our work (Crowell et al., 2017), we examined clusion and positive social interactions will provide
dynamic emotional interaction patterns among incentives for regulating negative emotions (e.g.,
mothers and their self-injuring, female adolescents guilt, shame; for a review, see, e.g., Heatherton, 2011).
during 10-minute conflict discussions. Using a non- In one study, Asian and European Americans were
linear dynamical systems approach, we found that exposed to either unpleasant or neutral pictures
mothers’ behaviors had a driving effect on self- while instructed to attend to or suppress generated
injuring adolescents’ behaviors and psychophysio- emotions (Murata et al., 2012). Asian Americans
logical responses. These driving relations were not demonstrated significantly greater decreases in pari-
observed among mothers and daughters in the con- etal late positive potential (LPP)—a neurological
trol group, providing evidence for theories that measure of emotional processing—during emotion
self-injuring adolescents are more emotionally reac- suppression tasks. This unique pattern of down-
tive and sensitive than typical controls. In a differ- regulation was so complete that the parietal LPP
ent study, mothers of self-injuring adolescents were returned to baseline approximately 2,000 ms post-
more likely than mothers of controls to match or stimulus, despite initial emotional reactions being
escalate conflict—only de-escalating conflict in re- at least as pronounced as those of European
sponse to highly aversive adolescent behavior. In Americans. These findings highlight cultural differ-
contrast, control mothers reliably de-escalated con- ences in emotion regulation between Asian and
flict, which may be one form of interpersonal emo- European Americans. Although such marked sup-
tion regulation (Crowell et al., 2013). These findings pression of emotional experiences among Asian
highlight the strong influence of dyadic interactions Americans may appear dysregulated to European
on individuals’ emotion generation, regulation, and Americans on a neurological level, this degree of
dysregulation, particularly among vulnerable ado- emotion regulation is consistent with cultural values
lescents at elevated risk for psychopathology. of high emotional control (Mauss & Butler, 2010).
Cultural Influences Synthesis and Future Directions

In European American culture, resisting group In summary, emotion generation, regulation, and
norms when they interfere with personal goals is dysregulation are multifaceted constructs that are
indicative of optimal social functioning (Markus & best understood from a developmental perspective.
Kitayama, 1991). Consequently, individuals are en- There is still ongoing debate about how to define
couraged to assert opinions and express emotions and conceptualize these terms, especially with
overtly. It follows that European Americans who regard to whether emotion generation and regula-
are depressed respond emotionally and physiologi- tion are separable. Although intertwined, it is pos-
cally in opposite patterns of those that are optimal sible to disentangle regulation of emotions from
for social functioning (e.g., anhedonia and dimin- their generation—especially when these constructs
ished physiological reactivity to emotionally evoca- are studied at the biological level of analysis. A lifes-
tive stimuli; Chentsova-Dutton et al., 2007; pan perspective also helps to elucidate important
Markus & Kitayama, 1991). This logic extends to distinctions between basic emotions and regulatory
Asian American culture as well, which values har- strategies. Specifically, there are early temperamen-
monious interdependence rather than individual- tal differences in emotion generation that are ob-
ity. Chentsova-Dutton and colleagues (2007) servable early in development. To some degree,
found that, in direct contrast with depressed emotional expressions and communications in
European Americans, depressed Asian Americans infancy could also be described as dysregulated,


a lthough this is more difficult to distinguish from Beauchaine, T. P., Hinshaw, S. P., & Bridge, J. A. (2019).
normative infant behavior. In contrast, emotion Nonsuicidal self-injury and suicidal behaviors in maltreated
girls with ADHD: The case for targeted prevention in
regulation is a maturational process that requires preadolescence. Clinical Psychological Science, 7, 643–667.
social inputs. Proximal environments, including doi:10.1177/2167702618818474
caregivers and siblings, play a critical role in Beauchaine, T. P., Klein, D. N., Crowell, S. E., Derbidge, C., &
shaping emotion regulation through soothing and Gatzke-Kopp, L. (2009). Multifinality in the development
nurturing in early development, and through con- of personality disorders: A biology × sex × environment
interaction model of antisocial and borderline traits.
flict de-escalation, praise, and responsive parenting Development and Psychopathology, 21, 735–770.
in childhood and adolescence. Beauchaine, T. P., Sauder, C. L., Derbidge, C. M., & Uyeji,
Future research should continue to examine L. L. (in press). Self-injuring adolescent girls exhibit
these three constructs across multiple levels of anal- insular cortex volumetric abnormalities that are similar to
ysis. Emotional processes are central to healthy de- those seen in adults with borderline personality disorder.
Development and Psychopathology. https://www.cambridge.
velopment and, when disrupted, heighten risk for org/core/journals/development-and-psychopathology/
a wide range of psychiatric diagnoses. Given the articleselfinjuring-adolescent-girls-exhibit-insular-cortex-
importance of close relationships in socializing emo- volumetric-abnormalities-that-are-similar-to-those-
tion regulation skills and strategies, scholars should seen-in-adults-with-borderline-personality-disorder/
continue to conduct dyadic, triadic, family, and DA24393F2BC925644156F8E795B675E9
Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as
systems-level research across development. These a transdiagnostic biomarker of psychopathology. International
studies have potential to elucidate social mechanisms Journal of Psychophysiology, 98, 338–350.
of risk and resilience, with potential to inform early Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion
intervention efforts and prevent psychopathology. regulation, and the latent structure of psychopathology:
An integrative and convergent historical perspective.
International Journal of Psychophysiology, 117, 108–111.
References Beauchaine, T. P., Zisner, A. R., & Sauder, C. L. (2017). Trait
Abe, J. A. A., & Izard, C. E. (1999). The developmental functions impulsivity and the externalizing spectrum. Annual Review of
of emotions: An analysis in terms of differential emotions Clinical Psychology, 13, 343–368.
theory. Cognition and Emotion, 13, 523–549. Blonigen, D. M., Hicks, B. M., Krueger, R. F., Patrick, C. J.,
Amstadter, A. B., Daughters, S. B., MacPherson, L., Reynolds, & Iacono, W. G. (2005). Psychopathic personality traits:
E. K., Danielson, C. K., Wang, F., . . . Lejuez, C. W. (2012). Heritability and genetic overlap with internalizing and
Genetic associations with performance on a behavioral externalizing psychopathology. Psychological Medicine, 35,
measure of distress intolerance. Journal of Psychiatric Research, 637–648.
46, 87–94. Brody, L. R. (1999). Gender, emotion, and the family. Cambridge,
Ashkanasy, N. M. (2003). Emotions in organizations: A multi- MA: Harvard University Press.
level perspective. In F. Dansereau & F. J. Yammarino (Eds.), Burke, J. D., & Stepp, S. D. (2012). Adolescent disruptive
Multi-level issues in organizational behavior and strategy (Vol. behavior and borderline personality disorder symptoms in
2, pp. 9–54). Bingley, UK: Emerald Group Publishing. young adult men. Journal of Abnormal Child Psychology, 40,
Bearden, C. E., Jawad, A. F., Lynch, D. R., Monterossso, J. R., 35–44.
Sokol, S., McDonald-McGinn, D. M., . . . Zackai, E. (2005). Butler, E. A. (2012). Emotion regulation in cultural context:
Effects of COMT genotype on behavioral symptomatology Implications for wellness and illness. In S. Barnow &
in the 22q11.2 Deletion Syndrome. Child Neuropsychology, N. Balkir (Eds.), Cultural variations in psychopathology: From
11, 109–117. research to practice (pp. 93–114). Boston, MA: Hogrefe
Beauchaine, T. P. (2001). Vagal tone, development, and Gray’s Publishing.
motivational theory: Toward an integrated model of Butler, E. A. (2015). Interpersonal affect dynamics: It takes two
autonomic nervous system functioning in psychopathology. (and time) to tango. Emotion Review, 7, 336–341.
Development and Psychopathology, 13, 183–214. Butler, E. A. (2017). Emotions are temporal interpersonal
Beauchaine, T. P. (2012). Physiological markers of emotion and systems. Current Opinion in Psychology, 17, 129–134.
behavior dysregulation in externalizing psychopathology. Butler, E. A., Lee, T. L., & Gross, J. J. (2007). Emotion regulation
Monographs of the Society for Research in Child Development, and culture: Are the social consequences of emotion
77, 79–86. suppression culture-specific? Emotion, 7, 30–48.
Beauchaine, T. P. (2015a). Future directions in emotion Casey, B. J., Giedd, J. N., & Thomas, K. M. (2000). Structural
dysregulation and youth psychopathology. Journal of Clinical and functional brain development and its relation to
Child and Adolescent Psychology, 44, 875–896. cognitive development. Biological Psychology, 54, 241–257.
Beauchaine, T. P. (2015b). Respiratory sinus arrhythmia: A Casey, B. J., Jones, R. M., & Hare, T. A. (2008). The adolescent
transdiagnostic biomarker of emotion dysregulation and brain. Annals of the New York Academy of Sciences, 1124,
psychopathology. Current Opinion in Psychology, 3, 43–47. 111–126.
Beauchaine, T. P., Constantino, J. N., & Hayden, E. P. (2018). Casey, B. J., Tottenham, N., Liston, C., & Durston, S. (2005).
Psychiatry and developmental psychopathology: Unifying Imaging the developing brain: What have we learned about
themes and future directions. Comprehensive Psychiatry, 87, cognitive development? Trends in Cognitive Sciences, 9,
143–152. 104–110.

Cervantes, C. A., & Callanan, M. A. (1998). Labels and Crowell, S. E., & Kaufman, E. A. (2016). Development of
explanations in mother-child emotion talk: Age and gender self-inflicted injury: Comorbidities and continuities with
differentiation. Developmental Psychology, 34, 88–98. borderline and antisocial personality traits. Development and
Chaplin, T. M. (2015). Gender and emotion expression: Psychopathology, 28, 1071–1088.
A developmental contextual perspective. Emotion Review, 7, Crowell, S. E., Puzia, M. E., & Yaptangco, M. (2015). The
14–21. ontogeny of chronic distress: Emotion dysregulation
Chaplin, T. M., Cole, P. M., & Zahn-Waxler, C. (2005). Parental across the life span and its implications for psychological
socialization of emotion expression: Gender differences and and physical health. Current Opinion in Psychology, 3,
relations to child adjustment. Emotion, 5, 80–88. 91–99.
Chentsova-Dutton, Y. E., Tsai, J. L., Chu, J. P., Rottenberg, J., Crowell, S. E., Yaptangco, M., & Turner, S. L. (2016). Coercion,
Gross, J. J., & Gotlib, I. H. (2007). Depression and invalidation, and risk for self-injury and borderline
emotional reactivity: Variation among Asian Americans of personality traits. In T. J. Dishion & J. J. Snyder (Eds.), The
East Asian decent and European Americans. Journal of Oxford handbook of coercive relationship dynamics (pp. 182–193).
Abnormal Psychology, 116, 776–785. New York, NY: Oxford University Press.
Cicchetti, D. (1984). The emergence of developmental Davidson, R. J. (2000). Affective style, psychopathology, and
psychopathology. Child Development, 55, 1–7. resilience: Brain mechanisms and plasticity. American
Cicchetti, D. (1993). Developmental psychopathology: Psychologist, 55, 1196–1214.
Reactions, reflections, projections. Developmental Review, De Brito, S. A., Mechelli, A., Wilke, M., Laurens, K. R.,
13, 471–502. Jones, A. P., Barker, G. J., . . . Viding, E. (2009). Size matters:
Cicchetti, D., Ackerman, B. P., & Izard, C. E. (1995). Emotions Increased grey matter in boys with conduct problems and
and emotion regulation in developmental psychopathology. callous-unemotional traits. Brain, 132, 843–852.
Development and Psychopathology, 7, 1–10. Diamond, L. M., & Aspinwall, L. G. (2003). Emotion regulation
Cole, P. M., Hall, S. E., & Hajal, N. J. (2017). Emotion across the life span: An integrative perspective emphasizing
dysregulation as a vulnerability to psychopathology. In self-regulation, positive affect, and dyadic processes. Motivation
T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent and Emotion, 27, 125–156.
psychopathology (3rd ed., pp. 346–386). Hoboken, NJ: Wiley. Dollar, J. M., Stifter, C. A., & Buss, K. A. (2017). Exuberant and
Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion inhibited children: Person-centered profiles and links to
regulation as a scientific construct: Methodological social adjustment. Developmental Psychology, 53, 1222–1229.
challenges and directions for child development research. Drabant, E. M., Hariri, A. R., Meyer-Lindenberg, A., Munoz,
Child Development, 75, 317–333. K. E., Mattay, V. S., Kolachana, B. S., . . . Weinberger, D. R.
Conradt, E., Adkins, D. E., Crowell, S. E., Monk, C., & (2006). Catechol O-methyltransferase val158met genotype
Kobor, M. S. (2018). An epigenetic pathway approach and neural mechanisms related to affective arousal and
to investigating associations between prenatal exposure to regulation. Archives of General Psychiatry, 63, 1396–1406.
maternal mood disorder and newborn neurobehavior. Eisenberg, N., Spinrad, T. L., & Eggum, N. D. (2010). Emotion-
Development and Psychopathology, 30, 881–890. related self-regulation and its relation to children’s
Corr, P. J. (2013). Approach and avoidance behaviour: Multiple maladjustment. Annual Review of Clinical Psychology, 6,
systems and their interactions. Emotion Review, 5, 285–290. 495–525.
Crowell, S. E., Baucom, B. R., McCauley, E., Potapova, N. V., Eme, R. (2015). Sex differences in the prevalence and expression
Fitelson, M., Barth, H., . . . Beauchaine, T. P. (2013). of externalizing behavior. In T. P. Beauchaine & S. P. Hinshaw
Mechanisms of contextual risk for adolescent self-injury: (Eds.), The Oxford handbook of externalizing spectrum
Invalidation and conflict escalation in mother-child disorders, 239–265. New York, NY: Oxford University Press.
interactions. Journal of Clinical Child and Adolescent Felix-Ortiz, A. C., Burgos-Robles, A., Bhagat, N. D., Leppla,
Psychology, 42, 467–480. C. A., & Tye, K. M. (2016). Bidirectional modulation of
Crowell, S. E., Baucom, B. R., Yaptangco, M., Bride, D., Hsiao, R., anxiety-related and social behaviors by amygdala projections
McCauley, E., & Beauchaine, T. P. (2014). Emotion to the medial prefrontal cortex. Neuroscience, 321, 197–209.
dysregulation and dyadic conflict in depressed and typical Gatzke-Kopp, L. M. (2011). The canary in the coalmine: The
adolescents: Evaluating concordance across psychophysiological sensitivity of mesolimbic dopamine to environmental
and observational measures. Biological Psychology, 98, 50–58. adversity during development. Neuroscience and Biobehavioral
Crowell, S. E., Beauchaine, T. P., McCauley, E. M., Smith, C. J., Reviews, 35, 794–803.
Stevens, A. L., & Sylvers, P. (2005). Psychological, autonomic, Gizer, I. R., Otto, J. M., & Ellingson, J. M. (2016). Molecular
and serotonergic correlates of parasuicide among adolescent genetics of the externalizing spectrum. In T. P. Beauchaine &
girls. Development and Psychopathology, 17, 1105–1127. S. P. Hinshaw (Eds.), The Oxford handbook of externalizing
Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C. J., spectrum disorders (pp. 149–169). New York, NY: Oxford
Vasilev, C. A., & Stevens, A. L. (2008). Parent-child University Press.
interactions, peripheral serotonin, and self-inflicted injury in Goldin, P. R., McRae, K., Ramel, W., & Gross, J. J. (2008).
adolescents. Journal of Consulting and Clinical Psychology, The neural bases of emotion regulation: Reappraisal and
76, 15–21. suppression of negative emotion. Biological Psychiatry, 63,
Crowell, S. E., Butner, J. E., Wiltshire, T. J., Munion, A. K., 577–586.
Yaptangco, M., & Beauchaine, P. (2017). Evaluating Gordis, E. B., Feres, N., Olezeski, C. L., Rabkin, A. N., &
emotional and biological sensitivity to maternal behavior Trickett, P. K. (2010). Skin conductance reactivity and
among self-injuring and depressed adolescent girls using respiratory sinus arrhythmia among maltreated and comparison
nonlinear dynamics. Clinical Psychological Science, 5, youth: Relations with aggressive behavior. Journal of Pediatric
272–285. Psychology, 35, 547–558.

Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment dopamine synthesis capacity in healthy subjects. American
of emotion regulation and dysregulation: Development, Journal of Psychiatry, 160, 904–910.
factor structure, and initial validation of the difficulties Luan, W., Hammond, L. A., Vuillermot, S., Meyer, U., & Eyles,
in emotion regulation scale. Journal of Psychopathology and D. W. (2018). Maternal vitamin D prevents abnormal
Behavioral Assessment, 26, 41–54. dopaminergic development and function in a mouse model
Gray, J. A. (1982). The neuropsychology of anxiety: An enquiry into of prenatal immune activation. Scientific Reports, 8, 9741.
the function of the septo-hippocampal system. New York, NY: Mann, J. J., Brent, D. A., & Arango, V. (2001). The neurobiology
Oxford University Press. and genetics of suicide and attempted suicide: A focus on the
Gray, J. A., & McNaughton, N. (2000). The neuropsychology of serotonergic system. Neuropsychopharmacology, 24, 467–477.
anxiety (2nd ed.). New York, NY: Oxford University Press. Markus, H. R., & Kitayama, S. (1991). Culture and the self:
Gray, S. A. O., Jones, C. W., Theall, K. P., Glackin, E., & Implications for cognition, emotion, and motivation.
Drury, S. S. (2017). Thinking across generations: Unique Psychological Review, 98, 224–253.
contributions of maternal early life and prenatal stress to Martel, M. (2013). Sexual selection and sex differences in the
infant physiology. Journal of the American Academy of Child prevalence of childhood externalizing and adolescent
and Adolescent Psychiatry, 56, 922–929. internalizing disorder. Psychological Bulletin, 139, 1221–1259.
Gross, J. J. (1998). The emerging field of emotion regulation: An Mauss, I. B., & Butler, E. A. (2010). Cultural context moderates
integrative review. Review of General Psychology, 2, 271–299. the relationship between emotion control values and
Gross, J. J. (2015). Emotion regulation: Current status and future cardiovascular challenge versus threat responses. Biological
prospects. Psychological Inquiry, 26, 1–26. Psychology, 84, 521–530.
Gross, J. J., & Feldman Barrett, L. (2011). Emotion generation McLaughlin, K. A., Alves, S., & Sheridan, M. A. (2014). Vagal
and emotion regulation: One or two depends on your point regulation and internalizing psychopathology among
of view. Emotion Review, 3, 8–16. adolescents exposed to childhood adversity. Developmental
Gross, J. J., Sheppes, G., & Urry, H. L. (2011). Emotion Psychobiology, 56, 1036–1051.
generation and emotion regulation: A distinction we should McRae, K., Misra, S., Prasad, A. K., Pereira, S. C., & Gross, J. J.
make (carefully). Cognition and Emotion, 25, 765–781. (2011). Bottom-up and top-down emotion generation:
Heatherton, T. F. (2011). Neuroscience of self and self-regulation. Implications for emotion regulation. Social Cognitive and
Annual Review of Psychology, 62, 363–390. Affective Neuroscience, 7, 253–262.
Herts, K. L., McLaughlin, K. A., & Hatzenbuehler, M. L. Mezulis, A. H., Crystal, S. I., Ahles, J. J., & Crowell, S. E.
(2012). Emotion dysregulation as a mechanism linking stress (2015). Examining biological vulnerability in environmental
exposure to adolescent aggressive behavior. Journal of Abnormal context: Parenting moderates effects of low resting respiratory
Child Psychology, 40, 1111–1122. sinus arrhythmia on adolescent depressive symptoms.
Hughes, A. E., Crowell, S. E., Uyeji, L., & Coan, J. A. (2012). Developmental Psychobiology, 57, 974–983.
A developmental neuroscience of borderline pathology: Monk, C. S., Telzer, E. H., Mogg, K., Bradley, B. P., Mai, X.,
Emotion dysregulation and social baseline theory. Journal of Louro, H. M., . . .
Pine, D. S. (2008). Amygdala and
Abnormal Child Psychology, 40, 21–33. ventrolateral prefrontal cortex activation to masked angry
Johnson, M. H., Posner, M. I., & Rothbart, M. K. (1991). faces in children and adolescents with generalized anxiety
Components of visual orienting in early infancy: Contingency disorder. Archives of General Psychiatry, 65, 568–576.
learning, anticipatory looking, and disengaging. Journal of Murata, A., Moser, J. S., & Kitayama, S. (2012). Culture shapes
Cognitive Neuroscience, 3, 335–344. electrocortical responses during emotion suppression. Social
Kagan, J. (2017). High reactive temperament, behavioral Cognitive and Affective Neuroscience, 8, 595–601.
inhibition, and vulnerability to psychopathology. In Ochsner, K. N., Ray, R. R., Hughes, B., McRae, K., Cooper,
T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and J. C., Weber, J., . . . Gross, J. J. (2009). Bottom-up and top-
adolescent psychopathology (3rd ed., pp. 213–236). Hoboken, down processes in emotion generation: Common and
NJ: Wiley. distinct neural mechanisms. Psychological Science, 20,
Kagan, J., & Snidman, N. (1999). Early childhood predictors of 1322–1331.
adult anxiety disorders. Biological Psychiatry, 46, 1536–1541. Owens, M. J., & Nemeroff, C. B. (1994). Role of serotonin in
Kim, H., Arnold, D. H., Fisher, P. H., & Zeljo, A. (2005). the pathophysiology of depression: Focus on the serotonin
Parenting and pre-schoolers’ symptoms as a function of child transporter. Clinical Chemistry, 40, 288–295.
gender and SES. Child and Family Behavior Therapy, 27, Panksepp, J. (1982). Toward a general psychobiological theory of
23–41. emotions. Behavioral and Brain Sciences, 5, 407–467.
Kim, H. S., Sherman, D. K., Mojaverian, T., Sasaki, J. Y., Park, Panksepp, J. (1998). The periconscious substrates of
J., Suh, E. M., & Taylor, S. E. (2011). Gene-culture consciousness: Affective states and the evolutionary origins of
interaction: Oxytocin receptor polymorphism (OXTR) and the SELF. Journal of Consciousness Studies, 5, 566–582.
emotion regulation. Social Psychological and Personality Panksepp, J., & Watt, D. (2011). What is basic about basic
Science, 2, 665–672. emotions? Lasting lessons from affective neuroscience.
Kurjak, A., Azumendi, G., Andonotopo, W., & Salihagic-Kadic, Emotion Review, 3, 387–396.
A. (2007). Three- and four-dimensional ultrasonography Plichta, M. M., & Scheres, A. (2014). Ventral-striatal
for the structural and functional evaluation of the fetal face. responsiveness during reward anticipation in ADHD and its
American Journal of Obstetrics and Gynecology, 196, 16–28. relation to trait impulsivity in the healthy population: A
Laakso, A., Wallius, E., Kajander, J., Bergman, J., Eskola, O., meta-analytic review of the fMRI literature. Neuroscience and
Solin, O., . . . Hietala, J. (2003). Personality traits and striatal Biobehavioral Reviews, 38, 125–134.

Plieger, T., Melchers, M., Vetterlein, A., Görtz, J., Kuhn, S., Sutton, S. K., & Davidson, R. J. (1997). Prefrontal brain
Ruppel, M., & Reuter, M. (2017). The serotonin transporter asymmetry: A biological substrate of the behavioral
polymorphism (5-HTTLPR) and coping strategies influence approach and inhibition systems. Psychological Science, 8,
successful emotion regulation in an acute stress situation: 204–210.
Physiological evidence. International Journal of Psychophysiology, Swann, A. C., Bjork, J. M., Moeller, F. G., & Dougherty, D. M.
114, 31–37. (2002). Two models of impulsivity: Relationship to
Price, C. J., & Crowell, S. E. (2016). Respiratory sinus arrhythmia personality traits and psychopathology. Biological Psychiatry,
as a potential measure in substance use treatment-outcome 51, 988–994.
studies. Addiction, 111, 615–625. Swanson, E. N., Owens, E. B., & Hinshaw, S. P. (2014).
Reissland, N., Francis, B., & Mason, J. (2013). Can healthy Pathways to self-harmful behaviors in young women with
fetuses show facial expressions of “pain” or “distress”? PLoS and without ADHD: A longitudinal examination of
One, 8, e65530. mediating factors. Journal of Child Psychology and Psychiatry,
Robinson, D. T. (2014). Comment: Growing a multilevel science 55, 505–515.
of emotion. Emotion Review, 6, 137–138. Takahashi, T., Chanen, A. M., Wood, S. J., Yücel, M., Tanino, R.,
Rogers, K. B., Schröder, T., & von Scheve, C. (2014). Dissecting Suzuki, M., . . . McGorry, P. D. (2009). Insular cortex volume
the sociality of emotion: A multilevel approach. Emotion and impulsivity in teenagers with first-presentation borderline
Review, 6, 124–133. personality disorder. Progress in Neuropsychopharmacology and
Rose, A. J., & Rudolph, K. D. (2006). A review of sex differences Biological Psychiatry, 33, 1395–1400.
in peer relationship processes: Potential trade-offs for the Thompson, R. A. (1993). Emotion regulation: A theme in search
emotional and behavioral development of girls and boys. of definition. Monographs of the Society for Research in Child
Psychological Bulletin, 132, 98–131. Development, 59, 25–52.
Rothbart, M. K. (1986). Longitudinal observation of infant Trost, S., Diekhof, E. K., Zvonik, K., Lewandowski, M., Usher, J.,
temperament. Developmental Psychology, 22, 356–365. Keil, M., . . . Gruber, O. (2014). Disturbed anterior prefrontal
Rothbart, M. K., Ahadi, S. A., & Hershey, K. L. (1994). control of the mesolimbic reward system and increased
Temperament and social behavior in childhood. Merrill- impulsivity in bipolar disorder. Neuropsychopharmacology, 39,
Palmer Quarterly, 40, 21–39. 1914–1923.
Sallis, H., Davey Smith, G., & Munafò, M. R. (2018). Genetics Viddal, K. R., Berg-Nielsen, T. S., Belsky, J., & Wichstrøm, L.
of biologically based psychological differences. Philosophical (2017). Change in attachment predicts change in emotion
Transactions of the Royal Society B: Biological Sciences, 373, regulation particularly among 5-HTTLPR short-allele
20170162. homozygotes. Developmental Psychology, 53, 1316–1329.
Schachter, S., & Singer, J. (1962). Cognitive, social, and Vohs, K. D., & Baumeister, R. F. (2016). Handbook of self-
physiological determinants of emotional state. Psychological regulation: Research, theory, and applications. New York, NY:
Review, 69, 379–399. Guilford Publications.
Schultz, W. (2002). Getting formal with dopamine and reward. Weems, C. F., Pina, A. A., Costa, N. M., Watts, S. E., Taylor,
Neuron, 36, 241–263. L. K., & Cannon, M. F. (2007). Predisaster trait anxiety and
Sheppes, G., Suri, G., & Gross, J. J. (2015). Emotion regulation negative affect predict posttraumatic stress in youths after
and psychopathology. Annual Review of Clinical Psychology, Hurricane Katrina. Journal of Consulting and Clinical
11, 379–405. Psychology, 75, 154–159.
Skowron, E. A., & Reinemann, D. H. S. (2005). Effectiveness of Wilson, S. R., Rack, J. J., Shi, X., & Norris, A. M. (2008).
psychological interventions for child maltreatment: A meta- Comparing physically abusive, neglectful, and non-
analysis. Psychotherapy: Theory, Research, Practice, Training, maltreating parents during interactions with their children:
42, 52–71. A meta-analysis of observational studies. Child Abuse and
Solmeyer, A. R., & Feinberg, M. E. (2011). Mother and father Neglect, 32, 897–911.
adjustment during early parenthood: The roles of infant Yaptangco, M., Crowell, S. E., Baucom, B. R., Bride, D. L., &
temperament and coparenting relationship quality. Infant Hansen, E. J. (2015). Examining the relation between
Behavior and Development, 34, 504–514. respiratory sinus arrhythmia and depressive symptoms in
Strauman, T. J. (2017). Self-regulation and psychopathology: emerging adults: A longitudinal study. Biological Psychology,
Toward an integrative translational paradigm. Annual Review 110, 34–41.
of Clinical Psychology, 13, 497–523. Zahn-Waxler, C., Shirtcliff, E. A., & Marceau, K. (2008).
Suess, P. E., Porges, S. W., & Plude, D. J. (1994). Cardiac vagal tone Disorders of childhood and adolescence: Gender and
and sustained attention in school-age children. Psychophysiology, psychopathology. Annual Review of Clinical Psychology, 4,
31, 17–22. 275–303.

CH A PTE R
Development of Emotion Dysregulation
8 in Developing Relationships
Ross A. Thompson and Sara F. Waters
Abstract
A developmental perspective to emotion dysregulation underscores the relational bases to developing

emotion regulation capacities. In this chapter, attachment theory and functionalist emotions theory
are discussed as theoretical foundations for understanding emotion dysregulation in the context of
developing relationships. In the subsequent discussion of central research literatures, the chapter
profiles family processes that contribute to the development of emotionally dysregulated behavior.
The interaction of biological and social processes is considered next in discussions of the physiological
synchrony between children and parents, the socialization of stress neurobiology, and children’s differential
susceptibility to environmental influences and its consequences for emotion regulation and dysregulation.
The chapter concludes with reflections on future directions, including the clinical implications of
considering developing problems in emotion dysregulation as problems not just of individual children
but also of relationships.
Keywords: development, relationships, attachment, functionalist emotions theory, family, differential

susceptibility, stress neurobiology, physiological synchrony
Introduction capacities to maintain satisfactory emotional balance

Psychological studies of emotion regulation and and self-regulation (Zaki & Williams, 2013). At the
dysregulation have naturally viewed these concepts end of life, older adults manage their social relation-
in terms of psychological adjustment. Because emo- ships for purposes of emotion regulation, particularly
tions are so important to thinking, motivation, and for maintaining positive affectivity (Carstensen, Fung,
sociability, well-adjusted individuals are capable of & Charles, 2003). Thus, emotion regulation and
autonomously managing their emotions, and failure dysregulation develop and function in a relational
to do so competently may be an indicator of context, not just within the individual.
psychopathology. But a developmental approach to Relationships can promote the growth of con-
emotion regulation and dysregulation offers a some- structive skills of emotion management, but they
what different perspective from this conventional can also lead to dysfunctional patterns of emotion
view. From the beginning of life when young in- dysregulation. When other people impose unman-
fants depend on others to manage their arousal, ageable emotional demands (as when children live
emotion regulation develops not individually but in in chronically violent homes) or undermine con-
the context of social relationships. Children rely on structive strategies of emotion self-management (as
others to foster manageable emotional experiences when a parent dismisses a child’s need for emotional
in which they can develop and practice their skills of support), for example, close relationships become
emotional self-control. Moreover, as literatures on associated with emotion dysregulation. The effects
social support, empathy, and romantic relationships of relationships on emotion dysregulation can be
underscore, other people remain important to adults’ observed throughout life (as research on family and
99
marital interaction documents) but are most readily between infants and caregivers, and the psychological
observed in the early years when young children are significance of such ties. Bowlby argued that humans
so dependent on others for managing their feelings. have been motivated to develop these attachments
Viewed in this light, emotion dysregulation may throughout evolution because of the importance of
not be solely a problem of individual adjustment, infant–caregiver proximity for protection, nurtur-
but may also reflect relational problems. Indeed, ance, and social learning. As attachment researchers
this view is at the cornerstone of the field of infant/ have learned more about early psychological devel-
early childhood mental health, which regards early opment, however, many have concluded that early
problems of psychological functioning as inherently attachments serve broader functions, including sup-
relational. It is captured in Winnicott’s famous line, porting emotion regulation that derives from an
“There is no such thing as a baby. . . you are describ- infant’s trust in an adult who responds sensitively,
ing a baby and someone” (Winnicott, 1957, p. 137). buffers stress, provides relief from distress, and
In this chapter we consider the development of manages environmental demands (Brumariu, 2015;
emotion dysregulation in developing relationships. Cassidy, 1994). Viewed from this perspective, secure
Our focus is primarily on the early years because attachments promote the growth of constructive
this is a formative period for growth of emotion forms of emotion self-regulation in several ways, in-
regulation and thus also a period of vulnerability to cluding the parent’s acceptance of the child’s feelings,
social influences that can promote emotion dysreg- willingness to communicate openly about them,
ulation. For this reason, developmental study of and coaching emotion regulation skills (Thompson,
early emotion regulation is also the study of risk for 2015). From these influences, children develop a
emotion dysregulation (see Garber & Dodge, 1991). greater understanding of emotion and its manage-
Yet some developmental processes that contribute ment, and develop a broader understanding of the
to emotion dysregulation are very different from role of emotions in the context of close relationships.
those that lead to skills in emotion management. The benefits of secure attachments are especially
We organize the chapter in this manner. In the noteworthy when contrasted with the kinds of emo-
section that follows, two central theoretical per- tion dysregulation apparent in insecure parent–child
spectives are considered: attachment theory and attachments, whether insecurity is manifested in
functionalist emotions theory. The section closes with resistant, avoidant, or disorganized responses. When
reflection on some unresolved theoretical issues. insecure-resistant infants are observed with their
The next section focuses on central findings and mothers, they exhibit self-evident signs of emotion
conclusions from the research literature, with par- dysregulation. For example, when stressed by a brief
ticular attention to interactions among social and separation, they have difficulty soothing even after
biological influences on developing emotion dys- the mother’s return and instead show continued and
regulation in relationships. The chapter concludes sometimes angry distress throughout reunion. By
with some ideas about future directions for this field contrast, insecure-avoidant infants are more placid
of research. during separations from their mothers, but their
behavior is belied by physiological indications of
Theoretical Perspectives on the strong arousal, suggesting that they minimize ex-
Development of Emotion Dysregulation pressions of distress to a caregiver who has been
Attachment theory and functionalist emotions theory relatively insensitive to these signals in the past
are two perspectives that frame current thinking (Spangler & Grossmann, 1993). Disorganized in-
about the development of emotion dysregulation in fants show the most atypical patterns of attachment
the context of developing relationships. The first fo- behavior including indications of disorientation,
cuses on the nature of early relationships and their inconsistent responses to their mothers (e.g., ap-
role in the development of self-regulation and emo- proach combined with avoidance), fearful behavior,
tion dysregulation. The second contributes a com- and/or inconsolability during reunion episodes.
plementary focus on the nature of emotion and its Attachment researchers believe that this indicates
management in the context of an individual’s trans- that disorganized infants lack a constructive strategy
actions with the social world. for engaging their mothers after separation because
their mothers are not reliable sources of safety and
Attachment Theory emotion management.
Attachment theory was formulated by Bowlby Considerable research conducted with infants,
(1969) to explain the development of emotional ties children, and adolescents confirms the advantages
100 Emotion Dysregul ation in Developing Rel ationships

afforded by a secure attachment in the development the more likely that child is to live in a family in
of emotion regulation. Securely attached children economic stress, with nearly half (46%) of young
tend to be more capable in managing their emo- children in the first 3 years living in poverty or
tions (especially in the company of a parent), have a in poor families (Jiang, Granja, & Koball, 2017).
more acute understanding of emotions (especially Considerable research drawn from the Family Stress
negative emotions), and are more likely to identify Model documents how economic stress contributes
and enlist constructive strategies of emotion man- to parental anxiety and depressive symptoms, in-
agement compared to insecurely attached children creased marital conflict, and higher levels of disen-
(Thompson, Virmani, Waters, Meyer, & Raikes, gaged, nonnurturant parenting (see Conger, Conger,
2013; Waters & Thompson, 2016; see also Brumariu, & Martin, 2010, for a review). More than one in
2015; Thompson, 2016, for reviews). Unfortunately, seven infants are exposed to major maternal depres-
attachment researchers have not explored as fully sion during their first year of life (Wisner et al.,
the different patterns of emotion dysregulation as- 2013). More significant risks derive from the high
sociated with the three insecure groups, although proportions of young children who are victims of
there are indications from several studies that disor- child maltreatment and enter foster care. Taken to-
ganized children are most likely to use dysfunctional gether, family conditions that contribute to the de-
strategies for coping with emotional arousal (e.g., velopment of emotion dysregulation in children are
catastrophizing) and are more vulnerable to fear and those characterized not only by hostility but also by
anxiety compared to children in the other groups parental disengagement, and these conditions are
(Brumariu, Kerns, & Seiberg, 2012; Spangler & far too common.
Zimmermann, 2014).
Attachment theory and research findings are Functionalist Emotions Theory
consistent with broader literatures on the impor- Drawing on Darwinian theory, most theories of
tance of attachment relationships as stress buffers, emotion are functionalist in orientation, emphasiz-
especially for human and animal young who are ing the adaptive purposes served by discrete emo-
least capable of coping with stressors on their own tions throughout human evolution. Definitions of
(Gunnar & Donzella, 2002). Attachment research emotion regulation are also functionalist, focused
is also consistent with studies showing that parental on personal, situational, and/or social goals achieved
sensitivity and responsiveness to distress are associ- by managing emotions and their expression.
ated with the development of more constructive Individuals regulate their emotions to feel better in
strategies for regulating negative emotion in infancy difficult situations, mobilize themselves to face
and childhood (Davidov & Grusec, 2006; Leerkes, difficult challenges, think more clearly, strengthen
Blankson, & O’Brien, 2009). When young children relationships, and accomplish other purposes. As
lack parental support, it is not just that they develop Thompson (1994) notes, individuals also regulate
poorer strategies for managing emotion; they also themselves to alter the temporal dynamics of emo-
exhibit behaviors indicative of emotion dysregulation even if they cannot change emotion valence.
tion, such as defiant noncompliance accompanied For example, they may reduce the duration of fear
by negative affect in response to parental requests or sadness, slow the escalation of anger or frustra-
(e.g., Leerkes et al., 2009). This is because the lack tion, prolong feelings of pleasure or well-being, or
of relational support not only denies young children achieve a more even and less volatile emotional
a stress buffer but also is itself a significant stressor demeanor. Indeed, emotion regulation may be used
at an age when children depend on parental nur- more often for these purposes than to change the
turance (Thompson, 2014). Consistent with attach- valence of feelings.
ment research, therefore, emotion dysregulation What does this mean for emotion dysregulation?
develops not only in contexts of parental harshness One way of defining emotion dysregulation is when
and negativity (e.g., Chang, Schwartz, Dodge, & an individual cannot manage his or her emotions,
McBride-Chang, 2003) but also in contexts of or manages them dysfunctionally. Either way, one
nonresponsiveness and emotional unavailability fails to regulate emotions or their expression ac-
to the child. cording to his or her goals. This is consistent with a
Such findings are important given the broad functionalist orientation and occurs when someone
range of circumstances faced by families with young “loses control” of his or her anger, cannot recover
children that can cause parents to be nonresponsive from enduring feelings of sadness or anxiety, has dif-
and emotionally unavailable. The younger a child is, ficulty experiencing happiness, undergoes disturbing
Thompson and Waters 101

mood swings, or responds emotionally in ways diate nor long-term goals, or when certain goals are
unsuited to immediate circumstances. Viewed in achieved at very high cost.
this light, it is easy to see how readily various kinds Third, there are situations that undermine an
of affective psychopathology are interpreted as individual’s capacity to adaptively regulate their
problems of emotion dysregulation. emotions to improve well-being, and in which im-
But a functionalist orientation to emotion com- mediate coping occurs at the cost of long-term dif-
plicates this view in several ways. First, there may be ficulty. These are conditions that heighten the risk
a difference between an individual’s goals in a par- for affective psychopathology and influence others’
ticular context and expectations of others for those perceptions of one being emotionally dysregulated.
goals. Stated differently, an observer may interpret In these situations, dysregulation arises, at least in
someone’s behavior as emotionally dysregulated by part, from emotionally insurmountable conditions
misconstruing the emotion goals the individual is that foster problems in emotion management. One
trying to achieve. An example is when an adolescent example is the experience of young children with a
or adult ruminates on events that cause sadness chronically depressed parent (Goodman & Gotlib,
because of sympathetic responses their sadness elic- 1999). Depressed mothers tend to be less positive
its from friends. To an observer, that person is not and more punitive with their children, engage in
regulating emotions very well, but viewed from that more critical and hostile behavior, and enmesh their
person’s perspective, emotion regulation is accom- children in their own affect by adopting negative
plishing its purpose of mobilizing social support. attributional biases toward their children, combined
It may often be true that children are perceived by with helplessness in remedying their own condition
adults as emotionally dysregulated when they are (Rogosch, Cicchetti, & Toth, 2004). Thus, in addi-
actually behaving as emotional tacticians to manage tion to being unsupportive and emotionally un-
their emotions, and their expression, to coerce, cajole, available, chronically depressed caregivers make it
or entice others to produce desired outcomes. difficult for children to effectively manage their own
Second, many social situations in which emotion emotions by involving the child in parental distress
is managed involve multiple goals, both immediate and enhancing children’s feelings of responsibility
and longer term, and these goals may be inconsistent. for it. Enmeshed in these circumstances, it may be
Individuals in these situations must often choose difficult for children, especially at young ages, to
which goals should guide their emotion regulatory engage in constructive emotion self-regulatory strat-
efforts at the cost of achieving other goals. Consider egies that might involve, for example, reappraising
a child who is bullied by a peer (or, for that matter, the situation or disengaging from it. As a conse-
an adult who is bullied by a coworker). Mobilizing quence, children with a chronically depressed mother
feelings of anger to resist intimidation may ac- not only are at heightened risk of depression but also
complish the immediate goal of self-defense but evince dysphoric affect, diminished self-concept, and
may undermine other relationships if people are of- poorer social competence—all of which contribute
fended by the angry display. Suppressing feelings of to emotionally dysfunctional behavior outside the
anger or fear to endure intimidation does little to home, including the classroom and with peers
reduce it in the future but may preserve ongoing rela- (Goodman & Gotlib, 1999).
tionships of value. Expressing distress to others to In some cases, children’s efforts to cope with im-
mobilize social support may provide immediate as- mediate circumstances create longer term emotional
sistance but may color how others perceive the self. dysfunction. Young children at risk for anxiety dis-
As this example illustrates, there may be different orders, for example, show hypervigilance in situa-
and potentially inconsistent immediate and longer tions associated with fearful events, attentional ori-
term outcomes of each strategy based on the indi- enting to anxiety-provoking stimuli, and a tendency
vidual’s power relative to that of the bully, beliefs to construe benign situations as disproportionately
and expectations of others in that setting, a person’s negative or threatening. These appraisal (and preap-
gender, and/or broader cultural and subcultural praisal) processes are exacerbated by influences from
values. Competent emotion regulation thus in- family members, who may themselves share a ten-
volves negotiating tradeoffs between multiple goals dency toward anxious symptoms, and serve the child’s
and accepting both the costs and benefits of specific preeminent self-regulatory strategy of avoiding
self-regulatory strategies. Emotion dysregulation anxiety-provoking situations, even though this has
in such contexts may occur when an individual’s dysfunctional long-term consequences by enhancing
self-regulatory strategies accomplish neither imme- rather than reducing anxious psychopathology

(Fox, Henderson, Marshall, Nichols, & Ghera, 2005; the context of its development. The traditional
Thompson, 2001). Without the kind of concerted psychological orientation to emotion dysregulation
family support that is a goal of family therapy, how- is to portray it as a component of psychological
ever, it is difficult to know how a young child can adjustment and as an individual characteristic that

better self-regulate in these circumstances. can be addressed through therapeutic intervention.

Children who are physically abused by their But functionalist emotions theory and attachment
caregivers also confront a tradeoff of emotion theory together argue that developing problems
self-regulatory goals. Children with a history of abuse, manifesting in emotionally dysregulated behavior
exposure to violence, and other trauma become must be interpreted in a relational context because
physiologically and emotionally hypersensitive to it is that context that shapes the emotional demands
cues of adult anger, with a lower threshold of de- on the child, the goals that the child might be seek-
tecting anger in adult voices and faces, and greater ing to accomplish through self-regulatory efforts, and
physiological reactivity when these cues are per- the outcomes of strategies the child enlists. Emotion
ceived (Pollak, 2008). These responses can serve dysregulation is, like insecure attachment, an adap-
emotion regulatory functions if they enable a child tation to a particular relational context. And al-
to anticipate an attack before it occurs and to be though these adaptations can create difficulties as
prepared to flee, although they also contribute to the child enters other relational contexts—such as
difficulty in managing emotion because negative problems in peer social competence exhibited by in-
emotions tend to quickly escalate to high inten- securely attached children and children exposed to
sity when they are evoked. In addition, outside chronic violence—this does not mitigate the impor-
the home their hypersensitivity to threat cues un- tance of understanding these adaptations within
dermines competent emotion management and is the relational frameworks in which they develop.
socially dysfunctional (Thompson, 2011). But it is As considered further later, addressing these devel-
difficult to think of any other adaptive strategy opmental challenges requires not only individual
children might enlist to cope with potential harm therapeutic intervention but also efforts to address
at home that does not carry these dysfunctional ex- relational bases of their development, such as in the
ternal consequences and threats to long-term emo- context of two-generation interventions.
tional development.
From a functionalist perspective, therefore, re- Current Methods and Findings
sponses that appear to be emotionally dysregulated— In this section, we profile contemporary advances
dysphoric affect, anxious avoidance, hypervigilance, in the developmental study of emotion dysregula-
and overreactivity to threat—might also be inter- tion. We turn first to studies of family processes
preted as deriving from efforts to cope with that contribute to the development of emotionally
circumstances that do not permit more adaptive dysregulated behavior. We consider next interac-
self-regulatory strategies, even though they also tions of biological and social processes in sections
have long-term costs to developmental compe- addressing the nature of the physiological syn-
tence. Viewed in this light, emotion regulation is a chrony between children and their caregivers, so-
double-edged sword because strategies that permit cialization of stress neurobiology, and children’s
immediate coping render children more vulnerable differential susceptibility to environmental influ-
to long-term problems (Thompson & Calkins, 1996). ences and their consequences for emotion regula-
Describing these children as emotionally dysregu- tion and dysregulation.
lated in more than a broadly descriptive sense over-
looks a thoughtful appraisal of the circumstances Family Processes
that shaped their emotional development, the mul- Considerable research has addressed how family
tiple and sometimes conflicting emotion goals that influences affect the development of emotion regu-
children might be coping with, and the challenges lation, although researchers have tended to be more
of managing emotionally insurmountable conditions. interested in the growth of self-regulatory compe-
Describing these children as emotionally dysregu- tency than on development of emotion dysregula-
lated also overlooks the important and sometimes tion. From this research, however, it is possible to
profound relational context in which efforts to discern at least three broad ways that family processes
manage emotions occur. contribute to emotionally dysregulated behavior in
An unresolved issue, therefore, is how to charac- children (Morris, Silk, Steinberg, Myers, & Robinson,
terize emotion dysregulation and its treatment in 2007; Thompson, 2013).

First, children acquire strategies of emotion ness at home was linked to adolescents’ internalizing
r egulation and patterns of emotionally dysregulated and externalizing symptoms, although for internal-
behavior from observations of other family members. izing symptoms, this effect was buffered by parents’
A young child with a parent who has an explosive supportive emotion coaching (Stocker, Richmond,
temper is likely to manifest anger similarly, espe- Rhoades, & Kiang, 2007). It is noteworthy that
cially if family members acquiesce in the face of parents’ negative expressiveness predicted both in-
such displays. Because of the influence of parents’ ternalizing and externalizing symptoms in youth,
manner of emotional expression on the broader reflecting its broad emotionally dysregulatory impact.
family climate, observational processes are likely to Third, consistent with the foregoing, the general
be especially influential in the development of emo- emotional climate of the family influences the devel-
tion dysregulation when parents’ emotional expres- opment of emotion dysregulation. Children’s emotion
sions are extreme. Silk, Shaw, Skuban, Oland, and self-regulation is disrupted by the overall emotional
Kovacs (2006) reported, for example, that offspring environment created by family interactions—the
of chronically depressed mothers tended to use more relative amounts of negative and positive expressiv-
passive, less competent styles of managing their ity by family members, for example, as well as the
emotions during mood induction compared to chil- unpredictability and emotional instability of the
dren who lived with nondepressed mothers. family climate. The influence of the family emo-
Second, parenting practices directly related to tional climate is illustrated by research based on
the socialization of emotion also influence the de- the Family Stress Model discussed earlier, in which
velopment of emotionally dysregulated behavior. economic stress promotes depressive and anxious
These socialization influences can include parents’ symptoms in adults, which become manifested in
active coaching of emotion self-regulation; their marital difficulties and aversive parent–child rela-
accepting, dismissive, or punitive reactions to chil- tionships—an emotional climate that contributes to
dren’s negative emotional expressions; and conver- children’s behavior problems (Conger et al., 2010).
sations about emotion and its management. In a The importance of the family emotional climate is
recent meta-analysis, Johnson, Hawes, Eisenberg, also reflected in studies of the effects of marital con-
Kohlhoff, and Dudeney (2017) concluded that flict on children. In the emotional security hypothesis
child conduct problems are predicted by parents’ developed by Cummings and Davies (2010), marital
nonsupportive emotion socialization practices, par- conflict disrupts children’s emotional security and
ticularly those directed toward children’s negative emotion regulation, causing children to develop
emotions, and that this influence is greater with heightened sensitivity to parental distress and anger,
younger children. Nonsupportive practices include become overinvolved in their parents’ conflicts,
minimizing or punishing children’s emotional ex- have difficulty managing the strong emotions that
pressions, refusing to talk about the meaning or conflict arouses, and show early signs of internal-
significance of children’s feelings, and frequent izing problems (Davies, Harold, Goeke-Morey, &
expressions of negative emotion, especially toward Cummings, 2002).
children. The authors emphasized that conduct Taken together, family processes can contribute
problems and nonsupportive emotion socialization both to adaptive emotion regulatory skills in children
practices become mutually influential over time, and to emotion dysregulation depending on how
and that socialization practices can have compound- parents act as examples of emotion regulation,
ing effects. These processes are illustrated in a study their emotion socialization practices, and the broader
by Mence and colleagues (2014), who found that in emotional climate of the family. Development of
families of toddlers with disruptive behavior prob- emotion dysregulation in the family derives not only
lems, parents exhibited hostile attributional biases from absence of support for competent self-regulation
and emotion flooding, as well as negative discipline but also from influences that heighten negative
practices. Children’s behavior problems and parents’ emotional reactivity, blunt children’s efforts to manage
unsupportive emotion socialization practices became their feelings, and dismiss, denigrate, or ignore chil-
mutually maintaining elements of a negative family dren’s feelings altogether.
environment.
Parents’ emotion socialization is also relevant to Physiological Synchrony
the development of children’s internalizing prob- One way that close relationships contribute to emo-
lems (Schwartz, Sheeber, Dudgeon, & Allen, 2012). tion regulation—or dysregulation—is through syn-
Mothers’ and fathers’ negative emotional expressive- chrony that develops between partners’ emotions,

behaviors, and even physiological responses. The As these studies illustrate, PS can be measured
importance of parent–child emotional and behav- using assessments of heart rate. Studies with young
ioral synchrony for children’s healthy social and children also commonly focus on respiratory sinus
emotional development has long been recognized arrhythmia (RSA), which quantifies changes in in-
(see Harrist & Waugh, 2002, for a review). More tervals between heart beats across respiratory cycles
recently, developmental scientists have begun to (i.e., inhalation and exhalation) and is a reliable
empirically examine the influences of physiological measure of parasympathetic nervous system activity.
synchrony on parent–child relationships. Their RSA at rest and RSA in response to emotionally
work is built on earlier studies of time-linked physi- evocative situations are indicative of individual
ological processes of social partners. In their foun- differences in emotion regulatory capacities (see
dational work, for example, Levenson and Gottman Beauchaine, 2015, for a review). Skin conductance
(1983; Gottman & Levenson, 2000) predicted dis- (SC), an index of sympathetic nervous system activ-
solution of marriage over the course of 14 years on ity, is also used in PS analyses. Salivary cortisol,
the basis of the synchrony of couples’ autonomic which indexes limbic hypothalamic-pituitary-adrenal
nervous system responses during conflict conversa- (L-HPA) axis activity, is another common measure
tions. Similarly, trajectories of mothers’ and infants’ used to study PS, but is more often used in samples
heart rate responses during stressful episodes varied of older children and adolescents than very young
as a function of their relationship quality (Donovan children (see Saxbe et al., 2014).
& Leavitt, 1985). During the past decade, research Studies of PS with very young children and their
on dyadic physiological processes has proceeded in parents typically use one of two procedures. In the
earnest. This is due, in part, to recent improve- first, physiological activity is measured during a
ments in physiological recording technology and, period of parent–child interaction that is briefly
more significantly, advances in statistical modeling interrupted by a stressor to the child (e.g., the
techniques for dynamic dyadic data analysis that adult stops responding to the child, a brief separa-
have allowed researchers to unlock the complexities tion from the parent), followed by a resumption
of these data (Butler, 2015; Crowell et al., 2017; of normal interaction. Using such a procedure,
Ferrer & Helm, 2013; Thorson, West, & Mendes, Ham and Tronick (2009) found that PS (measured
in press). by SC) was observed between mothers and their
Physiological synchrony (PS) can be defined as 5-month-olds during stress and was positively asso-
“any interdependent or associated activity identi- ciated with maternal sensitivity when normal inter-
fied in the physiological processes of two or more action resumed. A second study also showed that
individuals” (Palumbo et al., 2017, p. 100). This def- sensitive mothers and their 6-month-old babies
inition is useful because it subsumes more specific showed greater PS during the resumption of normal
descriptors of relational synchrony such as covaria- interaction, but this was not observed for other
tion (within time-point associations) and linkage mother–child dyads (Moore et al., 2009). Greater
(between time-point associations) and because it sensitivity may enable mothers to facilitate their
can be applied both to dyadic regulation and to children’s recovery from stress as they manage their
dysregulation. In her biobehavioral model of bond own emotions.
formation, Feldman (2012) argues that physiologi- In the second type of procedure, mothers undergo
cal and behavioral processes work together to foster an emotion induction, and physiological reactivity
organization of the early parent–child relationship of both partners is measured. Using this approach,
into a dyadic regulatory system that shapes chil- PS (measured by RSA) was observed when mothers
dren’s development. For instance, mothers and held their 3-month-olds as they underwent a paced
their 3-month-olds experienced synchronized heart breathing exercise (van Puyvelde et al., 2015). In an
rhythms during face-to-face interactions, and these experimental study, mothers and their 1-year-olds
episodes of PS co-occurred with episodes of increased were observed after mothers experienced a negative
affective synchrony (Feldman, Magori-Cohen, Galili, stress task. Mothers and infants exhibited PS (meas-
Singer, & Louzoun, 2011). Mothers with affective ured with cardiac indices) that increased over time,
symptoms—including depression and anxiety— a pattern not observed by mothers in a control
were less capable of establishing affective synchrony condition or mothers who experienced stressful events
with their infants, and this was associated with that ended positively (Waters, West, & Mendes,
infants’ poorer stress reactivity and fear regulation 2014). Waters and her colleagues suggested that this
(Feldman et al., 2009). kind of physiological synchrony between mothers

and babies can contribute to affective contagion in effects. Stressors can also be chronic experiences
shared experiences. In this example, infants shared that progressively wear down psychological and
physiological indicators of stress that their mothers physiological coping mechanisms. Developmental
experienced. In a follow-up study, PS (measured by research on emotion regulation has focused increas-
RSA) was observed for mother–infant dyads after ing attention on the latter types of stress in recent
mothers experienced a relaxation task but not for years for several reasons: such stressors affect more
dyads with mothers who experienced a negative children than traumatic stressors; they often occur
stress task (Waters, West, Karnilowicz, & Mendes, early in life with long-lasting consequences; and
2017). Taken together, evidence of physiological these consequences can derive from reorganization
synchrony in both normal interactions and stressful of stress neurocircuitry in the brain and the effects
conditions can be observed between mothers and of close relationships that can either exacerbate
their children in the first year, and this varies ac- stress or buffer it.
cording to maternal sensitivity, although evidence Stressful experiences have surprisingly early ef-
of PS also varies according to how it is measured. fects on development, beginning prenatally. For
Synchrony can contribute to stress contagion and example, mothers’ depression during pregnancy
also to shared recovery from it. was associated with heightened cortisol reactivity
Similar results are obtained with older children. when infants were observed 3 months after birth
During episodes of play and mild challenge, as they underwent a moderately stressful proce-
mothers and their preschool-age children exhibited dure (Oberlander et al., 2008). This illustrates a
PS (measured by RSA), but mother–child RSA kind of physiological synchrony complementary
was dyssynchronous (i.e., moved in opposite di- to the kinds previously discussed. These findings
rections) for children with externalizing problems are consistent with many other animal and human
(Lunkenheimer et al., 2015). In the same sample, PS studies describing “fetal programming” that occurs
was weaker for dyads with mothers who were highly in response to signals from the mother’s body con-
disengaged (Skoranski, Lunkenheimer, & Lucas- cerning nutritional sufficiency, stress, and other
Thompson, 2017). More research on these issues is aspects of the world into which the fetus will be
needed, however, in light of inconsistent findings in born (Davis & Thompson, 2014). They suggest that
the literature (see, e.g., Smith, Woodhouse, Clark, some of the foundations for emotion and stress
& Skowron, 2016). These studies indicate that the regulatory capacities are established in mother–child
quality of parent–child relationships is an impor- interaction very early. Sometimes these effects
tant moderator of physiological synchrony, which are exerted through epigenetic changes in neural
may help to account for the role of synchrony in the and neurohormonal systems that are implicated
development of emotion regulation and dysregula- in stress regulation and social affiliation (see
tion in early parent–infant interactions. Anacker, O’Donnell, & Meaney, 2014; Chapter 16,
There remains much more to be understood this volume).
about the meaning of PS for social-emotional devel- After birth, infants respond to their direct
opment. Physiological synchrony with a parent who experience of stressors. Because biological stress
experiences emotional psychopathology may pose systems—especially the L-HPA axis (discussed
risks for the development of emotional dysregula- previously)—are maturing during the early years,
tion, especially in young children, compared to self- they are particularly susceptible to the effects of
regulatory support afforded by PS with emotionally chronic or severe stress that may progressively tax
healthy parents. In addition, there is more to be system capacities over time. Among young children
known about the effects of context on PS, including living in poverty, for example, environmental char-
immediate physiological demands of situations, the acteristics such as poor housing quality, economic
quality of parent–child interactions during meas strain, and poor parenting were associated with dys-
urement, relational histories of parents and chil- regulated activity of the L-HPA axis from 7 months
dren, and characteristics of individuals. to 4 years of age (Blair et al., 2011). Moreover, toddlers
living in poor families characterized by interparen-
Socialization of Stress Neurobiology tal violence and mothers’ “emotional unavailability”
Emotion dysregulation arises, for many children and exhibited disruptions to normal L-HPA activity
adults, from stress. Stressors, such as traumatic events (Sturge-Apple, Davies, Cicchetti, & Manning, 2012).
that lead to posttraumatic psychopathology, can be In older children, higher cortisol levels were associ-
intense, overwhelming experiences that have lasting ated with lower family socioeconomic status, and

mothers of children with higher cortisol levels were Taken together, potentially enduring tendencies
more likely to have depressive symptoms (Lupien, toward emotion dysregulation can develop early in
King, Meaney, & McEwen, 2000). response to chronically stressful experiences. Behavior
These dysregulatory effects on stress neurobiol- and emotion dysregulation develop because of
ogy from chronic early stressful experiences are be- changes in multiple physiological systems that sys-
lieved to derive from adaptation of physiological temically adapt to environmental experiences that
systems to environmental conditions that begin signal persistent threat, challenge, and danger. Once
with processes of fetal programming, as earlier de- these emotional and physiological adaptations
scribed. Ordinary experiences of challenge and stress begin to develop, they alter children’s reactions even
help “tune” biological stress systems and strengthen in nonthreatening circumstances, such as school
coping. Chronic and severe early stress, however, classrooms. Consequently, children in these circum-
alters sensitivity of the L-HPA axis and other sys- stances often become identified as behaviorally
tems, in part through effects on limbic and cortical disruptive and difficult, and thus evoke aversive
processes that regulate L-HPA activity (Ulrich-Lai responses from others, which can exacerbate their
& Herman, 2009). One consequence of this dys- emotion regulatory problems.
regulation is that stress responding becomes hyper- What are the circumstances leading to these de-
reactive, with heightened responses to cues of threat velopmental adaptations in behavior and biology?
and danger along with rapid escalation of response. Researchers who examine the effects of early chronic
Behaviorally, this is manifested in self-regulatory stress most often study children in poverty, which,
problems that can be observed in children’s height- as earlier noted, is associated with poor housing
ened vigilance, emotional dysregulation, and com- quality, parental stress, interparental relationship
plementary problems in cognitive and attentional difficulties, disengaged and nonnurturant parent-
focus and difficulties in social functioning (Blair & ing, and poorer child care and school quality. Other
Raver, 2012). In some situations, however, chronic conditions studied by researchers include chronic
stress may result in neuro-adaptive “downregulation” maternal depression, foster care placement, interpa-
of the L-HPA axis (Doom & Gunnar, 2013). Thus, rental/domestic violence, and child maltreatment
rather than responding to threat in a hyperreactive and chronic neglect. Significantly, in most of these
manner, children show a lower cortisol response to circumstances, parents are either the agent of chronic
stressors, and sometimes exhibit a flattened diurnal stress or a victim along with the child, and are thus
cortisol pattern throughout the day. Some research- unable to protect the child. This underscores that
ers speculate that this alternative response pattern the absence of parental support is an important
reflects a biological stress system that shows signs of component of severe stress for young children be-
suppression or shutting down (Bruce, Gunnar, cause of children’s dependence on adults for protec-
Pears, & Fisher, 2013). tion and nurturance. Without parental support as a
There are other physiological changes associated stress buffer, children are more vulnerable to emo-
with recurrent experiences of severe stress. Chronic tion dysregulation.
stress is associated with immune suppression and Thus, it is important to recognize the beneficial
“proinflammatory tendencies,” which become in- effects that parental support can have for buffering
corporated into biological functioning (Miller, Chen, stress or remediating its effects on children (Hostinar,
& Parker, 2011). This helps to account for the sus- Sullivan, & Gunnar, 2014). In a study of families
ceptibility of children in difficult circumstances to living in rural poverty, for example, researchers
infectious agents, both acute and chronic. There is found that infants’ chronic exposure to domestic vi-
also growing evidence of epigenetic changes in gene olence was associated with elevated stress reactivity
expression associated with chronic stress that may by age 2 years. But when mothers were observed
help to account for some of the changes in stress behaving sensitively with their children in earlier
reactivity noted previously. The study earlier de- home observations, repeated exposure to domestic
scribed concerning the association of prenatal ma- violence was not associated with heightened stress
ternal depression with heightened stress reactivity reactivity for their children (Hibel, Granger, Blair,
in 3-month-olds was related, for example, to epige- Cox, & the Family Life Project Key Investigators,
netic changes in the activation of the glucocorticoid 2011). Consistent with the findings of research on
receptor gene detected when children were newborn, social support for adolescents and adults, reliable
a gene that is implicated in L-HPA axis function support from a parent is an important resource for
(Oberlander et al., 2008). emotion regulation in the early years.

Differential Susceptibility Difficult temperament, which is characterized
Psychological understanding of negative develop- by negative mood, reactivity, lack of rhythmicity,
mental outcomes has long been dominated by a and slow adaptability, was among the earliest identi-
focus on risk factors and vulnerabilities. Within the fied susceptibility factors (Belsky, Hsieh, & Crnic,
diathesis-stress model, for example, researchers ex- 1998). In a large national sample, harsh parenting
amine characteristics that make some individuals and deficient home environments predicted later
more likely to succumb to the sequelae of adversity behavior problems, whereas sensitive parenting was
compared to those who are more resilient. There is negatively associated with behavior problems, for
considerable work, for example, on vulnerabilities infants with difficult temperament compared to
and risk factors that contribute to the development those with average or easy temperament (Bradley &
of emotion dysregulation (e.g., Gazelle & Ladd, Corwyn, 2008). In another study, positive parent-
2003; Kim & Cicchetti, 2010). From this perspec- ing in early childhood was more predictive of first-
tive, some individuals have characteristics, such as grade academic success, social skills, peer status,
difficult temperament, that heighten vulnerability and strong relationships with teachers for children
to problems with emotion self-management com- who had more difficult temperaments in infancy
pared with others. (Dopkins Stright, Gallagher, & Kelley, 2008). Infants
However, this account may be incomplete. From with difficult temperaments had better adjustment
the perspective of differential susceptibility, indi- than less difficult infants when parenting quality
viduals vary not exclusively in vulnerability factors was high but poorer adjustment when parenting
but also in broader susceptibility to environmental was poorer.
influences (Belsky & Pluess, 2009). According to Notably, difficult temperament is not the only
differential susceptibility theorists, some people are dispositional susceptibility factor worth considering.
more readily influenced by their environments than Associations consistent with differential susceptibility
others. For more susceptible individuals, the envi- have also been found between parental effective guid-
ronment affects them “for better and for worse” ance and behavior problems for highly anger-prone
such that they experience highly negative outcomes children, but not for non-anger-prone children
when environments are stressful (consistent with (Smeekens, Riksen-Walraven, & van Bakel, 2007).
the diathesis-stress model), but also exhibit positive Other susceptibility factors include certain pat-
outcomes when environments are supportive. For terns of physiological responding. Earlier we dis-
others who are less susceptible to these environmen- cussed RSA as a biomarker of individual differences
tal influences, outcomes are only slightly moderated in emotion regulatory capacities. Conradt and col-
by environmental quality. Importantly, individuals leagues (2013) examined RSA as a potential suscep-
who are more susceptible to environmental influ- tibility factor in a sample of infants growing up in
ences are often viewed as being more vulnerable poverty. They found that secure attachment pre-
because research studies typically only focus on dicted the least behavior problems, and that disor-
their responses to adversity, not to both adverse ganized attachment predicted the greatest behavior
and supportive circumstances. Once they are stud- problems for children with high resting RSA, but
ied in both contexts, positive and negative out- these associations did not hold for children with low
comes associated with putative vulnerabilities can resting RSA. In the context of family economic dif-
be observed. ficulty, in other words, higher emotion regulatory
A growing body of research has identified dif- capability (indexed by high resting RSA) is associ-
ferential susceptibility factors in the form of phe- ated with infants’ greater adaptation to differences
notypic traits (e.g., temperament), neurobiological in the quality of care leading to attachment. In an-
characteristics (i.e., physiological responses), and other study, kindergarten-age children who had
genetics (i.e., genetic polymorphisms) (Belsky & strong RSA responses to a series of challenging tasks
Pluess, 2009). Research studies have identified the subsequently exhibited the greatest behavior prob-
differential influence of these factors in samples lems and lowest school engagement when they also
ranging from infancy through adolescence and young experienced family adversity, but the greatest school
adulthood. In many cases, characteristics that were engagement and fewest behavior problems when
traditionally portrayed as risk factors that enhance they did not experience adversity. Children who did
vulnerability are being reconceptualized as markers not have strong RSA responses to challenge did not
of environmental sensitivity, and this is apparent exhibit this for-better-and-for-worse set of associ-
from early in life. ations (Obradovic et al., 2010). Whether at rest or

in response to specific tasks, there is evidence of problems can contribute to emotion dysregulation
RSA as an indicator of a child’s susceptibility to at all ages. We propose that a relational orientation
the environment. can strengthen inquiry into the nature of emotion
Genetic variation can also constitute suscepti- dysregulation throughout life by contributing a
bility factors. Researchers have investigated several deeper understanding of the influence of other
candidate genes, most notably DRD4 gene poly- people—as providers of support, sources of stress,
morphisms. This dopamine receptor gene, particu- models of emotion regulation and dysregulation,
larly the allelic variant known as the 7-repeat allele, is evaluators of one’s feelings, and contributors to the
implicated in novelty seeking and impulsive be- general emotional climate of close relationships.
havior. In one study, toddlers’ 7-repeat allele showed With the predominant orientation of current research
an inverse association between the quality of par- on adult emotion regulation toward the functioning
enting and sensation seeking. In contrast, no such of individual strategies such as cognitive reappraisal
associations were found for children without the and emotional suppression (e.g., Gross, 2015), ex-
7-repeat allele (Sheese, Voelker, Rothbart, & Posner, pansion of the field to include attention to relational
2007). Others have also reported this for-better- influences would be worthwhile (see also Beauchaine
and-for-worse effect of parenting for children with & Zalewski, 2016).
the DRD4 7-repeat polymorphism compared to Expanding inquiry into the relational bases of
those without, underscoring the significance of emotion regulation and dysregulation is important
this Gene × Environment interaction (Bakermans- also for clinical intervention. When young children
Kranenburg & van Ijzendoorn, 2006; Windhorst are emotionally dysregulated, infant and early child-
et al., 2014). hood mental health practices are concertedly two-
The expanding research literature on differen- generational, enlisting the child’s parents and other
tial susceptibility challenges simple diathesis-stress relational partners (such as early education care
models by suggesting that characteristics typically providers) into therapeutic avenues to address the
portrayed as vulnerability factors may instead have relational bases for the child’s dysregulation (Zero
more complex associations with emotion dysregula- to Three, 2016). The importance of relationships to
tion. Viewing these characteristics instead as mark- emotion dysregulation is recognized also at older
ers of environmental sensitivity reorients researchers ages in marriage and family therapy. The predomi-
to elements of the environment that cause these nant approach to psychotherapy, however, is to
characteristics to be associated with positive or neg- treat the individual, which means that associated
ative developmental outcomes. It is no accident that issues of emotion dysregulation are decontextual-
most developmental research on differential suscep- ized from the relational processes that may have
tibility has emphasized the influence of parenting contributed to their development. Greater consid-
quality and family life, because these are the most eration of these relational processes in therapeutic
important elements of environmental influence, contexts is warranted.
especially to a young child. This has important A second conclusion also points toward a future
implications for intervention (as discussed further direction for the field. From research literatures fo-
later). Taken together, this research underscores that cused on the physiological synchrony of relational
vulnerability to emotion dysregulation is sometimes partners (with our focus on parents and children),
less in the child alone and more in the Child × socialization of stress neurobiology, and differential
Context interaction. susceptibility to environmental influences, we de-
scribed connections between relational experience
Synthesis and Future Directions and biological processes associated with emotion
Research described in this chapter supports the dysregulation. These connections are complex and
theoretical view with which we opened: emotion bidirectional: social experiences associated with stress
regulation and dysregulation develop in contexts of alter how biological stress systems function, making
relationships, and developing problems in emotion emotion dysregulation under challenging condi-
management are relational problems as well as indi- tions more or less likely; the social context can make
vidual difficulties. This conclusion, which has roots environmental susceptibility factors (such as diffi-
in attachment theory, is most readily evident in cult temperament) assets or liabilities for outcomes
studies with young children, but, as earlier noted, related to emotion dysregulation; social influences can
older children, youth, and adults also rely on others support or undermine emotion regulation through
for support in emotion regulation, and relational physiological synchrony shared by relational partners.

These research fields contribute a biological dimen- context. In other cases, emotion dysregulation derives
sion to understanding the development of emotion from the child’s physiological synchrony with an-
dysregulation and confirm the growing recognition other who is emotionally dysregulated. For children
that the traditional nature-versus-nurture dichot- who experience chronic stress, emotion dysregula-
omy is scientifically obsolete (Thompson, 2015). tion derives from complex emotional challenges
They also show that biological bases of emotion they face. From the functionalist orientation of this
dysregulation, whether in stress neurobiology, in- chapter, understanding these children as emotion-
dividual temperament, or genetic propensities, are ally dysregulated must lead to a more searching ex-
far more dynamic in their influence than earlier be- amination of the interaction of characteristics of the
lieved because of their continuous interaction with child and the social environment in the context of
experience. Further efforts to empirically elucidate the multiple emotion goals the child may be seek-
the interplay between social (especially relational) ing, implicitly or explicitly, to accomplish. Viewed
experience and biology is certainly warranted, espe- in this light, children’s emotional experiences can be
cially concerning the origins of differences in emo- appreciated and understood with all the complexity
tion dysregulation. Fortunately, continuing research and depth they warrant.
in fields such as molecular genetics, epigenetics,
and life history theory offer promise for further References
understanding. Anacker, C., O’Donnell, K. J., & Meaney, M. J. (2014). Early life
adversity and the epigenetic programming of hypothalamic-
Developmental interactions between social expe-
pituitary-adrenal function. Dialogues in Clinical Neuroscience,
rience and biology are also important for clinical 16, 321–333.
applications. The possibility that, from the per- Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H.
spective of differential susceptibility, children with a (2006). Gene-environment interaction of the dopamine D4
susceptibility factor such as the DRD4 7-repeat receptor (DRD4) and observed mater nal insensitivity
predicting externalizing behavior in preschoolers.
allele are likely to thrive in a more supportive social
Developmental Psychobiology, 48, 406–409.
context underlies therapeutic efforts focused on Bakermans-Kranenburg, M. J., van Ijzendoorn, M. H., Pihlman,
improving the caregiving context because these chil- F. T. A., Mesman, J., & Juffer, F. (2008). Experimental
dren might especially benefit from such efforts (see evidence for differential susceptibility: Dopamine D4 receptor
Bakermans-Kranenburg, van Ijzendoorn, Pihlman, polymorphism (DRD4 VNTR) moderates intervention
effects on toddlers’ externalizing behavior in a randomized
Mesman, & Juffer, 2008). In other clinical contexts,
controlled trial. Developmental Psychology, 44, 293–300.
recognition that prior experiences of chronic stress Beauchaine, T. (2015). Respiratory sinus arrhythmia: A
have dysregulated biological stress systems has ori- transdiagnostic biomarker of emotion dysregulation and
ented some therapeutic programs for young chil- psychopathology. Current Opinion in Psychology, 3, 43–47.
dren in foster care to measure the functioning of Beauchaine, T. P., & Zalewski, M. (2016). Physiological and
developmental mechanisms of emotional lability in coercive
the L-HPA axis and the security of attachment
relationships. In T. J. Dishion & J. J. Snyder (Eds.), The
relationships as indicators of therapeutic success Oxford handbook of coercive relationship dynamics (pp. 39–52).
(see review by Thompson, 2014). Understanding New York, NY: Oxford University Press.
emotion dysregulation as a multilevel process in- Belsky, J., Hsieh, K.-H., & Crnic, K. (1998). Mothering,
volving behavioral and biological factors contrib- fathering, and infant negativity as antecedents of boys’
externalizing problems and inhibition at age 3 years:
utes a multilevel orientation to clinical intervention
Differential susceptibility to rearing experience? Development
and promotes attention to multiple indicators of and Psychopathology, 10, 301–319.
therapeutic outcome. Belsky, J., & Pluess, M. (2009). Beyond diathesis stress:
Finally, the functionalist approach to under- Differential susceptibility to environmental influence.
standing emotion dysregulation is affirmed by the Psychological Bulletin, 135, 885–908.
Blair, C., & Raver, C. C. (2012). Child development in the
research literatures discussed in this chapter. Young
context of adversity: Experiential canalization of brain and
children who live in poverty, live with a depressed behavior. American Psychologist, 67, 309–318.
parent, possess a genetic vulnerability to impulsiv- Blair, C., Raver, C. C., Granger, D., Mills-Koonce, R., Hibel,
ity, and/or are born with a difficult temperament L., and the Family Life Project Key Investigators (2011).
are often emotionally dysregulated, but it is more Allostasis and allostatic load in the context of poverty in
early childhood. Development and Psychopathology, 23,
important to understand the strategies they enlist
845–857.
to manage their feelings in the contexts in which Bowlby, J. (1969). Attachment and loss, Vol. 1. Attachment. New
this occurs. In some cases, differential susceptibility York, NY: Basic Books.
means that children’s characteristics may or may not Bradley, R. H., & Corwyn, R. F. (2008). Infant temperament,
predict emotion dysregulation depending on the parenting, and externalizing behavior in first grade: A test of

the differential susceptibility hypothesis. Journal of Child Feldman, R. (2012). Parent-infant synchrony: A biobehavioral
Psychology and Psychiatry and Allied Disciplines, 49, 124–131. model of mutual influences in the formation of affiliative
Bruce, J., Gunnar, M. R., Pears, K. C., & Fisher, P. A. (2013). bonds. Monographs of the Society for Research in Child
Early adverse care, stress neurobiology, and prevention Development, 77, 42–51.
science: Lessons learned. Prevention Science, 14, 247–256. Feldman, R., Granat, A., Pariente, C., Kanety, H., Kuint, J., &
Brumariu, L. E. (2015). Parent-child attachment and emotion Gilboa-Schechtman, E. (2009). Maternal depression and
regulation. New Directions for Child and Adolescent anxiety across the postpartum year and infant social
Development, 148, 31–45. engagement, fear regulation, and stress reactivity. Journal of
Brumariu, L. E., Kerns, K. A., & Seibert, A. (2012). Mother- the American Academy of Child and Adolescent Psychiatry, 48,
child attachment, emotion regulation, and anxiety symptoms 919–927.
in middle childhood. Personal Relationships, 19, 569–585. Feldman, R., Magori-Cohen, R., Galili, G., Singer, M., &
Butler, E. A. (2015). Interpersonal affect dynamics. It takes two Louzoun, Y. (2011). Mother and infant coordinate heart
(and time) to tango. Emotion Review, 7, 336–341. rhythms though episodes of interaction synchrony. Infant
Carstensen, L. L., Fung, H. H., & Charles, S. T. (2003). Behavior and Development, 34, 569–577.
Socioemotional selectivity theory and the regulation of Ferrer, E., & Helm, J. L. (2013). Dynamical systems modeling of
emotion in the second half of life. Motivation and Emotion, physiological coregulation in dyadic interactions. International
27, 103–123. Journal of Psychophysiology, 88, 296–308.
Cassidy, J. (1994). Emotion regulation: Influences of attachment Fox, N. A., Henderson, H. A., Marshall, P. J., Nichols, K. E., &
relationships. In N. A. Fox (Ed.), The development of emotion Ghera, M. M. (2005). Behavioral inhibition: Linking
regulation and dysregulation: Biological and behavioral aspects. biology and behavior within a developmental framework.
Monographs of the Society for Research in Child Development, Annual Review of Psychology, 56, 235–262.
50(2–3), 228–249. Garber, J., & Dodge, K. A. (Eds.). (1991). The development of
Chang, L., Schwartz, D., Dodge, K. A., & McBride-Chang, C. emotion regulation and dysregulation. New York, NY:
(2003). Harsh parenting in relation to child emotion Cambridge University Press.
regulation and aggression. Journal of Family Psychology, 17, Gazelle, H., & Ladd, G. W. (2003). Anxious solitude and peer
598–606 exclusion: A diathesis-stress model of internalizing trajectories
Conger, R. D., Conger, K. J., & Martin, M. J. (2010). in childhood. Child Development, 74, 257–278.
Socioeconomic status, family processes, and individual Goodman, S. H., & Gotlib, I. H. (1999). Risk for psychopathology
development. Journal of Marriage and the Family, 72, in the children of depressed mothers: A developmental model
685–704. for understanding mechanisms of transmission. Psychological
Conradt, E., Measelle, J., & Ablow, J. C. (2013). Poverty, Review, 106, 458–490.
problem behavior, and promise: Differential susceptibility Gottman, J. M., & Levenson, R. W. (2000). The timing of
among infants reared in poverty. Psychological Science, 24, divorce: Predicting when a couple will divorce over a 14-year
235–242. period. Journal of Marriage and the Family, 62, 737–745.
Crowell, S. E., Butner, J., Wiltshire, T. J., Munion, A. K., Gross, J. J. (2015). Emotion regulation: Conceptual and empirical
Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating foundations. In J. J. Gross (Ed.), Handbook of emotion
emotional and biological sensitivity to maternal behavior regulation (2nd ed., pp. 3–20). New York, NY: Guilford.
among depressed and self-injuring adolescent girls using Gunnar, M., & Donzella, B. (2002). Social regulation of the
nonlinear dynamics. Clinical Psychological Science, 5, cortisol levels in early human development.
272–285. Psychoneuroendocrinology, 27, 199–220.
Cummings, E. M., & Davies, P. T. (2010). Children and marital Ham, J., & Tronick, E. (2009). Relational psychophysiology:
conflict: An emotional security perspective. New York, NY: Lessons from mother-infant physiology research on dyadically
Guilford. expanded states of consciousness. Psychotherapy Research, 19,
Davidov, M., & Grusec, J. E. (2006). Untangling the links of 619–632.
parental responsiveness to distress and warmth to child Harrist, A. W., & Waugh, R. M. (2002). Dyadic synchrony: Its
outcomes. Child Development, 77, 44–58. structure and function in children’s development.
Davies, P. T., Harold, G. T., Goeke-Morey, M. C., & Cummings, Developmental Review, 22, 555–592.
E. M. (2002). Child emotional security and interparental Hibel, L. C., Granger, D. A., Blair, C., Cox, M. J., & the Family
conflict. Monographs of the Society for Research in Child Life Project Key Investigators. (2011). Maternal sensitivity
Development, 67, 1–127. buffers the adrenocortical implications of intimate partner
Davis, E. P., & Thompson, R. A. (2014). Prenatal foundations: violence exposure during early childhood. Development and
Fetal programming of health and development. Zero to Three Psychopathology, 23, 689–701.
Journal, 34, 6–11. Hostinar, C. E., Sullivan, R. M., & Gunnar, M. R. (2014).
Donovan, W. L., & Leavitt, L. L. (1985). Physiologic assessment Psychobiological mechanisms underlying the social buffering
of mother-infant attachment. Journal of the American of the hypothalamic-pituitary-adrenocortical axis: A review
Academy of Child Psychiatry, 24, 65–70. of animal models and human studies across development.
Doom, J. R., & Gunnar, M. R. (2013). Stress physiology and Psychological Bulletin, 140, 256–282.
developmental psychopathology: Past, present, and future. Jiang, Y., Granja, M. R., & Koball, J. (2017). Basic facts about
Development and Psychopathology, 25, 1359–1373. low-income children: Children under 3 years, 2015. New York,
Dopkins Stright, A., Gallagher, K. C., & Kelley, K. (2008). NY: National Center for Children in Poverty, Columbia
Infant temperament moderates relations between maternal University Mailman School of Public Health. Retrieved on
parenting in early childhood and children’s adjustment in July 7, 2017, from http://www.nccp.org/publications/pdf/
first grade. Child Development, 79, 186–200. text_1171.pdf.

Johnson, A. M., Hawes, D. J., Eisenberg, N., Kohlhoff, J., & Saxbe, D. E., Margolin, G., Shapiro, L. S., Ramos, M.,
Dudeney, J. (2017). Emotion socialization and child conduct Rodriguez, A., & Iturralde, E. (2014). Relative influences:
problems: A comprehensive review and meta-analysis. Patterns of L-HPA axis concordance during triadic family
Clinical Psychology Review, 54, 65–80. interaction. Health Psychology, 33, 273–281.
Kim, J., & Cicchetti, D. (2010). Longitudinal pathways linking Schwartz, O. S., Sheeber, L. B., Dudgeon, P., & Allen, N. B.
child maltreatment, emotion regulation, peer relations, and (2012). Emotion socialization within the family environment
psychopathology. Journal of Child Psychology and Psychiatry, and adolescent depression. Clinical Psychology Review, 32,
51, 706–716. 447–453.
Leerkes, E. M., Blankson, A. N., & O’Brien, M. (2009). Sheese, B. E., Voelker, P. M., Rothbart, M. K., & Posner, M. I.
Differential effects of maternal sensitivity to infant distress (2007). Parenting quality interacts with genetic variation
and nondistress on social-emotional functioning. Child in dopamine receptor D4 to influence temperament in
Development, 80, 762–775. early childhood. Development and Psychopathology, 19,
Levenson, R. W., & Gottman, J. M. (1983). Marital interaction: 20139–21046.
Physiological linkage and affective exchange. Journal of Silk, J. S., Shaw, D. S., Skuban, E. M., Oland, A. A., & Kovacs,
Personality and Social Psychology, 45, 587–597. M. (2006). Emotion regulation strategies in offspring of
Lunkenheimer, E., Tiberio, S. S., Buss, K. A., Lucas-Thompson, childhood-onset depressed mothers. Journal of Child
R. G., Boker, S. M., & Timpe, Z. C. (2015). Coregulation of Psychology and Psychiatry, 47, 69–78.
respiratory sinus arrhythmia between parents and preschoolers: Skoranski, A. M., Lunkenheimer, E., Lucas-Thompson, R. G.
Differences by children’s externalizing problems. Developmental (2017). The effects of maternal respiratory sinus arrhythmia
Psychobiology, 57, 994–1003. and behavioral engagement on mother-child physiological
Lupien, S. J., King, S., Meaney, M. J., & McEwen, B. S. (2000). coregulation. Developmental Psychobiology, 59, 888–898.
Child’s stress hormone levels correlate with mother’s Smeekens, S., Riksen-Walraven, J. M., & van Bakel, H. J. A.
socioeconomic status and depressive state. Biological (2007). Multiple determinants of externalizing behavior in
Psychiatry, 48, 976–980. 5-year-olds: A longitudinal model. Journal of Abnormal
Mence, M., Hawes, D. J., Wedgwood, L., Morgan, S., Barnett, B., Psychology, 35, 347–361.
Kohlhoff, J., & Hunt, C. (2014). Emotional flooding and Smith, J. D., Woodhouse, S. S., Clark, C. A. C., & Skowron,
hostile discipline in the families of toddlers with disruptive E. A. (2016). Attachment status and mother-preschooler
behavior problems. Journal of Family Psychology, 28, 12–21. parasympathetic response to the Strange Situation procedure.
Miller, G. E., Chen, E., & Parker, K. J. (2011). Psychological Biological Psychology, 114, 39–48.
stress in childhood and susceptibility to the chronic diseases Spangler, G., & Grossmann, K. E. (1993). Biobehavioral
of aging: Moving toward a model of behavioral and biological organization in securely and insecurely attached infants.
mechanisms. Psychological Bulletin, 137, 959–997. Child Development, 64, 1439–1450.
Moore, G. A., Hill-Soderlund, A. L., Propper, C. B., Calkins, Spangler, G., & Zimmermann, P. (2014). Emotional and
S. D., Mill-Koonce, W. R., & Cox, M. J. (2009). Mother- adrenocortical regulation in early adolescence: Prediction
infant vagal regulation in the face-to-face still-face paradigm by attachment security and disorganization in infancy.
is moderated by maternal sensitivity. Child Development, 80, International Journal of Behavioral Development, 38, 1–13.
209–223. Stocker, C. M., Richmond, M. K., Rhoades, G. K., & Kiang, L.
Morris, A. S., Silk, J. S., Steinberg, L., Myers, S. S., & Robinson, (2007). Family emotional processes and adolescents’
L. R. (2007). The role of family context in the development adjustment. Social Development, 16, 310–325.
of emotion regulation. Social Development, 16, 361–388. Sturge-Apple, M. L., Davies, P. T., Cicchetti, D., & Manning,
Oberlander, T. F., Weinberg, J., Papsdorf, M., Grunau, R., Misri, L. G. (2012). Interparental violence, maternal emotional
S., & Devlin, A. M. (2008). Prenatal exposure to maternal unavailability and children’s cortisol functioning in family
depression, neonatal methylation of human glucocorticoid contexts. Developmental Psychology, 48, 237–249.
receptor gene (NR3C1) and infant cortisol stress responses. Thompson, R. A. (1994). Emotion regulation: A theme in search
Epigenetics, 3, 97–106. of definition. In N. A. Fox (Ed.), The development of emotion
Obradovic, J., Bush, N. R., Stamperdahl, J., Adler, N. E., & regulation and dysregulation: Biological and behavioral aspects.
Boyce, W. T. (2010). Biological sensitivity to context: The Monographs of the Society for Research in Child Development,
interactive effects of stress reactivity and family adversity 59 (2–3), 25–52 (Serial no. 240).
on socioemotional behavior and school readiness. Child Thompson, R. A. (2001). Childhood anxiety disorders from
Development, 81, 270–289. the perspective of emotion regulation and attachment. In
Palumbo, R. V., Marraccini, M. E., Weyandt, L. L., Wilder- M. W. Vasey & M. R. Dadds (Eds.), The developmental
Smith, O., McGee, H. A., Lui, S., & Goodwin, M. S. (2017). psychopathology of anxiety (pp. 160–182). Oxford, UK:
Interpersonal autonomic physiology: A systematic review of Oxford University Press.
the literature. Personality and Social Psychology Review, 21, Thompson, R. A. (2011). Emotion and emotion regulation: Two
99–141. sides of the developing coin. Emotion Review, 3, 53–61.
Pollak, S. D. (2008). Mechanisms linking early experience and Thompson, R. A. (2013). Socialization of emotion and emotion
the emergence of emotions: Illustrations from the study of regulation in the family. In J. Gross (Ed.), Handbook of emotion
maltreated children. Current Directions in Psychological regulation (2nd ed., pp. 173–186). New York, NY: Guilford.
Science, 17, 370–375. Thompson, R. A. (2014). Stress and child development. Future of
Rogosch, F. A., Cicchetti, D., & Toth, S. L. (2004). Expressed Children, 24, 41–59.
emotion in multiple subsystems of the families of toddlers Thompson, R. A. (2015). Relationships, regulation, and early
with depressed mothers. Development and Psychopathology, development. In R. M. Lerner (Ed.), Handbook of child
16, 689–709. psychology and developmental science, Vol. 3: Social and

emotional development (M. E. Lamb & C. Garcia Coll, Vol. Waters, S. F., West, T. V., Karnilowicz, H. R., & Mendes, W. B.
Eds., 7th ed., pp. 201–246). New York, NY: Wiley. (2017). Affect contagion between mothers and infants:
Thompson, R. A. (2016). Early attachment and later development: Examining valence and touch. Journal of Experimental
Reframing the questions. In J. Cassidy & P. R. Shaver (Eds.), Psychology: General, 146, 1043–1051.
Handbook of attachment (3rd ed., pp. 330–348). New York, Waters, S. F., West, T. V., & Mendes, W. B. (2014). Stress
NY: Guilford. contagion: Physiological covariation between mothers and
Thompson, R. A., & Calkins, S. (1996). The double-edged infants. Psychological Science, 25, 934–942.
sword: Emotional regulation for children at risk. Development Windhorst, D. A., Mileva-Seitz, V. R., Linting, M., Hofman, A.,
and Psychopathology, 8, 163–182. Jaddoe, V. W. V., Verhulst, F. C., Tiemeier, H., . . . Bakermans-
Thompson, R. A., Virmani, E., Waters, S. F., Meyer, S., & Raikes, Kranenburg, M. J. (2014). Differential susceptibility in a
A. (2013). The development of emotion self-regulation: The developmental perspective: DRD4 and maternal sensitivity
whole and the sum of the parts. In K. Barrett, N. A. Fox, predicting externalizing behavior. Developmental Psychobiology,
G. A. Morgan, D. J. Fidler, & L. A. Daunhauer (Eds.), 57, 35–49.
Handbook of self-regulatory processes in development (pp. 5–26). Winnicott, D. W. (1957). Further thoughts on babies as persons.
New York, NY: Taylor & Francis. In J. Hardenberg (Ed.), The child and the outside world:
Thorson, K. R., West, T. V., & Mendes, W. B. (in press). Studies in developing relationships (pp. 134–140). London,
Measuring physiological linkage in dyads: A guide to UK: Tavistock Publications (originally published 1947).
designing, implementing, and analyzing dyadic physiological Wisner, K. L., Sit, D. K. Y., McShea, M. C., Rizzo, D. M.,
studies. Psychological Methods. Zoretich, R. A., Hughes, C. L., . . . Hanusa, B. H. (2013).
Ulrich-Lai, Y. M., & Herman, J. P. (2009). Neural regulation of Onset timing, thoughts of self-harm, and diagnoses with
endocrine and autonomic stress responses. Nature Reviews postpartum women with screen-positive depression findings.
Neuroscience, 10, 397–409. JAMA Psychiatry, 70, 490–498.
van Puyvelde, M., Loots, G., Meys, J., Neyt, X., Mairesse, O., Zaki, J., & Williams, W. C. (2013). Interpersonal emotion
Simcock, D., & Pattyn, N. (2015). Whose clock makes yours regulation. Emotion, 13, 803–810.
tick? How maternal cardiorespiratory physiology influences Zero to Three. (2016). Early childhood mental health consultation:
newborns’ heart rate variability. Biological Psychology, 108, Policies and practices to foster the social-emotional development
132–141. of young children. Washington, DC: Author. Retrieved July
Waters, S. F., & Thompson, R. A. (2016). Children’s perceptions 17, 2017, from https://www.zerotothree.org/resources/1694-
of emotion regulation strategy effectiveness: Links with early-childhood-mental-health-consultation-policies-and-
attachment security. Attachment and Human Development, practices-to-foster-the-social-emotional-development-of-
18, 354–372. young-children.

CH A PT E R
Operant Reinforcement and
9 Development of Emotion
Dysregulation
Christina Gamache Martin, Maureen Zalewski, Grace Binion, and Jacqueline O’Brien
Abstract
Caregivers play a foundational role in the development of children’s emotion dysregulation. Yet,
because there are a multitude of ways in which parent behavior can intersect with children’s emotions,
the development of emotion dysregulation is complex. This chapter specifically examines the role of
operant reinforcement, where the way in which caregivers respond contingently to their children’s
expression of emotion influences child emotion dysregulation. It reviews (1) the central theoretical
models that explicate the process by which parental responses to children’s emotions reinforce
emotion dysregulation, (2) current evidence supporting these theories, and (3) interventions designed
to reduce emotion dysregulation through operant reinforcement processes. It emphasizes that, in
addition to unidirectional effects, operant reinforcement from a parent interacts with traits inherent
to the child, and parents and children mutually influence one another in ways that highlight the
transactional, dynamic processes underlying the development of emotion dysregulation. Limitations
and future directions are discussed.
Keywords: emotion dysregulation, operant reinforcement, development, parent-child interactions,

parental emotion socialization, coercion theory, invalidating environment
Introduction precursors to several forms of psychopathology

Emotion dysregulation is more than the absence of (McLaughlin, Hatzenbuehler, Mennin, & Nolen-
regulation. It is “a pattern of emotional experience Hoeksema, 2011). Given the centrality of emotion
and/or expression that interferes with appropriate dysregulation in the development and presentation
goal-directed behavior” (Beauchaine, 2015, p. 876). of psychopathology, it is critical to identify how
Moreover, there must be evidence of emotional ex- emotion dysregulation emerges during childhood.
pression that exceeds or differs from what would be Operant reinforcement, a primary theory of
warranted in a given context and for which regula- learning, is a critical tool in understanding how
tory abilities are inadequate for managing emotion, reinforcement patterns shape a child’s (in)ability to
while also avoiding equating expression of a nega- regulate emotion. Parenting can alter children’s abil-
tive emotion as being “emotionally dysregulated” ity or inability to regulate emotions over time. More
(Cole, Martin, & Dennis, 2004). Emotion dysregu- specifically, emotion dysregulation is shaped by
lation is a construct of interest within psychology ways in which caregivers respond contingently to
because emotion regulation deficits serve as a trans- a child’s expression of emotion and, in turn, how
diagnostic feature across most forms of psychopa- the child’s subsequent responses affect caregivers.
thology (Aldao, Nolen-Hoeksema, & Schweizer, Emotional expressions or experiences that encour-
2010). From this observation, it follows that dys- age or interfere with goal-directed behavior can be
regulated expression and maladaptive strategies positively reinforced (e.g., a caregiver only responds
for regulation of emotions during childhood are to a child’s extreme expression of negative emotion,
115
increasing the likelihood that the child will use and behavioral measures. Specific methods often
similar strategies in the future) or negatively rein- vary based on the developmental period assessed
forced (e.g., a child whines to avoid eating broccoli (Adrian, Zeman, & Vetis, 2011). For example, mea-
and then throws it on the floor; the parent then re- suring behavioral responses through observational
moves the broccoli, increasing the likelihood that methods is more common in young children,
the child will use similarly dysregulated strategies in whereas assessing subjective experience through
the future). self-report is more prevalent in older children and
The development of emotion dysregulation is adolescents. Researchers often measure facial,
complex because emotions and efforts to regulate bodily, or vocal cues associated with discrete emo-
emotions are multifaceted. In addition, there are a tions using laboratory tasks designed to elicit nega-
multitude of ways in which parent behavior inter- tive emotions. Then the corresponding emotional
sects with child emotions. The pairing of children’s expressions and any behavioral attempts to manage
emotions and regulatory efforts with positive and those emotions are coded (i.e., problem solving, dis-
negative reinforcement by parents can lay the foun- traction, disruptive behavior) so that attempts are
dation for emotion dysregulation during childhood. made to disentangle expression of negative emo-
Improved understanding of the mechanistic pro- tions from regulatory efforts. In contrast, internal
cesses that shape emotion dysregulation has also led experiences of emotion dysregulation are measured
to novel interventions that target children’s emo- via self-report and through physiological measures.
tional expression, promote effective regulation, and, More recently, self-report methodologies have been
importantly, intervene with parents to support ef- enhanced by the use of ecological momentary as-
fective responses to their child’s emotions (e.g., sessment (EMA), particularly with adolescents
Havighurst, Wilson, Harley, Prior, & Kehoe, 2010). (Shiffman, Stone, & Hufford, 2008), in which sam-
This chapter reviews theory, current evidence, pling occurs at various instances throughout the day
and interventions that target the development of to more accurately assess the dynamic nature of
emotion dysregulation in children. Specifically, we emotions. The most common physiological index of
will address the following questions: (1) What are emotion dysregulation is respiratory sinus arrhyth-
the central theoretical models linking parental mia (RSA). RSA, also known as vagal tone or heart
responses to children’s emotions with emotion dys- rate variability, is a measure of parasympathetic
regulation? (2) What is the current evidence sup- nervous system influence on cardiac activity. Higher
porting these theories? (3) How do interventions resting RSA has been linked consistently with emo-
targeting operant reinforcement processes provide tional stability, whereas lower resting RSA has been
additional evidence of mechanistic processes under- linked consistently with emotional lability and dys-
lying emotion dysregulation? (4) What are the limi- regulation (e.g., Beauchaine, Gatzke-Kopp, &
tations of the current literature and key next ques- Mead, 2007). Small decreases in RSA in response to
tions? Although beyond the focus of this chapter, it a stimulus or stressor (i.e., vagal withdrawal) have
is important to recognize that operant reinforce- been linked to effective emotion regulation (Calkins,
ment, in terms of positive and negative reinforce- Graziano, Berdan, Keane, & Degnan, 2008),
ment patterns, continues to develop within peer whereas larger decreases appear to mark significant
and romantic relationships and may replicate and dysregulation (e.g., Crowell et al., 2005).
maintain problematic patterns of emotion dysregu- While these measurement tools offer ways to
lation across the lifespan (see Dishion & Snyder, assess emotion dysregulation, they must be embed-
2016). The current chapter focuses on how operant ded within specific study designs to accurately in-
reinforcement in caregiver–child relationships shapes vestigate operant reinforcement of emotion dysreg-
child emotion dysregulation. ulation. Specifically, a parent’s response must follow
a child’s expression of emotion or regulatory strat-
Terms and Measurement Issues egy. Alternatively, reciprocal models that examine
Measurement tools are reviewed briefly because the dynamic reinforcement patterns between parent
definition of a construct is informed by the way in and child must measure transactional influences of
which it is measured (Larsen & Prizmic-Larsen, parents and children on each other across time.
2006). Emotion dysregulation is inherently multi- Interaction models examine how parenting affects
faceted because emotions entail full-system re- children’s emotion dysregulation in the context of
sponses. Therefore, measurement is accomplished another variable, such as child sex, trait characteris-
using a range of methods, including observational tics, or genetic predispositions. The dominant
116 Operant Reinforcement of Emotion Dysregul ation

coding strategies for observational data include main-effects models to better incorporate the role of
micro-coding, which examines reciprocal exchanges operant reinforcement, and how parent and child
that occur on brief time scales, and global coding, mutually influence one another’s emotion expres-
which is based on longer coding units and may sion and regulation.
require greater inference (Julien, Markman, &
Coercion theory was born from behavioral obser-
Lindahl, 1989). It is also common for researchers to vation and microanalytic coding of dyadic ex-
use self-report measures to assess typical parent re- changes in the homes of at-risk families (e.g.,
sponses to child emotion dysregulation. However, Patterson, Dishion, & Bank, 1984; Snyder, 1977).
this limits the ability to detect temporal links This model is presented in a functional-analytic
between child emotion dysregulation and parental frame in which children’s aversive behaviors are neg-
reinforcement. More recently, researchers have atively reinforced because they serve the function of
combined creative study designs and multimethod momentarily stopping their parents’ aversive behav-
approaches, which has promoted more rigorous iors (Beauchaine & Zalewski, 2016). As noted by
testing of key theories of operant reinforcement and Patterson, DeBaryshe, and Ramsey (1989, p. 330),
the development of emotion dysregulation. “the most important set of contingencies for coer-
cive behavior consist of escape conditioning [in
Theoretical Perspectives which] the child uses aversive behaviors to termi-
Three primary models examine how caregivers nate aversive intrusions by other family members.”
shape emotion dysregulation across childhood and Snyder further demonstrated that aggressive boys
adolescence by focusing on how parents respond become more likely to escalate conflict once in a
immediately after encountering a child’s emotion or dysregulated, irritable state (Snyder, Schrepferman,
regulation strategy. The first model emerged from & St. Peter, 1997), and that intense displays of
research on normative developmental processes and negative affect are more likely to cease conflict in
was the first to operationalize and promote rigorous aggressive dyads than in control dyads (Snyder,
measurement of children’s emotion regulation abili- Edwards, McGraw, Kilgore, & Holton, 1994). In
ties. Specifically, parental emotion socialization refers this way, children’s extreme emotion dysregulation,
to the way in which parents contribute to the devel- as manifested through aggression or violence, can be
opment of children’s emotion competence, includ- viewed as a subsequent outcome of reciprocal, aver-
ing emotion regulation (Morris, Silk, Steinberg, sive exchanges that occur repeatedly across develop-
Myers, & Robinson, 2007). While various theories ment in at-risk families.
of parental emotion socialization exist, researchers The invalidating environment model is rooted in
generally agree that parents shape emotion regula- Linehan’s (1993) biosocial theory that depicts a
tion by the way they (1) respond to a child’s emotion transactional model in which individual (e.g., trait
(emotionally contingent responses), (2) regulate vulnerability) and environmental factors (e.g., lack
their own emotions in front of their child (model- of support) transact over time to influence emotion
ing), (3) engage in parenting and form attachments dysregulation. Invalidating environments can be
with their child (family emotional climate), and (4) defined by four primary parenting characteristics:
talk directly about emotions and emotion regula- communications of inaccuracy, misattribution, dis-
tion with their child (emotion coaching; Morris couragement of negative emotional expression, and
et al., 2007). While emotion socialization theories oversimplification of problem solving (Cummins,
have been highly influential and have prompted re- Zalewski, Lewis, & Stepp, under review). Across
search on parental influences on children’s emotion these four types of responses, the parent communi-
regulation, they are focused predominantly on the cates that both internal experiences and public ex-
direct or main effects of parent to child. pressions of emotions are invalid and inappropriate.
In contrast to this unidirectional and normative In an invalidating environment, expressions of
developmental approach, two theoretical models emotion, such as fear or sadness, may only be at-
originating from different traditions, coercion theory tended to when they are extreme, while more mod-
and the invalidating environment model, describe erate displays of negative emotion are ignored or
children’s emotion dysregulation as both shaped by punished. This pattern both reinforces extreme dis-
and shaping parental behavior. Both emphasize re- plays of emotion and fails to provide scaffolding or
ciprocal and dynamic exchanges that contribute to tools necessary to facilitate regulation at lower levels
emotion dysregulation through behavioral rein- of distress. This leads the child to “oscillate between
forcement processes. These theories move beyond emotional inhibition on the one hand, and extreme
Martin, Zalewski, Binion, and O ’ Brien 117

emotional states on the other” (Linehan, 1993, r efocusing, cognitive reframing) would best facilitate
p. 51). When extreme displays of emotion do not 4- to 9-year-olds’ expressions of anger and sadness
appear valid for the given situation, however, they in the context of disappointment. Children were
tend to prompt further invalidating responses presented with a disappointing gift in the presence
from parents, thus creating a transactional pattern. of their mothers, and their mothers were instructed
Because the invalidating environment minimizes to respond naturally to their child’s emotional
the difficulties of solving one’s problems (e.g., expression—a component of emotion regulation

a pull-yourself-up-by-the-bootstraps approach), a (Dennis, Cole, Wiggins, Cohen, & Zalewski, 2009).
child does not learn distress tolerance or the ability The authors assessed mothers’ operant reinforce-
to set goals and expectations that are realistic and ment of emotional expression by coding child affect
achievable. Thus, as a consequence of both trait vul- in 10-second epochs; maternal responses were micro-
nerability and a lack of support from their environ- coded and time-synced to emotion expression
ment, emotionally dysregulated children struggle epochs to examine the influence of mothers’ regula-
to learn effective strategies for managing aversive tory strategies on children’s emotional expression in
emotional states. As a result, problematic behaviors, the following epoch. Mothers’ attempts to comfort
such as self-inflicted injury, begin to serve an emo- their children were not associated with children’s
tion regulatory function, which serves as a form of expressions of anger or sadness. Rather, for children
avoidance or escape from negative emotions. younger than age 8, maternal efforts at distraction
and refocusing children’s attention were associated
Current Findings with children immediately displaying less sadness.
Given the focus of this chapter, we limited our Moreover, when children and their mothers jointly
review to studies that (1) specifically assessed emo- engaged in cognitive reframing, children expressed
tion (dys)regulation or a primary component of less sadness and anger. Importantly, and in contrast
the construct, (2) were designed in such a way that to a transactional model, children’s expressed emo-
parental responses temporally preceded assessment tions did not predict which strategies were used by
of child emotion (dys)regulation, or (3) examined their mothers. Thus, in the context of a disappoint-
transactional models. Further, because emotion dys- ing experience, mothers who can effectively distract
regulation appears to precede diagnosable psycho- their young children by refocusing their attention
pathology, we focus predominantly on children’s or by facilitating joint cognitive reframing enhance
emotion dysregulation as opposed to psychopathol- their children’s abilities to regulate their feelings of
ogy. We implemented this criterion because psycho- sadness and anger.
pathology is often used as a proxy for emotion dys- Binion and Zalewski (in press) built upon this
regulation. Yet, we believe that it is clinically and study of children’s expressed emotion by also ob-
scientifically advantageous to maintain a distinction serving and micro-coding preschoolers’ regulatory
between the two constructs to better understand the behaviors in a frustration-eliciting Locked Box Task
development of emotion dysregulation. While we (Goldsmith & Rothbart, 1996), in which emotion-
permitted some studies to be framed as emotion ally regulated children typically engage in problem
regulation or a component of emotion regulation, solving when frustrated (Dennis, Cole, Wiggins,
instead of emotion dysregulation, we did so only Cohen, & Zalewski, 2009). This study, which
when study results suggested that certain parental oversampled mothers with extreme emotion dys-
responses predicted deficits in emotion regulation. regulation, assessed supportive maternal responses
Given that there are many ways to measure emotion (i.e., encouraging emotion expression or provision
dysregulation, we detail how it was operationalized in of helpful strategies) and unsupportive responses
each study. Finally, we organize this review in terms (i.e., minimizing or punishing emotion) to chil-
of the models tested: main-effects, interaction, and dren’s distress. Maternal supportive responses were
transactional models. associated with children’s attempts to engage in play
during the frustrating task, while maternal unsup-
Main-effects models portive responses were associated with children en-
Morris and colleagues (2011) sought to expand gaging in more disruptive behaviors, such as throw-
upon research delineating the benefits of supportive ing the locked box, leaving the room, and shouting
maternal responses (e.g., Cole, Dennis, Smith-Simon, at a research assistant, when frustrated. Thus, in ad-
& Cohen, 2008) by clarifying which specific dition to observed maternal support being associ-
supportive responses (i.e., comforting, attention ated with lower offspring expression of negative

emotion (Morris et al., 2011), the findings from this the conflict task. The authors also deconstructed
study suggest that mothers’ self-reported unsupport- maternal invalidation into punishing and dampen-
ive responses are associated with children engaging ing (i.e., minimizing) responses to a dolescent posi-
in more disruptive regulatory attempts in the con- tive affect, and found that when mothers responded
text of negative emotions. in punishing ways during event planning, males
A third study examined how parent emotion so- maintained longer durations of aversive behaviors
cialization shapes youth reactivity to negative events in the conflict task, while females were more likely
within peer and nonpeer contexts in a sample of to reciprocate their mothers’ dysphoric behaviors.
anxious youth aged 9 to 14 (Oppenheimer et al., Mothers’ dampening responses were unrelated to
2016). This study is noteworthy because most stud- adolescent emotion dysregulation, but were related
ies with older children rely solely on self-report. In to more frequent use of maladaptive emotion regu-
this case, however, the authors observed and micro- lation strategies in females. These findings suggest
coded parents’ supportive and unsupportive behav- that females may be at greater risk for emotion dys-
iors second by second during a 2-minute period regulation when mothers are less validating and
where the parent helped his or her child prepare for more invaliding of their daughters’ emotions, par-
a social-evaluative speech task. Parent responses to ticularly their positive emotions.
youth during this anxiety-provoking task were used Another study with self-injuring and control
to predict youth negative reactivity during 14 EMAs teens highlighted how mother invalidating and
of negative events across 5 days. Supportive parental aversive behaviors interacted with adolescent aver-
responses were associated with significantly less neg- sive behaviors during conflict to predict adolescent
ative affect for youth in response to negative peer emotion dysregulation, as indexed by RSA (Crowell
events compared to nonpeer events, suggesting that et al., 2013). Crowell and colleagues found that ado-
supportive parenting behaviors during an anxiety- lescents in dyads where both mother and adolescent
provoking task can buffer anxious children’s nega- exhibited high levels of aversive behavior showed
tive responses to stressful peer events. Taken to- the lowest resting RSA, which is indicative of greater
gether, the three studies reviewed here suggest that emotion dysregulation. However, in dyads where
supportive and unsupportive contingent maternal mothers showed high rates of aversive behavior but
responses may serve to shape children’s emotional the adolescent showed low aversive behavior, ado-
expression, level of reactivity, and regulation in the lescents had high RSA, which may have been pro-
context of distressing experiences across early child- tective. There were no differences in adolescent RSA
hood through early adolescence. for dyads with low-aversive mothers. It therefore
appears that maternal aversiveness may be particu-
Interaction models larly problematic for adolescent emotion dysregula-
Gender may be an important moderator to consider tion among more vulnerable adolescents. Moreover,
when examining how parents respond to children’s during conflict interactions, mothers of adolescents
regulation of emotion. Yap, Allen, and Ladouceur who engaged in self-injury had a higher probability
(2008) found gender effects in the context of mater- of matching or escalating the adolescent’s level of
nal socialization of positive affect. Adolescents and aversiveness. In contrast, mothers of control adoles-
mothers, in a high-risk sample, engaged in two in- cents were more likely to de-escalate conflict follow-
teraction tasks designed to elicit both positive (i.e., ing adolescent aversive behavior. Interestingly, the
event planning) and negative (i.e., conflict discus- only time self-injuring adolescents and their moth-
sion) affect, respectively. Emotion dysregulation was ers reliably deescalated conflict was in response to
operationalized as the frequency and duration of very high levels of aversive behavior from one an-
adolescent aversive or dysphoric behaviors, as well other. Crowell and colleagues suggested that nega-
as fewer positive behaviors in both mother–adolescent tive reinforcement of highly aversive behavior may
interactions. Maladaptive emotion regulation strat- function to reduce conflict in the short run but in
egies were also measured using adolescent self-report the long run likely increases and maintains emotion
on the Child Affect Questionnaire–Child Strategies dysregulation in both parent and child. Taken to-
(Garber, Braafladt, & Weiss, 1995). The study found gether, these findings suggest that treatment may be
that mothers’ validating responses to adolescents’ more beneficial when providers target both mother
displays of positive affect via self-report served as a and adolescent behaviors.
protective factor for males, who demonstrated less Genetic research provides an additional avenue
dysregulation of positive and negative affect during to examine how child characteristics interact with

the environment to influence emotion dysregulation. Perry, Mackler, Calkins, and Keane (2014) exam-
Specifically, research in this area has found that inse- ined the relation between maternal sensitivity and
cure attachment styles serve as a risk factor in ado- preschoolers’ emerging regulation capabilities, in-
lescents (Zimmermann & Spangler, 2016) carrying dexed by greater vagal withdrawal (i.e., decreased
one or two short 5-HTTLPR alleles, which are asso- RSA in response to a stressor), in a sample of 356
ciated with greater emotional vulnerability (Canli mother–child dyads oversampled for children at
& Lesch, 2007). Emotion regulation in adolescents risk for externalizing problems. At each time point,
was measured by their ability to engage in effective children’s vagal activity was measured while children
emotion regulation strategies while interacting with completed age-appropriate frustration tasks (i.e.,
their mothers during an emotion-eliciting com- the Locked Box Task at age 2½, the Impossibly
puter game task (Zimmermann & Spangler, 2016). Perfect Circles Task at age 4½, and the Not Sharing
Insecure attachment styles were associated with Task at age 5½). Maternal sensitivity was assessed at
greater emotion dysregulation, but only for youth each time point during pretend play and clean-up
with genetic vulnerability. For youth with secure tasks, which was later coded and assigned a global
attachment styles, there was no association between sensitivity code for the entire interaction. Results
genetic vulnerability and emotion dysregulation. supported a cross-lagged model, such that maternal
Similar to Crowell et al. (2013), these findings sensitivity when children were age 2½ was associ-
highlight how an emotional environment with less ated with children’s improved regulation (i.e.,
optimal contingent responses from parents (i.e., greater vagal withdrawal) at age 4½, which was in
aversive maternal behaviors and insecure attach- turn related to increased maternal sensitivity when
ments) is most problematic in terms of youths’ children were age 5½. Yates, Obradovic, and
emotion dysregulation when the youth are more Egeland (2010) similarly examined a transactional
vulnerable (i.e., aversiveness or genetic risk). model of parenting quality and child emotion dys-
regulation in an at-risk sample of children and their
Transactional models mothers. They observed child emotion dysregula-
During infancy, Kiel, Gratz, Moore, Latzman, and tion in the context of frustration with a series of
Tull (2011) found that mothers’ insensitive behav- problem-solving-tool tasks that increased in com-
iors increased in response to infant distress that plexity at age 2 and using Block’s Barrier Box Task
persisted for longer durations during the Strange (Harrington, Block, & Block, 1978) at age 3½.
Situation (Ainsworth, Blehar, Waters, & Wall, 1978), Parenting behaviors were likewise observed and
but only for mothers with high borderline personal- coded in terms of supportiveness, limit setting, and
ity disorder (BPD) features. In turn, infant distress quality of instruction/assistance during challenging
was more likely to follow displays of maternal nega- laboratory tasks at visits 1 and 2, while parenting
tive affect and maternal insensitive behaviors. The quality at child age 6 was assessed using the Home
opposite pattern was found for mothers low in BPD Observation for Measurement of the Environment
features, where they were more likely to respond to (Caldwell & Bradley, 1984). Their results supported
infant distress with positive affect, and infant dis- a transactional model in which parenting quality at
tress was less likely to be observed following mater- child age 2 predicted children’s emotion dysregula-
nal positive affect. This work not only supports a tion at age 3½, which in turn predicted poorer par-
main-effects model indicating that maternal re- enting quality at child age 6. This model was found
sponse to infant distress influences infants’ ability to to be a better fit for the data than a continuity
regulate emotion but also highlights how infant dis- model in which parenting quality at each time point
tress may evoke insensitive maternal responses, es- predicted parenting quality at the following time
pecially for more dysregulated mothers. This find- point. The results of these longitudinal studies pro-
ing underscores the crucial role of mothers’ ability vide support for the transactional model, demon-
to regulate their own emotions and to respond sen- strating that the development of child emotion
sitively in the face of infants’ negative affect in avert- dysregulation emerges over time, as a transaction
ing dysregulation in their children. This bidirec- between children’s aversive expression of emotion
tional relationship has also been supported with and parents’ aversive responses.
longitudinal data across early childhood. Finally, this same transactional pattern of
Two longitudinal studies explicate associations aversive parent–child interactions has been linked
between aversive parent–child transactions and to emotion dysregulation in middle childhood
child emotion dysregulation across early childhood. (Morelen & Suveg, 2012). Parents’ supportive and

unsupportive emotional responses, as well as chil- or mediator of change or (2) intervene directly on
dren’s adaptive and maladaptive emotion regulation operant reinforcement models by incorporating the
behaviors, were observed during four 5-minute parent and conceptualizing parental response to
emotional discussions about a time the child felt child emotion as a primary agent of change. We
angry, anxious, sad, and happy. Children were review three principal modes of clinical interven-
coded as having adaptive emotion regulation behav- tion: parent training interventions, developed from
iors when they verbally expressed their emotion, coercion theory; dual-generation interventions,
discussed emotion, or discussed a developmentally which incorporate parental emotion socialization;
appropriate emotion regulation strategy. In con- and interventions that target invalidating environ-
trast, maladaptive emotion regulation behaviors ments as a means to reduce emotion dysregulation
were coded when the child engaged in dysregulated in children and adolescents.
behavior such as whining, yelling, or making derog-
atory comments or when the child was rude. The Parent training interventions
results supported a transactional pattern between As evidence of parents’ role in children’s emotion
parent and child exchanges where children’s use of (dys)regulation across development has become more
adaptive emotion regulation behaviors tended to be prominent (e.g., Morris et al., 2007), many parent
followed by more supportive emotion responses by training interventions have shifted from focusing
parents, which were in turn followed by additional exclusively on parental-contingent responses to chil-
adaptive emotion regulation behaviors in children. dren’s problematic behaviors to also incorporating
This pattern of results was found across emotion emotion coaching or emotion socialization compo-
type and parent. In contrast, when examining the nents into their protocols. Parent training interven-
transactional pattern for children prone to using tions that incorporate these emotional components
maladaptive emotion regulation behaviors, unsup- for preschool-aged children with inattention, hy-
portive emotional responses from parents were only peractivity, and oppositional behaviors have shown
more common during the discussion of anger. These promising results for reducing children’s emotion
results appear to align with coercion theory where dysregulation. Specifically, Webster-Stratton and
the transactional nature between parent and child is colleagues found that mothers and fathers in the
escalatory, as would likely be the case with anger, as Incredible Years (IY) program reported significant
opposed to a discussion related to anxiety, sadness, improvements in their children’s emotion regula-
and happiness. tion skills at posttreatment compared to parents
In summary, results from the extant literature of waitlisted children (Webster-Stratton, Reid, &
support theories that operant reinforcement of emo- Beauchaine, 2011), and these treatment effects were
tion contributes to the development of emotion maintained at the 1-year follow-up (Webster-Stratton,
dysregulation. Although the majority of researchers Reid, & Beauchaine, 2013). These results suggest that
examined this process through a main-effects model, emotion socialization components can be added to
many scholars extended beyond such direct effects parent training interventions to help parents change
to examine child traits that affect parent-contingent the way they respond to their children’s emotions
responses to shape child emotion dysregulation. In and reduce child emotion dysregulation.
addition, several research groups examined the recip-
rocal effects of children on parents. Dual-generation interventions
Dual-generation interventions are those that inter-
Testing Operant Reinforcement Through vene at the level of both the child and the parent to
Clinical Interventions maximize benefits for the family by simultaneously
Clinical interventions, particularly those that use targeting parental and child psychopathology or
randomized controlled trial designs, offer a power- distress (Shonkoff & Fisher, 2013). Dual-generation
ful experimental tool by which to examine mecha- interventions target parents’ contingent responses
nistic processes. Thus, in lieu of an exhaustive review to child negative emotion, as well as the parent’s
of emotion dysregulation interventions, our goal own emotion dysregulation difficulties (i.e., parents
here is to provide another test of key theories by actively acquire emotion regulation skills). The aims
examining whether interventions targeting operant of these interventions are twofold: to reduce child
reinforcement processes have an effect on emotion emotion dysregulation and children’s externalizing
dysregulation. We focus on interventions that (1) behaviors, and to reduce parents’ own emotion
target parent emotion dysregulation as a moderator dysregulation.

Havighurst and her colleagues developed a did not mediate trauma treatment outcomes. They
widely studied dual-generation intervention for found support for the moderating role of emotion
parents and their preschool-aged children (Tuning dysregulation in the reduction of posttraumatic
into Kids [TIK]; Havighurst, Wilson, Harley, & stress disorder (PTSD) symptoms. Specifically, they
Prior, 2009) or adolescents (Tuning into Teens found that for children with low levels of emotion
[TINT]; Havighurst, Kehoe, & Harley, 2015). A dysregulation, PTSD symptom reduction was re-
primary aim of these interventions is to help parents ported at mid- and posttreatment, but for children
become more aware of their own emotions and to with high levels of emotion dysregulation, PTSD
“sit with” these emotions while simultaneously vali- symptom reduction was reported only at posttreat-
dating their child’s emotion and helping him or her ment. The timing of symptom reduction is impor-
to manage it as needed. Parents’ well-being is con- tant because the first phase of trauma treatment fo-
ceptualized as critical for their emotional availability cuses on teaching coping skills to manage emotion
and responsiveness to their child’s emotional needs dysregulation. These results suggest that for children
(Havighurst et al., 2009). In comparison to waitlist high in emotion dysregulation, the phase of treat-
control groups, results from the TIK (Havighurst ment designed to help children regulate their emo-
et al., 2010) and TINT (Havighurst et al., 2015) tions may only be effective for children with less
interventions, which coached contingent parental emotion dysregulation. However, children with low,
responses to children’s emotions, demonstrated in- medium, and high emotion dysregulation all dem-
creases in parental emotion awareness and decreases onstrated reductions in PTSD symptoms by post-
in parental emotion dysregulation while also in- treatment. Sharma-Patel and Brown (2016) specu-
creasing child knowledge of emotion and decreasing lated that these posttreatment reductions reflect the
child problematic behaviors. Finally, when compar- exposure component of treatment. Alternatively,
ing TIK to a parent training intervention and wait- these greater PTSD reductions found for children
list control, both treatments were equally effective high in emotion dysregulation might also result
(Duncombe et al., 2016). Despite the overall lack of from parents validating their emotions and experi-
difference in treatment outcomes across the inter- ences during the latter half of treatment. Children
ventions, when parents were more psychologically share their trauma narratives with their parents and
distressed, their children benefited more from the parents are coached to respond in validating ways.
TIK intervention, which focused on helping par- Thus, parents are coached to contingently respond
ents to become aware of their own emotions and to to their children’s expressions of negative emotion
contingently respond to their children’s expression in supportive ways, and children’s appropriate ex-
of emotion in ways that communicate understand- pression of negative affect is positively reinforced,
ing and acceptance. These results support the use encouraging future discussion about their abuse-
of a dual-intervention approach when parents are related emotions. A second alternative explanation
managing their own distress and psychopathology, relates to a methodological limitation, in that the
where responding contingently to children’s emo- authors only assessed parent report of child emotion
tions in a supportive manner (i.e., TIK) appears to dysregulation. Thus, it could be that parents with
be more beneficial than contingently responding to greater emotion dysregulation themselves were
their behaviors (i.e., parent training). more likely to perceive their children as more emo-
tionally dysregulated, especially during the earlier
Invalidating environment phases of treatment. Future research would benefit
Child abuse perpetrated by a family member or a from parsing out the benefits of exposure and vali-
child’s disclosure of abuse to a family member that dating responses from caregivers to determine the
is not fully believed or supported is an extreme ex- role of operant reinforcement in trauma treatment
ample of the invalidating environment. Evidence- for children, as well as assessing both parent and
based treatments for trauma emphasize affect regu- child report of children’s emotion dysregulation.
lation and incorporate parents coaching children in To date, results from studies incorporating pa-
regulating emotions and validating children’s nega- rental emotion socialization and coaching provide a
tive emotions related to the abusive experience. growing base of evidence suggesting that the ways in
Sharma-Patel and Brown (2016) examined the role which parents respond contingently to children’s
of child emotion regulation as a mediator and mod- emotions are important for children’s emotional
erator in trauma-specific treatment. Despite the competence and ability to regulate emotions. When
theorized mediating role of emotion regulation, it comparing interventions where the focus on contin-

gent responding is placed on child emotion versus (e.g., Crowell et al., 2017), which emphasize the
child behavior, these interventions appear to be emergence of emotion dysregulation as a transac-
equally effective but may differ based on parent tion between caregivers or other environmental in-
emotion dysregulation. In conjunction with this fluences and children. Studies seeking to test these
possibility, the finding by Kaminski, Valle, Filene, models must assess both children’s emotion dysregu-
and Boyle (2008) that parent training interventions lation and parenting, ideally at three or more time
that incorporate emotional communication are as- points across many months or years. Although such
sociated with the greatest increase in targeted par- studies are costly and difficult to conduct, they
enting behaviors or skills suggests that parents are more accurately assess bidirectional, reciprocal rela-
benefiting, and it may be that, in line with dual- tionships embedded within parent–child interac-
generation interventions, parents who are the most tions. Thus, the field can move forward by focusing on
dysregulated are benefiting more. transactional models to better understand the nuanced
relationships between the dynamic parent–child
Limitations and Future Directions interactions and their role in the emergence of
First, the extant literature is biased in its focus on emotion dysregulation.
mothers over fathers, despite findings that fathers Finally, to more fully understand all the various
play an integral role in child development (Lamb, ways in which emotion dysregulation develops, we
2010) and may respond differentially to child emo- need to better attend to other types of relationships,
tion (Klimes-Dougan et al., 2007). None of the such as peer and romantic relationships, particularly
studies reviewed were exclusive to fathers, and only for adolescents. It remains unknown whether emo-
two included fathers (e.g., Morelen & Suveg, 2012; tion dysregulation observed within the parent–child
Oppenheimer et al., 2016), with fathers making up relationship extends into other relationships or
5% of parents in one of the studies. In addition to whether an individual’s response varies across rela-
missing a valuable piece of the puzzle by not includ- tionships. Moreover, additional work is needed to
ing fathers or other coparents or caregivers in this answer the following questions related to parental-
research, excluding fathers makes it difficult to contingent response and the development of emo-
explore their influence on mothers’ contingent re- tion dysregulation: (1) Does the context (i.e., posi-
sponding. Examining potential differences in the tive, conflictual, emotionally distressing) in which
case of single parenting as compared to coparenting parents are responding to emotions or the type
is also recommended. Rather than continuing to of emotion matter? (2) In what ways does adversity
note the lack of fathers as a one-sentence limitation experienced by parents or children relate to how
or a direction for future research, researchers must parents respond to children’s emotions and across
make a conceptual shift and commit to better un- contexts? (3) What factors contribute to gender
derstanding the role of fathers in children’s develop- differences? (4) How do we most effectively enhance
ment of regulated and dysregulated emotion. our clinical treatments to better intervene in con-
Second, given the multifaceted nature of emo- flict escalation, as well as in more subtle cases of
tions and the multitude of ways that parental be- invalidation?
havior intersects with children’s emotions, more In addition to better addressing these limita-
theory-driven research is needed. Within the three tions, future intervention research should continue
primary theories reviewed, the majority of the to use dual-generation models to improve under-
extant research comes from the parental emotion standing of parent emotion dysregulation in child
socialization theory, which relies heavily on self-report treatment programs. Additional research is likewise
measures to assess parents’ contingent responses to necessary to determine whether the benefits of more
children’s emotions. This is problematic when the traditional parent training programs compared to
timing between the contingent response and the emotion socialization interventions depend on pa-
child’s expression of emotion or use of an emotion rental emotion dysregulation. If intervention results
regulation strategy is not immediate. Moreover, this depend on parent emotion dysregulation, it may be
work focuses predominantly on main effects from that more thorough assessments of children and
parent to child. Although we have highlighted re- their parents’ emotion dysregulation are needed in
search examining more complex parent–child pat- clinical settings to better match interventions with
terns of interactions, there is a relative dearth of ev- presenting problems in children and their parents.
idence for transactional models and in particular One area not yet examined is whether child emotion
those based on the invalidating environment theory dysregulation can be reduced solely by intervening

at the level of emotion dysregulation for the parent. Binion, G., & Zalewski, M. (in press). Maternal emotion
Our group is currently investigating this possibility dysregulation and the functional organization of preschooler’s
emotional expression and regulatory behaviors. Emotion.
using dialectical behavioral therapy skills with emo- Caldwell, B. M., & Bradley, R. H. (1984). Home observation for
tionally dysregulated mothers of preschool children. measurement of the environment. Little Rock, AR: University
In summary, emotion dysregulation is a transdi- of Arkansas at Little Rock.
agnostic feature across multiple forms of psychopa- Calkins, S. D., Graziano, P. A., Berdan, L. E., Keane, S. P., &
thology. Understanding its development is critical Degnan, K. A. (2008). Predicting cardiac vagal regulation in
early childhood from maternal-child relationship quality
for the translation of basic science to intervention during toddlerhood. Developmental Psychobiology, 50,
and treatment. Parents play a foundational role in 751–766.
the development of children’s emotion dysregula- Canli, T., & Lesch, K. P. (2007). Long story short: The serotonin
tion, where the way in which parents contingently transporter in emotion regulation and social cognition.
respond to their children’s expression of emotion Nature Neuroscience, 10, 1103–1109.
Cole, P. M., Dennis, T. A., Smith-Simon, K. E., & Cohen, L. H.
influences child emotion dysregulation. However, (2008). Preschoolers’ emotion regulation strategy
parents’ role is complex. In addition to this unidi- understanding: Relations with emotion socialization and
rectional effect, operant reinforcement from the child self-regulation. Social Development, 18, 324–352.
parent interacts with traits inherent to the child, Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion
and parents and children mutually influence one regulation as a scientific construct: Methodological challenges
and directions for child development research. Child
another in ways that highlight the transactional, dy- Development, 75, 317–333.
namic process underlying the development of emo- Crowell, S. E., Baucom, B. R., McCauley, E., Potapova, N. V.,
tion dysregulation. Multimethod approaches are Fitelson, M., Barth, H., . . . Beauchaine, T. P. (2013).
most advantageous for measuring emotion dysregu- Mechanisms of contextual risk for adolescent self-injury:
lation rigorously. Interventions incorporating meth- Invalidation and conflict escalation in mother-child
interactions. Journal of Clinical and Adolescent Psychology, 42,
ods to facilitate supportive contingent responses 467–480.
from parents in response to their children’s emo- Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C.,
tions have shown promising preliminary support. Stevens, A. L., & Sylvers, P. D. (2005). Psychological,
At the same time, our understanding of the devel- physiological, and serotonergic correlates of parasuicidal
opment of emotion dysregulation is primarily based behavior among adolescent girls. Development and
Psychopathology, 17, 1105–1127.
on main-effects models, providing ample opportu- Crowell, S. E., Butner, J., Wiltshire, T., Munion, A. K.,
nity for future research to clarify the complexity Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating
through which parental operant reinforcement in- emotional and biological sensitivity to maternal behavior
teracts and transacts with youth behaviors to mani- among depressed and self-injuring adolescent girls using
fest in child emotion dysregulation. nonlinear dynamics. Clinical Psychological Science, 5,
272–285.
Cummins, N., Zalewski, M., Lewis, J., & Stepp, S. D. (under
References review). A systematic review of negative parenting practices
Adrian, M., Zeman, J., & Veits, G. (2011). Methodological predicting borderline personality disorder: Are we measuring
implications of the affect revolution: A 35-year review of biosocial theory’s “invalidating environment”?
emotion regulation assessment in children. Journal of Dennis, T. A., Cole, P. M., Wiggins, C. N., Cohen, L. H., &
Experimental Child Psychology, 110, 171–197. Zalewski, M. (2009). The functional organization of
Ainsworth, M. D. S., Blehar, M. C., Waters, E., & Wall, S. preschool-age children’s emotion expressions and actions in
(1978). Patterns of attachment: A psychological study of the challenging situations. Emotion, 9, 520–530.
strange situation. Hillsdale, NJ: Erlbaum. Dishion, T. J., & Snyder, J. (2016). The Oxford handbook of
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). coercive relationship dynamics. New York, NY: Oxford
Emotion-regulation strategies across psychopathology: A University Press.
meta-analytic review. Clinical Psychology Review, 30, 217–237. Duncombe, M. E., Havighurst, S. S., Kehoe, C. E., Holland,
Beauchaine, T. P. (2015). Future directions in emotion dysregulation K. A., Frankling, E. J., & Stargatt, R. (2016). Comparing an
and youth psychopathology. Journal of Clinical Child and emotion- and a behavior-focused parenting program as part
Adolescent Psychology, 44, 875–896. of a multisystemic intervention for child conduct problems.
Beauchaine, T. P., Gatzke-Kopp, L., & Mead, H. K. (2007). Journal of Clinical Child and Adolescent Psychology, 45,
Polyvagal theory and developmental psychopathology: 320–334.
Emotion dysregulation and conduct problems from preschool Garber, J., Braafladt, N., & Weiss, B. (1995). Affect regulation in
to adolescence. Biological Psychology, 74, 174–184. depressed and nondepressed children and young adolescents.
Beauchaine, T. P., & Zalewski, M. (2016). Physiological and Development and Psychopathology, 7, 93–115.
developmental mechanisms of emotional lability in coercive Goldsmith, H., & Rothbart, M. K. (1996). Prelocomotor and
relationships. In T. J. Dishion & J. J. Snyder (Eds.), The locomotor laboratory temperament assessment battery (Lab-
Oxford handbook of coercive relationship dynamics (pp. 39–52). TAB; version 3.0, technical manual). Madison, WI: University
New York, NY: Oxford University Press. of Wisconsin, Department of Psychology.

Harrington, D., Block, J. H., & Block, J. (1978). Intolerance of Oppenheimer, C. W., Ladouceur, C. D., Waller, J. M., Ryan,
ambiguity in preschool children: Psychometric considerations, N. D., Allen, K. B., Sheeber, L., . . . Silk, J. S. (2016). Emotion
behavioral manifestations and parental correlates. socialization in anxious youth: Parenting buffers emotional
Developmental Psychology, 14, 242–256. reactivity to peer negative events. Journal of Abnormal Child
Havighurst, S. S., Kehoe, C. E., & Harley, A. E. (2015). Tuning Psychology, 44, 1267–1278.
in to teens: Improving parental responses to anger and Patterson, G. R., DeBaryshe, B., & Ramsey, E. (1989). A
reducing youth externalizing behavior problems. Journal of developmental perspective on antisocial behavior. American
Adolescence, 42, 148–158. Psychologist, 44, 329–335.
Havighurst, S. S., Wilson, K. R., Harley, A. E., & Prior, M. R. Patterson, G. R., Dishion, T. J., & Bank, L. (1984). Family
(2009). Tuning in to kids: An emotion-focused parenting interaction: A process model of deviancy training. Aggressive
program—initial findings from a community trial. Journal of Behavior, 10, 253–267.
Community Psychology, 37, 1008–1023. Perry, N. B., Mackler, J. S., Calkins, S. D., & Keane, S. P. (2014).
Havighurst, S. S., Wilson, K. R., Harley, A. E., Prior, M. R., & A transactional analysis of the relation between maternal
Kehoe, C. (2010). Tuning in to kids: Improving emotion sensitivity and child vagal regulation. Developmental
socialization practices in parents of preschool children— Psychology, 50, 784–793.
findings from a community trial. Journal of Child Psychology Sharma-Patel, K., & Brown, E. J. (2016). Emotion regulation
and Psychiatry, 51, 1342–1350. and self blame as mediators and moderators of trauma-
Julien, D., Markman, H. J., & Lindahl, K. M. (1989). A specific treatment. Psychology of Violence, 6, 400–409.
comparison of a global and a micro-analytic coding system: Shiffman, S., Stone, A. A., & Hufford, M. R. (2008). Ecological
Implications for future trends in studying interactions. momentary assessment. Annual Review of Clinical Psychology,
Behavioral Assessment, 11, 81–100. 4, 1–32.
Kaminski, J. W., Valle, L. A., Filene, J. H., & Boyle, C. L. Shonkoff, J. P., & Fisher, P. A. (2013). Rethinking evidence-based
(2008). A meta-analytic review of components associated practice and two-generation programs to create the future of
with parent training program effectiveness. Journal of early childhood policy. Development and Psychopathology, 25,
Abnormal Child Psychology, 36, 567–589. 1635–1653.
Kiel, E. J., Gratz, K. L., Moore, S. A., Latzman, R. D., & Tull, Snyder, J. J. (1977). Reinforcement analysis of interaction in
M. T. (2011). The impact of borderline personality pathology problem and nonproblem families. Journal of Abnormal
on mothers’ responses to infant distress. Journal of Family Psychology, 86, 528–535.
Psychology, 25, 907–918. Snyder, J., Edwards, P., McGraw, K., Kilgore, K., & Holton, A.
Klimes-Dougan, B., Brand, A. E., Zahn-Waxler, C., Usher, B., (1994). Escalation and reinforcement in mother-child
Hastings, P. D., Kendziora, K., & Garside, R. B. (2007). conflict: Social processes associated with the development
Parental emotion socialization in adolescence: Differences in of physical aggression. Development and Psychopathology, 6,
sex, age, and problem status. Social Development, 16, 326–342. 305–321.
Lamb, M. E. (2010). The role of the father in child development Snyder, J., Schrepferman, L., & St. Peter, C. (1997). Origins
(5th ed.). Hoboken, NJ: John Wiley & Sons. of antisocial behavior: Negative reinforcement and affect
Larsen, R. J., & Prizmic-Larsen, Z. (2006). Measuring emotions: dysregulation as socialization mechanisms in family
Implications of a multimethod perspective. In M. Eid & interaction. Behavior Modification, 21, 187–215.
E. Diener (Eds.), Handbook of multimethod measurement in Webster-Stratton, C. H., Reid, M. J., & Beauchaine, T. P. (2011).
psychology (pp. 337–351). Washington, DC: American Combining parent and child training for young children
Psychological Association. with ADHD. Journal of Clinical Child and Adolescent
Linehan, M. M. (1993). Cognitive-behavioral treatment of Psychology, 40, 191–203.
borderline personality disorder. New York, NY: Guilford Press. Webster-Stratton, C. H., Reid, M. J., & Beauchaine, T. P. (2013).
McLaughlin, K. A., Hatzenbuehler, M. L., Mennin, D. S., & One-year follow-up of combined parent and child
Nolen-Hoeksema, S. (2011). Emotion dysregulation and intervention for young children with ADHD. Journal of
adolescent psychopathology: A prospective study. Behaviour Clinical Child and Adolescent Psychology, 42, 251–261.
Research and Therapy, 49, 544–554. Yap, M. B., Allen, N. B., & Ladouceur, C. D. (2008). Maternal
Morelen, D., & Suveg, C. (2012). A real-time analysis of parent- socialization of positive affect: The impact of invalidation on
child emotion discussions: The interaction is reciprocal. adolescent emotion regulation and depressive
Journal of Family Psychology, 26, 998–1003. symptomatology. Child Development, 79, 1415–1431.
Morris, A. S., Silk, J. S., Morris, M. D., Steinberg, L., Aucoin, Yates, T. M., Obradović, J., & Egeland, B. (2010). Transactional
K. J., & Keyes, A. W. (2011). The influence of mother-child relations across contextual strain, parenting quality, and early
emotion regulation strategies on children’s expression of childhood regulation and adaptation in a high-risk sample.
anger and sadness. Developmental Psychology, 47, 213–225. Development and Psychopathology, 22, 539–555.
Morris, A. S., Silk, J. S., Steinberg, L., Myers, S. S., & Robinson, Zimmermann, P., & Spangler, G. (2016). Effects of Gene ×
L. R. (2007). The role of the family context in the Attachment interaction on adolescents’ emotion regulation
development of emotion regulation. Social Development, 16, and aggressive hostile behavior towards their mothers during
361–388. a computer game. Frontiers in Human Neuroscience, 10, 254.

CH A PT E R
Cognitive Processes and Risk
10 for Emotion Dysregulation
Hooria Jazaieri, Helen Uusberg, Andero Uusberg, and James J. Gross
Abstract
This chapter examines cognitive processes that underlie the development of emotion dysregulation.
It first introduces and defines key terms including emotion, emotion regulation, and emotion
dysregulation. It then introduces the authors’ theoretical perspective, the extended process model of
emotion regulation, which considers emotion generation and emotion regulation as valuation systems,
and describes core regulation processes, including regulation strategies. Next, using the extended
process model of emotion regulation as the guiding framework, the chapter discusses how emotion
dysregulation may occur during the identification, selection, implementation, and monitoring stages.
The chapter concludes by considering unresolved controversies and suggests several exciting avenues
for future research across basic and applied domains.
Keywords: cognitive processes, emotion, emotion regulation, emotion dysregulation, process model
Introduction Terms and Concepts

Skillful regulation of emotions is an essential com- Across time, disciplines, and subdisciplines, a vari-
ponent of adaptive functioning and mental health ety of terms have been used to refer to emotion and
(Gross & Muñoz, 1995). A corollary of this is that emotion-related processes. While there is no con-
emotion dysregulation is tied closely to psychopa- sensus regarding precise definitions of these terms,
thology (e.g., Cole, Michel, & Teti, 1994). In fact, it is important for researchers to be explicit regard-
systematic coding of psychological disorders in ing how they conceptualize emotion and emotion-
the Diagnostic and Statistical Manual for Mental related constructs (Gross, 2010; Gross & Barrett,
Disorders (DSM) suggests that affective distur- 2011). To follow, we provide our working definitions
bance is likely present in the diagnostic criteria for of emotion, emotion regulation, and emotion dys-
40% of psychological disorders (Jazaieri, Urry, & regulation.
Gross, 2013). Given the importance of this con-
struct, researchers have developed behavioral, Emotion
self-report, and daily assessments to monitor emo- Emotions arise when a person attends to a situation
tion dysregulation. Researchers have also devel- and then appraises it as being potentially important
oped efficacious treatments (e.g., dialectical behav- to current goals. It bears noting that attention and
ior therapy [DBT]; Linehan, 1993, 2015) designed appraisal of the situation need not occur within
to teach emotion regulation skills and tools. In this one’s conscious awareness. As emotions (e.g., fear,
chapter, we are interested in examining cognitive anger, sadness, joy) arise, they generally involve a set
processes that underlie development of emotion of loosely coupled experiential, behavioral, and
dysregulation. physiological (central and peripheral) responses.
127
This full-body response is typically referred to as either increasing or decreasing their magnitude,
“emotional reactivity.” The notion that emotions duration, or type. Second, regulation of emotions
arise and unfold over time is at the heart of most can occur through conscious and intentional pro-
contemporary conceptions of emotions, and there cesses or without conscious awareness and explicit
are commonly said to be four key steps in the intention (Gross & Thompson, 2007). Third, emo-
emotion-generative process: a situation that draws tion regulation processes cannot be deemed categor-
one’s attention, an evaluation or appraisal of the ically “good” or “bad,” as understanding the specific
situation, and a multisystem whole-body response context is necessary to evaluate whether emotion
(Gross & Thompson, 2007). regulation is adaptive or maladaptive in light of
Although emotions are often categorized into one’s goal(s).
binary groups (e.g., “good” vs. “bad,” “positive” vs.
“negative”), they are actually highly heterogeneous Emotion Dysregulation
in nature (Gross, Sheppes, & Urry, 2011). Any given We define emotion dysregulation as “a state in
emotion can sometimes be mild and hardly detect- which despite an individual’s best efforts, regulatory
able, while at other times it may be extraordinarily attempts are not achieving the individual’s emotion
intense and demanding of one’s attention. In one related goal(s) and the individual is unable to make
context, an emotion can be useful and adaptive, and necessary corrections to achieve the emotion related
in another context that very same emotion may be goal(s)” (Jazaieri et al., 2013, p. 587). Similar defini-
unhelpful and maladaptive. Emotions can be cognitions have been used by others, defining emotion
tively simple and at other times require a high level dysregulation as “the inability even when one’s best
of processing. They can be brief and fleeting and at efforts are applied, to change in a desired way emo-
other times more prolonged. tions cues, experiences, actions, verbal responses,
and/or nonverbal expressions under normative con-
Emotion Regulation ditions” (Neacsiu, Bohus, & Linehan, 2014, p. 493).
At times emotions are useful and adaptive—for ex- Beauchaine (2015) has similarly proposed that
ample, experiencing happiness while on vacation or emotion dysregulation is a “pattern of emotional
experiencing sadness when separated from someone experiences and/or expression that interferes with
you care for. However, at other times, emotions can appropriate goal-directed behavior” (p. 876).
be unhelpful and/or maladaptive (e.g., the specific It has been suggested that characteristics of emo-
emotion type, intensity, duration, and/or frequency tion dysregulation may include
are not well matched to the situation; Gross &
an excess of aversive emotional experiences, an
Jazaieri, 2014). During such times, people often at-
inability to regulate intense physiological arousal,
tempt to influence the specific emotion, its timing,
problems turning attention away from stimuli,
or how it is (or in some cases is not) experienced
cognitive distortions and failures in information
and/or expressed (Gross, 1998). This characterizes
processing, insufficient control of impulsive behaviors
emotion regulation, which involves the activation of
related to strong emotions, difficulties organizing and
a goal to regulate an emotion followed by recruit-
coordinating activities to achieve non-mood-
ment of strategies and tactics to achieve this goal.
dependent goals when emotionally aroused, and a
Sometimes the motivation for an individual to
tendency to “freeze” or dissociate under very high
engage in emotion regulation is driven by wanting
stress.
to simply feel better in a hedonic sense. For exam-
(Neacsiu et al., 2014, pp. 493–494)
ple, one may choose to downregulate anger because
the physical sensations are uncomfortable for the Others have suggested that emotion dysregula-
individual. At other times, the motivation to regu- tion is characterized by deficits in four specific areas:
late a particular emotion is driven by some other (1) (lack of ) awareness, understanding, and accept-
goal and altering the trajectory of an emotion ing of emotions; (2) (in)ability to engage in goal-
simply serves a means to an end. For example, one directed behaviors and inhibit impulsive behaviors
may choose to upregulate anger to garner attention when experiencing negative emotions; (3) (in)flexi-
from others and influence their behavior in a way ble use of situationally appropriate strategies to
that is consistent with one’s goals. modulate the intensity and/or duration of emo-
The scope of emotion regulation spans several tional response rather than to eliminate emotions
key dimensions. First, emotion regulation refers to entirely; and (4) (un)willingness to experience
changing both negative and positive emotions by negative emotions as part of pursuing meaningful
128 Cognitive Processes and Emotion Dysregul ation

activities in life (Gratz & Roemer, 2004, as cited by regulation (Gross, 2015). The extended process
Gratz, 2007, p. 1094). model uses the constructs of (1) hierarchical goal
Emotion dysregulation has been linked to representations (superordinate goals, focal goal,
psychopathology, especially mood and anxiety dis- subordinate goals, and actions) and (2) valuation
orders (e.g., Cole et al., 1994). When considering system (feedback control loops consisting of world
specific forms of psychopathology, emotion dysreg- [W], perception [P], valuation [V], and action
ulation has been defined in specific ways; for exam- [A] steps) to model the structure and dynamics of
ple, within the context of borderline personality emotion regulation. In the following three subsec-
disorder (BPD), Linehan (1993) defines emotion tions we consider (1) emotion generation and emo-
dysregulation as “high emotional vulnerability plus tion regulation as valuation systems, (2) four core
an inability to regulate emotions” (p. 43). Here processes in emotion regulation, and (3) emotion
emotional vulnerability is characterized as including regulation strategies.
(1) high sensitivity to emotional stimuli (e.g., react-
ing quickly and a low threshold for emotional reac- Emotion Generation and Emotion
tion), (2) emotional intensity (e.g., extreme emo- Regulation as Valuation Systems
tional reactions), and (3) slow return to baseline The extended process model of emotion regulation
(e.g., long-lasting reactions). Others have agreed views emotion regulation in the context of two
with Linehan’s emotion dysregulation definition interacting levels of valuation systems—one that is
within BPD and have suggested that individuals generating emotion and one that is seeking to influ-
who exhibit greater emotional reactivity and experience the emotion-generative process (Gross, 2015).
ence emotions more intensely may be at greater In the first-level valuation system, people encounter
risk for emotion dysregulation (Flett, Blankstein, & an internal or external world (W), which is selec-
Obertynski, 1996). Some clinical disorders have tively perceived (P; i.e., attention is deployed to
been characterized by “pervasive emotion dysregula- goal-relevant aspects of the world), valued (V; i.e.,
tion,” or the inability to regulate emotions across a appraised to be either helpful or unhelpful for current
wide range of emotional and situational contexts goals), and acted upon (A; i.e., the loosely coupled
(Neacsiu et al., 2014). changes in one’s subjective experience, physiology,
Emotion dysregulation occurs when a regulation and behavior that define emotion). In sum, emotion
strategy is maladaptive in some way (e.g., it creates is generated when a situation (internal or external)
more of the very emotion one is trying to regulate or occurs, attention is deployed, the meaning of the
the strategy creates a problematic secondary emo- situation is appraised, and a response occurs.
tion) and the individual is unable or unwilling to The second-level valuation system modulates
adapt his or her strategy, resulting in making the or regulates the first-level system of emotion. The
situation worse. However, it is important to keep in second-level valuation system also has a W→P→V→A
mind that emotional problems are not always the structure; however, the “W” of this cycle is the first-
result of emotion dysregulation (Sheppes, Suri, & level valuation system that is giving rise to emotion.
Gross, 2015). It is possible to simply experience Thus, when the person is experiencing an emotion
emotion problems (e.g., generation of problematic (W), he or she first “sees” or perceives (P) the emo-
emotions) without emotion dysregulation. For ex- tion, judges the emotion to be either good for me or
ample, a person may fail to recognize that an emo- bad for me (V), and then subsequently takes action
tion needs to be regulated in some way (emotion (A), which consists of generating an emotion regu-
regulation failure), or the individual may regulate lation goal (i.e., a goal to upregulate or downregu-
an emotion in an unhelpful, unskillful, or maladap- late the current emotion) and finding ways of
tive way (emotion misregulation) and yet not expe- achieving this goal.
rience emotion dysregulation. In other words, a The extended process model takes the perspective
person can experience emotion problems or emo- that emotion generation and emotion regulation
tion misregulation and then make necessary shifts, are integrated valuation systems that jointly facilitate
without resulting in emotion dysregulation. flexible pursuit of different goals. Specifically, emo-
tion generation monitors situations from the per-
Theoretical Perspectives spective of a set of primary goals and prepares the
To understand the role of cognitive processes in the individual for appropriate action (see Figure 10.1a;
development of emotion dysregulation, it is useful Uusberg, Uusberg, & Gross, in press; Gross, 2015).
to adopt the extended process model of emotion For example, we can consider how this loop generates
Jaz aieri, Uusberg, Uusberg, and Gross 129

the emotion of fear about a job interview. The W views emotion regulation as a second-level valua-
substep corresponds to the real or imagined situation system that helps to modulate the first-level
tion of stumbling with words while interviewing. system of emotion in such circumstances (see
The P substep corresponds to attending to goal- Figure 10.1b; Uusberg et al., in press). Thus, the
relevant aspects of the situation, including action regulation loop is able to assess one’s current emo-
affordances. For example, the interviewee may focus tion in light of one’s currently activated superordi-
on the implications of stumbling over her words nate goals and then helps to initiate a cascade of
and see few affordances for action at that point processes that are aimed at reducing any detected
beyond starting to cry or leaving the room. In the V discrepancies. This framework allows us to distin-
substep, features of the situation are appraised in guish among four stages of the emotion regulation
light of one’s current goals. The interviewee in our process, which we turn to next.
example may appraise stumbling over one’s words as
being incongruent with one’s goal of making a fa- Four Core Processes in Emotion Regulation
vorable impression on others. Finally, at the A sub- Emotion regulation is generally necessary when an
step the emotion loop activates changes in one’s ex- emotion (e.g., anxiety) is interfering with a goal
periential, physiological, and behavioral response (e.g., getting a job). To meet a goal, a person needs
systems and prepares the individual for action. The to solve this discrepancy by downregulating anxiety.
interviewee in our example becomes anxious, begins In the extended process model, we suggest that four
to sweat, and wishes to escape the situation. regulatory stages underlie this process: identifica-
While emotion shapes behavior in service of tion, selection, implementation, and monitoring (see
some goals that the individual values, this may si- Figure 10.2; Gross, 2015; Uusberg et al., in press).
multaneously cause conflict with other competing We further assume that the basic structure of a feed-
goals. At times the specific emotion type, intensity back control loop is helpful in understanding each
of the emotion, duration of the emotion, and/or stage of emotion regulation.
the frequency of the emotion becomes maladaptive The identification stage includes perception of
or in conflict with other goals. For example, the emotion generation and activation of a goal to regu-
Yerkes-Dodson Law (1908) would suggest that late this emotion. In this stage, a person is deciding
there would be an optimal level of anxious arousal whether or not the emotion he or she is experienc-
for an interviewee to experience; otherwise, having ing (or may experience in the future) needs to be
too little or too much anxiety would interfere with regulated in some way. There are three substeps of
one’s performance. The extended process model identification worth considering—perception (P),
(a) (b)
V
Attentional Cognitive
Deployment Change
V
Valuation P A
Response
P A Modulation
Perception Action a
V
Situation P A
W Selection &
World Modification
W
Figure 10.1 Emotion generation and emotion regulation as a two-level control system. Panel a. Emotion generation. A feedback
process attends to and appraises goal-relevant aspects of a situation to enact changes in multiple response systems. Black arrows
represent points at which emotion regulation can have an impact on emotion generation. Panel b. Emotion regulation. Another
feedback process compares the current emotion to the desired emotion and launches regulation strategies to minimize discrepancies.
The inset shows how panel a can be embedded in panel b for a full representation of emotion generation and emotion regulation.

Identification
V
Selection
V
P
Implementation
V
P
P A
W W W
Monitoring
Figure 10.2 Stages of emotion regulation. According to the extended process model, emotion regulation is initiated when a goal is
activated to change the ongoing emotion at the identification stage. Next, a broad regulation strategy is chosen at the selection
stage. The strategy is then enacted as a specific tactic suitable for the given situation at the implementation stage. This cycle can go
through multiple iterations, which are collectively viewed as a monitoring stage where the system maintains, switches, or stops one or
more aspects of the ongoing emotion regulation episode.
valuation (V), and action (A). Perception involves tactics that fit the situation (e.g., pause and take a
detecting the emotion (e.g., anxiety), valuation in- sip of cold water during the job interview). Getting
cludes determining whether the emotion is helpful from a general strategy to situation-specific tactics
or unhelpful for ongoing goal pursuits, and finally starts with the perceptual substep of the implemen-
the action substep involves activation of the goal to tation stage. At this point, a person is able to assess
regulate the emotion. Importantly, there are many available tactics and relevant situational constraints
points within the identification stage and each sub- and affordances. Then at the valuation substep a
step for emotion dysregulation to occur. person evaluates these tactics and the most promis-
Once a person identifies a regulatory goal, this ing ones are selected for implementation. The action
activates the selection stage. This stage involves a substep is the point at which an emotion regulation
valuation of available emotion regulation strategies strategy directly affects emotion generation. Thus,
from five broad families (situation selection, situa- implementation of an emotion regulation strategy
tion modification, attentional deployment, cogni- results in regulation of the first-level emotion-
tive change, and response modulation). By evaluat- generative valuation system. As in the prior stages,
ing candidate strategies with respect to situational there are many points at which emotion dysregula-
demands and available resources, the selection stage tion may occur.
results in an initial emotion regulation strategy pref- Each stage or loop continues to guide a person’s
erence. At the perception substep of the selection actions until his or her goal state is achieved or
stage, a person perceives the available regulation abandoned. This gives rise to the broader monitoring
strategies. Each strategy is evaluated during the val- stage, in which a person engages in ongoing evalua-
uation substep based on how effective the strategy is tion of whether to (1) keep implementing the cur-
expected to be in minimizing the gap between the rent emotion regulation behavior (“maintaining”);
current emotion and one’s goal in light of contex- (2) switch to a new emotion regulation goal, strat-
tual factors (e.g., cognitive and physiological re- egy, or tactic (“switching”); or (3) stop regulating
sources). After this valuation, the action substep altogether (“stopping”). As long as the action out-
activates the goal to use a particular strategy (e.g., puts of the three emotion regulation stages (identi-
response modulation). Here too, there are many fication, selection, and implementation) continue
points at which emotion dysregulation may occur. to minimize discrepancies between one’s emotion
At this point, the activated strategy is still a and current goal, the system will continue to engage
somewhat abstract representation of the individual’s in regulation. However, if the initially selected
desired end state. Thus, activation of the implemen- action substep does not produce expected results
tation stage allows a person to translate a general (e.g., anxiety is increasing or sufficient progress is
strategy (e.g., response modulation) into specific not being made), a person may consciously or

nconsciously choose to switch tactics, strategies, or
u terview. For instance, she could target the W sub-
goals, depending on the stage at which failure step in the emotion generation loop by cancelling
occurs. Emotion regulation switching means that a the job interview (situation selection) or preparing
goal is still activated but the specific strategy or note cards with answers to common questions to
tactic to achieve that goal (or the new goal) has been read from during the interview (situation modifica-
adjusted in light of the prior unfavorable results. If tion). She could target the P substep by thinking
an emotion falls below the threshold set by the iden- about the relaxing weekend ahead to distract herself
tification stage (e.g., through the new strategy’s ef- from attending to the threatening nature of the in-
fectiveness or changes in the situation or environ- terview (attentional deployment). She could target
ment) or if repeated efforts to regulate have failed, the V substep by construing the job interview as an
the goal to regulate the emotion may be abandoned opportunity to practice communicating her
or stopped. The monitoring stage—like the other thoughts and ideas to others rather than an impor-
stages—may also lead to emotion dysregulation. tant test of her competence as a person (cognitive
change). Finally, she could take a deep breath during
Emotion Regulation Strategies the job interview as a way of relaxing her body (re-
According to the process model, we categorize sponse modulation). We now turn to examining each
emotion regulation strategies based on where they of the five families of emotion regulation strategies
have their primary effect on emotion generation in greater detail.
(Figure 10.1a; Gross, 1998, 2015). As noted earlier
when discussing the implementation stage of emo- Situation Selection
tion regulation, regulatory processes can be organ With situation selection, the person is deciding
ized into five families (situation selection, situation whether to approach or avoid a situation based on
modification, attentional deployment, cognitive what the person hypothesizes the affective impact
change, and response modulation; Gross, 1998). may be. In general, people tend to avoid situations
Situation selection refers to efforts made to change that are likely to generate negative emotions and ap-
emotions by influencing the likelihood (increasing proach situations that are likely to generate positive
or decreasing) of encountering situations where a emotions. Empirically, it has been suggested that
particular emotion is likely to be elicited. Situation situation selection may be most effective for indi-
modification refers to efforts made to change emo- viduals who experience intense emotions and/or
tions by altering external, physical features within experience difficulty in regulating emotions in real
the environment. Both situation selection and situ- time (Webb, Lindquist, Jones, Avishai, & Sheeran,
ation modification have their impact on the “world” 2018). At times, however, the short-term emotion
(the W substep in the emotion generation process; regulatory goal of experiencing or not experiencing
Figure 10.1a). Attentional deployment refers to efforts an emotion comes at the expense of longer-term
made to change emotions by directing one’s atten- goals. This is exemplified by the detrimental effects
tion in a particular way to change one’s perception of behavioral avoidance, for instance, in the case of
of the situation (the P substep). Cognitive change anxiety disorders (e.g., Salters-Pedneault, Tull, &
refers to efforts made to alter one’s emotions by Roemer, 2004). Therefore, as with all strategies,
modifying the subjective meaning of the situation. situation selection must be evaluated within the
This is achieved by changing how the situation is present context and individual’s goals to understand
evaluated in light of current goals (the V substep). whether it is an adaptive strategy.
Finally, response modulation refers to efforts made to
alter physiological, experiential, or behavioral re- Situation Modification
sponses of an emotion in order to alter that emo- If the person chooses not to avoid the situation,
tion’s trajectory (the A substep). situation modification refers to adjusting external,
There is evidence that skillful implementation of physical parameters in the environment to influence
regulatory strategies is beneficial for emotional which emotions occur. People for a variety of rea-
health (for a meta-analysis see Webb, Miles, & sons enter situations where they want to regulate an
Sheeran, 2012). In any given situation, individuals emotion. For example, a person with anxiety about
can use one or any combination of emotion regula- germ-filled public restrooms may use a paper towel
tion strategies to influence their emotional state. to open the bathroom door, or a person anxious
Take the interviewee who is anxious about a job in- about giving a presentation may adjust the lighting

in the room so that the space is dim and more calm- tions to stressful, anxiety-provoking situations and
ing. While considerable guesswork is necessary to can lead to greater psychological flexibility and
anticipate the specific modifications that might emotional well-being (Gross & Thompson, 2007).
be necessary to change one’s emotions, research on Difficulty reappraising emotion-eliciting situa-
problem-focused coping (Lazarus & Folkman, 1984) tions is considered to be a core mechanism under-
and primary control (Rothbaum, Weisz, & Snyder, lying anxiety and mood disorders (Campbell-Sills
1982) suggests that efforts made to change emotions & Barlow, 2007). Researchers hypothesize that
through situation modification can be effective. some people, for a variety of reasons, may not have
the cognitive resources to engage in effective cog-
Attentional Deployment nitive change (Hofmann, Schmeichel, & Baddeley,
Where an individual chooses to place his or her at- 2012; Vohs & Heatherton, 2000). In general, cog-
tention can also have powerful effects on generation nitive reappraisal is considered to be one of the
of emotion. With attentional deployment, the more effective strategies for regulating emotions
person chooses how to allocate limited cognitive re- (Webb et al., 2012); however, there is some re-
sources between emotionally relevant and irrelevant search to suggest that when emotions are very in-
aspects of the situation. Given that emotions re- tense, reappraisal may be less effective (e.g.,
quire some capacity-limited central processing re- Sheppes & Gross, 2011).
sources (Brosch, Pourtois, & Sander, 2009; Pessoa
& Adolphs, 2010), changing the allocation of cogni- Response Modulation
tive resources devoted to the emotional aspects Response modulation refers to efforts to modify ex-
of the situation will also change the emotion. periential, behavioral, and/or physiological compo-
Attentional deployment can take several forms in- nents of an emotion after it has been generated.
cluding distraction (Van Dillen & Koole, 2007), Examples of response modulation can include
intense concentration (Csikszentmihalyi, 1975), useful tactics such as physical exercise, deep breath-
and rumination (Nolen-Hoeksema, 1991). For ex- ing, or drinking cold water, as well as less useful tac-
ample, in the case of distraction, a person who is tics such as eating sweets or consuming alcohol.
experiencing the emotion of anger during a meeting One of the most commonly studied forms of re-
may choose to redirect his or her attention to sponse modulation is expressive suppression, which
thoughts about a neutral topic (e.g., one’s grocery refers to efforts made to hide verbal and behavioral
list). Attentional deployment has been found to be expressions of emotion. Expressive suppression has
effective at reducing emotional intensity when been shown to have important consequences for re-
diverting attention (both overtly and covertly)
ducing positive (but not negative) emotions, in-
away from emotional stimuli (e.g., Augustine & creasing sympathetic nervous system responses,
Hemenover, 2009; Ochsner & Gross, 2005; Webb heightened amygdala activation, and worse memory,
et al., 2012). to name a few (see Gross, 2015). In short, expressive
suppression has been convincingly shown to have a
Cognitive Change range of negative inter- and intrapersonal conse-
This regulatory strategy involves using cognitive quences. But here too, it is important to keep in
skills (e.g., perspective taking, challenging interpre- mind that as with all strategies, response modula-
tations, reframing the situations) to modify the tion must be evaluated within a particular context
meaning of a stimulus or situation that gives rise to and personal goals to understand whether it is an
emotional reactions. Given that emotions depend adaptive or maladaptive strategy.
on our appraisals of various aspects of the situation
(e.g., how important it is, causes of the situation, Current Findings
anticipation of what might happen next, etc.), Here, we consider how each of the four stages in the
changing one or a series of interpretations about the extended process model of emotion regulation
situation will likely alter the course of the emotion. (identification, selection, implementation, and
Specifically, reappraisal (a common form of cogni- monitoring) can be used to explain adaptive and
tive change) entails utilizing cognitive and linguistic maladaptive emotion regulation (Gross, 2015;
processes to reframe or reinterpret the meaning of a Sheppes et al., 2015). Within the extended process
stimulus or situation in order to change emotions. model, emotion regulation difficulties can be traced
Cognitive reappraisal can modify emotional reac- to the functioning of different components of the

two-level valuation system (Gross, 2015; Sheppes times cause emotion regulation failures, though
et al., 2015; Uusberg et al., in press). Specifically, we these failures are not due to lack of awareness, but
review evidence related to each of the four stages— rather due to faulty valuation of the emotion. For
identification, selection, implementation, and example, in bipolar I (which is characterized by epi-
monitoring—and within each stage consider three sodes of mania or elevated mood) or bipolar II
substeps of perception, valuation, and action. (which is characterized by episodes of hypomania),
even if a person has the cognitive capacity to regu-
Identification Stage Difficulties late positive emotions when instructed (e.g., Gruber,
When the identification stage is working well, the Harvey, & Johnson, 2009), they often choose to not
individual is able to detect the emotion, accurately downregulate positive emotions (for a review see
place value on the emotion, and activate a regula- Gruber, 2011). Another potential issue in the valua-
tion goal. One of the difficulties that can occur tion substep is undervaluing regulation of lower in-
within the identification stage (at the perception tensity emotions. Therefore, while the person is
substage) is failing to detect that an emotion may aware of a lower intensity emotion, they may dis-
need regulating (lack of awareness or underrepre- miss the need or opportunity to regulate.
senting of emotional states). Therefore, the person Finally, emotion regulation problems can also
fails to activate a regulation goal in a situation where arise in the action substep of the identification loop,
it would be adaptive to do so. People vary in their which entails activating a goal to change emotion in
emotional awareness (Taylor, 1994), and these dif- some specific manner. At this substep the individual
ferences in emotional awareness can impede skillful may fail to take any action and choose to continue
emotion regulation. Another difficulty with percep- to not regulate. For example, take the feature of
tion is that people may have awareness but this learned helplessness in the context of major depres-
awareness is primarily for high-intensity emotions. sive disorder, whereby the individual has a sense of
For example, often when individuals report emo- (real or perceived) absence of control (powerless-
tion dysregulation, they report emotions going ness) over the outcome of a situation (e.g., Seligman,
“from 0 to 100” and then at times attempting to 1975), which may then interfere with translating the
regulate (unsuccessfully) the emotion once it is detected discrepancy between current and desired
around 100. Upon closer inspection, it is often the emotion into a regulatory goal. At other times
case that the emotion was present at lower intensi- people may only halfheartedly activate the goal to
ties (e.g., 30 or 40). However, the person was simply regulate the emotion, and depending on the inten-
not aware of the lower intensity emotion and there- sity of the emotion, this halfhearted effort to regu-
fore did not think about employing regulation ef- late may result in a regulation failure. To be effec-
forts. Another difficulty that may occur with per- tive, it is necessary to take action “all the way,”
ception is the issue of oversensitivity, which can also continuing to “turn the mind” toward being “will-
lead to unnecessary regulatory efforts. For example, ing” to take action in order to be effective (Linehan,
a hallmark feature of panic disorder is the tendency 1993, 2015).
to overrepresent subtle signs of one’s current emo-
tional state, which is often physiological in nature Selection Stage Difficulties
(Burns, 2007), such as having the thought “my When the selection stage is working well, the indi-
heart is racing so this must mean a panic attack is vidual is able to pick an optimal emotion regulation
eminent.” This misperception of identification of strategy for the current situation. However, in the
one’s emotional state triggers regulatory activity un- selection stage several sources of difficulty may exist.
necessarily, which may hinder pursuit of other goals. First, in the perceptual substep, a person may per-
Without adjustment, emotion dysregulation will ceive various emotion regulatory strategies. The in-
likely occur. dividual is essentially generating a hypothesis (by
Regulation failures can also occur in the valua- weighing the potential costs and benefits) regarding
tion substep. At times people overvalue certain which regulatory strategy will be most effective. In
emotional states and undervalue the goal to regulate addition to considering effectiveness, the person is
those emotions. For example, in general, people also considering which strategy he or she is willing
tend to shy away from downregulating positive and able to employ in the moment. In terms of will-
emotions when regulation of these positive emo- ingness, some strategies require greater cognitive
tions would potentially be skillful; thus, this can at resources to employ (e.g., cognitive change) over

others (e.g., situation selection). When considering question for future research on emotion dysregula-
ability, people have different repertories of emotion tion to consider.
regulatory strategies in their regulatory toolbox
(e.g., Aldao, Nolen-Hoeksema, & Schweizer, 2010) Implementation Stage Difficulties
or sometimes simply believe that they have few strat- Once an individual selects an emotion regulation
egies at their disposal (e.g., De Castella et al., 2013). strategy, the implementation stage is initiated. When
A person’s regulatory toolbox may be relatively the implementation stage is working well, the indi-
scarce, perhaps due to excessive reliance on only a vidual is able to translate the general strategy from
few strategies, whereas other individuals may have a the selection stage into specific tactics that are ap-
richer repertoire of regulatory strategies. propriate for the given situation. As with the prior
In terms of the valuation substep, people may stages, emotion regulation difficulties may arise at
overvalue short-term relief. Empirical evidence sug- each of the implementation stage’s substeps.
gests that some strategies are more effective in the One source of difficulty at this stage is that indi-
short run but may be less effective in the long run viduals may lack the skills necessary to implement
(e.g., attentional deployment; e.g., Paul, Kathmann, the specific tactics needed in the situation (e.g.,
& Riesel, 2016). Cognitive reappraisal, on the other Linehan, 1993, 2015). For example, a person may
hand, can help facilitate long-term adaptation to decide to use cognitive change, specifically cognitive
emotional stimuli but at some cost to immediate reappraisal. However, even if the person has been
effectiveness (MacNamara, Ochsner, & Hajcak, effective at utilizing cognitive reappraisal in the
2011). It could therefore be optimal to utilize a strat- past, perhaps in highly similar situations, the person
egy such as situation selection or attentional deploy- may be unable to effectively use cognitive reap-
ment when the immediate benefit of avoiding the praisal in the new context (e.g., due to varying emo-
situation outweighs the delayed cost of reduced ad- tional intensity, different goals, environmental fac-
aptation (e.g., eventual habituation to strong nega- tors, etc.). Alternatively, the person may be
tive emotions). On the other hand, choosing cogni- reappraising his or her thoughts but not actually
tive reappraisal may be more optimal if the believing the reappraisal, and thus the regulation of
immediate distress is manageable enough to be the emotion is ineffective. At other times the person
worth the delayed benefit of immediate relief. There may reappraise a thought only to have the thought
is some preliminary research to support this pattern come right back up (generally at a lower intensity)
of emotion regulation choice and it is an exciting again. With any given thought, reappraisal may not
area for continued research (e.g., Sheppes, 2014; be a one-shot effort, but instead may require re-
Sheppes et al., 2014). Maladaptive use of emotion peated attention.
regulation strategies could contribute to negative At the valuation substep, the person is evaluating
social, health, or occupational outcomes and is the tactics and selecting the most promising tactics
likely to be more pronounced among people who to implement. Contextual variables again (e.g.,
experience chronic emotion dysregulation. emotion intensity, cognitive resources, etc.) can in-
Finally, problems may also arise within the terfere with one’s ability to accurately value the situ-
action substep. One difficulty may be the belief that ation (over- or undervaluing), thus resulting in the
one cannot effectively utilize a particular emotion individual implementing an unsuccessful regulation
regulation strategy (referred to as low emotion reg- tactic. Due to the enormous range of potential be-
ulation self-efficacy), which has negative conse- haviors at this level, systematic research within this
quences for psychological health (De Castella et al., space is relatively limited (Uusberg et al., in press).
2013). Self-efficacy beliefs may shape how intensely Finally, the action substep may also give rise to
a person activates a particular regulation strategy problems if the specific tactic chosen is mismanaged
and can be modified through interventions (e.g., in its implementation. When considering psycho-
De Castella et al., 2015; Goldin et al., 2012). An pathology, many studies have documented the dif-
important question for researchers to consider is ficulties with implementation of tactics. For exam-
the relation between high emotion dysregulation ple, Heller and colleagues (2009) looked at
and low emotion regulation self-efficacy. One individuals with major depressive disorder and
might hypothesize that there would be a positive found that anhedonia in these individuals reflected
association between the two and potentially even a an inability to sustain activation in neural circuits
causal relationship. We find this to be an intriguing involved in positive affect and reward.

Monitoring Stage Difficulties match one’s initial regulatory goal. For example, in
Once the strategy has been selected and imple- the case of social anxiety disorder, the individual
mented, it must be monitored over time to evaluate may choose to approach anxiety-producing stimuli
the effectiveness and potential next action. When but may stop approaching or engaging prematurely
the monitoring stage is working well, the individual (Liebowitz, 1987). Delayed stopping (i.e., the strat-
is able to effectively monitor in real time—main- egy has already “worked”), on the other hand, is an
taining the strategy, switching the strategy in a interesting case where regulation efforts continue
timely fashion, or stopping regulation at an appro- well past the need for regulation. While the cost of
priate time. In general, maintaining, switching, and premature stopping is obvious, delayed stopping
stopping strategies can be considered maladaptive can have profound consequences as well. Depending
when their flexibility is either too low or too high. on the resources expended on extended regulation,
With regard to difficulties with maintaining the a person could create a secondary problem such as
strategy, at times a person will continue to use the increased physiological activation or unskillful in-
same strategy even though it is not effective in meet- terpersonal situations.
ing his or her goals. For example, in the case of
mood and anxiety disorders, the strategy of situa- Unresolved Controversies and
tion selection may be continually used even when it Future Directions
is counterproductive in achieving one’s goals (e.g., We have described a number of difficulties that may
Campbell-Sills & Barlow, 2007). At other times, occur in the identification, selection, implementation,
difficulties with maintenance occur because other and monitoring stages and specified the substep at
competing goals interfere with the goal to regulate. which these difficulties might occur. While the em-
This goal interference may change the initial trajec- pirical literature within many of these domains is
tory of regulating emotions and create potential scant (Sheppes et al., 2015), this opens up a number
emotional problems. of exciting avenues for future research.
When considering difficulties with switching, a
person must monitor in real time whether the se- Cognitive Processes and Clinical Disorders
lected strategy is sufficient for meeting his or her The extended process model is a promising organiz-
regulatory goals. Assuming one possesses a rich rep- ing framework for understanding how at times,
ertoire of regulatory strategies, the ability to recog- when cognitive processes go wrong, this can lead to
nize ineffective strategies opens up endless opportu- emotion dysregulation. It is important to note that
nities to utilize alternative strategies that may be there are still significant gaps in current understand-
more effective. However, if one’s repertoire of regu- ing about how different cognitive processes contrib-
latory strategies is limited, the individual may ute to various clinical disorders. For example, when
choose to “stay the course” even if ineffective (a case considering the four stages (identification, selec-
of “failure to switch”). Alternatively, if a person has tion, implementation, and monitoring), it is possi-
a rich repertoire and continually changes strategies ble that some clinical disorders are characterized by
and does not “settle” on a strategy or switches strate- difficulties in one, a combination of, or all four
gies prematurely, this can be problematic (“failure to stages. Then, within each stage, there are the sub-
settle”). At times, the context has shifted in some steps (perceptual, valuation, and action) and it is
way, requiring that the person switch strategies; possible that some diagnoses are characterized diffi-
however, the person may fail to switch given the culties different combinations of these. Thus, it is
new context. Additionally, if a person continually important for future research to begin to identify
switches strategies, he or she may get fatigued and specific difficulties among the stages and within
eventually give up on regulation goals. The ability to the substeps for various clinical disorders (Sheppes
engage in adaptive strategy switching has been as- et al., 2015).
sociated with healthy functioning in terms of one’s Relatedly, getting more precise about these diffi-
psychological health, including lower anxiety (Kato, culties for specific clinical disorders could have im-
2012). portant implications for our growing understanding
With regard to difficulties with stopping, prema- of clinical assessment and treatment. In terms of as-
ture or delayed stopping may be problematic. In the sessment, self-report questionnaires and clinician
instance of premature stopping, the person would interviews could more explicitly assess these areas of
be discontinuing the regulation strategy before the difficulty. In terms of treatment, specific interven-
emotion has had an opportunity to fully change to tions could be developed, or modules could be

added to existing interventions to provide individu- the individual is aware that regulation is taking
als with skills and tools to more skillfully address place. Recently there has been a growing interest in
these challenges. Emotion regulation efforts that are implicit, or more automatic and less effortful, forms
made by the individual, some maladaptive in of emotion regulation. For example, when probed
nature, may be part of the disorder itself (e.g., BPD; after the fact, people report using emotion regula-
Linehan, 1993). Knowing high-leverage points tion on a daily basis (Gross, Richards, & John,
could help streamline clinical interventions. 2006), suggesting some habitual pattern of emotion
regulation. Types of implicit regulation can include
Understanding Subclinical Difficulties inhibition of fear and regulation of emotional con-
We have suggested that people can experience emo- flict (Braunstein, Gross, & Ochsner, 2017; Etkin,
tion problems or emotion difficulties without expe- Büchel, & Gross, 2015).
riencing emotion dysregulation. People can also ex- Researchers are still examining effective ways to
perience emotion dysregulation at times without measure subjective experiences of implicit emotion
experiencing chronic emotion dysregulation. Much regulation without influencing or disrupting the
of the research on emotion dysregulation has exam- process. Neuroimaging tools have provided one
ined individuals with significant emotion dysregula- window into these processes; specifically, these stud-
tion compared with healthy individuals (e.g., Gratz, ies have found activation in the ventral anterior cin-
Rosenthal, Tull, Lejuez, & Gunderson, 2006). gulate cortex (vACC) and ventromedial prefrontal
Other researchers have compared clinical popula- cortex (vmPFC; e.g., Etkin et al., 2015). Additionally,
tions who differ in the extent of emotion dysregula- there are individual differences and contextual fac-
tion (e.g., Turk, Heimberg, Luterek, Mennin, & tors that differentiate those who readily engage in
Fresco, 2005). Finally, some have compared indi- emotion regulation versus those who find regula-
viduals who meet criteria for a clinical diagnosis tory efforts more effortful, which is also an interest-
characterized by emotion dysregulation with other ing area for continued research.
clinical disorders (without the hallmark feature of
emotion dysregulation) and healthy/nonclinical Conclusion
samples (e.g., Kuo & Linehan, 2009). In this chapter, we have examined some of the cog-
For a crisper empirical investigation of emo- nitive processes that may contribute to emotion
tional problems versus emotion dysregulation, regulation and dysregulation. We have argued that
future research may consider examining individuals by understanding how emotions are generated and
without psychopathology who also endorse experi- typically regulated, we can better understand how
encing some degree of unwanted emotion and emotion dysregulation occurs. Utilizing the ex-
emotion regulation problems (i.e., subclinical tended process model of emotion regulation as an
problems) with individuals who meet criteria for organizing framework (Gross, 2015), we have iden-
emotion dysregulation. Taking a dimensional ap- tified some of the areas where emotion dysregula-
proach (rather than looking at different groups of tion can arise and have made suggestions for future
people who meet criteria for various forms of psy- research, assessment, and treatment. Many gaps still
chopathology or looking at healthy/nonclinical exist in our understanding about how different cog-
samples) will help the field move toward a more nitive processes contribute to emotion dysregula-
direct empirical examination of potential differences tion; thus, there are a plethora of opportunities for
that may exist between those who experience various basic and applied researchers to contribute to cur-
degrees of emotion problems (without emotion rent understanding of emotion, emotion regulation,
dysregulation) and those who experience chronic and emotion dysregulation.
emotion dysregulation.
References
Implicit Versus Explicit Emotion Regulation Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
Much of the research conducted in the field (and Emotion-regulation strategies across psychopathology: A
cited throughout this chapter) focuses on explicit meta-analytic review. Clinical Psychology Review, 30, 217–237.
forms of emotion regulation. In explicit emotion Augustine, A. A., & Hemenover, S. H. (2009). On the relative
effectiveness of affect regulation strategies: A meta-analysis.
regulation, individuals are engaging in effortful reg-
Cognition and Emotion, 23, 1181–1220.
ulation. For example, in experimental settings, indi- Beauchaine, T. P. (2015). Future directions in emotion
viduals are instructed regarding which regulatory dysregulation and youth psychopathology. Journal of Clinical
strategy to use or which ones to choose from; thus, Child & Adolescent Psychology, 44, 875–896.

Braunstein, L. M., Gross, J. J., & Ochsner, K. N. (2017). Explicit Gross, J. J., & Jazaieri, H. (2014). Emotion regulation and
and implicit emotion regulation: A multi-level framework. psychopathology: An affective science perspective. Clinical
Social Cognitive and Affective Neuroscience, 12, 1545–1557. Psychological Science, 2, 387–401.
Brosch, T., Pourtois, G., & Sander, D. (2009). The perception Gross, J. J., & Muñoz, R. F. (1995). Emotion regulation and
and categorisation of emotional stimuli: A review. Cognition mental health. Clinical Psychology: Science and Practice, 2,
and Emotion, 24, 377–400. 151–164.
Burns, D. D. (2007). When panic attacks: The new, drug-free Gross, J. J., Richards, J. M., & John, O. P. (2006). Emotion
anxiety therapy that can change your life. New York, NY: regulation in everyday life. In D. K. Snyder, J. Simpson, &
Harmony Books. J. N. Hughes (Eds.), Emotion regulation in couples and
Campbell-Sills, L., & Barlow, D. H. (2007). Incorporating families: Pathways to dysfunction and health (pp. 13–35).
emotion regulation into conceptualizations and treatments Washington, DC: American Psychological Association.
of anxiety and mood disorders. In J. J. Gross (Ed.), Handbook Gross, J. J., Sheppes, G., & Urry, H. L. (2011). Emotion
of emotion regulation (pp. 542–559). New York, NY: Guilford generation and emotion regulation: A distinction we should
Press. make (carefully). Cognition and Emotion, 25, 765–781.
Cole, P. M., Michel, M. K., & Teti, L. O. (1994). The Gross, J. J., & Thompson, R. A. (2007). Emotion regulation:
development of emotion regulation and dysregulation: A Conceptual foundations. In J. J. Gross (Ed.), Handbook of
clinical perspective. Monographs of the Society for Research in emotion regulation (pp. 3–24). New York, NY: Guilford Press.
Child Development, 59, 73–100. Gruber, J. (2011). Can feeling too good be bad? Positive emotion
Csikszentmihalyi, M. (1975). Beyond boredom and anxiety: The persistence (PEP) in bipolar disorder. Current Directions in
experience of play in work and games. San Francisco, CA: Psychological Science, 20, 217–221.
Jossey-Bass. Gruber, J., Harvey, A. G., & Johnson, S. L. (2009). Reflective
De Castella, K., Goldin, P., Jazaieri, H., Ziv, M., Dweck, C. S., and ruminative processing of positive emotional memories in
& Gross, J. J. (2013). Beliefs about emotion: Links to bipolar disorder and healthy controls. Behaviour Research and
emotion regulation, well-being, and psychological distress. Therapy, 47, 697–704.
Basic and Applied Social Psychology, 35, 497–505. Heller, A. S., Johnstone, T., Shackman, A. J., Light, S. N.,
De Castella, K., Goldin, P., Jazaieri, H., Ziv, M., Heimberg, Peterson, M. J., Kolden, G. G., . . . Davidson, R. J. (2009).
R. G., Dweck, C. S., & Gross, J. J. (2015). Emotion beliefs Reduced capacity to sustain positive emotion in major
and cognitive behavioural therapy for social anxiety disorder. depression reflects diminished maintenance of fronto-striatal
Cognitive Behaviour Therapy, 44, 128–141. brain activation. Proceedings of the National Academy of
Etkin, A., Büchel, C., & Gross, J. J. (2015). The neural bases of Sciences, 106, 22445–22450.
emotion regulation. Nature Review Neuroscience, 16, 693–700. Hofmann, W., Schmeichel, B. J., & Baddeley, A. D. (2012).
Flett, G. L., Blankstein, K. R., & Obertynski, M. (1996). Affect Executive functions and self-regulation. Trends in Cognitive
intensity, coping styles, mood regulation expectancies, and Sciences, 16, 174–180.
depressive symptoms. Personality and Individual Differences, Jazaieri, H., Urry, H., & Gross, J. J. (2013). Affective disturbance
20, 221–228. and psychopathology: An emotion regulation perspective.
Goldin, P., Ziv, M., Jazaieri, H., Werner, K., Kraemer, H., Journal of Experimental Psychopathology, 4, 584–599.
Heimberg, R.G., & Gross, J. J. (2012). Cognitive reappraisal Kato, T. (2012). Development of the Coping Flexibility Scale:
self-efficacy mediates the effects of individual cognitive- Evidence for the coping flexibility hypothesis. Journal of
behavioral therapy for social anxiety disorder. Journal of Counseling Psychology, 59, 262–273.
Consulting and Clinical Psychology, 80, 1034–1040. Kuo, J. R., & Linehan, M. M. (2009). Disentangling emotion
Gratz, K. L. (2007). Targeting emotion dysregulation in the processes in borderline personality disorder: Physiological
treatment of self-injury. Journal of Clinical Psychology, 63, and self-reported assessment of biological vulnerability,
1091–1103. baseline intensity, and reactivity to emotionally evocative
Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment stimuli. Journal of Abnormal Psychology, 118, 531–544.
of emotion regulation and dysregulation: Development, Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal and coping.
factor structure, and initial validation of the Difficulties in New York, NY: Springer.
Emotion Regulation Scale. Journal of Psychopathology and Liebowitz, M. R. (1987). Social phobia. Modern Problems in
Behavioral Assessment, 26, 41–54. Pharmacopsychiatry, 22, 141–173.
Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., & Linehan, M. M. (1993). Cognitive-behavioral treatment of
Gunderson, J. G. (2006). An experimental investigation of borderline personality disorder. New York, NY: Guilford.
emotion dysregulation in borderline personality disorder. Linehan, M. M. (2015). DBT skills training manual (2nd ed.).
Journal of Abnormal Psychology, 115, 850–855. New York, NY: Guilford Press.
Gross, J. J. (1998). Antecedent- and response-focused emotion MacNamara, A., Ochsner, K. N., & Hajcak, G. (2011). Previously
regulation: Divergent consequences for experience, reappraised: The lasting effect of description type on picture-
expression, and physiology. Journal of Personality and Social elicited electrocortical activity. Social Cognitive and Affective
Psychology, 74, 224–237. Neuroscience, 6, 348–358.
Gross, J. J. (2010). The future's so bright, I gotta wear shades. Neacsiu, A. D., Bohus, M., & Linehan, M. M. (2014). Dialectical
Emotion Review, 2, 212–216. behavior therapy: An intervention for emotion dysregulation.
Gross, J. J. (2015). Emotion regulation: Current status and future In J. J. Gross (Ed.), Handbook of emotion regulation (2nd ed.,
prospects. Psychological Inquiry, 26, 1–26. pp. 491–507). New York, NY: Guilford Press.
Gross, J. J., & Barrett, L. F. (2011). Emotion generation and Nolen-Hoeksema, S. (1991). Responses to depression and their
emotion regulation: One or two depends on your point of effects on the duration of depressive episodes. Journal of
view. Emotion Review, 3, 8–16. Abnormal Psychology, 100, 569–582.

Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of Taylor, G. J. (1994). The alexithymia construct:
emotion. Trends in Cognitive Sciences, 9, 242–249. Conceptualization, validation, and relationship with basic
Paul, S., Kathmann, N., & Riesel, A. (2016). The costs of dimensions of personality. New Trends in Experimental and
distraction: The effect of distraction during repeated picture Clinical Psychiatry, 10, 61–74.
processing on the LPP. Biological Psychology, 117, 225–234. Turk, C. L., Heimberg, R. G., Luterek, J. A., Mennin, D. S., &
Pessoa, L., & Adolphs, R. (2010). Emotion processing and the Fresco, D. M. (2005). Emotion dysregulation in generalized
amygdala: From a “low road” to “many roads” of evaluating anxiety disorder: A comparison with social anxiety disorder.
biological significance. Nature Reviews Neuroscience, 11, 773–783. Cognitive Therapy and Research, 29, 89–106.
Rothbaum, F., Weisz, J. R., & Snyder, S. S. (1982). Changing the Uusberg, A., Uusberg, H., & Gross, J. J. (in press). Emotion
world and changing the self: A two-process model of perceived regulation. In A. Scarantino (Ed.), Routledge handbook of
control. Journal of Personality and Social Psychology, 42, 5–37. emotion theory. New York, NY: Taylor & Francis.
Salters-Pedneault, K., Tull, M. T., & Roemer, L. (2004). The role Van Dillen, L. F., & Koole, S. L. (2007). Clearing the mind: A
of avoidance of emotional material in the anxiety disorders. working memory model of distraction from negative
Applied and Preventive Psychology, 11, 95–114. emotion. Emotion, 7, 715–723.
Seligman, M. E. P. (1975). Helplessness: On depression, Vohs, K. D., & Heatherton, T. F. (2000). Self-regulatory failure:
development, and death. San Francisco, CA: W. H. Freeman. A resource-depletion approach. Psychological Science, 11,
Sheppes, G. (2014). Emotion regulation choice: Theory and 249–254.
findings. In J. J. Gross (Ed.), Handbook of emotion regulation Webb, T. L., Lindquist, K. A., Jones, K., Avishai, A., &
(2nd ed.). New York, NY: Guilford Press. Sheeran, P. (2018). Situation selection is a particularly
Sheppes, G., & Gross, J. J. (2011). Is timing everything? Temporal effective emotion regulation strategy for people who need
considerations in emotion regulation. Personality and Social help regulating their emotions. Cognition and Emotion, 32,
Psychology Review, 15, 319–331. 231–248.
Sheppes, G., Scheibe, S., Suri, G., Radu, P., Blechert, J., & Webb, T. L., Miles, E., & Sheeran, P. (2012). Dealing with
Gross, J. J. (2014). Emotion regulation choice: A conceptual feeling: A meta-analysis of the effectiveness of strategies
framework and supporting evidence. Journal of Experimental derived from the process model of emotion regulation.
Psychology: General, 143, 163–181. Psychological Bulletin, 138, 775–808.
Sheppes, G., Suri, G., & Gross, J. J. (2015). Emotion regulation Yerkes, R. M., & Dodson, J. D. (1908). The relation of strength
and psychopathology. Annual Review of Clinical Psychology, of stimulus to rapidity of habit-formation. Journal of
11, 379–405. Comparative Neurology and Psychology, 18, 459–482.

CH A PT E R
Interpersonal Processes and
11 the Development of Emotion
Dysregulation
Sarah A. Stoycos, Geoffrey W. Corner, Mona Khaled, and Darby Saxbe
Abstract
Emotion regulation and dysregulation often unfold within interpersonal contexts. Parent–child
relationships provide early scaffolding of emotion regulation processes. Parents attune to, and
influence, their children’s emotions, through pathways such as physical touch, infant cry, facial
expressions, and stress physiology. Interpersonal emotion regulation and dysregulation processes
continue to evolve within other close relationship contexts such as romantic couple relationships in
adulthood. Partners shape each other’s emotion regulation through stress contagion and physiological
interconnection, and through interactions that can be conflictual or supportive. This chapter reviews
the theoretical foundations and the existing literature describing how emotion regulation and
dysregulation take place within interpersonal relationships.
Keywords: emotion regulation, interpersonal, dyads, synchrony, attunement, stress contagion,

conflict, support
Introduction in emotion regulation and well-being (e.g., Gross &

Researchers have highlighted the reciprocal nature John, 2003; Ochsner & Gross, 2005), emphasizing
of emotion expression, perception, and modulation the role of emotion regulation in adaptive functioning.
within interpersonal groups. In The Expression of the Developmental researchers emphasize that infant
Emotions in Man and Animals (1872), Darwin pos- and child emotion regulation is almost exclusively
tulated that emotional facial expressions play a role an interpersonal process, and more recent reviews
in evolutionary survival and group dynamics. Later theorize that adolescent and adult emotion regula-
researchers furthered Darwin’s account by attempt- tion abilities remain interpersonal, rather than tran-
ing to parse out the intra- and interindividual func- sitioning to an intraindividual process (Rimé,
tionality of emotional expressions (Ekman, 1992, 2009). Indeed, for over a century psychologists, bi-
1993; Shariff & Tracy, 2011), theorizing that intrain- ologists, evolutionary scientists, sociologists, and
dividual emotion expression likely served to help anthropologists have studied the phenomena of in-
regulate the individual’s own physiological state terpersonal emotional expression, perception, and
(Susskind et al., 2008), and over time, emotion ex- regulation. This chapter will focus on various types
pression became linked with social communication. of interpersonal processes that contribute to emo-
Additionally, Bowlby’s (1969) and Harlow’s (1959) tion dysregulation, while acknowledging that dys-
seminal research on the role of emotion in dyadic regulation is only one side of the coin. Thus, we will
processes during infant development culminated in examine interpersonal processes leading to effective
attachment theory and an emphasis on parent–child emotion regulation to provide a context for emo-
relationships as foundational for adult expression, tion dysregulation as a deviation from adaptive pro-
perception, and regulation of emotions. James Gross cesses. We focus primarily on close dyadic relation-
and colleagues have studied individual differences ships, since the preponderance of research on
141
interpersonal emotional regulation and dysregula- language help facilitate the child’s socioemotional
tion has focused on dyads. We begin by describing development, even when the baby is too young to
interpersonal emotion transmission processes understand language (Rimé, 2009), and encourages
within parent–child dyads, including modalities bonding between infant and caregiver (Rilling,
such as touch, cry, facial expressions, and physiol- 2013). Over time, a baby learns that emitting cer-
ogy. We then move to the literature on adult couples tain emotional cues to others will elicit helping be-
and describe research on couple conflict and couple havior and facilitate getting their needs met. The
support. Finally, we conclude with recommenda- baby will also learn that certain others, especially
tions for further research. caregivers, are safe foundations, thereby creating an
enduring attachment. A healthy child learns that he
What Is Interpersonal Emotion Regulation or she can take risks, explore his or her environ-
and Dysregulation? ment, and return swiftly to his or her safe caregiver
Emotion regulation refers to the process of altering to return to a baseline emotional state.
one’s own or another’s emotional states, typically to Vital to this interpersonal process of emotion
reach a desired outcome (Gross & John, 2003; regulation is the caregiver’s ability to interpret the
Ochsner & Gross, 2005; Zaki & Williams, 2013). child’s emotional cues, respond appropriately, and
For example, two adults in a relationship might hug use affiliation rather than avoidance when an infant
and console each other when one partner is upset exhibits distress (Bowlby, 1969; Shaver & Klinnert,
about a troubling interaction at work. A parent may 1982; Dykas & Cassidy, 2011; Rilling & Young,
attempt to calm a crying infant by picking the baby 2014). The adult must be able to accurately process
up and rocking him or her back and forth. A pair of emotional cues and regulate his or her own emo-
athletes may hype each other up for competition. tions while also attending to the child’s needs
All of these are arguably adaptive interpersonal pro- (Rilling & Young, 2014; Rutherford, Wallace,
cesses that facilitate emotion regulation during chal- Laurent, & Mayes, 2015). A caregiver who struggles
lenging experiences. However, what happens when with emotion dysregulation or who has a history of
interpersonal dyadic processes are characterized by disrupted attachment relationships may struggle
emotion dysregulation? Perhaps adults in a relation- to scaffold his or her infant’s emotion regulation
ship direct their stress at each other through arguing (Dykas & Cassidy, 2011; Shah, Fonagy, & Strathearn,
instead of consoling; a parent yells at the child to 2010). Attachment researchers hypothesize that in-
stop crying instead of using touch to comfort; or dividual differences in caregiver responses to distress
athletes deflate each other’s confidence and readi- may act as a mechanism underlying transmission
ness to compete. Each interpersonal process has the of attachment patterns from caregiver to child.
potential to facilitate or hinder adaptive emotion Caregivers may be over- or underresponsive to their
regulation. Here, we review processes of interper- child’s distress, leading to intrusive or indifferent re-
sonal regulation and attunement within specific sponses instead of healthy reciprocity and syn-
types of social relationships, beginning with the chrony (Dykas & Cassidy, 2011; Feldman, 2012a).
parent–child relationship context. Interpersonal emotion regulation may begin to
occur during the transition to parenthood and early
The Role of Affiliative Bonds in Emotion postpartum period via biobehavioral feedback loops
Regulation: The Parent–Child Relationship between caregivers and infant (Feldman, Gordon,
Newborn babies are reliant upon caregivers for Schneiderman, Weisman, & Zagoory-Sharon,
physical, social, and emotional needs. Newborns 2010; Rutherford et al., 2015). Research has linked
have yet to develop language abilities and thus use mothers’ prenatal emotion dysregulation to the
emotional expression to elicit support for getting child’s behavioral functioning at three years old
their needs met. For example, a hungry baby may (Oberlander et al., 2010). Specifically, mothers who
cry to signal that he or she is hungry. A responsive were struggling with depression and taking antide-
caregiver can then meet the child’s needs by trying pressant medication during their third trimester
to decipher and respond to the newborn’s emotional were more likely to have children with internalizing
signal. With the crying baby, the caregiver may problems in early childhood. Furthermore, mothers
speak to the baby in soothing tones or pick the baby with depression in the third trimester who were also
up, providing physical contact intended to help the depressed three years postpartum had children with
baby. This use of physical contact, attention, and higher rates of externalizing symptoms (Oberlander
142 Interpersonal Processes and Emotion Dysregul ation

et al., 2010). Children exposed to prenatal anxiety contact that exhibited changes in oxytocin differed
have double the risk of internalizing and external- for mothers and fathers: mothers showed associa-
izing symptoms and conduct problems later in tions with affectionate touch (e.g., hugs, kisses),
childhood (O’Connor, Heron, Golding, Glover, & while fathers showed associations with stimulatory
ALSPAC Study Team, 2003; Van den Bergh & touch (e.g., touching infant with toys; Feldman
Marcoen, 2004). The intergenerational transmis- et al., 2010). Another form of touch linked with ox-
sion of emotion dysregulation likely has multifac- ytocin release and bonding is breastfeeding. One
eted causes, including genes, epigenetic and physi- study found that mothers who were breastfeeding,
ological effects of stress on the developing fetus, and compared to mothers who were formula-feeding,
interpersonal processes in early infancy. Importantly, had greater neural responding in brain regions asso-
adults with internalizing disorders respond differ- ciated with empathy and parent–child bonding at
ently to emotional cues, and perceive negative facial one month postpartum, and that this was related to
expressions more negatively than healthy controls more sensitive parenting (P. Kim et al., 2011). The
(Stein et al., 2010). Those with internalizing prob- authors hypothesized that a mechanism for greater
lems also have more difficulty recognizing and re- positive parenting may be the close physical contact
sponding to their own infant’s cry, showing distinct provided during breastfeeding, and that this physi-
patterns of neural recruitment relative to healthy ological touch helped regulate the mother’s own
controls (Laurent & Ablow, 2012a). emotions so that she could attune to the child’s
needs (P. Kim et al., 2011).
How Do Parents and Infants Attune? Given that touch facilitates bond formation via
Mechanisms of Interpersonal Emotion biobehavioral feedback loops, creating opportuni-
Transmission ties for caregivers to connect with their infant
Physical Touch through physical contact could support parental
During the transition to parenthood, adults ideally investment in infant rearing, which in turn could
develop an affiliative response to baby cues that oth- support development of healthy emotion regula-
erwise may have been aversive (Rilling, 2013; Rilling tion. In addition to encouraging continued parental
& Young, 2014). Physical touch has been shown to involvement, touch also plays a fundamental role in
facilitate bond formation and development of helping a child attach to the parents. Researchers
healthy attachments in mammals. Physical touch have identified the role of touch and parenting be-
between caregiver and offspring has been linked haviors as a mechanism for the cross-generational
with positive development, attachment, and transmission of oxytocin levels—supporting bond
bonding in premature infants and their parents formation, social reciprocity, empathy, and social
(Feldman, Weller, Sirota, & Eidelman, 2003). engagement in children (Feldman et al., 2010;
Greater maternal–child physical touch has also Weisman et al., 2012). Weisman and colleagues
been linked with the child having stronger brain (2012) found that intranasal oxytocin administra-
connectivity and reactivity in regions involved in the tion to fathers was linked with fathers’ increased use
regulation of emotion (Brauer, Xiao, Poulain, of touch, shared eye gaze, and synchrony with the
Friederici, & Schirmer, 2016), and mother–child infant, and that this was linked with increases in
touch acted as a stress buffer for teens (Lougheed, infant social engagement and oxytocin levels. The
Koval, & Hollenstein, 2016). Indeed, research sup- authors suggest a reciprocal association between
ports the role of physical touch in helping both parent and child biology and behavior.
child and mother regulate emotionally.
Touch may contribute to caregiver–child trans- Infant Cry
mission of emotion regulation and social readiness In addition to touch, infant vocalizations also serve
via biobehavioral feedback of the oxytocinergic as a strategy by which infants signal their needs to
system (Feldman et al., 2010; Weisman, Zagoory- caregivers. Infant cry sounds are typically regarded
Sharon, & Feldman, 2012). Another study investi- as aversive and unpleasant, and yet caregivers must
gating the role of oxytocin and parent-specific tactile override their emotional responses to their infant’s
contact found that both mothers and fathers have cries to soothe the infant effectively. One of the
similar baseline levels of oxytocin, with relative most basic functions of infant cry is to ensure prox-
increases seen after experiencing touch with the imity of their caregiver; infants cry more when away
infant (Feldman et al., 2010). The type of tactile from their mothers (Bell & Ainsworth, 1972), and
Stoycos, Corner, Khaled, and Saxbe 143

mothers can recognize their own infant’s cry (Proverbio, Brignone, Matarazzo, Del Zotto, &
(Formby, 1967), suggesting that the communicative Zani, 2006) and have heightened reactivity to
function of infant cry is reciprocal and bidirectional. infant affect (Nishitani, Doi, Koyama, & Shinohara,
Although some species can generate cry sounds that 2011). This suggests that parenthood may promote
indicate specific needs (e.g., hunger vs. separation heightened awareness of infant facial cues.
vs. cold), human cry sounds can be more challeng- Individual differences in parent ability to accurately
ing to differentiate, which requires that caregivers identify and respond with affiliative behavior to
identify potential sources of their child’s distress. infant distress faces and cues may be tied with the
The challenge of interpreting infant distress can child’s emotion regulation development. For exam-
frustrate caregivers, especially for those with poor ple, infants of mothers with internalizing disorders
emotion regulation skills (Barr, 2012). (e.g., depression) exhibit heightened reactivity to
Although in most cases caregivers are able to angry faces and less synchrony with their mothers
learn to effectively reduce their children’s distress, (Feldman, 2012a). Similarly, researchers have found
excessive infant crying is known to be one of the differential neural responses in new parents, based
most frequent triggers of child abuse (Carbaugh, on the type of attachment behavior exhibited by the
2004). The physiological hyperreactivity hypothesis infant (Laurent & Ablow, 2012b). For example,
suggests that parents’ excessive psychophysiological mothers of infants exhibiting insecure attachment
reactivity to children’s distress might motivate ag- behaviors maintained greater activation in brain re-
gressive and abusive parenting behavior (McCanne gions linked to emotional saliency, pain, and emo-
& Hagstrom, 1996); in other words, parents who tional memory in response to their infant’s cry (see
become overaroused by cry sounds may be unable Laurent & Ablow, 2012b for full results). This re-
to modulate their own and their children’s distress. search highlights again the bidirectional relation
Similar accounts have focused on cognitive rather between parent and child development of emotion
than physiological processes, suggesting that par- regulation, behavior, and physiology.
ents’ interpretations of infant cry as hostile or inten-
tionally annoying may also heighten risk for abuse Stress Physiology
(Crouch, Skowronski, Milner, & Harris, 2008). Adrenocortical attunement, or linkage in the stress
Although the literature on how parents respond to hormone cortisol, which is produced by the limbic-
infant cry sounds is relatively small, there is some hypothalamic-pituitary-adrenal (L-HPA) axis, has
evidence that autonomic (e.g., skin conductance), been observed in parent–child dyads (Granger et al.,
behavioral (e.g., handgrip force), and affective (e.g., 1998; Hibel, Granger, Blair, & Cox, 2009; Hibel,
frustration and annoyance) reactivity to crying are Granger, Blair, Finegood, & The Family Life Project
all associated with risk for child abuse (Reijman Key Investigators, 2015; Papp, Pendry, & Adam,
et al., 2016). Although not all frustrated caregivers 2009). This may represent a modality by which
will maltreat their infants, caregiver reactivity to parents and children transmit stress or arousal
infant distress may represent a form of interpersonal states to each other. Although some studies have
emotion dysregulation with a range of consequences suggested that L-HPA axis linkage is stronger when
for the caregiver–infant bond. parent–child dyads show more sensitivity, proxim-
ity, and closeness (Atkinson et al., 2013; Sethre-
Facial Expressions Hofstad, Stansbury, & Rice, 2002; van Bakel &
Infant facial expressions represent another salient Riksen-Walraven, 2008), other studies have found
infant cue by which emotion is transmitted within heightened L-HPA axis linkage within high-stress
caregiver–child dyads. The ability of parents to track contexts such as domestic violence (Hibel et al.,
and respond to their infant’s facial expressions has 2009) and maternal depression (Laurent, Ablow, &
been linked with stronger coordination of physio- Measelle, 2011). Similarly, several studies have re-
logical systems (heart rate in mother in infant) and ported stronger parent–child L-HPA linkage when
shows similar positive feedback loops as touch does, parents show lower levels of sensitivity and reciproc-
but without touch being required (Feldman, ity with their children (Pratt et al., 2017; Saxbe
2012b). Studies examining parent response to emo- et al., 2017) and when dyads report higher levels of
tional infant faces have found that parents, com- negative affect (Papp et al., 2009). Several studies
pared to nonparents, are better at discerning changes using experimental designs have added to this liter-
in the degree of distress level on an infant face ature. In one, mothers of infants were randomized

to either a negative or positive evaluation task within parent–child dyads, friendship dyads, and
(Waters, West, & Mendes, 2014). Both tasks elicited group dynamics. Thus, many insights from research
physiological reactivity in mothers, but mothers’ on couples may generalize to other interpersonal
reactivity only transmitted to infants—that is, contexts.
predicted infants’ physiological reactivity upon re-
union—in the negative evaluation condition. In a Physiological Stress Contagion within
follow-up study, the extent of transmission between Couples
mothers and infants was moderated by touch, such As with the parent–child literature, a growing
that infants who sat in their mothers’ lap showed number of researchers have found evidence for
stronger physiological linkage than infants who physiological linkage within couples. For example,
were in a high chair during the task (Waters, West, in a study in which married couples provided mul-
Karnilowicz, & Mendes, 2017). tiple cortisol samples a day over three days, Saxbe
In another study, researchers randomized moth- and Repetti (2010) found positive correlations be-
ers to a positive or a conflictual discussion with their tween husbands and wives. This finding has been
romantic partners (Hibel & Mercado, 2017). replicated by other researchers, both within natural-
Maternal cortisol reactivity to the conflict task, but istic daily diary studies (Liu, Rovine, Klein, &
not to the positive task, predicted infants’ cortisol Almeida, 2013; Papp, Pendry, Simon, & Adam,
reactivity to an in-lab challenge. These experimen- 2013) and in laboratory studies (Laws, Sayer,
tal studies corroborate naturalistic findings that Pietromonaco, & Powers, 2015; Saxbe et al., 2014).
parent–infant physiological transmission is bol- Within the couples’ literature, physiological linkage
stered within stressful contexts. Shared stress re- within systems associated with stress responding
sponses may be adaptive from an evolutionary (e.g., sympathetic and L-HPA systems) has been
perspective, helping to convey information about most consistently associated with relationship dys-
risky environments that might require heightened function (Timmons, Margolin, & Saxbe, 2015).
vigilance. However, chronic physiological stress Positive associations in cortisol have been linked
contagion may represent a form of interpersonal with relationship distress (Liu et al., 2013; Saxbe &
emotion dysregulation in which dyads fail to Repetti, 2010), intimate partner aggression (Saxbe
regulate, and instead exacerbate, each other’s
et al., 2015), and decreased empathy and increased
stress states. risk of relationship dissolution (Schneiderman,
Kanat-Maymon, Zagoory-Sharon, & Feldman,
The Role of Affiliative Bonds in Emotion 2014). Levenson and Gottman (1983) have sug-
Regulation: Romantic Partner Relationships gested that more strongly linked couples engage in
Parent–child relationships are typically the first negative affect reciprocity, in which partners become
meaningful attachment relationship and serve as a locked in escalating exchanges of negative emotion
staging ground for emerging emotion regulation and stress. In other words, rather than modulating
and dysregulation. However, individuals form other each other’s negative emotions or stress states, dyads
close affiliations across the lifespan that continue to that show stronger linkage may be more reactive to
contribute to interpersonal emotion regulation and each other and show stress contagion rather than
dysregulation (Rutherford et al., 2015; Crowell, stress buffering. In keeping with this idea, a study of
Puzia, & Yaptangco, 2015). In many adults, the parents of an infant found that stronger L-HPA axis
couple relationship becomes central, serving as a linkage between the members of the couple was as-
“stable base” for growth and exploration while also sociated with greater risk of intimate partner aggres-
providing a consistent interpersonal context for sion (Saxbe et al., 2015).
processing emotional experiences. Many of the
same modalities reviewed earlier—touch, vocaliza- Negative Emotion and Conflict within
tion, facial expressions, and physiology—help to Couples
transmit emotions between partners. In addition, All close relationships inevitably include conflict; cou-
researchers have studied two types of couple interac- ples’ ability to manage and rebound from conflict is a
tion that are relevant to emotion dysregulation: crucial feature of a successful, satisfying relationship.
conflict and support. Conflict may escalate, and Individuals who have difficulty regulating internal
support may buffer, interpersonal emotion dysregu- emotional experiences may be more likely to experi-
lation. Conflict and support are also important ence negative affect and interpersonal conflict. Indeed,

emotion dysregulation may mediate intergenerational a critical factor in understanding how partners’
transmission of relationship conflict, as exemplified personalities affect their satisfaction with one another.
by one study finding that the children of parents with Difficulty regulating emotions during conflict
poor emotion regulation skills were more likely to can affect relationship satisfaction, and repeated
show emotion dysregulation themselves, which in emotion dysregulation can increase risk for intimate
turn predicted greater interpartner conflict in their partner violence. Factors related to intimate partner
adult romantic relationships (H. K. Kim, Pears, aggression include an inability to manage extreme
Capaldi, & Owen, 2009). However, the amount of emotional reactions such as intense anger, losing
conflict is not the only factor that predicts poor re- control, and difficulty with verbal expression (see
lationship outcomes. Failure to effectively handle Neal & Edwards, 2015 for a full review). Adolescent
disagreements and prevent conflict escalation is also couples in which at least one partner is psychologi-
important (Seiffge-Krenke & Burk, 2015). Emotion cally or physically aggressive exhibit more jealousy,
dysregulation within couple conflict is an important higher rates of conflict, and more maladaptive
marker of dissatisfaction within the relationship coping strategies (Seiffge-Krenke & Burk, 2015).
and may be a precursor to more detrimental and Not surprisingly, adolescent partners who are
dangerous behaviors, such as partner aggression mutually aggressive show the poorest relationship
and violence. functioning, emotion dysregulation, high levels of
Emotion dysregulation tends to have a cyclical conflict, lack of trust and acceptance for their partner,
relationship with negative emotionality. An individ- and lack of insight. Similarly, distressed married
ual who struggles to effectively integrate emotional couples tend to engage in negative and aggressive
experiences may express more negative affect, poten- interactions and are unable to manage their con-
tially due to the link between developmental forma- flicts constructively, exemplifying difficulty with
tion of emotion dysregulation and later internalizing emotion dysregulation (Goldstein, 2011; O’Leary
disorders or insecure attachments (Rutherford et al., et al., 1989). This can trigger a vicious cycle, in
2015; Zimmer-Gembeck et al., 2017). In the midst which emotion dysregulation leads to distress, and
of intense negative affect, individuals may have diffi- partners experiencing relational distress consequently
culty managing these negative emotions, and thus struggle to manage disagreements and emotional
become dysregulated. Additionally, partners’ nega- reactions. Therefore, targeting emotion dysregula-
tive moods can be “contagious,” and couples who are tion within couples can be a valuable point of
dissatisfied may intensify one another’s negative intervention to help diminish relationship distress,
affect. For example, using daily diary data, Saxbe and contagion of negative mood states, and subsequent
Repetti (2010) found that individuals’ negative risk for intimate partner violence.
mood states were associated with their partners’ neg-
ative mood states at the same time. However, within- Supportive Interactions within Couples
couple correlations in negative mood were weaker Although a troubled marriage can lead to emotional
among couples who reported higher relationship sat- and physiological dysregulation and depression and
isfaction, suggesting that relationship quality can have a negative impact on health (Robles & Kiecolt-
buffer negative mood transmission within couples. Glaser, 2003; Whisman, 2001), a satisfying relation-
Thus, couple characteristics may prevent negative ship can potentially be helpful or even protective
moods from escalating into conflict. Additionally, (Cutrona, 1996). When dealing with stress, sadness,
some characteristics of each partner may impact re- or other negative emotions, supportive interactions
lationship satisfaction, such as individual personality with a spouse or significant other may have an ame-
and compatibility of both partners’ personalities. liorative effect. In fact, research suggests that mar-
While personality shapes the way an individual in- ried people, on the whole, tend to live longer than
teracts with and responds to his or her partner, it also nonmarried individuals (Manzoli, Villari, Pirone, &
affects his or her ability to regulate internal emo- Boccia, 2007), which suggests that beneficial pro-
tional experiences. Vater and Schröder-Abé (2015) cesses may be occurring in the marital context.
found that emotion regulation during a laboratory Researchers have operationalized supportive pro-
couple conflict discussion mediated the association cesses in a variety of ways and have studied support
between personality and long-term relationship sat- across contexts and populations. We focus on the
isfaction, indicating that a couple’s ability to regulate importance of support in two contexts in which
their emotional reactions during disagreements is there is high risk for emotion dysregulation and

in which couples typically encounter challenges suggests that support may be more valuable for
together: illness and the transition to parenthood. women than men (Kiecolt-Glaser & Newton,
Next, we review specific processes through which 2001).
partners can help each other in adverse circum-
stances. Support from a Partner during the
Transition to Parenthood
Support from a Partner during Illness Pregnancy and the transition to parenthood is an-
Several studies have begun to illuminate effects of other critical time for research on partner support.
partner support in times of illness and disentangle Much of this research has focused on support pro-
unique effects of different types of support. For the vided by men when their partners are pregnant or
purposes of this chapter, we will focus on couples soon after the birth of their child. A longitudinal
coping with a partner with cancer. A qualitative study focusing specifically on effective social sup-
study of women with a life-threatening diagnosis of port, which includes indices of both quality and
cancer found that type of support was important, quantity, found that partner support was associated
with emotional support being the most commonly with less concurrent anxiety and reductions in
desired and offered. Furthermore, “mutuality” in anxiety across pregnancy (Rini, Dunkel Schetter,
romantic relationships, which is defined as a recip- Hobel, Glynn, & Sandman, 2006). Additionally,
rocal intellectual and emotional openness between perceptions of effective social support were pre-
partners, was also highly valued (Sormanti & dicted by both individual (e.g., attachment,
Kayser, 2000). In addition to emotional support, individualism–collectivism orientation) and couple-
other kinds of support (i.e., informational support level characteristics (e.g., intimacy, equity), sug-
and instrumental support) are valuable for women gesting that perceptions of effective support may be
coping with a breast cancer diagnosis and treatment influenced by the personality and experiences of
(Kinsinger, Laurenceau, Carver, & Antoni, 2011). the person reporting it. Furthermore, a qualitative
Specifically, perceptions of emotional and instru- study found that partner support continues to be
mental support from a partner were associated with important in childbirth experiences, with female
concurrent and longitudinal relationship satisfac- partners endorsing the value of their partner’s pres-
tion. Moreover, emotional and informational sup- ence and support provided by the partner during
port were associated with fewer sexual difficulties birth (Somers-Smith, 1999).
following treatment. Emotional support from a ro- The postpartum period is another time of high
mantic partner is also helpful for women recently stress. Thorp, Krause, Cukrowicz, and Lynch (2004)
diagnosed with breast cancer (Pistrang & Barker, found that mothers who were unsatisfied with their
1995). Importantly, however, the mere provision of partners’ support, specifically instrumental support,
support may not be sufficient to affect adjustment experienced more stress. This association was par-
in illness. Rini and colleagues (2011) found that tially mediated by demand–withdraw communica-
quality of partner support, rather than quantity of tion, suggesting that this kind of interaction pattern
support, was associated with less distress in patients may be particularly problematic. Many new moth-
who received hematopoietic stem cell transplanta- ers also experience symptoms of postpartum depres-
tion. The relation between perceived partner sup- sion. Misri, Kostaras, Fox, and Kostaras (2000)
port and psychosocial adjustment may also be bidi- tested the impact of partner involvement in treat-
rectional; higher levels of partner-provided ment of postpartum depression in a randomized
emotional support predict subsequent depressive controlled trial. Specifically, new fathers attended
symptoms, but depressive symptoms also predict several sessions with their partners, and interven-
subsequent perceptions of support (Talley, Molix, tion content included psychoeducation around in-
Schlegel, & Bettencourt, 2010). Individual charac- strumental support and positive interactions. They
teristics may also be important in determining the found that, compared with treatment that did not
effects of partner support. For example, partner include a partner, women receiving this interven-
support appears to be a stronger predictor of health- tion showed greater improvements in postpartum
related quality of life in female compared with male depressive symptoms. In a related study, women ex-
cancer patients (Gustavsson-Lilius, Julkunen, & periencing the loss of a pregnancy endorse a desire
Hietanen, 2007), a finding that is consistent with for support from their partner (Corbet-Owen,
literature on social support and marriage, which 2003). This is consistent with research showing that

avoiding talking about the shared loss of a child and Rogge (2017) found an association between
tends to predict higher levels of grief in one’s partner expressions of compassion and emotional well-being
(Stroebe et al., 2013). for both partners. Another recent study found that
partners’ moment-to-moment displays of compas-
Behaviors Underlying Support sion moderated concordance in heart rates over the
from a Partner course of a discussion about an emotionally signifi-
In addition to elucidating the consequences of part-
cant loss experience. Specifically, couples’ heart rates
ner support, it is important to determine the char-
were more closely linked when the partner listening
acteristics of a supportive interaction. This enables
to a loss experience was being less compassionate
us to discuss what support looks like in real life and
(Corner et al., 2018). This same study found that
on a moment-to-moment basis. Kirschbaum,
partners sharing a loss exhibited decreases in heart
Klauer, Filipp, and Hellhammer (1995) studied the
rate over the course of the discussion, whereas part-
effect of partner support before a version of the Trier
ners listening to a loss showed increases.
Social Stress Test, a laboratory paradigm in which
Overall, the empirical literature supports the
participants were required to speak in front of a
value of positive interactions in couples. Thus, not
panel about their qualifications for a hypothetical
only can negative interactions contribute to devel-
vacant job position. They instructed partners to be
opment of emotion dysregulation, but also positive
as helpful as possible during the ten minutes leading
interactions may be helpful or even protective.
up to this task, provided psychoeducation about
A variety of processes may occur in the context of a
emotional and instrumental support, and told part-
supportive interaction between partners. These in-
ners to use their own understanding of the partici-
clude the provision of emotional, instrumental,
pants’ coping preferences to inform how they pro-
and information support, as well as the expression
vide support. Men, but not women, showed an
of compassion. Importantly, it is also possible that
attenuated physiological stress response (i.e., less of
partner support, in certain instances, can be exces-
an increase in cortisol after the task) when sup-
sive (Brock & Lawrence, 2009), and provision of
ported by their partners. Importantly, supportive
support may be most effective when it is accom-
partners were instructed to avoid physical touch,
plished subtly and when it goes unnoticed by the
and when Ditzen and colleagues (2007) used a sim-
recipient (i.e., “invisible support”; Bolger, Zuckerman,
ilar Trier Social Stress paradigm but included both
& Kessler, 2000). This suggests that determining
“verbal support” and “physical contact” conditions,
what kind of partner support is “effective” is likely
they found that women showed lower heart rates
complicated. Additionally, associations between
and cortisol responses to stress when they received
partner support and psychological outcomes appear
physical touch from their partners. Thus, an effec-
to be bidirectional, and a variety of individual and
tive supportive interaction may look different for
relationship characteristics influence the provision
men and women.
of, perceptions of, and responses to partner support,
Another study examining partner support in a
including attachment styles of both members of the
conflict discussion behaviorally coded positive
dyad (Cobb, Davila, & Bradbury, 2001; Simpson,
emotional and instrumental supportive behavior,
Rholes, & Nelligan, 1992). Future research needs to
defined on the Social Support Interaction Coding
continue studying moment-to-moment behavioral
System as reassurance, consoling, encouragement,
components of supportive interactions between
and helpful suggestions or advice (Pasch, Harris,
partners, as well as moderators and mediators of as-
Sullivan, & Bradbury, 2004). The authors found
sociations between partner support and psychoso-
that higher levels of partner support in a conflict
cial outcomes.
discussion conducted soon after marriage were as-
sociated with lower levels of negative emotion in Conclusion
a subsequent conflict discussion one year later In conclusion, emotion regulation and dysregula-
(Sullivan, Pasch, Johnson, & Bradbury, 2010). This tion are deeply interpersonal processes. These pro-
study also provided preliminary evidence that posi- cesses may first develop within the scaffolding
tive emotions, including empathy, may mediate the provided by parent–child relationships, and then
association between partner support and later mari- continue to evolve within other close relationships
tal satisfaction and stability. A related literature sug- such as romantic couple relationships in adulthood.
gests the importance of exhibited compassion be- Both parent–child and couple relationships are
tween partners. In a daily diary study, Reis, Maniaci, characterized by social synchrony (Feldman, 2007),

or the reciprocal exchange of nonverbal cues within Bowlby, J. (1969). Attachment and loss: Vol. 1. Attachment.
interpersonal interactions. Atzil, Hendler, and New York, NY: Basic Books.
Brauer, J., Xiao, Y., Poulain, T., Friederici, A. D., & Schirmer, A.
Feldman (2014) suggest that social synchrony is (2016). Frequency of maternal touch predicts resting activity
learned initially in parent–child dyads and then and connectivity of the developing social brain. Cerebral
generalizes, affecting a person’s ability to engage in Cortex, 26, 3544–3552.
supportive, empathic, and satisfying relationships as Brock, R. L., & Lawrence, E. (2009). Too much of a good thing:
an adult. The ability to coordinate nonverbal cues Underprovision versus overprovision of partner support.
Journal of Family Psychology, 23, 181–192.
and responses with a partner can facilitate forma- Carbaugh, S. F. (2004). Understanding shaken baby syndrome.
tion of affiliative bonds and may depend on skilled Advanced Neonatal Care, 4, 105–116.
detection and regulation of one’s own and others’ Cobb, R. J., Davila, J., & Bradbury, T. N. (2001). Attachment
emotional states. The coordination or regulation of security and marital satisfaction: The role of positive
cues can extend “under the skin” and include stress perceptions and social support. Personality and Social
Psychology Bulletin, 27, 1131–1143.
physiology (Timmons, Margolin, & Saxbe, 2015) in Corbet-Owen, C. (2003). Women’s perceptions of partner
addition to touch, vocalization, and facial expres- support in the context of pregnancy loss(es). South African
sion. Within the couples’ literature, research on Journal of Psychology, 33, 19–27.
conflict and support helps to elucidate a range of Corner, G. W., Saxbe, D. E., Chaspari, T., Rasmussen, H. F.,
interactions that facilitate emotional expression and Perrone, L., Pettit, C., . . . Margolin, G. (2018). Compassion in
a heartbeat: Physiology during couples’ loss discussions. Journal
regulation within dyads. of Social and Personal Relationships. Advance online publication.
Individual differences in affiliative response to Crouch, J. L., Skowronski, J. J., Milner, J. S., & Harris, B.
distress cues are closely tied with disruptions in social (2008). Parental responses to infant crying: The influence of
synchrony. For example, in postpartum depression child physical abuse risk and hostile priming. Child Abuse
or other clinical disorders, there may be a disruption and Neglect, 32, 702–710.
Crowell, S. E., Puzia, M. E., & Yaptangco, M. (2015). The
in coordination of behavioral responses within ontogeny of chronic distress: Emotion dysregulation across
dyads, which perturbs biobehavioral feedback loops, the life span and its implications for psychological and
potentially perpetuating emotion dysregulation. physical health. Current Opinion in Psychology, 3, 91–99.
Finally, although shaped by early attachment experi- Cutrona, C. E. (1996). Social support in couples. Thousand Oaks,
ences, emotion regulation skills are potentially mu- CA: SAGE Publications.
Darwin, C. (1872). The expression of emotions in man and animals.
table in adulthood and may be an important target London, England: Murray.
for intervention. Many psychotherapies, such as dia- Ditzen, B., Neumann, I. D., Bodenmann, G., von Dawans, B.,
lectical behavior therapy, specifically focus on emo- Turner, R. A., Ehlert, U., & Heinrichs, M. (2007). Effects of
tion recognition, expression, and regulation within different kinds of couple interaction on cortisol and heart
interpersonal contexts (Linehan, Tutek, Heard, & rate responses to stress in women. Psychoneuroendocrinology,
32, 565–574.
Armstrong, 1994). Future research could explore Dykas, M. J., & Cassidy, J. (2011). Attachment and the processing
short-term and long-term implications of interper- of social information across the life span: Theory and
sonal emotion dysregulation, including the potential evidence. Psychological Bulletin, 137, 19–46.
intergenerational transmission of emotion dysregu- Ekman, P. (1992). Are there basic emotions? Psychological Review,
lation from parents to children. 99, 550–553.
Ekman, P. (1993). Facial expression and emotion. American
Psychologist, 48, 384–392.
References Feldman, R. (2007). Parent-infant synchrony and the
Atkinson, L., Gonzalez, A., Kashy, D. A., Santo Basile, V., construction of shared timing: Physiological precursors,
Masellis, M., Pereira, J., & Levitan, R. (2013). Maternal developmental outcomes, and risk conditions. Journal of
sensitivity and infant and mother adrenocortical function Child Psychology and Psychiatry, 48, 329–354.
across challenges. Psychoneuroendocrinology, 38, 2943–2951. Feldman, R. (2012a). Oxytocin and social affiliation in humans.
Atzil, S., Hendler, T., & Feldman, R. (2014). The brain basis of Hormones and Behavior, 61, 380–391.
social synchrony. Social Cognitive and Affective Neuroscience, Feldman, R. (2012b). Parent–infant synchrony: A biobehavioral
9, 1193–1202. model of mutual influences in the formation of affiliative
Barr, R. G. (2012). Preventing abusive head trauma resulting bonds. Monographs of the Society for Research in Child
from a failure of normal interaction between infants and Development, 77, 42–51.
their caregivers. Proceedings of the National Academy of Feldman, R., Gordon, I., Schneiderman, I., Weisman, O., &
Sciences, 109, 17294–17301. Zagoory-Sharon, O. (2010). Natural variations in maternal and
Bell, S. M., & Ainsworth, M. D. S. (1972). Infant crying and paternal care are associated with systematic changes in oxytocin
maternal responsiveness. Child Development, 43, 1171–1190. following parent-infant contact. Psychoneuroendocrinology, 35,
Bolger, N., Zuckerman, A., & Kessler, R. C. (2000). Invisible 1133–1141.
support and adjustment to stress. Journal of Personality and Feldman, R., Weller, A., Sirota, L., & Eidelman, A. I. (2003).
Social Psychology, 79, 953–961. Testing a family intervention hypothesis: The contribution of

mother-infant skin-to-skin contact (kangaroo care) to family stress response profiles. Developmental Psychopathology, 23,
interaction, proximity, and touch. Journal of Family 521–538.
Psychology, 17, 94–107. Laws, H. B., Sayer, A. G., Pietromonaco, P. R., & Powers, S. I.
Formby, D. (1967). Maternal recognition of infant’s cry. (2015). Longitudinal changes in spouses’ HPA responses:
Developmental Medicine and Child Neurology, 9, 293–98. Convergence in cortisol patterns during the early years of
Goldstein, S. E. (2011). Relational aggression in young adults’ marriage. Health Psychology, 34, 1076–1089.
friendships and romantic relationships. Personal Relationships, Levenson, R. W., & Gottman, J. M. (1983). Marital interaction:
18, 645–656. Physiological linkage and affective exchange. Journal of
Granger, D. A., Serbin, L. A., Schwartzman, A. E., Lehoux, P., Personality and Social Psychology, 45, 587–597.
Cooperman, J., & Ikeda, S. (1998). Children’s salivary Linehan, M. M., Tutek, D. A., Heard, H. L., & Armstrong,
cortisol, internalizing behavior problems, and family H. E. (1994). Interpersonal outcome of cognitive behavioral
environment: Results from the Concordia Longitudinal treatment for chronically suicidal borderline patients.
Risk Project. International Journal of Behavioral Development, American Journal of Psychiatry, 151, 1771–1776.
22, 707–728. Liu, S., Rovine, M. J., Klein, L. C., & Almeida, D. M. (2013).
Gross, J. J., & John, O. P. (2003). Individual difference in Synchrony of diurnal cortisol pattern in couples. Journal of
two emotion regulation processes: Implications for affect, Family Psychology, 27, 579–588.
relationships, and well-being. Journal of Personality and Lougheed, J. P., Koval, P., & Hollenstein, T. (2016). Sharing the
Social Psychology, 85, 348–362. burden: The interpersonal regulation of emotional arousal in
Gustavsson-Lilius, M., Julkunen, J., & Hietanen, P. (2007). mother-daughter dyads. Emotion, 16, 83–93.
Quality of life in cancer patients: The role of optimism, Manzoli, L., Villari, P., Pirone, G. M., & Boccia, A. (2007).
hopelessness, and partner support. Quality of Life Research, Marital status and mortality in the elderly: A systematic review
16, 75–87. and meta-analysis. Social Science and Medicine, 64, 77–94.
Harlow, H. F. (1959). Love in infant monkeys. Scientific McCanne, T. R., & Hagstrom, A. H. (1996). Physiological
American, 200, 68–74. hyperreactivity to stressors in physical child abusers and
Hibel, L. C., Granger, D. A., Blair, C., & Cox, M. J. (2009). individuals at risk for being physically abusive. Aggression and
Intimate partner violence moderates the association between Violent Behavior, 1, 345–358.
mother–infant adrenocortical activity across an emotional Misri, S., Kostaras, X., Fox, D., & Kostaras, D. (2000). The
challenge. Journal of Family Psychology, 23, 615–625. impact of partner support in the treatment of postpartum
Hibel, L. C., Granger, D. A., Blair, C., Finegood, E. D., & The depression. Canadian Journal of Psychiatry, 45, 554–558.
Family Life Project Key Investigators. (2015). Maternal-child Neal, A. M., & Edwards, K. M. (2015). Perpetrators’ and victims’
adrenocortical attunement in early childhood: Continuity attributions for IPV: A critical review of the literature.
and change. Developmental Psychobiology, 57, 83–95. Trauma, Violence, & Abuse, 18, 239–267.
Hibel, L. C., & Mercado, E. (2017). Marital Conflict Predicts Nishitani, S., Doi, H., Koyama, A., & Shinohara, K. (2011).
Mother-to-Infant Adrenocortical Transmission. Child Differential prefrontal response to infant facial emotions in
Development, 1–16. mothers compared with non-mothers. Neuroscience Research,
Kiecolt-Glaser, J. K., & Newton, T. L. (2001). Marriage and 70, 183–188.
health: His and hers. Psychological Bulletin, 127, 472–503. Oberlander, T. F., Papsdorf, M., Brain, U. M., Misri, S., Ross,
Kim, H. K., Pears, K. C., Capaldi, D. M., & Owen, L. D. C., & Grunau, R. E. (2010). Prenatal effects of selective
(2009). Emotion dysregulation in the intergenerational serotonin reuptake inhibitor antidepressants, serotonin
transmission of romantic relationship conflict. Journal of transporter promoter genotype (SLC6A4), and maternal
Family Psychology, 23, 585. mood on child behavior at 3 years of age. Archives of Pediatric
Kim, P., Feldman, R., Mayes, L. C., Eicher, V., Thompson, N., Adolescent Medicine, 164, 444–451.
Leckman, J. F., & Swain, J. E. (2011). Breastfeeding, brain Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of
activation to own infant cry, and maternal sensitivity. Journal emotion. Trends in Cognitive Sciences, 9, 242–249.
of Child Psychology and Psychiatry, 52, 907–915. O’Connor, T. G., Heron, J., Golding, J., Glover, V., & ALSPAC
Kinsinger, S. W., Laurenceau, J., Carver, C. S., & Antoni, M. Study Team (2003). Maternal antenatal anxiety and
(2011). Perceived partner support and psychosexual adjustment behavioral/emotional problems in children: A test of a
to breast cancer. Psychology and Health, 26, 1571–1588. programming hypothesis. Journal of Child Psychology and
Kirschbaum, C., Klauer, T., Filipp, S. H., & Hellhammer, D. H. Psychiatry, 44, 1025–1036.
(1995). Sex-specific effects of social support on cortisol and O’Leary, K. D., Barling, J., Arias, I., Rosenbaum, A., Malone, J.,
subjective responses to acute psychological stress. Psychosomatic & Tyree, A. (1989). Prevalence and stability of marital
Medicine, 57, 23–31. aggression between spouses: A longitudinal analysis. Journal
Laurent, H. K., & Ablow, J. C. (2012a). A cry in the dark: of Consulting and Clinical Psychology, 57, 263–268.
Depressed mothers show reduced neural activation to their Papp, L. M., Pendry, P., & Adam, E. K. (2009). Mother-
own infant’s cry. Social Cognitive and Affective Neuroscience, adolescent physiological synchrony in naturalistic settings:
7, 125–134. Within-family cortisol associations and moderators. Journal
Laurent, H. K., & Ablow, J. C. (2012b). The missing link: of Family Psychology, 23, 882–894.
Mothers’ neural response to infant cry related to infant Papp, L. M., Pendry, P., Simon, C. D., & Adam, E. K. (2013).
attachment behaviors. Infant Behavior and Development, 35, Spousesʼ cortisol associations and moderators: Testing
761–772. physiological synchrony and connectedness in everyday life.
Laurent, H. K., Ablow, J. C., & Measelle, J. (2011). Risky shifts: Family Process, 52, 284–298.
How the timing and course of mothers’ depressive symptoms Pasch, L. A., Harris, K. M., Sullivan, K. T., & Bradbury, T. N.
across the perinatal period shape their own and infants’ (2004). The social support interaction coding system. In

P. Kerig & D. Baucom (Eds.), Couple observational coding hormones shape conflict dialog and relationship duration
systems. Mahwah, NJ: Lawrence Erlbaum. at the initiation of romantic love. Social Neuroscience, 9,
Pistrang, N., & Barker, C. (1995). The partner relationship in 337–351.
psychological response to breast cancer. Social Science and Seiffge-Krenke, I., & Burk, W. J. (2015). “Bad romance”: Links
Medicine, 40, 789–797. between psychological and physical aggression and
Pratt, M., Apter-Levi, Y., Vakart, A., Kanat-Maymon, Y., relationship functioning in adolescent couples. Behavioral
Zagoory-Sharon, O., & Feldman, R. (2017). Mother-child Science, 5, 305–323.
adrenocortical synchrony: Moderation by dyadic relational Sethre-Hofstad, L., Stansbury, K., & Rice, M. A. (2002).
behavior. Hormones and Behavior, 89, 167–175. Attunement of maternal and child adrenocortical response to
Proverbio, A. M., Brignone, V., Matarazzo, S., Del Zotto, M., & child challenge. Psychoneuroendocrinology, 27, 731–747.
Zani, A. (2006). Gender and parental status affect the visual Shah, P. E., Fonagy, P., & Strathearn, L. (2010). Is attachment
cortical response to infant facial expression. Neuropsychologia, transmitted across generations? The plot thickens. Clinical
44, 2987–2999. Child Psychology and Psychiatry, 15, 329–345.
Reijman, S., Bakermans-Kranenburg, M. J., Hiraoka R., Crouch, Shariff, A. F., & Tracy, J. L. (2011). What are emotion expressions
J. L., Milner, J. S., Alink, L. R. A. & van IJzendoorn, M. H. for? Current Directions in Psychological Science, 20, 395–399.
(2016). Baseline functioning and stress reactivity in Shaver, P., & Klinnert, M. (1982). Schachter’s theories of
maltreating parents and at-risk adults: Review and meta- affiliation and emotion: Implications of developmental
analyses of autonomic nervous system studies, Child research. Review of Personality and Social Psychology, 3, 37–71.
Maltreatment, 21(4), 327–342. Simpson, J. A., Rholes, W. S., & Nelligan, J. S. (1992). Support
Reis, H. T., Maniaci, M. R., & Rogge, R. D. (2017). seeking and support giving within couples in an anxiety-
Compassionate acts and everyday emotional well-being provoking situation: The role of attachment styles. Journal of
among newlyweds. Emotion, 17, 751–763. Personality and Social Psychology, 62, 434–446.
Rilling, J. K. (2013). The neural and hormonal basis of human Somers-Smith, M. J. (1999). A place for the partner? Expectations
parental care. Neuropsychologia, 51, 731–747. and experiences of support during childbirth. Midwifery, 15,
Rilling, J. K., & Young, L. J. (2014). The biology of mammalian 101–108.
parenting and its effect on offspring social development. Sormanti, M., & Kayser, K. (2000). Partner support and changes
Science, 345, 771–776. in relationships during life-threatening illness: Women’s
Rimé, B. (2009). Emotion elicits the social sharing of emotion: perspectives. Journal of Psychosocial Oncology, 18, 45–66.
Theory and empirical review. Emotion Review, 1, 60–85. Stein, A., Arteche, A., Lehtonen, A., Craske, M., Harvey, A.,
Rini, C., Dunkel Schetter, C., Hobel, C. J., Glynn, L. M., & Counsell, N., & Murray, L. (2010). Interpretation of infant
Sandman, C. A. (2006). Effective social support: Antecedents facial expression in the context of maternal postnatal
and consequences of partner support during pregnancy. depression. Infant Behavior and Development, 33, 273–278.
Personal Relationships, 13, 207–229. Stroebe, M., Finkenauer, C., Wijngaards-de Meij, L., Schut, H.,
Rini, C., Redd, W. H., Austin, J., Moster, C. E., Meschian, van den Bout, J., & Stroebe, W. (2013). Partner-oriented
Y. M., Isola, L., & DuHamel, K. N. (2011). Effectiveness of self-regulation among bereaved parents: The costs of holding
partner social support predicts enduring psychological in grief for the partner’s sake. Psychological Science, 24,
distress after hematopoietic stem cell transplantation. Journal 395–402.
of Consulting and Clinical Psychology, 79, 64–74. Sullivan, K. T., Pasch, L. A., Johnson, M. D., & Bradbury, T. N.
Robles, T. F., & Kiecolt-Glaser, J. K. (2003). The physiology of (2010). Social support, problem-solving, and the longitudinal
marriage: Pathways to health. Physiology and Behavior, 79, course of newlywed marriage. Journal of Personality and
409–416. Social Psychology, 98, 631–644.
Rutherford, H. J. V., Wallace, N. S., Laurent, H. K., & Mayes, Susskind, J. M., Lee, D. H., Cusi, A., Feiman, R., Grabski, W.,
L. C. (2015). Emotion regulation in parenthood. & Anderson, A. K. (2008). Expressing fear enhances sensory
Developmental Review, 36, 1–14. acquisition. Nature Neuroscience, 11, 843–850.
Saxbe, D. E., Adam, E. K., Schetter, C. D., Guardino, C. M., Talley, A., Molix, L., Schlegel, R. J., & Bettencourt, A. (2010).
Simon, C., McKinney, C. O., & Shalowitz, M. U. (2015). The influence of breast cancer survivors’ perceived partner
Cortisol covariation within parents of young children: social support and need satisfaction on depressive symptoms:
Moderation by relationship aggression. Psychoneuroendocrinology, A longitudinal analysis. Psychology and Health, 25, 433–449.
62, 121–128. Thorp, S. R., Krause, E. D., Cukrowicz, K. C., & Lynch, T. R.
Saxbe, D. E., Golan, O., Ostfeld-Etzion, S., Hirschler- (2004). Postpartum support, demand-withdraw
Guttenberg, Y., Zagoory-Sharon, O., & Feldman, R. (2017). communication, and maternal stress. Psychology of Women
HPA axis linkage in parent-child dyads: Effects of parent sex, Quarterly, 28, 362–369.
autism spectrum diagnosis, and dyadic relationship behavior. Timmons, A. C., Margolin, G., & Saxbe, D. E. (2015).
Developmental Psychobiology, 59, 776–786. Physiological linkage in couples and its implications for
Saxbe, D. E., Margolin, G., Spies Shapiro, L., Ramos, M., individual and interpersonal functioning: A literature review.
Rodriguez, A., & Iturralde, E. (2014). Relative influences: Journal of Family Psychology, 29, 720–731.
Patterns of HPA axis concordance during triadic family Van Bakel, H. J., & Riksen-Walraven, J. M. (2008).
interaction. Health Psychology, 33, 273–281. Adrenocortical and behavioral attunement in parents with
Saxbe, D. E., & Repetti, R. (2010). No place like home: Home 1-year-old infants. Developmental Psychobiology, 50, 196–201.
tours correlate with daily patterns of mood and cortisol. Van den Bergh, B. R. H., & Marcoen, A. (2004). High antenatal
Personality and Social Psychology Bulletin, 36, 71–81. maternal anxiety is related to ADHD symptoms, externalizing
Schneiderman, I., Kanat-Maymon, Y., Zagoory-Sharon, O., & problems, and anxiety in 8- and 9-year-olds. Child Development,
Feldman, R. (2014). Mutual influences between partners’ 75, 1085–1097.

Vater, A., & Schröder-Abé, M. (2015). Explaining the physiological and behavioral readiness for social engagement.
link between personality and relationship satisfaction: Biological Psychiatry, 72, 982–989.
Emotion regulation and interpersonal behavior in Whisman, M. A. (2001). The association between depression and
conflict discussions. European Journal of Personality, 29, marital dissatisfaction. In S. R. H. Beach (Ed.), Marital and
201–215. family processes in depression: A scientific foundation for clinic
Waters, S. F., West, T. V., Karnilowicz, H. R., & Mendes, W. B. practice (pp. 3–24). Washington, DC: American Psychological
(2017). Affect contagion between mothers and infants: Association.
Examining valence and touch. Journal of Experimental Zaki, J., & Williams, W. C. (2013). Interpersonal emotion
Psychology: General, 146, 1043–1051. regulation. Emotion, 13(5), 803–810.
Waters, S. F., West, T. V., & Mendes, W. B. (2014). Stress Zimmer-Gembeck, M. J., Webb, H. J., Pepping, C. A., Swan,
contagion: Physiological covariation between mothers and K., Merlo, O., Skinner, E. A., . . . Dunbar, M. (2017). Is
infants. Psychological Science, 25, 934–942. parent-child attachment a correlate of children’s emotion
Weisman, O., Zagoory-Sharon, O., & Feldman, R. (2012). regulation and coping? International Journal of Behavioral
Oxytocin administration to parent enhances infant Development, 41, 74–93.

CH A PTE R
Respiratory Sinus Arrhythmia as a
12 Transdiagnostic Biomarker of
Emotion Dysregulation
Theodore P. Beauchaine and Ziv E. Bell
Abstract
Over the past two decades, emotion dysregulation—defined as the inability to dampen strong
emotional responses in the service of goal-directed behavior—has emerged as a consistent,
transdiagnostic vulnerability to psychopathology. Although specific forms of dysregulated emotion vary
across disorders (e.g., exuberance, anger, and related approach emotions in externalizing disorders;
anxiety, panic, and related avoidance emotions in internalizing disorders), deficits in dampening
emotional responses help define many psychiatric conditions. Peripherally, emotion dysregulation is
often marked by low tonic (resting) parasympathetic nervous system (PNS) activity, as indexed by
respiratory sinus arrhythmia (RSA). In fact, hundreds of studies conducted to date have found low RSA
across diverse forms of psychopathology (e.g., anxiety disorders, autism spectrum disorder, conduct
disorder, depression, panic disorder, psychotic disorders). Associations between psychopathology
and RSA reactivity to laboratory tasks are less consistent. However, wide variability in tasks and
psychophysiological methods may explain some of these inconsistencies. This chapter provides an
updated summary of this literature, ending with discussion of methodological issues.
Keywords: emotion dysregulation, psychopathology, respiratory sinus arrhythmia, biomarker, emotion

regulation, parasympathetic nervous system, anxiety disorders, depression, panic disorder, psychotic
disorders
Introduction disorders (e.g., Berking et al., 2011), to name but a

Most psychiatric disorders are characterized by few (see also Dixon-Gordon, Haliczer, & Conkey;
some form of emotion dysregulation (Aldao, Nolen- Garland, Bell, Atchley, & Froeliger; Hostinar &
Hoeksema, & Schweizer, 2010; Beauchaine, 2015a; Cicchetti; Kaufman & Crowell; Kerig; Neuhaus;
Cole, Hall, & Hajal, 2013). Internalizing disorders Racine & Horvath; Shader & Beauchaine; Wallace
(e.g., depression, panic), for example, are character- & Docherty, this volume).
ized by dysregulated anxious and fearful reactions Notably, specifying associations between emo-
to real or perceived threat, whereas externalizing tion dysregulation and psychopathology is a histor-
disorders (e.g., conduct problems, delinquency) are ically recent development. Throughout much of
characterized by dysregulated angry and aggressive the 20th century, dominant theoretical models es-
reactions to frustration and social provocation poused by U.S. psychologists favored behavioral
(Beauchaine, 2015b). Dysregulated emotional reac- and cognitive explanations for psychopathology—
tions are also implicated in many other forms of often eschewing emotional processes because emotion
psychopathology, including borderline personality was difficult to quantify using available technologies
disorder (e.g., Carpenter & Trull, 2013), self-inflicted (see Beauchaine & Zisner, 2017). Beginning in the
injury (e.g., Crowell et al., 2017), eating disorders mid-1990s, however, this state of affairs began to
(e.g., Haynos & Fruzzetti, 2011), and substance use change. Advances in electrophysiological recording,
153
hormonal assays, and neuroimaging made objective 2007; McLaughlin, Rith-Najarian, Dirks, &
assessment of emotion possible, producing a rich Sheridan, 2015) among children, adolescents, and
literature in which emotional states are quantified adults. We focus specifically on literature in which
and studied systematically (e.g., Cicchetti & RSA—measured at rest or in response to emotional
Rogosch, 2012; Crowell et al., 2017; Hajcak, challenge—is used to evaluate emotion dysregula-
MacNamara, Foti, Ferri, & Keil, 2013; Lapate et al., tion among those with various forms of psychopa-
2017). As a result, research on emotion regulation thology. We note that this literature is extensive and
and dysregulation has flourished in the 21st century cannot be reviewed comprehensively in a single
(Adrian, Zeman, & Veits, 2011). chapter. In fact, in a recent meta-analysis on RSA
As articulated by authors throughout this reactivity in psychopathology, an initial literature
volume, emotion regulation (ER) comprises bio- search yielded over 4,000 articles (Beauchaine et al.,
logical, cognitive, social, and behavioral processes 2018). Our goal here is to summarize major find-
that shape and modulate one’s experience and ex- ings. After doing so, we outline key methodological
pression of emotions in the service of adaptive, goal- issues critical to research assessing RSA, before dis-
oriented behaviors (see Thompson, 1990, 1994). cussing future directions for research on RSA as a
However, despite the importance of ER for adaptive biomarker of emotion dysregulation.
human function, quantifying emotion regulatory
processes becomes problematic if we attempt to do Respiratory Sinus Arrhythmia and Emotion
so by inferring emotion regulation from the absence Dysregulation
of maladaptive behaviors and emotional reactions RSA refers to cyclic, respiratory-linked variation in
(see Cole, Martin, & Dennis, 2004; Ramsook, heart beats, as quantified in the R-R interval time
Cole, & Fields-Olivieri, this volume). In contrast, series (see Figure 12.1; Berntson et al., 1997; Zisner
emotion dysregulation—defined as experiences and & Beauchaine, 2016). RSA can be indexed in several
expressions of emotion that interfere with adaptive, ways (see Shader et al., 2018), all of which capture
goal-directed behavior (see Beauchaine & Gatzke- high-frequency heart rate variability (HF-HRV).
Kopp, 2012)—is often easier to quantify through Given appropriate stimulus conditions and quanti-
direct observation (e.g., Beauchaine, 2015b; Cole fication, HF-HRV indexes parasympathetic-linked
et al., 2013). Strong emotional reactions can be ob- inhibitory influence on cardiac activity and reactiv-
served and measured in laboratory settings via be- ity (Beauchaine, 2001; Berntson et al., 1997;
havior observation and physiological reactivity, and Grossman, Karemaker, & Wieling, 1991; Ritz,
depending on context, self-reports. Most contem- 2009). Full explanation of RSA quantification is
porary research uses multiple measures, including beyond the scope of this chapter; interested readers
behavioral, psychophysiological, and/or neural, to are referred to recent, comprehensive reviews
examine correlates and mechanisms of emotion dys- (Laborde, Mosley, & Thayer, 2017; Shader et al.,
regulation, particularly emotional reactions that are 2018; Zisner & Beauchaine, 2016).
experienced too intensely and/or too enduringly to
be adaptive (Beauchaine, 2015b; Beauchaine & Foundational Theoretical Models
Bell; Brown, Conradt, & Crowell; Jazaieri, Uusberg, Although a few studies appeared before the 1990s,
Uusberg, & Gross; Leshin & Lindquist; Martin, research on RSA as a peripheral biomarker of emo-
Zalewski, Binion, & O’Brien; Speed & Hajcak; tion regulation and dysregulation began in earnest
Rappaport, Hawn, Overstreet, & Amstadter; following a foundational paper by Porges, Doussard-
Stoycos, Corner, Khaled, & Saxbe; Thompson & Roosevelt, and Maiti (1994), who linked RSA spe-
Waters, this volume). cifically to emotion regulatory processes. This paper
In this chapter, we summarize current litera- was soon followed by Porges’s (1995) elaborate theo-
ture on respiratory sinus arrhythmia (RSA) as a retical model in which he presented a phylogenetic
peripheral, physiological biomarker of emotion reg- account of brainstem development that distin-
ulation and dysregulation. RSA has been quantified guished between a reptilian “vegetative” branch and
in literally thousands of studies designed to evaluate a mammalian “smart” branch of the vagus nerve.
emotional processes and their relations to typical According to Porges, the vegetative vagus, shared by
and atypical development (see, e.g., Shader et al., both reptiles and mammals, is mediated by the
2018), vulnerability to adversity (e.g., El-Sheikh, dorsal motor nucleus (DMNX) and produces heart
Harger, & Whitson, 2001), and existing psychopa- rate slowing (bradycardia) during orienting re-
thology (e.g., Beauchaine, Gatzke-Kopp, & Mead, sponses. In contrast, the smart vagus evolved in
154 Respiratory Sinus Arrhy thmia as Biomarker

R-R1 R-R2 R-R3 R-R4 R-R5
R R R R R R
T T T T T
P P P P P P
Q Q Q Q Q
Q
S S S S S S
Figure 12.1 Time series of heart beats collected from a standard electrocardiogram (ECG). QRS complexes, P-waves, and T-waves
are marked. Respiratory sinus arrhythmia indexes periodic lengthening and shortening of R-R intervals across successive breathing
cycles.
mammals, is mediated by the nucleus ambiguus in each case, deficient top-down inhibition of the
(NA), and provides for rapid mobilization responses subcortex by one or more functional subdivisions of
in contexts of environmental challenge. Porges con- the PFC is observed. This suggestion is supported
tended that moment-to-moment vagal modulation by neuroimaging findings of altered functional con-
of cardiac activity is a precondition for evolution of nectivity between (1) specific subcortical (striatum)
complex social behaviors among mammals, since and cortical structures (e.g., dorsolateral PFC, ante-
fight/flight (F/F) reactions need to be inhibited to rior cingulate) implicated in externalizing disorders
engage effectively with friendly conspecifics. In a and (2) specific subcortical (amygdala) and cortical
series of papers, Porges invoked the “vagal brake” structures (e.g., ventrolateral PFC, ventromedial
metaphor to describe inhibitory functions on car- PFC) implicated in internalizing disorders (for
diac output of the PNS, especially during social in- recent reviews, see Beauchaine, 2015b; Beauchaine
teractions (e.g., Porges, 1995, 2007). & Zisner, 2017; Heatherton, 2011; Tone, Garn, &
Although Porges’s (1995, 2007) phylogenetic ac- Pine, 2016).
count of PNS function has been debated (e.g., Thayer and Lane (2000) introduced neurovis-
Grossman & Taylor, 2007), polyvagal theory ush- ceral integration theory (NIT), which specifies a
ered in a new generation of research on physiological neural network through which PFC function regu-
markers of ER and emotion dysregulation (see lates RSA. According to NIT, a central autonomic
Appelhans & Luecken, 2006; Beauchaine, 2001; network—including the ventromedial PFC and an-
Beauchaine & Zisner, 2017). Porges’s perspective terior cingulate cortex—provides top-down regula-
provided researchers with a mechanistic theory from tion of cardiac function via the vagus nerve. Since
which to launch studies linking RSA to emotion reg- 2000, Thayer and colleagues (e.g., Thayer, Hansen,
ulatory processes across development, including as- Saus-Rose, & Johnsen, 2009) have elaborated and
sociations between RSA and psychopathology. extended NIT in a series of pharmacologic blockade
and neuroimaging studies. These studies demon-
Contemporary Theoretical Models strate associations between resting RSA and perfor-
Since publication of Porges’s (1995, 2007) theory, mance on executive function tasks that recruit the
considerable elaboration on likely neural substrates PFC, including sustained attention and continuous
of RSA has emerged. Much of this research links performance tasks (see Beauchaine & Thayer, 2015).
RSA to prefrontal cortex (PFC) function, with Thus, understanding associations between RSA and
brainstem nuclei outlined by Porges serving as the psychopathology may help elucidate transdiagnos-
final common pathway of efferent neural traffic tic neural underpinnings of psychopathology and
from the PFC to the heart (e.g., Thayer & Lane, treatment response. RSA is of course easier to meas-
2000). According to this perspective, low RSA and ure than central nervous system function in diverse
emotion dysregulation—both of which are ob- contexts, and with clinical and developmental sam-
served in many forms of psychopathology—emerge ples who have difficulty participating in neuroimag-
from insufficient top-down cortical (PFC) modula- ing studies.
tion of subcortically generated affective responding Although further validation of NIT is needed,
(see Beauchaine, 2015a, 2015b). Although emo- support for the hypothesis that RSA activity and
tional predispositions differ across subtypes of psy- reactivity fall at least in part under prefrontal con-
chopathology (e.g., anxiety, fear, panic, anger, etc.), trol has emerged. For example, in a recent review
Beauchaine and Bell 155

of studies conducted among healthy adults who & Kaess, 2016), mania (Henry, Minassian, Paulus,
performed mental stress tasks that recruit the PFC, Geyer, & Perry, 2010), schizophrenia (e.g., Clamor,
Castaldo et al. (2015) found modest associations Lincoln, Thayer, & Koenig, 2016), and self-harm
between task performance and RSA. Similarly, in a (Crowell et al., 2005). Thus, as outlined in the in-
recent meta-analysis of 123 studies, Holzman and troductory paragraphs of this chapter, low resting
Bridgett (2017) found modest associations be- RSA is a transdiagnostic biomarker of psychopa-
tween RSA and performance on self-regulation thology (Beauchaine, 2015a, 2015b). Conversely,
tasks—including those that recruit ER and execu- high resting RSA correlates positively with social
tive control. function among children (Diamond, Fagundes, &
Linking RSA to ER capabilities and PFC func- Butterworth, 2012; Eisenberg et al., 2008), execu-
tion is important for several reasons. First, it dovetails tive function among adults (Thayer et al., 2009),
with an extensive literature on prefrontal substrates and resilience to various forms of stress throughout
of self-regulation, emotion, and executive control life (e.g., El-Sheikh et al., 2001; Souza et al., 2013).
more broadly (e.g., Dixon, Thiruchselvam, Todd, & Even among those who suffer from various forms of
Christoff, 2017; Heatherton, 2011; Nigg, 2017). diagnosable psychopathology, resting RSA corre-
Second, tying emotion regulatory capacity to both lates with individual differences in adaptive social
(1) the PFC, which develops throughout childhood function (e.g., Patriquin, Scarpa, Friedman, &
and adolescence (Tau & Peterson, 2010), and (2) Porges, 2013).
its functional interconnections with subcortical
structures that mature somewhat earlier (Brain Social and Developmental Influences on
Development Cooperative Group, 2012), is con- Resting Respiratory Sinus Arrhythmia
sistent with neuromaturational models that link Among typically developing children, RSA increases
compromised PFC development to emerging diffi- linearly from infancy to midadolescence, peaks in
culties with impulse control and self-regulation in late adolescence and young adulthood, then de-
adolescence and beyond (e.g., De Brito et al., 2009; creases gradually across the lifespan (Alkon, Boyce,
Heller, Cohen, Dreyfuss, & Casey, 2016). Davis, & Eskenazi, 2011; Shader et al., 2018).2
Differences in resting RSA between typically devel-
Resting Respiratory Sinus Arrhythmia oping children and children with internalizing and
and Psychopathology externalizing disorders are often not evident in pre-
Low resting RSA is observed in an impressively long school but are observed consistently by later child-
list of psychiatric disorders among children, adoles- hood and adolescence (e.g., Beauchaine et al., 2007;
cents, and adults (see Beauchaine, 2001, 2015a; Koenig et al., 2016). This likely reflects a failure in
Beauchaine & Thayer, 2015; Shader et al., 2018). normal maturation of emotion regulation and its
Over the last 20 years, such findings have been re- physiological substrates for children with psychopa-
ported for (1) internalizing conditions including thology.
depression (Kemp et al., 2010; Koenig, Kemp, Development of both emotion regulation and
Beauchaine, Thayer, & Kaess, 2016; Rottenberg, resting RSA are affected by environmental influ-
2007),1 generalized anxiety (Chalmers, Quintana, ences in childhood and adolescence. In fact, most
Abbott, & Kemp, 2014), panic (Asmundson & measures of emotion regulation are moderately her-
Stein, 1994), phobias (Åhs, Sollers, Furmark, itable, suggesting considerable socialization (e.g.,
Fredrikson, & Thayer, 2009), posttraumatic stress Goldsmith, Pollak, & Davidson, 2008). Consistent
(Meyer et al., 2016), and obsessive-compulsive dis- with this interpretation, a growing body of research
order (Pittig, Arch, Lam, & Craske, 2013); (2) ex- indicates that emotion regulation, other forms of
ternalizing conditions including attention-deficit self-regulation, and related executive functions are
hyperactivity disorder (ADHD; Beauchaine et al., shaped strongly across development by environ-
2013), conduct disorder (CD; Beauchaine et al., mental influences, especially parent–child relation-
2007), callous-unemotional traits (de Wied, van ship dynamics (e.g., Beauchaine & Zalewski, 2016;
Boxtel, Matthys, & Meeus, 2012), and substance Bell & Calkins, 2000; Breaux, McQuade, Harvey,
use (Harte & Meston, 2014; Ingjaldsson, Laberg, & & Zakarian, 2018; Bernier, Carlson, & Whipple,
Thayer, 2003); and (3) various other conditions in- 2010; Smith, Calkins, & Keane, 2006; see also
cluding autism spectrum disorder (ASD; Neuhaus, Beauchaine & Bell; Brown, Conradt, & Crowell;
Bernier, & Beauchaine, 2014), borderline personal- Hostinar & Cicchetti; Jazaieri, Uusberg, Uusberg,
ity disorder (BPD; Koenig, Kemp, Feeling, Thayer, & Gross; Leshin & Lindquist; Martin, Zalewski,

Binion, & O’Brien; Speed & Hajcak; Rappaport, in RSA are noteworthy given well-established
Hawn, Overstreet, & Amstadter; Shader & associations between RSA and ER outlined previ-
Beauchaine; Stoycos, Corner, Khaled, & Saxbe; ously, and given associations between low resting RSA
Thompson & Waters, this volume). Such findings and prospective vulnerability to worsening emotion
are unsurprising given a large literature linking en- dysregulation and both internalizing and external-
vironmental enrichment to structural and func- izing psychopathology into adolescence (e.g., Vasilev,
tional integrity of the PFC across development in Crowell, Beauchaine, Mead, & Gatzke-Kopp, 2009;
both animals and humans (see Baroncelli et al., Yaroslavsky, Rottenberg, & Kovacs, 2013).
2010; Blair, 2016).
Family relationship dynamics in particular ex- Respiratory Sinus Arrhythmia Reactivity
hibit concurrent and prospective associations with and Psychopathology
children and adolescents’ resting RSA. Ineffective According the phylogenetic account described
parenting, including inconsistent discipline and earlier, PNS inhibition of cardiac reactivity is an
corporal punishment, are associated with low rest- evolutionary precondition for social affiliation,
ing RSA among adolescents, whereas positive par- which requires mammals to suppress F/F respond-
enting and parental involvement are associated with ing (Porges, 1995, 2007). Thus, competent emotion
high resting RSA (Graham, Scott, & Weems, 2017). regulation—at least in social contexts—should be
As reviewed elsewhere, such associations emerge in marked by limited vagal withdrawal (Beauchaine,
part through negative reinforcement of emotional 2001). In contrast, under conditions of real or per-
lability and associated physiological dysregulation ceived social threat, the PNS—via the vagus
in at-risk families (Beauchaine, 2018; Beauchaine & nerve—withdraws its inhibitory influence, allowing
Zalewski, 2016; Crowell et al., 2013). the sympathetic nervous system (SNS) to mobilize
Given that both emotion regulation and dysreg- unopposed in the service of F/F responding. In such
ulation are shaped strongly by environment— situations, PNS withdrawal is near complete, and
including parent–child relationship dynamics—one RSA is almost fully abolished (Berntson et al., 1997;
might expect changes in children’s RSA in response Porges, 1995). The PNS therefore suppresses cardiac
to effective family interventions, and interventions output when social engagement is adaptive and po-
that target children’s ER directly. Although inter- tentiates cardiac output when fighting or fleeing is
ventions targeting children’s ER are less common adaptive. To the extent that socioemotional prob-
than such interventions for adolescents and adults lems and associated F/F reactions characterize psy-
(see Kehoe & Havighurst; Winiarski, Brown, Karnik, chopathology, RSA reactivity should index emotion
& Brennan, this volume), recent findings indicate regulatory capacity (Beauchaine, 2012; Shader et al.,
considerable promise. For example, our research 2018). For example, PNS withdrawal to unthreaten-
group recently completed an externalizing intervening social stimuli could potentiate F/F responding
tion in which we targeted children’s ER, as indexed when social affiliative behaviors are adaptive. Several
by behavior observations, parent reports, teacher studies reveal such patterns of RSA reactivity among
reports, and RSA. The intervention taught children externalizing samples (e.g., Beauchaine, Katkin,
strategies for regulating their emotions, including Strassberg, & Snarr, 2001; Beauchaine et al., 2007;
coping with anger, social problem solving, and ef- Fortunato, Gatzke-Kopp, & Ram, 2013; Hamilton
fective communication of emotions. Parents learned & Alloy, 2016) and among those with anxiety and
effective emotion coaching aimed at helping their panic disorders (e.g., Chalmers et al., 2014; Pittig
children understand, interpret, and cope with their et al., 2013). In both cases, dysregulated emotion—
own and others’ emotions (see Gottman, Katz, & albeit of different forms—interferes with adaptive
Hooven, 1997). Children improved at posttreat- social function.
ment on all measures of externalizing behavior and It should be noted, however, that links between
ER, with large effect sizes (Beauchaine et al., 2013; RSA reactivity and psychopathology are far less con-
Webster-Stratton, Reid, & Beauchaine, 2011). More sistent than links between resting RSA and psychopa-
important for purposes of this chapter, these behav- thology (Balzarotti, Biassoni, Colombo, & Ciceri,
ioral and emotional improvements were accompa- 2017; Beauchaine et al., 2018; Shader et al., 2018;
nied by increases in resting RSA that were over 20 Zisner & Beauchaine, 2016). Although several studies
times larger than age-normative developmental indicate excessive RSA withdrawal during lab tasks
shifts (Bell, Shader, Webster-Stratton, Reid, & among internalizing and externalizing samples (e.g.,
Beauchaine, 2018). Intervention-induced changes Beauchaine et al., 2001; Crowell et al., 2005; de Wied

et al., 2012), and although internalizing–externalizing (e.g., Crowell et al., 2013; Snyder, 1977; Snyder,
comorbidity is associated with greater RSA with- Edwards, McGraw, Kilgore, & Holton, 1994;
drawal than either internalizing or externalizing dis- Snyder, Schrepferman, & St. Peter, 1997). Recent
orders alone (Calkins, Graziano, & Keane, 2007; findings from multiple research groups indicate that
Pang & Beauchaine, 2013), other studies indicate during dyadic interactions in high-risk families,
associations between low RSA reactivity and symp- emotionally dysregulated children and adolescents
toms of psychopathology (e.g., Brugnera et al., exhibit exquisite physiological sensitivity to their
2017; Graziano & Derefinko, 2013; Obradović, parents’ evocative behaviors. For example, Crowell
Bush, Stamperdahl, Adler, & Boyce, 2010), and still et al. (2017) found that self-injuring adolescent girls—
others find no associations at all (e.g., Musser et al., all of whom reported poor emotion regulation—
2011; Negrao, Bipath, van der Westhuizen, & displayed greater behavioral and RSA reactivity to
Viljoen, 2011; Pittig et al., 2013). As we have re- their mothers’ aversive behaviors than their depressed-
viewed elsewhere (Beauchaine et al., 2018; Shader only and healthy control peers. In a much younger
et al., 2018; Zisner & Beauchaine, 2016), there are sample of three- to five-year-olds, Skowron et al.
several methodological and sample ascertainment (2011) reported lower RSA during a mother–child
issues that contribute to such heterogeneity of find- dyadic interaction task for children with histories of
ings. We discuss these further under the heading physical abuse compared with controls. Thus, availa-
Methodological Considerations. First, however, we ble data, although limited, suggest that aversive so-
summarize existing literature on social and develop- cialization mechanisms are associated with both
mental influences on RSA reactivity. emotional lability and excessive RSA withdrawal
among children and adolescents during social ex-
Social and Developmental Influences on changes with parents. Notably, studies with infants
Respiratory Sinus Arrhythmia Reactivity indicate that maternal socialization of children’s
Specifying developmental trajectories in RSA reac- RSA reactivity begins as early as six months of age
tivity is more challenging than doing so for resting (Moore et al., 2009).
RSA because different tasks are often used by differ-
ent research groups, because similar tasks can evoke Methodological Considerations
very different responses at different ages, and be- As noted earlier, considerable heterogeneity exists
cause emotion regulation improves across child- among studies that examine RSA as a marker of
hood and adolescence (see Beauchaine & Webb, emotion dysregulation and psychopathology. This is
2017; Zisner & Beauchaine, 2016). In a recent arti- especially the case for RSA reactivity. Recent litera-
cle that combined data from five existing studies of ture reviews and meta-analyses suggest that this het-
children and adolescents (N = 559), all of whom erogeneity is systematic, and attributable at least in
underwent negative emotion inductions, we found part to (1) the nature of tasks used to elicit RSA re-
steep decreases in RSA reactivity from ages 4 to activity (e.g., attention allocation vs. negative emo-
17 years (Shader et al., 2018). Such data are consistent tion induction), (2) differences in the nature of
with the notion that children and adolescents samples recruited (clinical vs. high risk), (3) RSA
become better able to regulate their physiological quantification methods, and (4) measurement issues
reactions to negative emotion as they mature. (Beauchaine et al., 2018; Shader et al., 2018). Next,
Developmental trajectories in RSA reactivity to we briefly discuss each of these issues in turn. More
other types of tasks (e.g., attention allocation, posi- extended discussions of methodological issues in
tive emotion inductions) are less clear but are not as psychophysiology research can be found elsewhere
relevant for assessing emotion dysregulation, the (Beauchaine & Webb, 2017; Zisner & Beauchaine,
topic of this chapter. 2016).
Compared with the literature on resting RSA,
fewer studies address social correlates of RSA reac- Selection of Tasks
tivity. However, socialization mechanisms of emo- Over the past two decades or so, many task conditions
tional lability are almost certainly relevant given have been used to elicit RSA reactivity in psycho-
functional relations between F/F responding and pathology research. These include negative emo-
PNS withdrawal. It has long been known that emotion evocation tasks (e.g., Crowell et al., 2005),
tional lability is shaped and maintained by negative attention allocation tasks (e.g., Suess et al., 1994),
reinforcement mechanisms (i.e., escape condition- problem-solving tasks (e.g., El-Sheikh, 2005), ex-
ing) in high-risk families of both boys and girls ecutive function tasks (e.g., Marcovitch et al., 2010),

and positive mood inductions (e.g., Fortunato et al., are less consistent, similar patterns have been
2013), among others. Notably, RSA reactivity is reported (e.g., Crowell et al., 2005, 2017; Levine,
often interpreted as a biomarker of emotion regula- Fleming, Piedmont, Cain, & Chen, 2016).
tion, regardless of task conditions. This is prob- Of note, Shader et al. (2018), in a large sample of
lematic because physiological markers of specific children and adolescents (N = 559), found that low
psychological constructs are valid insofar as those resting RSA differentiated between those with and
psychological constructs are elicited (see National without clinical levels of externalizing psychopa-
Advisory Mental Health Council Workgroup on thology, even though the sample-wide correlation
Tasks and Measures for Research Domain Criteria, between RSA reactivity and externalizing scores was
2016; Zisner & Beauchaine, 2016). In the case of small and nonsignificant. This suggests that rela-
RSA reactivity, inferences about emotion regula- tions between RSA reactivity and psychopathology
tion/dysregulation should be derived from strong may be swamped in nonclinical samples by normal
negative emotion induction tasks (see Beauchaine, variation in responding (see Zisner & Beauchaine,
2015b). This does not mean that other tasks aren’t 2016). Thus, in the case of RSA reactivity, inferences
useful in making inferences about other psycholog- about those with psychopathology may not be valid
ical processes. For example, modest RSA reactivity when extrapolated from those with ordinary varia-
appears to be a valid peripheral index of attentional tion in or only mildly elevated symptoms. Indeed,
capacity during sustained attention tasks (Suess et al., individual differences in internalizing and external-
1994; see also Beauchaine, 2001). Yet we cannot izing scores are distributed normally, and low to
infer emotion regulation from tasks that do not intermediate scores better reflect temperamental

elicit emotional responses. tendencies such as shyness and exuberance—not
Consistent with this perspective, RSA reactivity psychopathology (e.g., Degnan et al., 2011).
among those with diverse forms of psychopathology
is most pronounced during negative emotion in- Respiratory Sinus Arrhythmia
ductions (Beauchaine et al., 2018; Graziano & Quantification
Derefinko, 2013). Furthermore, inducing different RSA can be quantified in a number of ways. The
emotions yields emotion-specific patterns of RSA simplest approaches capture HRV in the time
reactivity (Fortunato et al., 2013; Kreibig, 2010; domain by evaluating beat-to-beat differences in the
Rainville, Bechara, Naqvi, & Damasio, 2006). R-R time series (see Figure 12.1). There are several
Thus, although RSA reactivity is a promising bio- such methods, including standard deviation of R-R
marker of emotion regulation, any such inferences intervals and mean successive difference in R-R in-
are valid only when stimulus conditions are chosen tervals, among others. The most common is root
appropriately. mean square of successive differences (RMSSD),
which is preferred over other time-domain metrics
Sample Characteristics for statistical reasons that are beyond the scope of
When studies are grouped into those conducted this discussion (Berntson, Lozano, & Chen, 2005).
with clinical samples versus those conducted with Most research on RSA among those with psy-
high-risk and normative samples, it becomes appar- chopathology uses frequency domain assessment.
ent that associations between excessive RSA reactiv- Common frequency domain approaches include
ity and psychopathology derive primarily from fast Fourier transform (FFT) analysis and autore-
clinical groups. Several studies show, for example, gressive (AR) spectral analysis (Poliakova et al.,
that children, adolescents, and adults with clinical 2014). Both of these spectral analytic methods
levels of externalizing behaviors exhibit greater RSA quantify the amount, or “power,” of HRV in specific
withdrawal to emotion evocation than their peers frequency bands. FFT and AR convert R-R time
(e.g., Beauchaine, Hong, & Marsh, 2008; series into spectral density functions. As shown in
Beauchaine et al., 2001, 2007; de Wied et al., Figure 12.2, these methods can be used to isolate
2012; Mezzacappa et al., 1996). In contrast, in nor- and distinguish between RSA and other sources of
mative and high-risk samples, externalizing symp- HRV that are not of PNS origin.
toms often either correlate with less RSA withdrawal For adult participants, spectral density functions
during lab tasks or show no association with RSA are typically subdivided into low-frequency (<0.04
withdrawal (e.g., Dietrich et al., 2007; Obradović Hz), midfrequency (0.04 to 0.15 Hz), and high-
et al., 2010). Although associations between RSA frequency HRV (0.15 to 0.50 Hz) bands. At normal
reactivity and diagnosable internalizing disorders
adult breathing rates, high-frequency HRV yields

FFT spectrum (Welch’s periodogram: 256 s window with 50% overlap)
0.03
0.02
PSD (s2/Hz)
0.01
0.15Hz 0.33Hz
0
0 0.1 0.2 0.3 0.4 0.5
Frequency (Hz)
Figure 12.2 Spectral density plot of heart rate variability collected from a typical 4-year-old. Given normal respiration rates in this
age range, respiratory sinus arrhythmia (RSA), which indexes parasympathetic nervous system (PNS)-linked cardiac activity—is
captured by the frequency band spanning 0.33 and 0.50 Hz. Above 0.50 Hz, there is no appreciable spectral power. Below 0.33 Hz,
spectral power is not respiratory related, and therefore not PNS linked. Note that when an adult respiratory frequency of 0.15 Hz is
used, excess noise is added to the RSA estimate, as indicated by the double-headed arrow (see text for details). Frequency (Hz) is
plotted along the x-axis, and power spectral density is plotted along the y-axis. Reproduced from Shader et al. (2018) with permission
from Cambridge University Press.
an estimate of RSA. Notably, however, children to and exceeding 10 minutes are often most effective
breathe much faster than adults, so the high- for minimizing physiological arousal (e.g., Jennings,
frequency band must be adjusted to capture RSA Kamarck, Stewart, Eddy, & Johnson, 1992). When
accurately (see Figure 12.1). Since preschoolers re- a resting state is not achieved, baseline RSA is
spire at over twice the rate of adults, this is not a -underestimated, which in turn underestimates
trivial concern (Zisner & Beauchaine, 2016). RSA reactivity to subsequent tasks, since reactivity
To date, many studies have used respiration is quantified as baseline minus task. Such effects
bands appropriate for adults when quantifying RSA are especially important to minimize in psychopa-
among preschoolers, middle schoolers, and adoles- thology research. For example, failure to collect
cents. This results in overestimates of resting RSA true baseline RSA data from participants who
and underestimates of RSA reactivity (Shader et al., arrive at the lab anxious or angry may result in
2018). Although specific implications for our underestimates of both resting RSA and RSA
understanding of RSA–emotion regulation and
reactivity.
RSA–psychopathology relations across develop- In research with children, it is common to use al-
ment are not fully clear, literature-wide biases in ternative baseline conditions in which participants
estimates of RSA and RSA reactivity may exist, es- engage in minimally demanding tasks, such as color
pecially for younger samples. At the very least, this detection (Jennings et al., 1992), or watch quiet, age-
adds measurement error to existing data, which appropriate videos (e.g., Sulik, Eisenberg, Silva,
could explain some null findings. Spinrad, & Kupfer, 2013). These approaches follow
from common assumptions that children with inter-
Measurement Issues nalizing or externalizing disorders cannot tolerate true
Several additional measurement issues should be baselines, or that young children, regardless of their
considered when collecting and interpreting RSA level of functioning, cannot tolerate true baselines.
data. Among these, baseline conditions during Notably, however, even moderate levels of attention
which resting RSA is assessed stand out as particularly allocation alter RSA (see Beauchaine, 2001).
important. As a general rule in psychophysiology Accordingly, true baselines are preferred. Although
research, resting, tonic measures should be collected 10 minutes is long for young children, even pre-
following a movement- and stimulus-free baseline schoolers with ADHD tolerate five-minute base-
condition that is long enough to induce a resting lines well given the novelty of lab visits (e.g., Crowell
but wakeful state (Obrist, 1981). These are often re- et al., 2006).
ferred to as “true” baselines and are designed to Finally, in our recent meta-analysis we
minimize effects of endogenous and exogenous (Beauchaine et al. 2018) found that adherence to
stressors on resting physiological activity. Extensive standards set forth by the Task Force of the European
research indicates that extended quiet baselines up Society of Cardiology and the North American

Society of Pacing and Electrophysiology (1996) was Acknowledgment
associated with larger effect sizes in studies of RSA Work on this chapter was supported by grant DE025980 from
reactivity in psychopathology. Among other recom- the National Institutes of Health, and by the National Institutes
of Health Science of Behavior Change (SoBC) Common Fund.
mendations, Task Force guidelines include (1) ex-
tended quiet baselines during which participants do
not engage in activities, (2) electrocardiogram Notes
(ECG) sampling rates of at least 512 Hz, and (3) use 1. Some have suggested that low RSA among depressed adults
results from antidepressant treatment (e.g., O’Regan, Kenny,
of commercially produced ECG equipment and Cronin, Finucane, & Kearney, 2015; Kemp et al., 2014).
standard electrode placement. The finding that ad- However, unmedicated, physically healthy individuals with
herence to these guidelines was associated with major depression also show low RSA (e.g., Kemp, Quintana,
larger effect sizes suggests once again that measure- Felmingham, Matthews, & Jelinek, 2012).
ment error is responsible for at least some null find- 2. In adulthood, age-related declines in RSA in adulthood are
offset by physical fitness (Byrne, Fleg, Vaitkevicius, Wright, &
ings in the literature. Porges, 1996).
Conclusion
References
In this chapter, we summarize literature indicating Adrian, M., Zeman, J., & Veits, G. (2011). Methodological
that resting RSA marks emotion regulation capac- implications of the affect revolution: A 35-year review of
ity, and excessive RSA reactivity marks in vivo emo- emotion regulation assessment in children. Journal of
tion dysregulation. We also review socialization Experimental Child Psychology, 110, 171–197.
Åhs, F., Sollers, J. J., Furmark, T., Fredrikson, M., & Thayer, J. F.
mechanisms through which emotion dysregulation
(2009). High-frequency heart rate variability and cortico-
develops and is maintained. Because emotion dys- striatal activity in men and women with social phobia.
regulation is a transdiagnostic feature of many psy- NeuroImage, 47, 815–820.
chiatric disorders, low resting RSA is often observed Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
among those with psychopathology. Although the Emotion-regulation strategies across psychopathology:
A meta-analytic review. Clinical Psychology Review, 30,
literature is more mixed regarding RSA reactivity,
217–237.
we discuss a number of potential explanations for Alkon, A., Boyce, W. T., Davis, N. V., & Eskenazi, B. (2011).
heterogeneity of findings, including diversity of Developmental changes in autonomic nervous system resting
eliciting tasks, clinical versus nonclinical nature of and reactivity measures in Latino children from 6 to 60
samples, methods used to quantify RSA, and preci- months of age. Journal of Developmental and Behavioral
Pediatrics, 32, 668–677.
sion of measurement.
Appelhans, B. M., & Luecken, L. J. (2006). Heart rate variability
Existing literature demonstrates that RSA is a as an index of regulated emotional responding. Review of
useful measure for assessing emotion regulation and General Psychology, 10, 229–240.
dysregulation, especially when used with data col- Asmundson, G. J., & Stein, M. B. (1994). Vagal attenuation in
lected across other levels of analysis (e.g., self-report, panic disorder: An assessment of parasympathetic nervous
system function and subjective reactivity to respiratory
informant report, behavior observation, dyadic in-
manipulations. Psychosomatic Medicine, 56, 187–193.
teractions). In fact, most contemporary studies of Balzarotti, S., Biassoni, F., Colombo, B., & Ciceri, M. R. (2017).
emotion regulation and dysregulation use multiple Cardiac vagal control as a marker of emotion regulation in
measures (see Beauchaine, 2015b). Although we do healthy adults: A review. Biological Psychology, 130, 54–66.
not recommend inferring emotion dysregulation Baroncelli, L., Braschi, C., Spolidoro, M., Begenisic, T., Sale, A.,
& Maffei, L. (2010). Nurturing brain plasticity: Impact of
solely from RSA, physiological measures provide
environmental enrichment. Cell Death and Differentiation,
certain advantages over self- and informant reports 17, 1092–1103.
since they are objective. Beauchaine, T. P. (2001). Vagal tone, development, and Gray’s
Given the heterogeneity of findings for RSA motivational theory: Toward an integrated model of
reactivity, one concern is that it could be abandoned autonomic nervous system functioning in psychopathology.
Development and Psychopathology, 13, 183–214.
as a physiological index of emotion regulation and
Beauchaine, T. P. (2012). Physiological markers of emotion and
dysregulation. We assert that such abandonment behavior dysregulation in externalizing psychopathology.
would be premature, and that RSA reactivity Monographs of the Society for Research in Child Development,
holds considerable promise if issues of measure- 77, 79–86.
ment precision and quantification are addressed Beauchaine, T. P. (2015a). Respiratory sinus arrhythmia: A
transdiagnostic biomarker of emotion dysregulation and
in future research. We look forward to such re-
psychopathology. Current Opinion in Psychology, 3, 43–47.
search in the years to come given the utility of Beauchaine, T. P. (2015b). Future directions in emotion
RSA as a transdiagnostic biomarker of emotion dysregulation and youth psychopathology. Journal of Clinical
regulation and dysregulation. Child and Adolescent Psychology, 44, 875–896.

Beauchaine, T. P. (2018). Nonsuicidal self-injury and suicidal precursors of young children’s executive functioning. Child
behaviors in girls: The case for targeted prevention in Development, 81, 326–339.
preadolescence. Manuscript under revision. Berntson, G. G., Bigger, J. J., Eckberg, D. L., Grossman, P.,
Beauchaine, T. P., Bell, Z., Knapton, E., McDonough-Caplan, Kaufmann, P. G., Malik, M., . . . van der Molen, M. W.
H., Shader, T., & Zisner, (2018). Respiratory sinus (1997). Heart rate variability: Origins, methods, and
arrhythmia reactivity across empirically-based structural interpretive caveats. Psychophysiology, 34, 623–648.
categories of psychopathology: A meta-analysis. Manuscript Berntson, G. G., Lozano, D. L., & Chen, Y. J. (2005). Filter
under revision. properties of root mean square successive difference
Beauchaine, T. P., & Gatzke-Kopp, L. M. (2012). Instantiating (RMSSD) for heart rate. Psychophysiology, 42, 246–252.
the multiple levels of analysis perspective in a program Blair, C. (2016). Developmental science and executive function.
of study on externalizing behavior. Development and Current Directions in Psychological Science, 25, 3–7.
Psychopathology, 24, 1003–1018. Brain Development Cooperative Group. (2012). Total and
Beauchaine, T. P., Gatzke-Kopp, L. M., & Mead, H. K. (2007). regional brain volumes in a population-based normative
Polyvagal theory and developmental psychopathology: sample from 4 to 18 years: The NIH MRI Study of Normal
Emotion dysregulation and conduct problems from preschool Brain Development. Cerebral Cortex, 22, 1–12.
to adolescence. Biological Psychology, 74, 174–184. Breaux, R. P., McQuade, J. D., Harvey, E. A., & Zakarian, R. J.
Beauchaine, T. P., Gatzke-Kopp, L. M., Neuhaus, E., Chipman, (2018). Longitudinal associations of parental emotion
J., Reid, M. J., & Webster-Stratton, C. (2013). Sympathetic- socialization and children’s emotion regulation: The
and parasympathetic-linked cardiac function and prediction moderating role of ADHD symptomatology. Journal of
of externalizing behavior, emotion regulation, and prosocial Abnormal Child Psychology, 46, 671–683.
behavior among preschoolers treated for ADHD. Journal of Brugnera, A., Zarbo, C., Adorni, R., Tasca, G. A., Rabboni, M.,
Consulting and Clinical Psychology, 81, 481–493. Bondi, E., . . . Sakatani, K. (2017). Cortical and cardiovascular
Beauchaine, T. P., Hong, J., & Marsh, P. (2008). Sex differences responses to acute stressors and their relations with
in autonomic correlates of conduct problems and aggression. psychological distress. International Journal of Psychophysiology,
Journal of the American Academy of Child and Adolescent 114, 38–46.
Psychiatry, 47, 788–796. Byrne, E. A., Fleg, J. L., Vaitkevicius, P. V., Wright, J., & Porges,
Beauchaine, T. P., Katkin, E. S., Strassberg, Z., & Snarr, J. S. W. (1996). Role of aerobic capacity and body mass index
(2001). Disinhibitory psychopathology in male adolescents: in the age-associated decline in heart rate variability. Journal
Discriminating conduct disorder from attention-deficit/ of Applied Physiology, 81, 743–750.
hyperactivity disorder through concurrent assessment of Calkins, S. D., Graziano, P. A., & Keane, S. P. (2007). Cardiac
multiple autonomic states. Journal of Abnormal Psychology, vagal regulation differentiates among children at risk for
110, 610–624. behavior problems. Biological Psychology, 74, 144–153.
Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as Carpenter, R. W., & Trull, T. J. (2013). Components of emotion
a transdiagnostic biomarker of psychopathology. International dysregulation in borderline personality disorder: A review.
Journal of Psychophysiology, 98, 338–350. Current Psychiatry Reports, 15, 335.
Beauchaine, T. P., & Webb, S. J. (2017). Developmental processes Castaldo, R., Melillo, P., Bracale, U., Caserta, M., Triassi, M., &
and psychophysiology. In J. T. Cacioppo, L. G. Tassinary, & Pecchia, L. (2015). Acute mental stress assessment via short
G. G. Berntson (Eds.), Handbook of psychophysiology (4th ed., term HRV analysis in healthy adults: A systematic review
pp. 495–510). New York, NY: Cambridge University Press. with meta-analysis. Biomedical Signal Processing and Control,
Beauchaine, T. P., & Zalewski, M. (2016). Physiological and 18, 370–377.
developmental mechanisms of emotional lability in coercive Chalmers, J. A., Quintana, D. S., Abbott, M. J., & Kemp, A. H.
relationships. In T. J. Dishion & J. J. Snyder (Eds.), The (2014). Anxiety disorders are associated with reduced heart
Oxford handbook of coercive relationship dynamics (pp. 39–52). rate variability: A meta-analysis. Frontiers in Psychiatry, 5, 80.
New York, NY: Oxford University Press. Cicchetti, D., & Rogosch, F. A. (2012). Gene × Environment
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion interaction and resilience: Effects of child maltreatment
regulation, and the latent structure of psychopathology: An and serotonin, corticotropin releasing hormone, dopamine,
integrative and convergent historical perspective. International and oxytocin genes. Development and Psychopathology, 24,
Journal of Psychophysiology, 119, 108–118. 411–427.
Bell, K. L., & Calkins, S. D. (2000). Relationships as inputs and Clamor, A., Lincoln, T. M., Thayer, J. F., & Koenig, J. (2016).
outputs of emotion regulation. Psychological Inquiry, 11, Resting vagal activity in schizophrenia: Meta-analysis of
160–163. heart rate variability as a potential endophenotype. British
Bell, Z., Shader, T. M., Webster-Stratton, C., Reid, M. J., & Journal of Psychiatry, 208, 9–16.
Beauchaine, T. P. (2018). Improvements in negative parenting Cole, P. M., Hall, S. E., & Hajal, N. J. (2013). Emotion
mediate changes in children’s autonomic responding dysregulation as a risk factor for psychopathology. In
following a preschool intervention for ADHD. Clinical T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent
Psychological Science, 6, 134–144. psychopathology (2nd ed., pp. 341–373). Hoboken, NJ:
Berking, M., Margraf, M., Ebert, D., Wupperman, P., Hofmann, Wiley.
S. G., & Junghanns, K. (2011). Deficits in emotion- Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion
regulation skills predict alcohol use during and after regulation as a scientific construct: Methodological challenges
cognitive-behavioral therapy for alcohol dependence. Journal and directions for child development research. Child
of Consulting and Clinical Psychology, 79, 307–318. Development, 75, 317–333.
Bernier, A., Carlson, S. M., & Whipple, N. (2010). From Crowell, S. E., Baucom, B. R., Potapova, N. V., McCauley, E.,
external regulation to self-regulation: Early parenting Fittleson, M., Barth, H., . . . Beauchaine, T. P. (2013).

Mechanisms of contextual risk for adolescent self-injury: Goldsmith, H. H., Pollak, S. D., & Davidson, R. J. (2008).
Emotion invalidation and conflict escalation in mother-child Developmental neuroscience perspectives on emotion
interactions. Journal of Clinical Child and Adolescent regulation. Child Development Perspectives, 2, 132–140.
Psychology, 42, 467–480. Gottman, J. M., Katz, L. F., & Hooven, C. (1997). Meta-emotion:
Crowell, S., Beauchaine, T. P., Gatzke-Kopp, L., Sylvers, P., How families communicate emotionally. Mahwah, NJ:
Mead, H., & Chipman-Chacon, J. (2006). Autonomic Erlbaum.
correlates of attention-deficit/hyperactivity disorder and Graham, R. A., Scott, B. G., & Weems, C. F. (2017). Parenting
oppositional defiant disorder in preschool children. Journal behaviors, parent heart rate variability, and their associations
of Abnormal Psychology, 115, 174–178. with adolescent heart rate variability. Journal of Youth and
Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C., Adolescence, 46, 1089–1103.
Stevens, A. L., & Sylvers, P. (2005). Psychological, Graziano, P., & Derefinko, K. (2013). Cardiac vagal control and
autonomic, and serotonergic correlates of parasuicidal children’s adaptive functioning: A meta-analysis. Biological
behavior in adolescent girls. Development and Psychopathology, Psychology, 94, 22–37.
17, 1105–1127. Grossman, P., Karemaker, J., & Wieling, W. (1991). Prediction of
Crowell, S. E., Butner, J., Wiltshire, T. J., Munion, A. K., tonic parasympathetic cardiac control using respiratory sinus
Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating arrhythmia: The need for respiratory control. Psychophysiology,
emotional and biological sensitivity to maternal behavior 28, 201–216.
among depressed and self-injuring adolescent girls using Grossman, P., & Taylor, E. W. (2007). Toward understanding
nonlinear dynamics. Clinical Psychological Science, 5, respiratory sinus arrhythmia: Relations to cardiac vagal tone,
272–285. evolution and biobehavioral functions. Biological Psychology,
De Brito, S. A., Mechelli, A., Wilke, M., Laurens, K. R., Jones, 74, 263–285.
A. P., Barker, G. J., . . . Viding, E. (2009). Size matters: Hajcak, G., MacNamara, A., Foti, D., Ferri, J., & Keil, A.
Increased grey matter in boys with conduct problems and (2013). The dynamic allocation of attention to emotion:
callous-unemotional traits. Brain, 132, 843–852. Simultaneous and independent evidence from the late
Degnan, K. A., Hane, A. A., Henderson, H. A., Moas, O. L., positive potential and steady state visual evoked potentials.
Reeb-Sutherland, B. C., & Fox, N. A. (2011). Longitudinal Biological Psychology, 92, 447–455.
stability of temperamental exuberance and social-emotional Hamilton, J. L., & Alloy, L. B. (2016). Atypical reactivity of heart
outcomes in early childhood. Developmental Psychology, 47, rate variability to stress and depression across development:
765–780. Systematic review of the literature and directions for future
de Wied, M., van Boxtel, A., Matthys, W., & Meeus, W. (2012). research. Clinical Psychology Review, 50, 67–79.
Verbal, facial and autonomic responses to empathy-eliciting Harte, C. B., & Meston, C. M. (2014). Effects of smoking
film clips by disruptive male adolescents with high versus low cessation on heart rate variability among long-term male
callous–unemotional traits. Journal of Abnormal Child smokers. International Journal of Behavioral Medicine, 21,
Psychology, 40, 211–223. 302–309.
Diamond, L. M., Fagundes, C. P., & Butterworth, M. R. Haynos, A. F., & Fruzzetti, A. E. (2011). Anorexia nervosa as a
(2012). Attachment style, vagal tone, and empathy during disorder of emotion dysregulation: Evidence and treatment
mother–adolescent interactions. Journal of Research on implications. Clinical Psychology Science and Practice, 18,
Adolescence, 22, 165–184. 183–202.
Dietrich, A., Riese, H., Sondeijker, F. E., Greaves-Lord, K., van Heatherton, T. F. (2011). Neuroscience of self and self-regulation.
Roon, A. M., Ormel, J., .
.
.
Rosmalen, J. G. (2007). Annual Review of Psychology, 62, 363–390.
Externalizing and internalizing problems in relation to Heller, A. S., Cohen, A. O., Dreyfuss, M. F. W., & Casey, B. J.
autonomic function: A population-based study in (2016). Changes in cortico-subcortical and subcortico-
preadolescents. Journal of the American Academy of Child and subcortical connectivity impact cognitive control to
Adolescent Psychiatry, 46, 378–386. emotional cues across development. Social Cognitive and
Dixon, M. L., Thiruchselvam, R., Todd, R., & Christoff, K. Affective Neuroscience, 11, 1910–1918.
(2017). Emotion and the prefrontal cortex: An integrative Henry, B. L., Minassian, A., Paulus, M. P., Geyer, M. A., &
review. Psychological Bulletin, 143, 1033–1081. Perry, W. (2010). Heart rate variability in bipolar mania and
El-Sheikh, M. (2005). Stability of respiratory sinus arrhythmia schizophrenia. Journal of Psychiatric Research, 44, 168–176.
in children and young adolescents: A longitudinal Holzman, J. B., & Bridgett, D. J. (2017). Heart rate variability
examination. Developmental Psychobiology, 46, 66–74. indices as bio-markers of top-down self-regulatory
El-Sheikh, M., Harger, J., & Whitson, S. M. (2001). Exposure to mechanisms: A meta-analytic review. Neuroscience and
interparental conflict and children’s adjustment and physical Biobehavioral Reviews, 74, 233–255.
health: The moderating role of vagal tone. Child Development, Ingjaldsson, J., Laberg, J., & Thayer, J. (2003). Reduced heart
72, 1617–1636. rate variability in chronic alcohol abuse: Relationship with
Eisenberg, N., Fabes, R. A., Murphy, B., Maszk, P., Smith, M., & negative mood, chronic thought suppression, and compulsive
Karbon, M. (2008). The role of emotionality and regulation drinking. Biological Psychiatry, 54, 1427–1436.
in children’s social functioning: A longitudinal study. Child Jennings, J. R., Kamarck, T., Stewart, C., Eddy, M., & Johnson,
Development, 66, 1360–1384. P. (1992). Alternate cardiovascular baseline assessment
Fortunato, C. K., Gatzke-Kopp, L. M., & Ram, N. (2013). techniques: Vanilla or resting baseline. Psychophysiology, 29,
Associations between respiratory sinus arrhythmia reactivity 742–750.
and internalizing and externalizing symptoms are emotion Kemp, A. H., Brunoni, A. R., Santos, I. S., Nunes, M. A.,
specific. Cognitive, Affective, and Behavioral Neuroscience, 13, Dantas, E. M., de Figueiredo, R. C., . . . Lotufo, P. A.
238–251. (2014). Effects of depression, anxiety, comorbidity, and

antidepressants on resting-state heart rate and its variability: hyperactivity disorder (ADHD). Journal of Abnormal Child
An ELSA-Brasil cohort baseline study. American Journal of Psychology, 39, 841–852.
Psychiatry, 171, 1328–1334. National Advisory Mental Health Council Workgroup on Tasks
Kemp, A. H., Quintana, D. S., Felmingham, K. L., Matthews, and Measures for Research Domain Criteria. (2016).
S., & Jelinek, H. F. (2012). Depression, comorbid anxiety Behavioral assessment methods for RDoC constructs. Bethesda,
disorders, and heart rate variability in physically healthy, MD: National Institute of Mental Health.
unmedicated patients: Implications for cardiovascular risk. Negrao, B. L., Bipath, P., van der Westhuizen, D., & Viljoen, M.
PLoS One, 7, e30777. (2011). Autonomic correlates at rest and during evoked
Kemp, A. H., Quintana, D. S., Gray, M. A., Felmingham, K. L., attention in children with attention-deficit/hyperactivity
Brown, K., & Gatt, J. M. (2010). Impact of depression and disorder and effects of methylphenidate. Neuropsychobiology,
antidepressant treatment on heart rate variability: A review 63, 82–91.
and meta-analysis. Biological Psychiatry, 67, 1067–1074. Neuhaus, E., Bernier, R., & Beauchaine, T. P. (2014). Social
Koenig, J., Kemp, A., Beauchaine, T. P., Thayer, J. F., & Kaess, skills, internalizing and externalizing symptoms, and
M. (2016). Depression and resting state heart rate variability respiratory sinus arrhythmia in autism. Journal of Autism and
in children and adolescents: A systematic review and meta- Developmental Disorders, 44, 730–737.
analysis. Clinical Psychology Review, 46, 136–150. Nigg, J. T. (2017). Annual Research Review: On the relations
Koenig, J., Kemp, A. H., Feeling, N. R., Thayer, J. F., & Kaess, M. among self-regulation, self-control, executive functioning,
(2016). Resting state vagal tone in borderline personality effortful control, cognitive control, impulsivity, risk-taking,
disorder: A meta-analysis. Progress in Neuro-Psychopharmacology and inhibition for developmental psychopathology. Journal
and Biological Psychiatry, 64, 18–26. of Child Psychology and Psychiatry, 58, 361–383.
Kreibig, S. D. (2010). Autonomic nervous system activity in Obradović, J., Bush, N. R., Stamperdahl, J., Adler, N. E., &
emotion: A review. Biological Psychology, 84, 394–421. Boyce, T. (2010). Biological sensitivity to context: The
Laborde, S., Mosley, E., & Thayer, J. F. (2017). Heart rate interactive effects of stress reactivity and family adversity on
variability and cardiac vagal tone in psychophysiological socioemotional behavior and school readiness. Child
research—Recommendations for experiment planning, Development, 81, 270–289.
data analysis, and data reporting. Frontiers in Psychology, Obrist, P. A. (1981). Cardiovascular psychophysiology. New York,
8, 213. NY: Plenum.
Lapate, R. C., Samaha, J., Rokers, B., Hamzah, H., Postle, B. R., O'Regan, C., Kenny, R. A., Cronin, H., Finucane, C., &
& Davidson, R. J. (2017). Inhibition of lateral prefrontal Kearney, P. M. (2015). Antidepressants strongly influence the
cortex produces emotionally biased first impressions: A relationship between depression and heart rate variability:
TMS/EEG study. Psychological Science, 28, 942–953. Findings from The Irish Longitudinal Study on Ageing.
Levine, J. C., Fleming, R., Piedmont, J. I., Cain, S. M., & Chen, Psychological Medicine, 45, 623–636.
W. J. (2016). Heart rate variability and generalized anxiety Pang, K. C., & Beauchaine, T. P. (2013). Longitudinal patterns of
disorder during laboratory-induced worry and aversive autonomic nervous system responding to emotion evocation
imagery. Journal of Affective Disorders, 205, 207–215. among children with conduct problems and/or depression.
Marcovitch, S., Leigh, J., Calkins, S. D., Leerks, E. M., O’Brien, Developmental Psychobiology, 55, 698–706.
M., & Blankson, A. N. (2010). Moderate vagal withdrawal in Patriquin, M. A., Scarpa, A., Friedman, B. H., & Porges, S. W.
3.5-year-old children is associated with optimal performance (2013). Respiratory sinus arrhythmia: A marker for positive
on executive function tasks. Developmental Psychobiology, 52, social functioning and receptive language skills in children
603–608. with autism spectrum disorders. Developmental Psychobiology,
McLaughlin, K. A., Rith-Najarian, L., Dirks, M. A., & Sheridan, 55, 101–112.
M. A. (2015). Low vagal tone magnifies the association Pittig, A., Arch, J. J., Lam, C. W., & Craske, M. G. (2013). Heart
between psychosocial stress exposure and internalizing rate and heart rate variability in panic, social anxiety,
psycho-pathology in adolescents. Journal of Clinical Child obsessive–compulsive, and generalized anxiety disorders at
and Adolescent Psychology, 44, 314–328. baseline and in response to relaxation and hyperventilation.
Meyer, P. W., Müller, L. E., Zastrow, A., Schmidinger, I., Bohus, International Journal of Psychophysiology, 87, 19–27.
M., Herpertz, S. C., & Bertsch, K. (2016). Heart rate Poliakova, N., Dionne, G., Dubreuil, E., Ditto, B., Pihl, R. O.,
variability in patients with post-traumatic stress disorder or Pe´russe, D., . .
.
Boivin, M. (2014). A methodological
borderline personality disorder: Relationship to early life comparison of the Porges algorithm, fast Fourier transform,
maltreatment. Journal of Neural Transmission, 123, 1107–1118. and autoregressive spectral analysis for the estimation of
Mezzacappa, E., Tremblay, R. E., Kindlon, D., Saul., J. P., heart rate variability in 5-month-old infants. Psychophysiology,
Arseneault, L., Pihl, R. O., & Earls, F. (1996). Relationship 51, 579–583.
of aggression and anxiety to autonomic regulation of heart Porges, S. W. (1995). Orienting in a defensive world: Mammalian
rate variability in adolescent males. Annals of the New York modifications of our evolutionary heritage. A polyvagal
Academy Sciences, 794, 376–378. theory. Psychophysiology, 32, 301–318.
Moore, G. A., Hill-Soderlund, A. L., Propper, C. B., Calkins, Porges, S. W. (2007). The polyvagal perspective. Biological
S. D., Mills-Koonce, W. R., & Cox, M. J. (2009). Mother- Psychology, 74, 116–143.
infant vagal regulation in the face-to-face still-face paradigm Porges, S. W., Doussard-Roosevelt, J. A., & Maiti, A. K. (1994).
is moderated by maternal sensitivity. Child Development, 80, Vagal tone and the physiological regulation of emotion.
209–223. Monographs of the Society for Research in Child Development,
Musser, E. D., Backs, R. W., Schmitt, C. F., Ablow, J. C., Measelle, 59, 167–186.
J. R., & Nigg, J. T. (2011). Emotion regulation via the Rainville, P., Bechara, A., Naqvi, N., & Damasio, A. R. (2006).
autonomic nervous system in children with attention-deficit/ Basic emotions are associated with distinct patterns of

cardiorespiratory activity. International Journal of Task Force of the European Society of Cardiology and the
Psychophysiology, 61, 5–18. North American Society of Pacing and Electrophysiology.
Ritz, T. (2009). Studying noninvasive indices of vagal control: (1996). Heart rate variability: Standards of measurement,
The need for respiratory control and the problem of target physiological interpretation, and clinical use. Circulation,
specificity. Biological Psychology, 80, 158–168. 93, 1043–1065.
Rottenberg, J. (2007). Cardiac vagal tone in depression: A Tau, G. Z., & Peterson, B. S. (2010). Normal development of
critical analysis. Biological Psychology, 74, 200–211. brain circuits. Neuropsychopharmacology, 35, 147–168.
Shader, T. M., Gatzke-Kopp, L. M., Crowell, S. E., Reid, M. J., Thayer, J. F., Hansen, A. L., Saus-Rose, E., & Johnsen, B. H.
Thayer, J. F., Vasey, M. W., . . . Beauchaine, T. P. (2018). (2009). Heart rate variability, prefrontal neural function, and
Quantifying respiratory sinus arrhythmia: Effects of cognitive performance: The neurovisceral integration
misspecifying breathing frequencies across development. perspective on self-regulation, adaptation, and health. Annals
Development and Psychopathology, 30, 351–366. of Behavioral Medicine, 37, 141–153.
Skowron, E. A., Loken, E., Gatzke-Kopp, L. M., Cipriano-Essel, Thayer, J. F., & Lane, R. D. (2000). A model of neurovisceral
E. A., Woehrle, P. L., Van Epps, J. J., . . . Ammerman, R. T. integration in emotion regulation and dysregulation. Journal
(2011). Mapping cardiac physiology and parenting processes of Affective Disorders, 61, 201–216.
in maltreating mother-child dyads. Journal of Family Thompson, R. A. (1990). Emotion and self-regulation. In
Psychology, 25, 663–674. R. A. Thompson (Ed.), Nebraska Symposium on Motivation:
Smith, C. L., Calkins, S. D., & Keane, S. P. (2006). The relation Vol. 36. Socioemotional development (pp. 383–483). Lincoln,
of maternal behavior and attachment security to toddlers’ NE: University of Nebraska Press.
emotions and emotion regulation. Research in Human Thompson, R. A. (1994). Emotion regulation: A theme in search
Development, 3, 21–31. of definition. Monographs of the Society for Research in Child
Snyder, J. J. (1977). Reinforcement analysis of interaction in Development, 59, 25–52.
problem and nonproblem families. Journal of Abnormal Tone, E. B., Garn, C. L., & Pine, D. S. (2016). Anxiety
Psychology, 86, 528–535. regulation: A developmental psychopathology perspective. In
Snyder, J., Edwards, P., McGraw, K., Kilgore, K., & Holton, A. D. Cicchetti (Ed.), Developmental psychopathology, Vol. 2:
(1994). Escalation and reinforcement in mother-child Developmental neuroscience (3rd ed., pp. 523–556). Hoboken,
conflict: Social processes associated with the development of NJ: Wiley.
physical aggression. Development and Psychopathology, 6, Vasilev, C. A., Crowell, S. E., Beauchaine, T. P., Mead, H. K., &
305–321. Gatzke-Kopp, L. M. (2009). Correspondence between
Snyder, J., Schrepferman, L., & St. Peter, C. (1997). Origins of physiological and self-report measures of emotion
antisocial behavior: Negative reinforcement and affect dysregulation: A longitudinal investigation of youth with
dysregulation as socialization mechanisms in family and without psychopathology. Journal of Child Psychology
interaction. Behavior Modification, 21, 187–215. and Psychiatry, 50, 1357–1364.
Souza, G. G. L., Magalhães, L. N., Da Cruz, T. A. R., Webster-Stratton, C., Reid, M. J., & Beauchaine, T. P. (2011).
Mendonça-De-Souza, A. C. F., Duarte, A. F. A., Fischer, Combining parent and child training for young children
N. L., . . . Figueira, I. (2013). Resting vagal control and with attention-deficit/hyperactivity disorder. Journal of
resilience as predictors of cardiovascular allostasis in Clinical Child and Adolescent Psychology, 40, 191–203.
peacekeepers. Stress, 16, 377–383. Yaroslavsky, I., Rottenberg, J., & Kovacs, M. (2013). The utility
Suess, P. E., Porges, S. W., & Plude, D. J. (1994). Cardiac vagal of combining RSA indices in depression prediction. Journal
tone and sustained attention in school-age children. of Abnormal Psychology, 122, 314–321.
Psychophysiology, 31, 17–22. Zisner, A., & Beauchaine, T. P. (2016). Psychophysiological
Sulik, M. J., Eisenberg, N., Silva, K. M., Spinrad, T. L., & methods and developmental psychopathology. In
Kupfer, A. (2013). Respiratory sinus arrhythmia, shyness, D. Cicchetti (Ed.), Developmental psychopathology. Vol. 2:
and effortful control in preschool-age children. Biological Developmental neuroscience (3rd ed., pp. 832–884). Hoboken,
Psychology, 92, 241–248. NJ: Wiley.

CH A PTE R
Event-Related Potentials
13 and Emotion Dysregulation
Brittany C. Speed and Greg Hajcak
Abstract
Emotion dysregulation is a common feature of many psychological disorders. To date, however, most
research evaluating emotion regulation has been limited to self-report assessments. Event-related
potentials (ERPs) are well suited to disentangle discrete aspects of emotional processing that are
critical to understanding both healthy and aberrant emotional functioning. This chapter focuses on
a particular ERP component, the late positive potential (LPP), and reviews evidence that the LPP
is modulated by emotional content and is sensitive to various emotion regulation strategies. Next,
studies leveraging the LPP to examine individual differences in emotional processing in the context
of psychopathology are reviewed. Finally, this chapter discusses methodological limitations of past
research and current gaps in our understanding, including suggestions for future research using ERPs
to study emotion dysregulation.
Keywords: event-related potential, late positive potential, emotion, regulation, depression, anxiety,
trauma, substance use
Introduction been described as a transdiagnostic factor of

There are many ways to conceptualize emotion and psychopathology (Fairholme et al., 2013; Kring &
emotion regulation. In this chapter we consider Sloan, 2009), as most psychiatric disorders involve
emotions as transient changes in one’s subjective the e xperience of emotions that are too intense or
experience, behavior, and physiology that result too prolonged to be adaptive (Beauchaine, 2012;
from motivationally salient internal or external cues Beauchaine, Gatzke-Kopp, & Mead, 2007).
(Gross, 2015; Lang, 1995). In turn, emotion regula- Most early research on emotion and emotion
tion reflects the initiation of a goal to modify one’s regulation relied on subjective reports of emotional
experiential, behavioral, and/or physiological emo- experience (Clore, 1994; Diener, 2000; Watson,
tional response tendencies to facilitate adaptive be- 2000), since self-report measures are convenient
havior (Gross, 1998; Gross, Sheppes, & Urry, 2011; and not limited to assessment of current emotions.
Thompson, 1990). Therefore, emotion dysregulation However, as reflected in broader conceptualizations
can be conceptualized as any pattern of emotional of emotion, subjective experience is only one part of
experience and/or expression that interferes with the multifaceted processes outlined previously.
appropriate goal-directed behavior (Beauchaine, Moreover, evidence demonstrates that when indi-
2012; Beauchaine, Gatzke-Kopp, & Mead, 2007). viduals report on their current experiences of emo-
This definition of emotion dysregulation includes tion versus their past, future, or “typical” emotional
abnormalities at any stage in processes of emotion experiences, they tend to use different sources of in-
generation, including reactivity, and/or subsequent formation (e.g., experiential information vs. gener-
regulation. We therefore review work that addresses alized beliefs), resulting in important discrepancies
each of these processes. Emotion dysregulation has across different types of self-reports (Robinson &
167
Clore, 2002). Thus, it is necessary to use multimethod many other psychophysiological measures (Breiter
assessments that leverage different dependent meas- et al., 1996; Codispoti & De Cesarei, 2007; Codispoti,
ures to more comprehensively assess emotional pro- Ferrari, & Bradley, 2006, 2007), potentiation of
cesses and their regulation. LPPs to emotional relative to neutral stimuli does
Meaningful changes in emotional processing not habituate over repeated presentations (Codispoti
occur rapidly, and electrocortical measures derived et al., 2006; Levinson, Speed & Hajcak, in prepara-
from event-related potentials (ERPs) are an ideal tion). It has been proposed that the LPP indexes
method for studying neural correlates of emotional sustained attention and engagement with emotional
processing (Weinberg, Ferri, & Hajcak, 2013). ERPs content (Hajcak, MacNamara, & Olvet, 2010;
represent near-instantaneous event-locked activity Hajcak & Olvet, 2008; Hajcak et al., 2011; Weinberg
of large and synchronous neural populations— & Hajcak, 2011b).
which is ideal for quantifying rapid changes in A variety of motivationally salient stimuli elicit
brain activity. In fact, ERPs can be used to track LPPs, such as emotional scenes, faces, and words
neural changes in response to emotional stimuli on (Cuthbert et al., 2000; Dillon, Cooper, Grent-‘t-
a millisecond-by-millisecond basis, making it pos- Jong, Woldorff, & LaBar, 2006; Eimer & Holmes,
sible to effectively isolate and quantify core aspects 2007; Schupp, Cuthbert, et al., 2004; Speed,
of emotion reactivity and emotion regulation. Levinson, Gross, Kiosses, & Hajcak, 2017). In
Furthermore, compared to other neuroimaging addition, emotional modulation of LPPs appear to
techniques, ERPs are relatively inexpensive, have be independent of perceptual features of stimuli, in-
few contraindications, and are well tolerated in cluding size (De Cesarei & Codispoti, 2006), and
both young and old populations. other perceptual characteristics (Bradley, Hamby,
Several distinct ERPs are modulated by emotional Low, & Lang, 2007). Previous work indicates that
stimuli, such as the P200 and the P300 (Carretie, emotional modulation of LPPs reflects the emo-
Hinojosa, Martin-Loeches, Mercado, & Tapia, 2004; tional intensity of stimulus content, and is not due
Crowley & Colrain, 2004; Huang & Luo, 2006; merely to stimulus novelty, perceptual differences,
Lifshitz, 1966; Mini, Palomba, Angrilli, & Bravi, or expectation violations. Emotional modulation of
1996; Naumann, Bartussek, Diedrich, & Laufer, the LPP is subject to genetic influence (Weinberg,
1992; Schupp, Junghöfer, Weike, & Hamm, 2004). Venables, Proudfit, & Patrick, 2015), and thus,
Although these ERPs appear to index early attention magnitude differences in LPPs may specify a herita-
to salient information, they are not well suited to ble biomarker of individual differences in emotional
capture changes in emotional responses that result processing. It is important to note that psychometric
from emotion regulation. Accordingly, we focus on evaluations of LPPs to emotional scenes and adjec-
the late positive potential (LPP), which can be used tives indicate good test–retest reliability and internal
to assess both emotional processing as it unfolds over consistency, supporting its appropriateness for the
time and emotion regulatory processes. Although study of individual differences in emotional proc-
the LPP has been used to study individual differences essing (Auerbach, Bondy, et al., 2016; Codispoti
across various psychiatric disorders, we focus on the et al., 2006; Moran, Jendrusina, & Moser, 2013).
most commonly examined disorders, including de- Unlike many more transient ERPs, emotional
pression, anxiety, substance abuse/dependence, and modulation of LPPs is sustained throughout stimu-
posttraumatic stress disorder. lus presentation (i.e., for several seconds; see Hajcak
et al., 2010) and can be observed for as long as 1,000
The Late Positive Potential: From ms after stimulus offset (Hajcak & Olvet, 2008).
Emotional Reactivity to Regulation The time course of LPPs supports the argument that
The LPP is a positive deflection maximal at central- emotional content not only captures but also holds
parietal midline recording sites that begins by 200 attention (Vuilleumier, 2005). Spatially, LPPs appear
ms after stimulus onset (Foti, Hajcak, & Dien, to shift over the course of emotional processing,
2009). As depicted in Figure 13.1, the LPP is poten- beginning with a parietally maximal distribution
tiated by emotional (e.g., pleasant, unpleasant) that progresses to a centrally maximal distribution.
compared to neutral stimuli, and the LPP magnitude This “frontalization” may suggest that earlier
remains potentiated for the duration of stimulus versus later segments of LPPs reflect separable com-
presentation (Cuthbert, Schupp, Bradley, Birbaumer, ponents (Foti et al., 2009; Hajcak et al., 2011;
& Lang, 2000; Hajcak & Olvet, 2008; Hajcak, MacNamara, et al., 2009). Indeed, earlier segments
Weinberg, MacNamara, & Foti, 2011). Unlike of the LPP (300 to 600 ms) appear to represent
168 Event-Rel ated Potentials and Emotion Dysregul ation

CPz
Amplitude (µV)
5
10
15 Pleasant
Neutral
Unpleasant
20
0 200 400 600 800 1,000

Time (msec)
Pleasant-Neutral –3 Unpleasant-Neutral
+2
+7
+15
Figure 13.1 Top: Grand averaged event-related potential (ERP) waveforms at electrode site CPz elicited during passive viewing
of pleasant, neutral, and unpleasant pictures. Picture onset occurred at 0 msec. Negative voltage changes are plotted as upward
deflections. Bottom: Voltage maps for pleasant minus neutral and unpleasant minus neutral comparisons at t = 700 msec. The figure is
based on data collected by Hajcak and Nieuwenhuis (2006).
more automatic processing of emotional content, example, studies that use open-ended (i.e., nonspe-
whereas later segments (600 ms and beyond) may cific) instructions to reduce the intensity of negative
represent more deliberative engagement with stimu- emotions show that LPPs to unpleasant pictures are
lus content (Olofsson, Nordin, Sequeira, & Polich, attenuated during regulation relative to control
2008; Weinberg & Hajcak, 2011b; Weinberg, conditions (Krompinger et al., 2008; Moser et al.,
Hilgard, Bartholow, & Hajcak, 2012). Previous re- 2006). In an evaluation of effects of cognitive reap-
search demonstrates that the duration of LPPs can praisal on LPPs, Hajcak and Nieuwenhuis (2006)
be manipulated using instructions that encourage demonstrated that LPP magnitude was substan-
participants to maintain previously viewed stimuli tially reduced when participants were instructed to
in working memory, supporting the argument that reinterpret unpleasant pictures using cognitive re-
more sustained aspects of LPPs index intentional appraisal relative to when participants were in-
engagement with emotional stimuli (Hajcak et al., structed to simply attend to unpleasant picture
2010; Thiruchselvam, Hajcak, & Gross, 2012). content (see Figure 13.2). Furthermore, reduction
Critically, LPPs are sensitive to various emotion in LPP amplitude during reappraisal was correlated
regulation strategies, making them ideal for study- positively with reductions in self-reported emotional
ing individual differences in emotion regulation intensity following reappraisal. Parvaz, MacNamara,
(Foti & Hajcak, 2008; Hajcak & Nieuwenhuis, Goldstein, and Hajcak (2012) found similarly that
2006; Krompinger, Moser, & Simons, 2008; Moser, LPPs in response to unpleasant pictures were re-
Hajcak, Bukay, & Simons, 2006; Thiruchselvam, duced following instructions to use cognitive
Blechert, Sheppes, Rydstrom, & Gross, 2011). For reappraisal compared to unpleasant pictures that
Speed and Hajcak 169

CPz Attend-Reappraise
–5 –3
0
Amplitude (µV) +2
10 +7
15
0 500 1,000 1,500 2,000 +15
Time (msec)
Reappraise Attend
Figure 13.2 Left: Grand averaged event-related potential (ERP) waveforms at electrode site CPz associated with unpleasant pictures
during cognitive reappraisal (solid line) and focused attention (dashed line). Picture onset occurred at 0 msec. Negative voltage changes
are plotted as upward deflections. Shaded gray areas represent 100-msec windows in which the reappraise late positive potential (LPP)
differed reliably from the attend LPP. Right: Voltage map for the attend minus reappraise comparison at t = 700 msec. The figure is
based on data collected by Hajcak and Nieuwenhuis (2006).
were viewed normally. This effect appears to be when faces were presented in unattended locations.
independent of methodological differences across Extending these findings, Eimer, Holmes, and
studies, such as how (visual vs. auditory) and when McGlone (2003) found that LPPs are potentiated
(before vs. after picture onset) reappraisal instruc- to faces displaying six basic emotions (angry, dis-
tions are provided (Hajcak & Nieuwenhuis, 2006; gusted, fearful, happy, sad, and surprised) relative to
Parvaz et al., 2012). For instance, one study pro- neutral, but only when faces are the focus of direct
vided auditory reappraisal frames before picture attention (see also Keil, Moratti, Sabatinelli,
viewing (i.e., “preappraisal”) and found that LPPs Bradley, & Lang, 2005). These findings are poten-
were reduced in response to unpleasant pictures tially important, since shifting spatial attention is a
that followed neutral descriptions, compared to relatively common and effective strategy for regulat-
LPPs elicited by unpleasant pictures that fol- ing emotion. For example, when instructed to de-
lowed negative descriptions (Foti & Hajcak, crease emotions to unpleasant images, participants
2008). Replicating and extending these findings, frequently look at unimportant or nonemotional
MacNamara and colleagues (2009) found that areas of pictures—and such changes in gaze account
LPPs were potentiated when neutral pictures were for significant variance in brain activity as assessed
preappraised in negative terms, demonstrating by functional magnetic resonance imaging (fMRI;
that effects of appraisal on LPPs are not specific to van Reekum et al., 2007). Similarly, LPP magnitude
unpleasant pictures. Furthermore, cognitive reap- is reduced when participants’ gaze is directed to
praisal attenuates LPPs when participants view low-arousal aspects of unpleasant pictures com-
words linked to negative autobiographical memo- pared to when their gaze is directed to high-arousal
ries (Speed et al., 2017. This suggests that cognitive parts of pictures (Dunning & Hajcak, 2009;
reappraisal is an effective strategy in reducing LPPs Hajcak, Dunning, & Foti, 2009). Thus, volitional
elicited by idiographic stimuli. Together, these redirection of spatial attention appears to be an ef-
findings illustrate that changing the meaning of an fective strategy for altering LPP magnitude during
emotional stimulus, via reappraisal or preappraisal, processing of visual emotional information. These
can alter amplitudes of LPPs. findings suggest that altering the meaning of or
In addition to cognitive reappraisal, manipulations modifying attention to an emotional stimulus can
of visual attention can effectively modulate LPPs. modify the magnitude of LPPs.
For example, when pictures of neutral or fearful Emotional modulation of LPPs can be observed
faces were presented in attended locations during a in children as young as 5 years (Hajcak & Dennis,
spatial attention task, participants demonstrated a 2009), making it possible to study developmental
potentiated LPP to fearful relative to neutral faces changes in emotional processing over the lifespan.
(Holmes, Vuilleumier, & Eimer, 2003). However, the Evaluations of developmental differences reveal that
effect of emotion expression on LPPs was eliminated younger (18 to 26 years) and older (60 to 77 years)

adults display comparable modulation of LPPs The self-referential encoding task (SRET; Rogers,
when viewing emotional compared to neutral Kuiper, & Kirker, 1977) has been used to investigate
pictures, and comparable regulation of LPPs to depressogenic self-referential biases in depression.
emotional pictures (Langeslag & Van Strien, In this task, participants are asked to make judgments
2010). Notably, childhood and adolescence are regarding whether positive (e.g., happy, excited) or
characterized by considerable reorientation in af- negative (e.g., loser, worthless) adjectives are self-
fective processing and changes in cognitive control descriptive. Past research reveals that depressed adults
(E. E. Nelson, Leibenluft, McClure, & Pine, 2005; and adolescents demonstrate potentiated LPPs to
Luna, Padmanabhan, & O’Hearn, 2010), raising negative relative to positive adjectives during the
questions about when specific emotion regulation SRET, whereas nondepressed individuals display
skills are acquired, and trajectories of their func- potentiated LPPs to positive relative to negative ad-
tioning. Data suggest that older children (8 to jectives (Auerbach, Stanton, Proudfit, & Pizzagalli,
10 years) can effectively use directed reappraisal to 2015; Shestyuk & Deldin, 2010). Thus, depressed
reduce LPP amplitude to unpleasant pictures adolescents and adults exhibit abnormal neural re-
(DeCicco, O’Toole, & Dennis, 2014; Dennis & sponses to negative compared to positive stimuli in
Hajcak, 2009). However, young children (5 to the SRET. Furthermore, never-depressed children
7 years) do not display reduced LPPs to unpleasant and adolescents who are at elevated risk for depres-
pictures using directed reappraisal (Babkirk, Rios, sion based on maternal life history of MDD also
& Dennis, 2015; DeCicco et al., 2014; Dennis & display potentiated LPPs to negative words during
Hajcak, 2009). Thus, this cognitive ability may the SRET—an effect that is independent of current
not emerge until ages 8 to 9, though within-subjects depressive symptoms (Speed, Nelson, Auerbach,
comparisons are needed before strong conclusions Klein, & Hajcak, 2016). Increased risk for depres-
are drawn. Babkirk and colleagues (2015) evaluated sion is therefore associated with more elaborative
individual differences in emotion regulation ability processing of negative information, which may be
among children ages 5 to 10 years by comparing important for the development of negative schemas
those who displayed reappraisal-induced reductions and reflect vulnerability for depression.
in LPPs to those who did not, and found that chil- Although depressed individuals and those who
dren who showed reductions in the LPP using reap- are at risk exhibit increased LPPs to negative relative
praisal displayed more adaptive emotion regulation to positive words, studies that use standardized
strategies both concurrently and 2 years later. These emotional picture sets typically find that LPPs are
data provide support for the LPP as a useful index of attenuated in response to both pleasant and unpleas-
emotion regulatory capacity in children, which may ant stimuli among depressed individuals (for a review
help in early identification of those at increased risk see Proudfit, Bress, Foti, Kujawa, & Klein, 2015).
for development of emotional problems. Although this pattern of emotional responding ap-
pears to run counter to descriptions of depression, it
Emotion Dysregulation in is consistent with the Emotion Context-Insensitivity
Psychopathology: Evidence (ECI) model proposed by Rottenberg and colleagues
from the Late Positive Potential (Rottenberg & Gotlib, 2004; Rottenberg, Gross, &
Depression Gotlib, 2005). According to this model, emotional
Major depressive disorder (MDD) is characterized dysfunction in MDD is best understood as lack of
by pronounced feelings of sadness and/or loss of engagement with emotional stimuli in the environ-
pleasure in previously enjoyed activities (American ment. In an early study involving passive viewing of
Psychiatric Association, 2013). Oftentimes, MDD emotional words, individuals with MDD showed
involves a combination of increased negative affec- blunted LPPs to both pleasant and unpleasant emo-
tivity (e.g., irritability) and decreased positive af- tional words, although the LPP to neutral words did
fectivity (e.g., anhedonia). Consequently, it stands not differ (Blackburn, Roxborough, Muir, Glabus,
to reason that depressed individuals should dem- & Blackwood, 1990). In addition, Kayser and
onstrate increased reactivity to mood-congruent colleagues found that patients with MDD demon-
negative stimuli and decreased reactivity to mood- strated blunted LPPs when viewing unpleasant
incongruent positive stimuli. To some extent, this pictures of dermatological disease (Kayser, Bruder,
is consistent with data derived from depressed in- Tenke, Stewart, & Quitkin, 2000). Consistent with
dividuals when they evaluate the personal relevance these early studies, a growing body of research
of verbally presented word stimuli. suggests that both MDD and elevated depressive

symptoms are associated with reduced LPPs to responding on experimental tasks (Dillon, Ritchey,
positive and negative emotional stimuli among both Johnson, & LaBar, 2007; Richards & Gross, 2000;
children and adults (Foti, Olvet, Klein, & Hajcak, Richards, Butler, & Gross, 2003; Sheppes, Catran, &
2010; Kujawa, MacNamara, Fitzgerald, Monk, & Meiran, 2009). For example, LPPs are potentiated
Phan, 2015; MacNamara, Kotov, & Hajcak, 2016; on trials immediately following cognitive reappraisal,
Weinberg, Perlman, Kotov, & Hajcak, 2016). and magnitudes of LPPs following reappraisal are
Notably, blunted LPPs to emotional stimuli may be associated positively with depressive symptoms
associated with a specific subgroup of depressed in- (Parvaz, Moeller, Goldstein, & Proudfit, 2015). This
dividuals who experience early-onset depression. suggests that cognitive reappraisal may require
Weinberg and colleagues (2016) found that only greater engagement of top-down resources among
patients with early-onset depression (first episode depressed individuals.
before age 18 years) displayed reduced LPPs to pos- Others have examined LPPs to evaluate individ-
itive and negative pictures, whereas individuals with ual differences in emotional reactivity and regula-
adult-onset depression exhibited LPPs that were tion associated with suicidality—a common and
comparable to never-depressed controls. These find- severe symptom of depression (and several other
ings were evident despite similar clinical presenta- psychiatric disorders). Among a clinical sample of
tions of symptoms across depressed groups at the individuals with anxiety and/or unipolar depressive
time of the study, suggesting that variability in the disorders and healthy controls, current severity of
LPP to emotional stimuli may reflect a specific phe- suicidal ideation was associated with blunted LPPs
notype of early-onset depression. to both rewarding and threatening images across all
Consistent with the notion that emotion context participants, even when controlling for other symp-
insensitivity is a risk factor for depression, blunted toms of depression (Weinberg et al., 2016). These
LPPs to emotional faces and scenes are observed in data may suggest that disengagement from emotional
children of parents with lifetime histories of depres- stimuli—as indexed by LPPs—may be linked to su-
sion (Kujawa, Hajcak, Torpey, Kim, & Klein, 2012; icidality across diagnostic boundaries. Furthermore,
B. D. Nelson, Perlman, Hajcak, Klein, & Kotov, regardless of current suicidal ideation, outpatients
2015) and among adolescent girls with low positive who have attempted suicide exhibit blunted LPPs
emotionality—a personality trait associated with to threatening pictures, but not rewarding or neu-
risk for depression (Speed et al., 2015). Furthermore, tral pictures (Weinberg, May, Klonsky, Kotov, &
in a prospective study of girls ages 8 to 14 years at Hajcak, 2017). Thus, diminished reactivity to threat
baseline, when controlling for initial depressive specifically may distinguish suicide attempters from
symptoms, blunted LPPs to emotional pictures in- ideators. Data also suggest that suicidal ideation is
teracted with increased negative life events to pre- associated with abnormalities in using adaptive
dict increases in depressive symptoms 2 years later emotion regulation strategies, including cognitive
(Levinson, Speed, & Hajcak, 2017). Therefore, data reappraisal. For example, undergraduates with his-
from at-risk children and adolescents suggest that tories of suicidal ideation show larger LPPs to dys-
blunted LPPs to emotional stimuli may be a prom- phoric images during cognitive reappraisal (Kudinova
ising biomarker of vulnerability to depression fol- et al., 2016).
lowing stress. To summarize, depressed individuals display po-
Taken together, evidence from SRET and pas- tentiated LPPs when viewing negative relative to
sive viewing paradigms indicate that depressed and positive adjectives during the SRET, indicating neg-
at-risk individuals experience aberrant emotional ative self-referential bias. In contrast, when viewing
processing. However, there is a paucity of ERP re- emotional pictures that are not self-referential, those
search investigating abnormalities in effortful (i.e., with depression and those with histories of suicidal
explicit) emotion regulation in depressed individ- ideation show blunted LPPs to both negative and
uals. In a small community sample of children ages positive stimuli, reflecting disengagement from
5 to 10 years, anxious/depressed symptoms were salient environmental information. Although few
associated positively with larger LPPs during di- studies have used LPPs to examine abnormalities in
rected reappraisal, suggesting that children with effortful regulation in depression, there is some
elevated internalizing symptoms are less able to evidence that depressive symptoms and suicidal

regulate their reactions to unpleasant images ideation are associated with larger LPPs during and
(Dennis & Hajcak, 2009). Of note, engaging in following cognitive reappraisal, suggesting difficul-
effortful cognitive reappraisal can affect subsequent ties using cognitive reappraisal to reduce negative

emotion. However, more research on effortful spider phobia exhibit potentiated LPPs to spider
regulation is needed using clinically depressed and at- stimuli relative to other negative stimuli during an
risk samples, ideally comparing more than one type early time window (340 to 770 ms), but not during
of regulation strategy to more thoroughly evaluate a later time window (800 to 1,500 ms). This may
the nature of emotion dysregulation in depression. reflect a maladaptive emotion regulation strategy
(avoidance) that prevents habituation to feared
Anxiety stimuli (Leutgeb et al., 2009). Individuals who
Depression and anxiety are often comorbid and complete exposure therapy display potentiated and
share many features (Goldberg, Krueger, Andrews, sustained LPPs to spider stimuli, consistent with the
& Hobbs, 2009). Nevertheless, evidence from LPP possibility that exposure therapy reduces avoidance
studies suggests that depression and anxiety differ (Leutgeb et al., 2009). This finding has been repli-
somewhat in emotion dysregulation. In contrast to cated in individuals with generalized anxiety disor-
depression, anxiety is associated with potentiated der, who were characterized by a potentiated early
LPPs to unpleasant pictures among both children neural response (P100) to unpleasant compared to
and adults—an effect that may reflect heightened neutral pictures, and an attenuated later LPP to un-
reactivity toward threat (Kujawa et al., 2015; pleasant compared to neutral pictures relative to
MacNamara et al., 2016; MacNamara & Hajcak, healthy controls. This supports the argument that
2010). LPPs are potentiated to participant-specific anxious individuals experience early hypervigilance
fears, such as pictures of spiders in both adults and to threatening stimuli followed by failure to engage
children with spider phobias (Kolassa, Musial, Mohr, in elaborative processing (Weinberg & Hajcak,
Trippe, & Miltner, 2005; Leutgeb, Schäfer, Köchel, 2011a). In addition to using maladaptive emotion
Scharmüller, & Schienle, 2010; Leutgeb, Schäfer, & regulation strategies, some individuals with anxiety
Schienle, 2009; Michalowski et al., 2009; Miltner may experience difficulty using adaptive emotion
et al., 2005), pictures of faces in individuals with regulation strategies, such as cognitive reappraisal.
social anxiety (Moser, Huppert, Duval, & Simons, For instance, Paul and colleagues (2016) observed that
2008; Mühlberger et al., 2009), disorder-relevant in contrast to healthy controls, patients with OCD
pictures in patients with obsessive-compulsive disor- were unable to reduce the magnitude of their LPPs
der (OCD; Paul, Simon, Endrass, & Kathmann, to unpleasant and disorder-relevant pictures using
2016), and aversive pictures in individuals with gen- cognitive reappraisal—an effect that was associated
eralized anxiety disorder (GAD; MacNamara & with less frequent use of reappraisal in daily life.
Hajcak, 2010). In an outpatient sample, MacNamara Taken together, this research highlights the im-
and colleagues (2016) found that both diagnoses and portance of assessing both anxious and depressive
symptoms of GAD were associated with potentiated symptoms when examining individual differences
LPPs to unpleasant pictures, controlling for MDD in emotion dysregulation, as these frequently co-
diagnoses, whereas MDD was associated with morbid disorders may be characterized by differing
blunted LPPs to unpleasant pictures. Consistent patterns of reactivity to aversive stimuli. Moreover,
with studies among adults, adolescents with anxiety individual differences in the time course of the LPP
disorders exhibit potentiated LPPs to angry and fear- might be leveraged to understand important
ful faces compared to healthy controls, an effect that changes in emotional processing that unfold over
is also modulated by depressive symptoms, such that time, such as maladaptive vigilance-avoidance pat-
higher depressive symptoms were associated with terns, which could be targeted in treatment. Finally,
reduced LPPs to angry faces in both groups (Kujawa much like research on depression, there is scant evi-
et al., 2015). Notably, potentiated LPPs to angry dence regarding regulation deficits in anxiety using
faces predicted better treatment response to both the LPP.
cognitive-behavioral therapy (CBT) and antidepres-
sant medication, even accounting for pretreatment Posttraumatic Stress Disorder
anxiety severity (Bunford et al., 2017). Thus, in- Emotion dysregulation is a core feature of PTSD
creased LPPs to threatening images may be a useful (Etkin & Wager, 2007). Several symptoms of PTSD,
biomarker for identifying individuals most likely to including intrusive traumatic memories, avoidance
respond to treatment. of trauma-related cues, and abnormal reactivity
There is also evidence that individuals with pho- (e.g., heightened arousal, emotional numbing;
bias display an attentional pattern of early vigilance American Psychiatric Association, 2013), indicate
followed by avoidance to feared stimuli. Those with that emotion dysfunction may occur at several

ifferent stages in emotional processing, and that
d faces, possibly due to numbing or avoidance,
significant heterogeneity in the type of emotion dys- may therefore be linked to both diagnoses and
regulation may exist across individuals. Therefore, it specific symptom dimensions of PTSD (e.g.,

is not entirely surprising that evidence regarding the re-experiencing).
nature of emotion dysfunction using the LPP is Extending beyond reactivity, Fitzgerald et al.
equivocal (for a review see Lobo et al., 2015). For (2016), using a cross-sectional design comparing
example, when using a passive picture-viewing par- emotion regulation ability in combat veterans with
adigm in an undergraduate sample, Lobo et al. and without PTSD, found no group differences in
(2014) found that greater symptoms were associated LPPs before or during cognitive reappraisal to nega-
positively with LPPs to unpleasant relative to neu- tive pictures. Rather, reappraisal resulted in similar
tral pictures. Symptom severity therefore was associ- reductions of LPPs in both veterans with and veterans
ated with heightened reactivity to negative stimuli. without PTSD. In contrast, smaller reductions in
Similarly, individuals with PTSD display potenti- LPPs during reappraisal to negative images, relative
ated LPPs when viewing trauma-specific questions to when viewing negative images, were associated
relative to neutral questions (Wessa, Jatzko, & Flor, with greater PTSD symptoms 1 year later among
2006). Combat veterans with PTSD symptoms combat-exposed veterans—even controlling for
show potentiated early-window LPPs to trauma- baseline PTSD, depression, and anxiety symptoms
related smells (e.g., diesel fuel), and increased LPP (Fitzgerald et al., 2017). Thus, although individuals
amplitudes to these scents are associated with with PTSD may not experience difficulties using
greater reduction in symptoms following treatment cognitive reappraisal to decrease negative emotion
(Bedwell et al., 2017). Thus, PTSD is associated with compared to individuals without PTSD, difficulties
heightened LPP reactivity to trauma-related cues, in down-regulating negative emotion may be a
and emotional modulation of LPPs might serve as a useful predictor of symptom change among combat-
treatment response moderator. However, more re- exposed veterans.
search is needed using larger, more representative In sum, variation in LPP effects across studies
samples. In addition, Fitzgerald et al. (2017) found supports the notion that PTSD is a heterogeneous
that potentiated LPPs to negative relative to neutral disorder. Individuals with PTSD vary greatly in
pictures during a baseline assessment predicted ele- their experience of emotion dysregulation (e.g.,
vated re-experiencing symptoms over the next year. blunted reactivity, heightened reactivity, reappraisal
Thus, individual differences in emotional reactivity deficits), and important changes in specific symptoms
may relate to changes in specific symptoms over time. may occur within individuals over time. Inconsistent
Notably, there is some evidence that individual dif- findings may be partially due to methodological
ferences in emotional processing prior to trauma may differences, including task and stimuli used to elicit
predict who is most likely to experience symptoms. LPPs, timing of assessments (cross-sectional vs.
For example, among children exposed to a natural longitudinal), and differences in types of symptoms
disaster, potentiated LPPs to negative images— examined (e.g., clinical diagnoses, overall symptom
assessed prior to the disaster—prospectively pre- severity, specific symptom severity). Therefore,
dicted psychiatric symptom severity in the six months whether individuals with PTSD demonstrate
following the disaster (Kujawa et al., 2016). elevated or reduced emotional reactivity and regula-
In contrast, other studies using emotional pic- tory abilities may depend on the type of emotional
ture viewing paradigms have failed to find differ- stimuli used to elicit the LPP and the relative role of
ences in LPPs between combat veterans with and specific symptom dimensions.
without PTSD (Fitzgerald et al., 2016; Wessa,
Karl, & Flor, 2005; Woodward et al., 2015). Some Substance Abuse and Dependence
studies using an emotional face-matching para- For most substances, neurobiological models of
digm in combat-exposed veterans found that vet- addiction are based on the notion that drugs co-opt
erans with PTSD displayed smaller LPPs to angry then modify reward processing by increasing the
faces relative to veterans without PTSD (DiGangi motivational salience of drug-related cues and by
et al., 2017; MacNamara, Post, Kennedy, Rabinak, & reducing the motivational salience of non-drug-
Phan, 2013). In addition, MacNamara et al. (2013) related cues (Koob & Volkow, 2010; Volkow, Koob,
found that LPPs in response to fearful faces were & McLellan, 2016). Because LPPs are thought to
associated negatively with intrusive (re-experiencing) reflect increased processing of motivationally salient
symptoms. Blunted processing of negative emotional stimuli (see earlier section, The Late Positive Potential:

From Emotional Reactivity to Regulation), it is of substances. In addition, consistent with studies
unsurprising that several studies have examined
that find that cognitive regulation strategies can
abnormalities in LPPs to drug-related stimuli
reduce drug craving (Kober, Kross, Mischel, Hart,
among individuals with substance use disorders & Ochsner, 2010), cognitive reappraisal and dis-
(SUDs). Evidence from early studies suggests that traction reduce the magnitude of LPPs to smok-
drug-related pictures elicit larger LPPs compared to ing cues among both light and heavy smokers
neutral pictures in individuals with alcohol (Littel & Franken, 2011). Thus, effective regula-
(Namkoong, Lee, Lee, Lee, & An, 2004), cannabis tion of craving-associated cues is marked by LPP
(Nickerson et al., 2011), cocaine (Dunning et al., responses among individuals with differing levels
2011; Franken, Hulstijn, Stam, Hendriks, & van of dependency.
den Brink, 2004; Franken et al., 2008; van de Laar, In sum, studies of LPPs are consistent with
Licht, Franken, & Hendriks, 2004), and heroin models of drug addiction, which specify potentiated
(Franken, Stam, Hendriks, & van den Brink, 2003; processing of drug-related stimuli at the expense of
Yang, Zhang, & Zhao, 2015) use disorders. Thus, non-drug-related motivationally salient reinforcers
these individuals show increased sustained attention (Koob & Volkow, 2010; Volkow et al., 2016). As
to addiction-related stimuli. Furthermore, increased with work in depression and anxiety, there remains
LPPs to cocaine pictures are associated with cocaine limited understanding as to whether individuals
craving (Franken et al., 2003). with SUDs exhibit abnormalities in explicit emo-
Extending these findings, studies show that indi- tion regulation as indexed by the LPP, as the major-
viduals with opiate use disorder display increased ity of studies have only examined reactivity.
LLP responding to drug-related stimuli and decreased
responding to non-drug-related (i.e., pleasant) Summary and Future Directions
stimuli compared to controls (Lubman, Allen, The LPP is a sustained positive deflection in the
Peters, & Deakin, 2008; Lubman et al., 2009). stimulus-locked ERP in response to emotional
Similarly, individuals with cocaine use disorders compared to neutral stimuli. Modulation of the
display potentiated early LPPs to cocaine-related LPP reflects motivational salience of stimulus con-
pictures relative to controls, and blunted LPPs to tent, which is subject to modification using various
standardized pleasant and unpleasant pictures emotion regulation strategies. Given its unique abil-
(Dunning et al., 2011). Evidence suggests that ity to differentiate between various stages of emo-
smokers who display potentiated LPPs to cigarette- tional processing that occur over relatively short
related cues compared to pleasant pictures are less periods of time, the LPP is ideally suited to examine
likely to achieve long-term (6-month) smoking individual differences in emotional reactivity and
abstinence following intervention, compared to
regulation associated with psychopathology and
smokers who display potentiated LPPs to pleasant various forms of emotion dysregulation. Indeed,
pictures relative to cigarette-related cues (Versace emotional processing abnormalities during emo-
et al., 2012). Therefore, individual differences in tional picture viewing are observed using LPPs
sensitivity to reward-related cues, as indexed by the across depression, anxiety, PTSD, and SUDs.
LPP, may be useful in predicting long-term out- Collectively, these data suggest that the LPP could
comes (for a review see Moeller & Paulus, 2017). be leveraged further as a transdiagnostic biomarker
Indeed, studies of individuals with substance use of emotion dysregulation.
disorders show that blunted LPPs to normative Studies of individual differences have, by and
pleasant stimuli predict future relapse and drug use large, examined emotional reactivity rather than
(Lubman et al., 2009; Versace et al., 2012, 2017). emotion regulation. This imbalance indicates an
Thus, blunted responding to naturally rewarding important opportunity for future research to exam-
stimuli may be a vulnerability to continued use. ine both processes in tandem. Emotion dysregula-
There are also data indicating that abstinence re- tion is an important feature of many psychological
verses magnitude differences in LPPs between drug- problems, including eating disorders, personality
related and pleasant stimuli in treatment-seeking disorders, and behavioral disturbances in children
individuals with cocaine use disorder (Parvaz et al., (just to name a few). However, few objective exami-
2017). Taken together, it appears that individual dif- nations of emotional processing using the LPP have
ferences in LPPs to drug versus emotional stimuli been conducted in these populations, despite signif-
may indicate clinical progress. However, it remains icant opportunities. For example, individuals with
unclear if findings generalize across different types anorexia nervosa display increased LPPs to extremely

underweight bodies relative to other body types, few studies have used Davidson’s metrics to evaluate
suggesting abnormalities in motivated attention affective chronometry using the LPP, data suggest
toward body shapes (Horndasch et al., 2017. In that the time course of LPPs prompted by emotional
addition, although emotion dysregulation is a
stimuli can be modified by cognitive instructions
hallmark of borderline personality disorder (BPD; (Hajcak & Olvet, 2008; Hajcak et al., 2010).
Conklin, Bradley, & Westen, 2006; Glenn & Therefore, in addition to examining LPP magnitude,
Klonsky, 2009), studies examining emotional proc- future studies might benefit from evaluating the
essing abnormalities in BPD using the LPP are rare. time course of LPPs to differentiate specific aspects
One study investigated negative bias in BPD using of emotional processing that might be abnormal in
a forced-choice facial expression recognition task various forms of psychopathology.
and found that patients demonstrated blunted early A general limitation of emotion regulation studies
responding (P300) to predominantly happy faces, using ERPs is that they have relied on standardized
but not predominantly angry faces (Hidalgo et al., emotional words, picture sets, and films (Buhle et al.,
2016). In addition, ERP evidence obtained during 2014; Dillon et al., 2006; Gross, 2002; Hajcak et al.,
the SRET indicates that female youth with BPD 2010; Schupp, Flaisch, Stockburger, & Junghöfer,
show negative self-referential bias, as indexed by a 2006). Appraisal theories suggest that self-relevance
potentiated LPP to negative relative to positive ad- of stimuli affects the intensity of resulting emotions,
jectives (Auerbach, Tarlow, et al., 2016). Thus, ado- which in turn influence the success of regulation at-
lescents with BPD allocate greater resources when tempts (Ellsworth & Scherer, 2003). Thus, although
processing negative self-referential information, simi- there is strong evidence that adults can use cognitive
lar to individuals with depression. To date, however, reappraisal successfully to alter emotional respond-
no studies have used the LPP to evaluate emotion ing to standardized emotional stimuli, and that re-
regulation abilities among those with BPD. Linehan’s sponding to such stimuli has important associations
(1993) biosocial theory argues that individuals with with psychopathology, there may be important dif-
BPD display abnormalities at several stages of ferences in one’s initial reactivity and ability to use
processing, including heightened reactivity, greater various emotion regulation strategies to self-relevant
emotional intensity, and slow return to baseline, yet versus standardized stimuli. For example, investiga-
these aspects of the disorder are difficult to disen- tions on emotional processing in depression find
tangle using traditional self-report, behavioral, or differential modulation of the LPP depending on
fMRI measures. Future research on BPD might use whether emotional pictures or self-descriptive ad-
LPPs to evaluate aspects of emotion dysfunction jectives are used (e.g., see Foti et al., 2010; Shestyuk
proposed by Linehan and elaborated and extended & Deldin, 2010). Using a novel word-viewing ERP
by her and her colleagues (Crowell, Beauchaine, & paradigm, we recently asked participants to identify
Linehan, 2009). neutral and emotionally charged autobiographical
It is well established that quantifying the magni- memories and generate keywords unique to each
tude of LPPs is useful for evaluating individual memory (Speed et al., 2017). Consistent with studies
differences in emotional reactivity and emotion
using standardized stimuli, the LPP was potentiated
regulation. However, there are other potentially
when viewing words linked to negative compared to
valuable ways in which LPPs might be used to study neutral memories. In addition, LPPs elicited by words
emotion regulation (Tracy, Klonsky, & Proudfit, related to negative memories were reduced following
2014). Similar to Linehan (1993), Davidson (1998) cognitive reappraisal compared to normal reactivity,
described several metrics for quantifying emotional demonstrating that the LPP can assess successful
responding in terms of affective chronometry. For ex- down-regulation of neural activity using idiographic
ample, the time it takes for an emotional response stimuli. Consistent with the notion that idiographic
to reach its maximum may vary in important ways stimuli are more salient than other stimuli, effect
between individuals, and Davidson refers to this sizes following cognitive reappraisal were smaller
metric as rise time to peak. Correspondingly, recovery than traditional studies using standardized stimuli.
time is a metric that refers to the time it takes to However, internal consistency of the LPP to nega-
return from the maximum response to baseline. In tive idiographic words during emotion regulation
addition, the amount of time that responding re- was poor. Future studies are needed to further eval-
mains above a threshold, or the duration of response, uate and optimize psychometric properties of LPPs
is an important component of affective chronome- in emotion regulation paradigms, particularly when
try that can be evaluated using the LPP. Although using idiographic stimuli—assuming the goal is to

examine individual differences (Hajcak, Meyer, & Babkirk, S., Rios, V., & Dennis, T. A. (2015). The late positive
Kotov, 2017). Furthermore, within-participant stud- potential predicts emotion regulation strategy use in school-
aged children concurrently and two years later. Developmental
ies using different types of stimuli and different mo- Science, 18, 832–841.
dalities (see Brown & Cavanagh, 2017) are needed Beauchaine, T. P. (2012). Physiological markers of emotion and
to determine how the nature of emotional stimuli behavior dysregulation in externalizing psychopathology.
(standardized vs. idiographic, visual vs. auditory) Monographs of the Society for Research in Child Development,
affect healthy, disordered, and at-risk individuals. 77, 79–86.
Beauchaine, T. P., Gatzke-Kopp, L., & Mead, H. K. (2007).
Most of the research reviewed previously examined Polyvagal theory and developmental psychopathology:
emotion dysregulation in psychopathology using Emotion dysregulation and conduct problems from
passive viewing paradigms, which provides impor- preschool to adolescence. Biological Psychology, 74, 174–184.
tant information regarding individual differences in Bedwell, J., Bohil, C., Neider, M., Gramlich, M., Neer, S., &
motivated attention and emotional reactivity. Studies Beidel, D. (2017). The late positive potential response to
olfactory stimuli in combat veterans with posttraumatic
that have examined emotion regulation abilities stress disorder. Biological Psychiatry, 81, S51–S52.
have typically focused on individual differences in Blackburn, I. M., Roxborough, H. M., Muir, W. J., Glabus, M.,
cognitive reappraisal or distraction—or have allowed & Blackwood, D. H. R. (1990). Perceptual and physiological
participants to determine their own strategy. dysfunction in depression. Psychological Medicine, 20,
Although these studies provide important informa- 95–103.
Bradley, M. M., Hamby, S., Low, A., & Lang, P. J. (2007). Brain
tion on effects of regulation strategies on LPPs in potentials in perception: Picture complexity and emotional
general, the type of emotion regulation strategy arousal. Psychophysiology, 44, 364–373.
used may affect neural responding differently, and Breiter, H. C., Etcoff, N. L., Whalen, P. J., Kennedy, W. A.,
different strategies may have distinct long-term Rauch, S. L., Buckner, R. L., . . . Rosen, B. R. (1996).
consequences. For example, Thiruchselvam and
Response and habituation of the human amygdala during
visual processing of facial expression. Neuron, 17, 875–887.
colleagues (2011) found that distraction resulted in Brown, D. R., & Cavanagh, J. F. (2017). The sound and the fury:
faster reduction of LPP magnitude compared to Late positive potential is sensitive to sound affect.
cognitive reappraisal; however, upon re-exposure to Psychophysiology, 54(12), 1812–1825.
the negative stimuli, distraction history was associ- Buhle, J. T., Silvers, J. A., Wager, T. D., Lopez, R., Onyemekwu,
ated with a larger LPP compared to cognitive reap- C., Kober, H., . . . & Ochsner, K. N. (2014). Cognitive
reappraisal of emotion: A meta-analysis of human
praisal, suggesting that distraction had different neuroimaging studies. Cerebral Cortex, 24, 2981–2990.
shorter versus longer term effects on the LPP. One Bunford, N., Kujawa, A., Fitzgerald, K. D., Swain, J. E., Hanna,
could imagine that this difference varies across G. L., Koschmann, E., . . . & Phan, K. L. (2017). Neural
individuals. To further elucidate these important reactivity to angry faces predicts treatment response in
differences and better understand the nature of pediatric anxiety. Journal of Abnormal Child Psychology,
45(2), 385–395.
emotion dysregulation in psychopathology, future Carretie, L., Hinojosa, J. A., Martin-Loeches, M., Mercado, F., &
research is required to compare the effects of different Tapia, M. (2004). Automatic attention to emotional stimuli:
types of emotion regulation strategies on the LPP Neural correlates. Human Brain Mapping, 22, 290–299.
and to evaluate how such differences are associated Clore, G. L. (1994). Why emotions are never unconscious. In
with real-world emotional functioning and psycho- P. Ekman & R. J. Davidson (Eds.), The nature of emotion:
Fundamental questions (pp. 285–290). New York, NY:
pathology. Oxford University Press.
Codispoti, M., & De Cesarei, A. (2007). Arousal and attention:
References Picture size and emotional reactions. Psychophysiology, 44,
American Psychiatric Association. (2013). Diagnostic and statistical 680–686.
manual of mental disorders (5th ed.). Arlington, VA: Author. Codispoti, M., Ferrari, V., & Bradley, M. (2006). Repetitive
Auerbach, R. P., Bondy, E., Stanton, C. H., Webb, C. A., picture processing: Autonomic and cortical correlates. Brain
Shankman, S. A., & Pizzagalli, D. A. (2016). Self-referential Research, 1068, 213–220.
processing in adolescents: Stability of behavioral and ERP Codispoti, M., Ferrari, V., & Bradley, M. (2007). Repetition and
markers. Psychophysiology, 53, 1398–1406. event-related potentials: Distinguishing early and late
Auerbach, R. P., Stanton, C. H., Proudfit, G. H., & Pizzagalli, processes in affective picture perception. Journal of Cognitive
D. A. (2015). Self-referential processing in depressed Neuroscience, 19, 577–586.
adolescents: A high-density event-related potential study. Conklin, C. Z., Bradley, R., & Westen, D. (2006). Affect
Journal of Abnormal Psychology, 124, 233–245. regulation in borderline personality disorder. Journal of
Auerbach, R. P., Tarlow, N., Bondy, E., Stewart, J. G., Aguirre, Nervous and Mental Disease, 194, 69–77.
B., Kaplan, C., . . . Pizzagalli, D. A. (2016). Electrocortical Crowell, S. E., Beauchaine, T. P., & Linehan, M. (2009). A
reactivity during self-referential processing in female youth biosocial developmental model of borderline personality:
with borderline personality disorder. Biological Psychiatry: Elaborating and extending Linehan’s theory. Psychological
Cognitive Neuroscience and Neuroimaging, 1, 335–344. Bulletin, 135, 495–510.

Crowley, K. E., & Colrain, I. M. (2004). A review of the evidence Fitzgerald, J. M., Gorka, S. M., Kujawa, A., DiGiani, J. A.,
for P2 being an independent component process: Age, sleep Proescher, E., Greenstein, J. E., . . . Phan, K. L. (2017). Neural
and modality. Clinical Neurophysiology, 115, 732–744. indices of emotional reactivity and regulation predict course
Cuthbert, B. N., Schupp, H. T., Bradley, M. M., Birbaumer, N., of PTSD symptoms in combat-exposed veterans. Progress in
& Lang, P. J. (2000). Brain potentials in affective picture Neuro-Psychopharmacology and Biological Psychiatry. Advance
processing: Covariation with autonomic arousal and affective online publication.
report. Biological Psychology, 52, 95–111. Fitzgerald, J. M., MacNamara, A., DiGangi, J. A., Kennedy,
Davidson, R. J. (1998). Affective style and affective disorders: A. E., Rabinak, C. A., Patwell, R., . . . Phan, K. L. (2016). An
Perspectives from affective neuroscience. Cognition and electrocortical investigation of voluntary emotion regulation
Emotion, 12, 307–330. in combat-related posttraumatic stress disorder. Psychiatry
De Cesarei, A., & Codispoti, M. (2006). When does size not Research: Neuroimaging, 249, 113–121.
matter? Effects of stimulus size on affective modulation. Foti, D., & Hajcak, G. (2008). Deconstructing reappraisal:
Psychophysiology, 43, 207–215. Descriptions preceding arousing pictures modulate the
DeCicco, J. M., O’Toole, L. J., & Dennis, T. A. (2014). Cognitive subsequent neural response. Journal of Cognitive Neuroscience,
reappraisal in children: An ERP study using the late positive 20, 977–988.
potential. Developmental Neuropsychology, 39, 497–515. Foti, D., Hajcak, G., & Dien, J. (2009). Differentiating neural
Dennis, T. A., & Hajcak, G. (2009). The late positive potential: response to emotional pictures: Evidence from temporal-
A neurophysiological marker for emotion regulation in spatial PCA. Psychophysiology, 46, 521–530.
children. Journal of Child Psychology and Psychiatry, 50, Foti, D., Olvet, D. M., Klein, D. N., & Hajcak, G. (2010).
1373–1383. Reduced electrocortical response to threatening faces in major
Diener, E. (2000). Subjective well-being: The science of depressive disorder. Depression and Anxiety, 27, 813–820.
happiness and a proposal for a national index. American Franken, I. H., Dietvorst, R. C., Hesselmans, M., Franzek, E. J.,
Psychologist, 55, 34–43. Van De Wetering, B. J., & Van Strien, J. W. (2008). Cocaine
DiGangi, J. A., Burkhouse, K. L., Aase, D. M., Babione, J. M., craving is associated with electrophysiological brain responses
Schroth, C., Kennedy, A. E., . . . Phan, K. L. (2017). An to cocaine-related stimuli. Addiction Biology, 13, 386–392.
electrocortical investigation of emotional face processing in Franken, I. H., Hulstijn, K. P., Stam, C. S. J., Hendriks, V. M.,
military-related posttraumatic stress disorder. Journal of & Brink, W. V. D. (2004). Two new neurophysiological
Psychiatric Research, 92, 132–138. indices of cocaine craving: Evoked brain potentials and cue
Dillon, D. G., Cooper, J. J., Grent-‘t-Jong, T., Woldorff, M. G., modulated startle reflex. Journal of Psychopharmacology, 18,
& LaBar, K. S. (2006). Dissociation of event-related 544–552.
potentials indexing arousal and semantic cohesion during Franken, I. H., Stam, C. J., Hendriks, V. M., & van den Brink,
emotional word encoding. Brain and Cognition, 62, 43–57. W. (2003). Neurophysiological evidence for abnormal
Dillon, D. G., Ritchey, M., Johnson, B. D., & LaBar, K. S. cognitive processing of drug cues in heroin dependence.
(2007). Dissociable effects of conscious emotion regulation Psychopharmacology, 170, 205–212.
strategies on explicit and implicit memory. Emotion, 7, Glenn, C. R., & Klonsky, E. D. (2009). Emotion dysregulation
354–365. as a core feature of borderline personality disorder. Journal of
Dunning, J. P., & Hajcak, G. (2009). See no evil: Directing Personality Disorders, 23, 20–28.
visual attention within unpleasant images modulates the Goldberg, D. P., Krueger, R. F., Andrews, G., & Hobbs, M. J.
electrocortical response. Psychophysiology, 46, 28–33. (2009). Emotional disorders: Cluster 4 of the proposed
Dunning, J. P., Parvaz, M. A., Hajcak, G., Maloney, T., Alia- meta-structure for DSM-V and ICD-11: Paper 5 of 7 of the
Klein, N., Woicik, P. A., . . . Goldstein, R. Z. (2011). Motivated thematic section: ‘A proposal for a meta-structure for DSM-V
attention to cocaine and emotional cues in abstinent and and ICD-11.’ Psychological Medicine, 39, 2043–2059.
current cocaine users—An ERP study. European Journal of Gross, J. J. (1998). The emerging field of emotion regulation: An
Neuroscience, 33, 1716–1723. integrative review. Review of General Psychology, 2, 271–299.
Eimer, M., & Holmes, A. (2007). Event-related brain potential Gross, J. J. (2002). Emotion regulation: Affective, cognitive, and
correlates of emotional face processing. Neuropsychologia, 45, social consequences. Psychophysiology, 39, 281–291.
15–31. Gross, J. J. (2015). Emotion regulation: Current status and future
Eimer, M., Holmes, A., & McGlone, F. P. (2003). The role of prospects. Psychological Inquiry, 26, 1–26.
spatial attention in the processing of facial expression: An Gross, J. J., Sheppes, G., & Urry, H. L. (2011). Emotion
ERP study of rapid brain responses to six basic emotions. generation and emotion regulation: A distinction we should
Cognitive, Affective, and Behavioral Neuroscience, 3, 97–110. make (carefully). Cognition and Emotion, 25, 765–781.
Ellsworth, P. C., & Scherer, K. R. (2003). Appraisal processes Hajcak, G., & Dennis, T. A. (2009). Brain potentials during
in emotion. In R. J. Davidson, K. R. Scherer, & affective picture processing in children. Biological Psychology,
H. H. Goldsmith (Eds.), Handbook of affective sciences 80, 333–338.
(pp. 572–595). New York, NY: Oxford University Press. Hajcak, G., Dunning, J. P., & Foti, D. (2009). Motivated and
Etkin, A., & Wager, T. D. (2007). Functional neuroimaging of controlled attention to emotion: Time-course of the late
anxiety: A meta-analysis of emotional processing in PTSD, positive potential. Clinical Neurophysiology, 120, 505–510.
social anxiety disorder, and specific phobia. American Journal Hajcak, G., MacNamara, A., & Olvet, D. M. (2010). Event-
of Psychiatry, 164, 1476–1488. related potentials, emotion, and emotion regulation: An
Fairholme, C. P., Nosen, E. L., Nillni, Y. I., Schumacher, J. A., Tull, integrative review. Developmental Neuropsychology, 35,
M. T., & Coffey, S. F. (2013). Sleep disturbance and emotion 129–155.
dysregulation as transdiagnostic processes in a comorbid Hajcak, G., Meyer, A., & Kotov, R. (2017). Psychometrics
sample. Behaviour Research and Therapy, 51, 540–546. and the neuroscience of individual differences: Internal

consistency limits between-subjects effects. Journal of natural disaster on psychiatric symptoms in children.
Abnormal Psychology, 126(6), 823–834. Biological Psychiatry, 80, 381–389.
Hajcak, G., & Nieuwenhuis, S. (2006). Reappraisal modulates Kujawa, A., Hajcak, G., Torpey, D., Kim, J., & Klein, D. N.
the electrocortical response to unpleasant pictures. Cognitive, (2012). Electrocortical reactivity to emotional faces in
Affective, and Behavioral Neuroscience, 6, 291–297. young children and associations with maternal and paternal
Hajcak, G., & Olvet, D. M. (2008). The persistence of attention depression. Journal of Child Psychology and Psychiatry, 53,
to emotion: Brain potentials during and after picture 207–215.
presentation. Emotion, 8, 250–255. Kujawa, A., MacNamara, A., Fitzgerald, K. D., Monk, C. S., &
Hajcak, G., Weinberg, A., MacNamara, A., & Foti, D. (2011). Phan, K. L. (2015). Enhanced neural reactivity to threatening
ERPs and the study of emotion. In S. J. Luck & faces in anxious youth: Evidence from event-related potentials.
E. Kappenman (Eds.), Handbook of event-related potential Journal of Abnormal Child Psychology, 43, 1493–1501.
components (pp. 441–474). New York, NY: Oxford University Lang, P. J. (1995). The emotion probe: Studies of motivation and
Press. attention. American Psychologist, 50, 372–385.
Hidalgo, N. A. I., Oelkers-Ax, R., Nagy, K., Mancke, F., Bohus, Langeslag, S. J., & Van Strien, J. W. (2010). Comparable
M., Herpertz, S. C., & Bertsch, K. (2016). Time course of modulation of the late positive potential by emotion regulation
facial emotion processing in women with borderline in younger and older adults. Journal of Psychophysiology, 24,
personality disorder: An ERP study. Journal of Psychiatry and 186–197.
Neuroscience, 41, 16–26. Leutgeb, V., Schäfer, A., Köchel, A., Scharmüller, W., & Schienle,
Holmes, A., Vuilleumier, P., & Eimer, M. (2003). The processing A. (2010). Psychophysiology of spider phobia in 8- to
of emotional facial expression is gated by spatial attention: 12-year-old girls. Biological Psychology, 85, 424–431.
Evidence from event-related brain potentials. Cognitive Brain Leutgeb, V., Schäfer, A., & Schienle, A. (2009). An event-related
Research, 16, 174–184. potential study on exposure therapy for patients suffering
Horndasch, S., Kratz, O., Van Doren, J., Graap, H., Kramer, R., from spider phobia. Biological Psychology, 82, 293–300.
Moll, G. H., & Heinrich, H. (2017). Cue reactivity towards Levinson, A. R., Speed, B. C., & Hajcak, G. (2017). The late
bodies in anorexia nervosa–common and differential effects positive potential moderates the prospective relationship
in adolescents and adults. Psychological Medicine. Advance between life stressors and depressive symptoms in adolescent
online publication. females. Journal of Clinical Child and Adolescent Psychology.
Huang, Y. X., & Luo, Y. J. (2006). Temporal course of Advance online publication.
emotional negativity bias: An ERP study. Neuroscience Levinson, A. R., Speed, B. C., & Hajcak, G. (in preparation).
Letters, 398, 91–96. Towards a more reliable ERP: Psychometric properties of
Kayser, J., Bruder, G. E., Tenke, C. E., Stewart, J. E., & Quitkin, the late positive potential to repeated versus assorted
F. M. (2000). Event-related potentials (ERPs) to hemifield pictures.
presentations of emotional stimuli: Differences between Lobo, I., David, I. A., Figueira, I., Campagnoli, R. R., Volchan, E.,
depressed patients and healthy adults in P3 amplitude and Pereira, M. G., & de Oliveira, L. (2014). Brain reactivity to
asymmetry. International Journal of Psychophysiology, 36, unpleasant stimuli is associated with severity of posttraumatic
211–236. stress symptoms. Biological Psychology, 103, 233–241.
Keil, A., Moratti, S., Sabatinelli, D., Bradley, M. M., & Lang, Lobo, I., Portugal, L. C., Figueira, I., Volchan, E., David, I.,
P. J. (2005). Additive effects of emotional content and spatial Pereira, M. G., & de Oliveira, L. (2015). EEG correlates of
selective attention on electrocortical facilitation. Cerebral the severity of posttraumatic stress symptoms: A systematic
Cortex, 15, 1187–1197. review of the dimensional PTSD literature. Journal of
Kober, H., Kross, E. F., Mischel, W., Hart, C. L., & Ochsner, Affective Disorders, 183, 210–220.
K. N. (2010). Regulation of craving by cognitive strategies Lifshitz, K. (1966). The averaged evoked cortical response to
in cigarette smokers. Drug and Alcohol Dependence, 106, complex visual stimuli. Psychophysiology, 3, 55–68.
52–55. Linehan, M. (1993). Cognitive-behavioral treatment of borderline
Kolassa, I. T., Musial, F., Mohr, A., Trippe, R. H., & Miltner, personality disorder. New York, NY: Guilford.
W. H. (2005). Electrophysiological correlates of threat Littel, M., & Franken, I. H. (2011). Intentional modulation of
processing in spider phobics. Psychophysiology, 42, 520–530. the late positive potential in response to smoking cues by
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of cognitive strategies in smokers. PLoS One, 6, e27519.
addiction. Neuropsychopharmacology, 35, 217–238. Lubman, D. I., Allen, N. B., Peters, L. A., & Deakin, J. W.
Kring, A. M., & Sloan, D. M. (Eds.). (2009). Emotion regulation (2008). Electrophysiological evidence that drug cues have
and psychopathology: A transdiagnostic approach to etiology and greater salience than other affective stimuli in opiate
treatment. New York, NY: Guilford Press. addiction. Journal of Psychopharmacology, 22, 836–842.
Krompinger, J. W., Moser, J. S., & Simons, R. F. (2008). Lubman, D. I., Yücel, M., Kettle, J. W., Scaffidi, A., MacKenzie, T.,
Modulations of the electro-physiological response to pleasant Simmons, J. G., & Allen, N. B. (2009). Responsiveness
stimuli by cognitive reappraisal. Emotion, 8, 132–137. to drug cues and natural rewards in opiate addiction:
Kudinova, A. Y., Owens, M., Burkhouse, K. L., Barretto, K. M., Associations with later heroin use. Archives of General
Bonanno, G. A., & Gibb, B. E. (2016). Differences in Psychiatry, 66, 205–212.
emotion modulation using cognitive reappraisal in Luna, B., Padmanabhan, A., & O’Hearn, K. (2010). What has
individuals with and without suicidal ideation: An ERP fMRI told us about the development of cognitive control
study. Cognition and Emotion, 30, 999–1007. through adolescence? Brain and Cognition, 72, 101–113.
Kujawa, A., Hajcak, G., Danzig, A. P., Black, S. R., Bromet, MacNamara, A., Foti, D., & Hajcak, G. (2009). Tell me about
E. J., Carlson, G. A., . . . Klein, D. N. (2016). Neural reactivity it: Neural activity elicited by emotional pictures and
to emotional stimuli prospectively predicts the impact of a preceding descriptions. Emotion, 9, 531–543.

MacNamara, A., & Hajcak, G. (2010). Distinct electrocortical Nickerson, L. D., Ravichandran, C., Lundahl, L. H., Rodolico,
and behavioral evidence for increased attention to threat J., Dunlap, S., Trksak, G. H., & Lukas, S. E. (2011). Cue
in generalized anxiety disorder. Depression and Anxiety, 27, reactivity in cannabis-dependent adolescents. Psychology of
234–243. Addictive Behaviors, 25, 168–173.
MacNamara, A., Kotov, R., & Hajcak, G. (2016). Diagnostic Olofsson, J. K., Nordin, S., Sequeira, H., & Polich, J. (2008).
and symptom-based predictors of emotional processing in Affective picture processing: An integrative review of ERP
generalized anxiety disorder and major depressive disorder: findings. Biological Psychology, 77, 247–265.
An event-related potential study. Cognitive Therapy and Parvaz, M. A., MacNamara, A., Goldstein, R. Z., & Hajcak, G.
Research, 40, 275–289. (2012). Event-related induced frontal alpha as a marker of
MacNamara, A., Post, D., Kennedy, A. E., Rabinak, C. A., & lateral prefrontal cortex activation during cognitive reappraisal.
Phan, K. L. (2013). Electrocortical processing of social Cognitive, Affective, and Behavioral Neuroscience, 12, 730–740.
signals of threat in combat-related post-traumatic stress Parvaz, M. A., Moeller, S. J., Goldstein, R. Z., & Proudfit, G. H.
disorder. Biological Psychology, 94, 441–449. (2015). Electrocortical evidence of increased post-reappraisal
Michalowski, J. M., Melzig, C. A., Weike, A. I., Stockburger, J., neural reactivity and its link to depressive symptoms. Social,
Schupp, H. T., & Hamm, A. O. (2009). Brain dynamics in Cognitive, and Affective Neuroscience, 10, 78–84.
spider-phobic individuals exposed to phobia-relevant and Parvaz, M. A., Moeller, S. J., Malaker, P., Sinha, R., Alia-Klein,
other emotional stimuli. Emotion, 9, 306–315. N., & Goldstein, R. Z. (2017). Abstinence reverses EEG-
Miltner, W. H., Trippe, R. H., Krieschel, S., Gutberlet, I., indexed attention bias between drug-related and pleasant
Hecht, H., & Weiss, T. (2005). Event-related brain potentials stimuli in cocaine-addicted individuals. Journal of Psychiatry
and affective responses to threat in spider/snake-phobic and and Neuroscience, 42, 78–86.
non-phobic subjects. International Journal of Psychophysiology, Paul, S., Simon, D., Endrass, T., & Kathmann, N. (2016).
57, 43–52. Altered emotion regulation in obsessive–compulsive disorder
Mini, A., Palomba, D., Angrilli, A., & Bravi, S. (1996). as evidenced by the late positive potential. Psychological
Emotional information processing and visual evoked brain Medicine, 46, 137–147.
potentials. Perceptual and Motor Skills, 83, 143–152. Proudfit, G. H., Bress, J. N., Foti, D., Kujawa, A., & Klein,
Moeller, S. J., & Paulus, M. P. (2017). Toward biomarkers of the D. N. (2015). Depression and event-related potentials:
addicted human brain: Using neuroimaging to predict Emotional disengagement and reward insensitivity. Current
relapse and sustained abstinence in substance use disorder. Opinion in Psychology, 4, 110–113.
Progress in Neuro-psychopharmacology and Biological Psychiatry, Richards, J. M., Butler, E. A., & Gross, J. J. (2003). Emotion
80 Part B, 143–154. regulation in romantic relationships: The cognitive
Moran, T. P., Jendrusina, A. A., & Moser, J. S. (2013). The consequences of concealing feelings. Journal of Social and
psychometric properties of the late positive potential during Personal Relationships, 20, 599–620.
emotion processing and regulation. Brain Research, 1516, Richards, J. M., & Gross, J. J. (2000). Emotion regulation and
66–75. memory: The cognitive costs of keeping one’s cool. Journal of
Moser, J. S., Hajcak, G., Bukay, E., & Simons, R. F. (2006). Personality and Social Psychology, 79, 410–424.
Intentional modulation of emotional responding to Robinson, M. D., & Clore, G. L. (2002). Belief and feeling:
unpleasant pictures: An ERP study. Psychophysiology, 43, Evidence for an accessibility model of emotional self-report.
292–296. Psychological Bulletin, 128, 934–960.
Moser, J. S., Huppert, J. D., Duval, E., & Simons, R. F. (2008). Rogers, T. B., Kuiper, N. A., & Kirker, W. S. (1977). Self-
Face processing biases in social anxiety: An electrophysiological reference and the encoding of personal information. Journal
study. Biological Psychology, 78, 93–103. of Personality and Social Psychology, 35, 677–688.
Mühlberger, A., Wieser, M. J., Herrmann, M. J., Weyers, P., Rottenberg, J., & Gotlib, I. H. (2004). Socioemotional functioning
Tröger, C., & Pauli, P. (2009). Early cortical processing of in depression. In M. Power (Ed.), Mood disorders: A handbook
natural and artificial emotional faces differs between lower of science and practice (pp. 61–77). Hoboken, NJ: Wiley.
and higher socially anxious persons. Journal of Neural Rottenberg, J., Gross, J. J., & Gotlib, I. H. (2005). Emotion
Transmission, 116, 735–746. context insensitivity in major depressive disorder. Journal of
Namkoong, K., Lee, E., Lee, C. H., Lee, B. O., & An, S. K. Abnormal Psychology, 114, 627–639.
(2004). Increased P3 amplitudes induced by alcohol-related Schupp, H., Cuthbert, B., Bradley, M., Hillman, C., Hamm, A.,
pictures in patients with alcohol dependence. Alcoholism: & Lang, P. (2004). Brain processes in emotional perception:
Clinical and Experimental Research, 28, 1317–1323. Motivated attention. Cognition and Emotion, 18, 593–611.
Naumann, E., Bartussek, D., Diedrich, O., & Laufer, M. (1992). Schupp, H. T., Flaisch, T., Stockburger, J., & Junghöfer, M.
Assessing cognitive and affective information processing (2006). Emotion and attention: Event-related brain potential
functions of the brain by means of the late positive complex studies. Progress in Brain Research, 156, 31–51.
of the event-related potential. Journal of Psychophysiology, 6, Schupp, H. T., Junghöfer, M., Weike, A. I., & Hamm, A. O.
285–298. (2004). The selective processing of briefly presented affective
Nelson, E. E., Leibenluft, E., McClure, E. B., & Pine, D. S. pictures: An ERP analysis. Psychophysiology, 41, 441–449.
(2005). The social re-orientation of adolescence: A neuroscience Sheppes, G., Catran, E., & Meiran, N. (2009). Reappraisal (but
perspective on the process and its relation to psychopathology. not distraction) is going to make you sweat: Physiological
Psychological Medicine, 35, 163–174. evidence for self-control effort. International Journal of
Nelson, B. D., Perlman, G., Hajcak, G., Klein, D. N., & Psychophysiology, 71, 91–96.
Kotov, R. (2015). Familial risk for distress and fear disorders Shestyuk, A. Y., & Deldin, P. J. (2010). Automatic and strategic
and emotional reactivity in adolescence: An event-related representation of the self in major depression: Trait and state
potential investigation. Psychological Medicine, 45, 2545–2556. abnormalities. American Journal of Psychiatry, 167, 536–544.

Speed, B. C., Levinson, A. R., Gross, J. J., Kiosses, D. N., & Vuilleumier, P. (2005). How brains beware: Neural mechanisms
Hajcak, G. (2017). Emotion regulation to idiographic of emotional attention. Trends in Cognitive Sciences, 9,
stimuli: Testing the Autobiographical Emotion Regulation 585–594.
Task. Neuropsychologia. Advance online publication. Watson, D. (2000). Mood and temperament. New York, NY:
Speed, B. C., Nelson, B. D., Auerbach, R. P., Klein, D. N., & Guilford Press.
Hajcak, G. (2016). Depression risk and electrocortical Weinberg, A., Ferri, J., & Hajcak, G. (2013). Interactions
reactivity during self-referential emotional processing in 8 to between attention and emotion: Insights from the late
14 year-old girls. Journal of Abnormal Psychology, 125, 607–619. positive potential. In M. D. Robinson, E. R. Watkins, &
Speed, B. C., Nelson, B. D., Perlman, G., Klein, D. N., E. Harmon-Jones (Eds.), Handbook of cognition and emotion
Kotov, R., & Hajcak, G. (2015). Personality and emotional (pp. 35–54). New York, NY: Guilford Press.
processing: A relationship between extraversion and the Weinberg, A., & Hajcak, G. (2011a). Electrocortical evidence
late positive potential in adolescence. Psychophysiology, 52, for vigilance-avoidance in generalized anxiety disorder.
1039–1047. Psychophysiology, 48, 842–851.
Thiruchselvam, R., Blechert, J., Sheppes, G., Rydstrom, A., & Weinberg, A., & Hajcak, G. (2011b). The late positive potential
Gross, J. J. (2011). The temporal dynamics of emotion predicts subsequent interference with target processing.
regulation: An EEG study of distraction and reappraisal. Journal of Cognitive Neuroscience, 23, 2994–3007.
Biological Psychology, 87, 84–92. Weinberg, A., Hilgard, J., Bartholow, B. D., & Hajcak, G.
Thiruchselvam, R., Hajcak, G., & Gross, J. J. (2012). Looking (2012). Emotional targets: Evaluative categorization as a
inward: Shifting attention within working memory function of context and content. International Journal of
representations alters emotional responses. Psychological Psychophysiology, 84, 149–154.
Science, 23, 1461–1466. Weinberg, A., May, A. M., Klonsky, E. D., Kotov, R., & Hajcak, G.
Thompson, R. A. (1990). Emotion and self-regulation. In (2017). Decreased neural response to threat differentiates
R. A. Thompson (Ed.), Nebraska Symposium on Motivation: patients who have attempted suicide from nonattempters
Vol. 36. Socioemotional development (pp. 383–483). Lincoln, with current ideation. Clinical Psychological Science, 5(6),
NE: University of Nebraska Press. 952–963.
Tracy, J. L., Klonsky, E. D., & Proudfit, G. H. (2014). How Weinberg, A., Perlman, G., Kotov, R., & Hajcak, G. (2016).
affective science can inform clinical science: An introduction Depression and reduced neural response to emotional
to the special issue. Clinical Psychological Science, 2, 371–386. images: Distinction from anxiety, and importance of
Van de Laar, M. C., Licht, R., Franken, I. H., & Hendriks, V. M. symptom dimensions and age of onset. Journal of Abnormal
(2004). Event-related potentials indicate motivational Psychology, 125, 26–39.
relevance of cocaine cues in abstinent cocaine addicts. Weinberg, A., Venables, N. C., Proudfit, G. H., & Patrick, C. J.
Psychopharmacology, 177, 121–129. (2015). Heritability of the neural response to emotional
van Reekum, C. M., Johnstone, T., Urry, H. L., Thurow, M. E., pictures: Evidence from ERPs in an adult twin sample.
Schaefer, H. S., Alexander, A. L., & Davidson, R. J. (2007). Social, Cognitive, and Affective Neuroscience, 10, 424–434.
Gaze fixations predict brain activation during the voluntary Wessa, M., Jatzko, A., & Flor, H. (2006). Retrieval and emotional
regulation of picture-induced negative affect. Neuroimage, processing of traumatic memories in posttraumatic stress
36, 1041–1055. disorder: Peripheral and central correlates. Neuropsychologia,
Versace, F., Engelmann, J. M., Deweese, M. M., Robinson, J. D., 44, 1683–1696.
Green, C. E., Lam, C. Y., . . . Cinciripini, P. M. (2017). Wessa, M., Karl, A., & Flor, H. (2005). Central and peripheral
Beyond cue reactivity: Non-drug-related motivationally psychophysiological responses to trauma-related cues in
relevant stimuli are necessary to understand reactivity to subclinical posttraumatic stress disorder: A pilot study.
drug-related cues. Nicotine and Tobacco Research, 19, 663–669. Experimental Brain Research, 167, 56–65.
Versace, F., Lam, C. Y., Engelmann, J. M., Robinson, J. D., Woodward, S. H., Shurick, A. A., Alvarez, J., Kuo, J., Nonyieva,
Minnix, J. A., Brown, V. L., & Cinciripini, P. M. (2012). Y., Blechert, J., . . . Gross, J. J. (2015). A psychophysiological
Beyond cue reactivity: Blunted brain responses to pleasant investigation of emotion regulation in chronic severe
stimuli predict long-term smoking abstinence. Addiction posttraumatic stress disorder. Psychophysiology, 52, 667–678.
Biology, 17, 991–1000. Yang, L., Zhang, J., & Zhao, X. (2015). Implicit processing of
Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). heroin and emotional cues in abstinent heroin users: Early
Neurobiologic advances from the brain disease model of and late event-related potential effects. American Journal of
addiction. New England Journal of Medicine, 374, 363–371. Drug and Alcohol Abuse, 41, 237–245.

CH A PTE R
Neuroimaging of Emotion
14 Dysregulation
Joseph C. Leshin and Kristen A. Lindquist
Abstract
Affective neuroscience, the study of neural mechanisms that give rise to emotional experiences in
humans and animals, has a short but rich history. Almost three decades old, affective neuroscience
has predominantly taken two theoretical approaches to understanding the brain bases of human
emotions, and thus, two stances on the brain bases of emotion dysregulation. One approach, the
traditional approach, argues that specific emotions are hardwired in human biology with specific
neural underpinnings or signatures for said emotions. The second approach, a psychological constructionist
approach, argues that each experienced emotion emerges not from a specific, dedicated anatomical
circuit, but from an interplay of broad networks in the brain that are involved in general operations of
the mind. This chapter provides an overview of these two theoretical approaches with a specific focus
on functional magnetic resonance imaging (fMRI) findings. It concludes with evidence suggesting how
emotion dysregulation may arise and links this work to clinical fMRI investigations of anxiety disorders.
It closes by suggesting future directions affective neuroscience may take to better understand processes
underlying dysregulated emotions.
Keywords: affective neuroscience, emotion dysregulation, emotions, psychological constructionism,

brain, mind, functional MRI, anxiety disorders, constructed emotion theory
Introduction nderlie emotion dysregulation. Much of this

u
Emotion dysregulation is a core feature of almost research follows the traditional model of emotion,
every major form of psychopathology across the which assumes largely discrete anatomical bases of
lifespan (Beauchaine, 2015a; Insel, 2014; Kring, 2008; particular emotion categories (e.g., fear), with the
Kring & Mote, 2016). It underlies maladapt ive assumption that functional abnormalities of these
decision making (Lee, 2013; Sharp, Monterosso, & anatomical structures (e.g., excessive amygdala ac-
Montague, 2012) and maladaptive interpersonal tivation) result in emotional dysregulation (e.g.,
behaviors (Kring, 2008), and is often a source of anxiety). In this chapter, we discuss evidence for and
distress for individuals who experience it (Bylsma, against the traditional model, and offer a new
Taylor-Clift, & Rottenberg, 2011; Kashdan & Steger, approach—the theory of constructed emotion (TCE;
2006; Myin-Germeys et al., 2009). Understanding Barrett, 2017a, 2017b; Lindquist, 2013). In contrast
etiopathophysiologies of emotion dysregulation to traditional approaches, the TCE suggests that
would therefore provide insight into mechanisms each experienced emotion emerges not from a
underlying myriad maladies. specific, dedicated anatomical circuit, but from an
For the past 25 or so years, human neuroimaging interplay of broad networks in the brain that are
studies in the field of affective neuroscience have involved in general operations of the mind. Instances
evaluated the functional neuroanatomical bases of each emotion category (i.e., fear, anger, happi-
of emotions in attempts to identify processes that ness, etc.) are represented by a pattern within these
183
networks that is situation specific and individually localization to subcortical and other structures
different. Taking a constructionist approach, we (unlike EEG, MEG, and fNIRS). Subcortical struc-
discuss evidence of how dysregulation within these tures play a key role in most theories of emotion
networks may result in dysregulation of emotions. (e.g., Damasio et al., 2000; MacLean, 1949;
We begin our chapter by describing terms and Panksepp, 2016; Panksepp & Watt, 2011; cf. Kober
concepts. Next, we outline the two theoretical et al., 2008) and fMRI can image these deep brain
approaches that have guided neuroimaging research structures—often with high spatial resolution
on emotion for the past 25 years: the traditional, (Satpute, Wager, et al., 2013). In contrast, EEG,
anatomically given circuit-based view and the TCE. MEG, and fNIRS offer exceptional temporal reso-
With these theoretical perspectives in mind, we lution and are therefore better suited for answering
discuss what affective neuroscience suggests about questions about “when” activation occurs during
mechanisms underlying human emotion and its the experience of emotion. Temporal dynamics of
dysregulation. We conclude with evidence suggesting neural processing are surely of interest to emotion
how emotion dysregulation may arise, and link this researchers, and more research is needed in this area
work to clinical investigations of anxiety disorders. (see, e.g., Heller & Casey, 2016; Lee, Lindquist, &
Although we recognize there are myriad ways that Nam, 2017; Waugh, Hamilton, & Gotlib, 2010). As
emotion dysregulation affects well-being, behavior, we note later, some recent evidence on network
and psychopathology, we focus specifically on these properties of brain activation using fMRI combines
disorders for illustrative purposes. We close by sug- spatial and temporal domains by examining se-
gesting future directions that affective neuroscience quences of regional brain activation during emotions.
may take to better understand processes underlying Next, we define what we mean by “emotion,” as
dysregulated emotions, conceptually linking the the term is used differently among psychologists/
constructionist approach to other recent attempts neuroscientists, clinicians, and practitioners—and
to identify basic processes that underlie multiple even among affective neuroscientists. We differenti-
disorders (e.g., the Research Domain Criteria [RDoC] ate between what we call “emotions” and “affect.”
approach; Insel, 2014). Whereas “emotions” describe discrete experiences of
specific states, as named with words such as “sadness,”
Terms and Concepts “fear,” and “anger,” (often called “discrete emotions”;
This chapter is about neuroimaging of emotion Keltner, Ekman, Gonzaga, & Beer, 2003), “affect”
dysregulation, but we should first clarify how we is used to describe more general feelings that range
use the terms “neuroimaging,” “emotion,” and in positivity–negativity and activation–deactivation
“dysregulation.” In general, “neuroimaging” refers (see Barrett & Bliss-Moreau, 2009; Barrett, 2016;
to any technology that allows researchers to create Lindquist, 2013; Russell, 2003). We consider affect
images of neural structure or function. In this chap- as constitutive of emotions insofar as affect is a basic
ter, we review the literature on human functional “ingredient” that underlies all emotional experiences
neuroimaging—technologies that generate images of (i.e., all emotions can be described as having
neural processes related to mental states among live, some degree of pleasantness–unpleasantness and
waking human subjects. We focus specifically on activation–deactivation; Barrett & Bliss-Moreau,
functional magnetic resonance imaging (fMRI), 2009; Lindquist, 2013; Lindquist, Wager, Kober,
which assesses changes in blood oxygenation to Bliss-Moreau, & Barrett, 2012; Lindquist, Satpute,
estimate blood flow to specific regions of the brain Wager, Weber, & Barrett, 2016; Russell, 2009).
while humans experience mental states (e.g., fear). Finally, we describe our definition of emotion
Blood flow reflects corresponding changes in activity dysregulation, which is largely but not fully consistent
(both excitation and inhibition) to neural populations with the definition used throughout this volume
in brain tissue (see Logothetis, 2008). Although (i.e., patterns of emotional experience and/or
there are other methods of functional neuroimaging expression that interfere with goal-directed behavior;
(e.g., positron emission tomography [PET], electro- see Beauchaine, 2015b). By some definitions, dys-
encephalography [EEG], magnetoencephalography regulation is the opposite of regulation. Yet regulation
[MEG], functional near-infrared spectroscopy is used differently throughout the emotion and
[fNIRS]), we focus on fMRI for two reasons. First, affective neuroscience literature. In affective neuro-
most recent neuroimaging studies of human emo- science, research on regulation often refers to explicit
tion use fMRI because it does not require injection attempts by an individual to control or change his
of radioactive tracers (like PET) and affords good or her emotions (Gross & Thompson, 2007). There
184 Neuroimaging of Emotion Dysregul ation

is a large body of imaging research on explicit neuroscience (see Barrett, 2017a; Barrett & Satpute,
regulation of emotion (see Ochsner & Gross, 2008; in press; Gendron & Barrett, 2009) and derives in
Buhle et al., 2014). This research focuses primarily part from the common assumption that our experi-
on how effortful, “cognitive” control processes asso- ences of the world reveal underlying mechanisms
ciated with prefrontal cortex (PFC) function can (Ross & Ward, 1996). In the case of our emotions,
downregulate functional activity of subcortical since fear and sadness are experienced as distinct, we
structures such as the amygdala, which—along with are likely to assume that these categories of emotion
other subcortical structures—are canonically associ- derive from different psychological and neural
ated with emotion (e.g., Adolphs, 1999; Panksepp, mechanisms. This inference—the idea that catego-
2016; Phelps & LeDoux, 2005). This literature is ries are distinct and the idea that they each have
important, and is linked closely with emotion dys- their own mechanism—is rooted in essentialism.
regulation in psychopathology across the lifespan Essentialism is the human tendency to ascribe
(e.g., Beauchaine, 2015a; Berking & Wupperman, dedicated causal mechanisms to “categories” of
2012; Martin & Dahlen, 2005) and to other rela- observable phenomena—in this case different

tional and social outcomes (e.g., Gross & John, 2003). emotions (see Gelman, 2009a, 2009b). This trans-
We use the term “regulation” in its broader sense to lates into the belief that fear and sadness, for in-
refer to normative emotional processes. We believe stance, must be associated with different feelings
that before one studies explicit emotion regulation and behaviors and each derives from discrete mech-
or impairments in related processes, it is important anisms in the brain (see Lindquist, Siegel, Quigley,
to understand neural processes that contribute & Barrett, 2013).
normatively to emotions in healthy individuals In affective neuroscience, the traditional view is
across daily life.1 We therefore spend most of this codified in basic emotion theory, which argues that
chapter discussing processes associated with regu- emotions such as sadness, fear, and anger are cate-
lated emotion, and use this as a jumping-off point gories of experience that exist across species as
for exploring how those same processes may become evolved mechanisms, are present at birth in humans,
dysregulated in anxiety disorders. Of course, emo- and are universal across cultures (see Barrett, 2006a;
tion dysregulation is likely to be transdiagnostic Ekman & Cordaro, 2011; Panksepp & Watt, 2011;
across other disorders (Beauchaine, 2015a, 2015b; Tracy & Randles, 2011). The basic emotion per-
Beauchaine & Zisner, 2017). spective argues that at least some categories of
emotional experience (fear, sadness, anger, happi-
Theoretical Perspectives: Competing ness, disgust) evolved to motivate responses to
Theories of Brain Bases survival-linked contexts throughout phylogeny

of Human Emotions (Ekman & Cordaro, 2011; Panksepp & Watt, 2011).
Theories are much more than sets of explanations These basic emotions are thought by some to
for how emotions operate—they are philosophical constitute foundations for all human emotional
lenses through which observations are made, hy- experiences (including more complex “secondary
potheses are generated, studies are designed, and emotions”) and cannot be broken down into con-
data are interpreted (Kuhn, 1977). At only two and stituent parts (Ekman & Cordaro, 2011; Panksepp,
a half decades old, affective neuroscience is still a 1982; Panksepp & Watt, 2011).
young discipline, and is still reliant on assumptions
made since its inception (see also Kuhn, 1961). Neural Bases of Emotions
Thus, we begin by discussing traditional approaches Traditional theories of emotion sometimes suggest
to understanding brain bases of human emotion, that each basic emotion category corresponds to a
outlining how these approaches began the study of specific, inherited, and anatomically dictated mech-
emotion dysregulation among adults (and, by ex- anism within the central nervous system (see Tracy &
tension, children). We then describe the more recent Randles, 2011). Over the years, this idea has taken
theory of constructed emotion (Barrett, 2017a, multiple forms that manifest in the literature on
2017b; Lindquist, 2013), including its hypotheses emotion regulation and dysregulation.
regarding how emotion and dysregulation emerge. Maclean (1949) famously proposed the “triune
brain” concept, which is rooted in essentialist beliefs
The Traditional Approach about emotion versus reason that still shape—
The traditional approach to understanding emotion however implicitly—theory and interpretation of
has a long history in psychology, medicine, and neural data. The triune brain concept localizes
Leshin and Lindquist 185

emotion categories, such as fear, to limbic and amygdala is the brain locus of fear (LeDoux, 1995)
brainstem structures deep within subcortical regions or a key part of an encapsulated, anatomically de-
(e.g., amygdala, striatum) and separates these fined subcortical circuit for this emotion (Davis,
processes from cognitive processes involved in
1992; Fanselow, 1994; Panksepp, 1998; Tovote,
cognition, planning, and self-regulation (functions Fadok, & Lüthi, 2015).
associated with areas of the PFC). At the base of this The most compelling studies linking fear and
three-part system lies the “reptilian” brain that gen- amygdala activation are those in which amygdala
erates “primitive” emotions (e.g., anger, fear). Above lesions in animals, such as rats, abolish freezing
this system is the “visceral brain” that elaborates the behavior (e.g., Blanchard & Blanchard, 1972), a
“social” emotions (e.g., “contempt,” “embarrassment,” behavior commonly considered a fearful or defensive
etc.). Finally, the neocortex, the topmost system, is response. There are two concerns with this interpre-
typically the basis for cognitive functions and attrib- tation, one philosophical and the other empirical.
uted to regulatory processes. First, linking adaptive behaviors in nonhuman
Despite the legacy of the triune brain concept, animals with complex emotional experiences in

research on brain evolution suggests that the triune humans can be problematic (LeDoux, 2012, 2013)
brain concept is at best a heuristic; among mam- as it cannot be verified whether nonhuman animal
mals, there is no “limbic system” that is functionally emotional behaviors are subjectively similar to con-
separate from other parts of the brain (see Chanes & scious human emotions (see Barrett, 2017c for a dis-
Barrett, 2016; Pessoa, 2008). Moreover, the mam- cussion). More important, it is now empirically
malian brain did not develop in a linear, one-region- clear that the amygdala is not specific to defensive
above-the-next fashion. Instead, as the human brain responses (e.g., Paré & Quirk, 2017). Rather, the
evolved, it fundamentally reorganized, with new amygdala is involved more generally in behavioral
connections between subcortical nuclei, limbic, engagement “that governs transactions between
paralimbic, and cortical tissue created across pri- mammals and their environments: whether or not
mate evolution (see Barbas, 1995; Striedter, 2005). to engage with (or disengage from) stimuli or situa-
Although debate on brain evolution is far from tions” (Paré & Quirk, 2017, p. 6). That is, amygdala
closed, most experts agree that the triune brain con- activation occurs during behavioral outputs to mo-
cept does not accurately describe functional neuro- tivationally relevant stimuli (Amir, Lee, Headley,
anatomy. Herzallah, & Paré, 2015). This interpretation ex-
Nonetheless, the triune brain concept, in combi- plains why the amygdala is also active during non-
nation with basic emotion models (e.g., Ekman, fear states such as reward (Baxter & Murray, 2002)
1992; Izard, 1992), facilitated initial hypotheses and when dictating behavioral responses to nona-
about emotion-specific subcortical brain structures versive yet uncertain stimuli (Herry et al., 2007).
within the subcortex and limbic tissue (Panksepp, Research with humans has also been invoked in
1998). It is beyond the scope of this chapter to ascribing the amygdala as the brain basis of fear. In
review each of the subcortical, limbic, and paralimbic humans, amygdala damage produces disruptions to
regions or circuits that have been linked to specific aversive conditioning (LaBar, LeDoux, Spencer, &
basic emotions (see Barrett et al., 2007; Lindquist Phelps, 1995), the recognition of fearful expressions
et al., 2012; and Panksepp, 1998, 2016 for reviews). (Adolphs, Tranel, Damasio, & Damasio, 1995;
Instead, we focus attention on the amygdala–fear Adolphs, Damasio, Tranel, & Damasio, 1996), and
link, which is the best known and perhaps most some experiences of fear (e.g., in a haunted house;
historically influential hypothesis about the neural Feinstein, Adolphs, Damasio, & Tranel, 2011).
circuitry of emotion. However, more recent findings suggest these links are
The amygdala was considered an essential part of not consistent or specific enough to suggest that the
a dedicated neural circuit involved in perception and amygdala is the brain basis of fear. For instance,
experience of fear following early animal research the amygdala is not involved consistently in “fear
demonstrating its role in neophobia (Klüver & conditioning” and extinction across human neuro-
Bucy, 1937), aversive conditioning (“fear learning”; imaging studies; roughly half of studies reviewed
Davidson & Irwin, 1999; LeDoux, Cicchetti, failed to report amygdala activation (Sehlmeyer
Xagoraris, & Romanski, 1990), extinction (Falls, et al., 2009), suggesting a more complex role for the
Miserendino, & Davis, 1992), and freezing behavior amygdala in learning about aversive stimuli than
(e.g., Blanchard & Blanchard, 1972). Together, previously assumed. In the case of perceiving fearful
these led early researchers to conclude that the facial expressions, complete amygdala lesions do not

abolish accurate perceptions when patients are given experiments, people, and time). Importantly, the
the added instruction to look at the eyes of fearful patterns found across instances for, say, fear do not
faces (Adolphs et al., 2005). In addition, there are replicate one another, meaning that there is not a
significant increases in amygdala activation follow- stable “biomarker” for this emotion category (Clark-
ing presentation of isolated fearful faces, but not Polner et al., 2016). A second point is logical; MVPA
when those faces are shown with complete bodies, analyses can differentiate the brain’s representation
which should presumably be an even clearer fearful of semantic categories such as “athletes” versus
signal (Poyo Solanas et al., 2017). Finally, patients “buildings” (Huth, Nishimoto, Vu, & Gallant, 2012),
with bilateral amygdala lesions are able to experi- but humans are less likely to essentialize the clearly
ence fear when deprived of oxygen, suggesting that socially constructed category of “athletes” than the
all instances of fearful experience are not abolished body-based category of “emotions” (see Lindquist,
by amygdala lesions (Feinstein et al., 2013). A meta- Gendron, Oosterwijk, & Barrett, 2013) and so
analysis of neuroimaging experiments in healthy scientists do not conclude that they have found
humans identifies amygdala activation in roughly “biomarkers” for categories such as “athletes.” Finally,
30% of data points that induce fearful experiences MVPA studies identify a functional pattern but do
(Lindquist et al., 2012), so it is not activated consist not say whether those brain regions are working to-
ently during fearful experiences in humans. Rather, gether as a distinct circuit, or even whether those
the amygdala is most consistently activated in fear brain regions have functional connections to one
inductions involving external (visual, auditory) another. It would be more compelling to identify
stimuli as opposed to internally generated states of networks of regions that have known anatomical
fear (Lindquist et al., 2012). Nor is the amygdala connectivity and are consistently and specifically
specific to fear—it activates during other emotions associated with the experience of specific emotions.
(Lindquist et al., 2012) and during attention to We (Touroutoglou, Lindquist, Dickerson, &
motivationally relevant stimuli more generally
Barrett, 2015) attempted to identify whether brain
(Cunningham & Brosch, 2012). Like the nonhu- regions that showed consistent functional activation
man animal findings (e.g., Paré & Quirk, 2017), for specific emotions (from the Vytal & Hamann,
these findings suggest that the amygdala is playing a 2010 meta-analysis) were each part of their own,
more general psychological function and is not spe- emotion-specific anatomical network, or whether
cific to the emotion category fear. they formed broader networks that were not specific
Finally, the traditional approach to emotion can to emotions. We used resting state functional con-
be observed in recent neuroimaging findings that nectivity, which reveals chronic functional connec-
rely on multivariate pattern-based analyses (MVPA) tions between brain regions known to be undergirded
based in machine learning to examine whether a by anatomical connections (i.e., white matter tracts
pattern of brain activity across the whole brain can measured through diffusion tractography in humans
“diagnose” or serve as a “biomarker” of which emo- or in retrograde tracer injections in nonhuman
tion a person is experiencing (e.g., Kassam, Markey, primate brains; (Deco, Jirsa, & McIntosh, 2011;
Cherkassky, Loewenstein, & Just, 2013, Kragel & Hermundstad et al., 2013; Pernice, Staude,
LaBar, 2015; Saarimäki et al., 2015). These approaches Cardanobile, & Rotter, 2011; van den Heuvel et al.,
move beyond simple 1:1 relations between specific 2009). Using brain regions that consistently activate
brain regions and emotion categories to argue that for specific discrete emotions as seeds in resting state
neural circuits for emotion exist in complex patterns networks, we failed to reveal evidence for emotion-
in the brain. It is easy to assume that identifying a specific, anatomically defined brain networks. For
pattern for a specific category reveals the neuroana- instance, a region of the left amygdala that was con
tomical basis of that category, yet there are multiple sistently associated with fear in the meta-analytic
problems with this interpretation (see Clark-Polner, summary (Vytal & Hamann, 2010) did not form a
Johnson, & Barrett, 2016). The first problem is sta- fear-specific network. Rather, it was functionally
tistical. A pattern that successfully distinguishes the connected to areas that form part of a broader
members of one category from the members of an- “salience network” (cf. Seeley et al., 2007) identified
other (at a significant level) is not a “signature” or across species (Touroutoglou et al., 2016). Activation
“biomarker” but is instead a statistical summary of a within this salience network is generally associated
sample of instances (instances of fear induced in one with aversive states (e.g., Hayes & Northoff, 2011;
experiment) drawn from a greater population of Lindquist et al., 2016), attention (Menon & Uddin,
instances (other instances of fear across other 2010), and behavioral avoidance (Menon, 2011).

Critically, we found that the regions that showed structures (e.g., the amygdala) or failures of the
consistent activation across multiple negative cortex to regulate such structures as the basis of
emotions (fear, anger, disgust, and sadness) were emotion dysregulation (see Etkin & Wager, 2007).
part of this anatomically constrained salience net- Other studies explicitly focus on dysregulation of a
work (Touroutoglou et al., 2015), underscoring the “fear circuit.” Here we again focus our attention on
hypothesis that the salience network contributes to the fear–amygdala link, which has led to over 150
multiple types of emotional experiences. publications examining the role of the amygdala in
In sum, the literature increasingly suggests that fear and anxiety. We are not arguing that the amyg-
specific emotion categories do not map consistently dala is uninvolved in the neural etiology of anxiety
and specifically to certain anatomical circuity. This disorders; rather, we suggest that it is far from clear
finding is convergently revealed using neuroimag- that amygdala dysregulation represents dysregula-
ing in humans (for meta-analyses, see Kober et al., tion in a “fear circuit” as such. Rather, the amygdala
2008; Lindquist et al., 2012; Touroutoglou et al., may be playing a more basic role that is general to
2015; Vytal & Hamann, 2010; Wager et al., 2015) multiple emotion categories and is transdiagnostic
and also in studies that use causal methods in both across disorders, a point we delve into later.
humans (e.g., using electrical stimulation; Guillory Following the traditional model, emotion dys-
& Bujarski, 2014) and nonhuman animals (see regulation arises in part from dysfunction within
Barrett et al., 2007). Furthermore, and as men- the “limbic system,” including structures such as the
tioned previously, studies in nonhuman animals amygdala in anxiety and from the failure of the
reveal anatomical circuitry supporting certain cortex to regulate such structures. For instance,
adapt ive behaviors (for a review see Panksepp, heightened amygdala activation is observed across
1998), but the interpretation that these circuits are patients with social anxiety disorder (Birbaumer
the circuits for complex categories such as human et al., 1998; Furmark et al., 2004; Phan, Fitzgerald,
fear, disgust, anger, and so forth is problematic (see Nathan, & Tancer, 2006; Stein, Goldin, Sareen,
Barrett et al., 2007; LeDoux, 2012, 2013). For in- Zorrilla, & Brown, 2002) and posttraumatic stress
stance, there are elegantly worked-out circuits for disorder2 (PTSD; Rauch et al., 2000; Shin, Rauch,
escape (Vazdarjanova & McGaugh, 1998), freezing & Pitman, 2006). Interestingly, heightened amyg-
(LeDoux, 2007), and fighting (e.g., offensive dala activation to negative stimuli is also observed in
attack—Lin et al., 2011; defensive aggression—
anxiety-prone individuals who are otherwise con-
Motta et al., 2009), but the neural circuit for a sidered healthy (Stein, Simmons, Feinstein, &
behavior is not the neural circuit for an emotion per Paulus, 2007). Consistent with the role of PFC in
se (e.g., Barrett, 2012; Barrett et al., 2007; LeDoux, regulating the amygdala, diminished amygdala ac-
2012). A problem with this logic is that an animal tivity during emotion regulation tasks is associated
might perform multiple behaviors when faced with with increased cortical thickness and greater white
a potential threat (i.e., a “fearful” situation): it matter connectivity within prefrontal cortical areas
might flee, freeze, or fight. This introduces the prob- (Foland-Ross et al., 2010; Kim et al., 2011), suggest-
lem of having many fear circuits (e.g., Gross & ing that structural differences in the PFC predict
Canteras, 2012) and poses an inductive problem for reduced amygdala activity. In pathological anxiety,
the science of emotion and psychopathology since it patients show reduced functional connectivity be-
is unclear which fear circuit is the correct one to tween the amygdala and frontocortical areas, such
study when examining psychopathology. This said, as the orbitofrontal cortex (Hahn et al., 2011).
it is likely that circuits for these adaptive behaviors Patients with PTSD show a diminished ability to
form a more basic “element” in emotional experiences extinguish conditioned fear as compared to healthy
by combining with other more basic psychological controls, which is associated with weak recruitment
“elements.” This idea is consistent with the psycho- of prefrontal cortical areas and reduced amygdala
logical constructionist account we discuss next. inhibition (Milad et al., 2009; Kolassa & Elbert,
Limitations with the traditional view aside, in- 2007), and connectivity between the PFC and
vestigations of emotion dysregulation typically hew amygdala improves following successful treatment
to these traditional assumptions about the brain (see Clark & Beck, 2010 for a review).
basis of emotions by assuming that dysregulation Together, these findings suggest that subcortical
derives from dysregulation of an emotion-specific and cortical structures, or some interplay between
brain area or circuit. For instance, much research them, are important to regulated emotions.
focuses on increased reactivity within subcortical However, recent work suggests that the traditional

approach may provide too narrow a lens for generally (Lindquist & Barrett, 2012). These
hypothesis testing and interpretation when it comes approaches emerged in the history of psychology in
to understanding processes underlying emotional attempts to explain failures of traditional approaches
dysregulation. A recent meta-analysis (Sprooten et al., to account for existing empirical data on emotion
2017) of 537 studies of case-control clinical exami- (see Lindquist, 2013).
nations of mental disorders (including anxiety The TCE draws from patterns of data described
disorders, schizophrenia, bipolar disorder, major
in the literature on emotions, without appealing to
depressive disorder, and obsessive-compulsive disor- essentialist assumptions. The TCE and psychologi-
der) containing observations derived from 21,427 cal constructionist models before it (see Duffy, 1941;
participants calls the central role of the amygdala in Hunt, 1941; James, 1890; Schachter & Singer, 1962;
anxiety disorders into question. The meta-analysis Wundt, 1897/1998; see Gendron & Barrett, 2009
found some evidence for greater amygdala activa- and Lindquist, 2013 for a historical review) recog-
tion in anxiety disorders, but only when those stud- nize that emotions do not have their own specific
ies that used region-of-interest (ROI) analyses were behavioral action tendencies (Baumeister, DeWall,
considered in the analysis. ROIs are a priori locations Vohs, & Alquist, 2010; DeWall, Baumeister, Chester,
in the brain that are queried for activation during & Bushman, 2016), facial behaviors (Jack, Garrod,
analysis, oftentimes using more lenient statistics. Yu, Caldara, & Schyns, 2012; Jack, Sun, Delis,
This is one manner by which traditional notions Garrod, & Schyns, 2016), peripheral physiological
about brain function can influence the literature: signatures (Siegel et al., 2018), or causal mecha-
Traditional assumptions about emotion–brain link- nisms in the brain (Guillory & Bujarski, 2014;
ages cause researchers to look to the amygdala for Lindquist et al., 2012; Wager et al., 2015). These ap-
what would otherwise be subthreshold activation, proaches also recognize heterogeneity within each
and when such activation is found, it is concluded emotion category. For instance, although traditional
that amygdala dysfunction is central to a disorder. approaches assume that “fear” names a set of in-
However, when meta-analyzing studies that per- stances that share a key set of features with a
formed whole-brain analyses without an a priori common causal mechanism, some instances of fear
focus and using stricter statistical thresholds, there feel good and some feel bad (Wilson-Mendenhall,
was not a strong link between greater amygdala ac- Barrett, & Barsalou 2014), some involve an increase
tivity and anxiety disorders across the literature. In in heart rate and some involve a decrease (Kreibig,
fact, the link between amygdala activity and other 2010), and some involve activity within the amyg-
disorders (e.g., bipolar disorder) was relatively dala and some do not (Lindquist et al., 2012; Wager,
stronger when considering whole-brain analyses. In Barrett, et al., 2008). Neural concomitants of differ-
contrast, structures such as the thalamus and hippo- ent fear states (e.g., fear in a social context versus
campus, which are less frequently linked to anxiety, fear in a physical context) are as dissimilar as neural
showed relatively greater activation across anxiety concomitants of fear versus anger (Wilson-
(Sprooten et al., 2017). Of course, these findings Mendenhall, Barrett, & Barsalou, 2013b). The TCE
come from a single meta-analysis, but they converge thus attempts to describe both similarities in objective
with recent arguments that psychiatric disorders measures (i.e., behaviors, facial expressions, peripheral
arise not from emotion-specific circuits but from a physiology, brain activity; Barrett, 2006a, 2006b;
set of common large-scale brain networks (Menon, Barrett & Wager, 2006; Lindquist, 2013; Russell,
2011). This idea is articulated in a constructionist 2003) that exist between different emotion categories
approach to mind–brain correspondence (Lindquist and differences that exist within emotion categories
& Barrett, 2012). (Kreibig, 2010; Siegel et al., in press; Wilson-
Mendenhall et al., 2013a), all the while explaining
Constructionism: Emotions as Emergent why people subjectively experience emotions as
Phenomena relatively distinct from one another (e.g., people by
An alternative approach to understanding brain and large experience fear as distinct from disgust;
bases of emotion and, by extension, emotion dys- although see Barrett, 2006c for a discussion of in-
regulation is the theory of constructed emotion dividual differences).
(TCE). The TCE is part of the broader class of The TCE achieves this by defining emotions as
“psychological constructionist” approaches to emo- loose, fuzzy categories that are imposed by the
tion (see Gendron & Barrett, 2009 for a historical minds’ perceivers and emerge from a set of objec-
review) and mind–brain correspondence more tively measurable basic “elements” of the mind. One

such element is core affect. Core affect is a product of Barrett & Bar, 2009) or internal sensations of core
the brain’s attempts to maintain homeostasis by affect (e.g., Lindquist & Barrett, 2008). The TCE
marshalling changes in the body in relation to exter- thus shares much in common with predictive ap-
nal events (see Barrett, 2017a; Kleckner et al., 2017). proaches to the mind (e.g., Clark, 2013; Friston,
Experientially, core affect can be described as feel- 2010; Hohwy, 2013; Lupyan & Clark, 2015) insofar
ings of activation or deactivation of the autonomic as it hypothesizes that top-down information from
nervous system and feelings of pleasantness or un- prior experience is used to assign meaning to core
pleasantness (see Barrett & Bliss-Moreau, 2009; affect and produce discrete experiences of emotion
Barrett, 2016; Diener, Larsen, Levine, & Emmons, (anger, fear, etc.). Consistent with the TCE, catego-
1985; Duffy, 1957; Lindquist, 2013; Ortony, Clore, rization yields subjective differentiation of emo-
& Collins, 1988; Russell, 2003; Watson & Tellegen, tions, even when the underlying physiology is not
1985). Marshalling body changes to maintain ho- categorical. How people categorize their affective
meostasis is experienced as activating and, depend- states drives self-reported emotional experiences
ing on the context, sometimes unpleasant (e.g., in (Jamieson, Mendes, Blackstock, & Schmader, 2010;
the face of a threat). In other cases, it might be ex- Kirkland & Cunningham, 2012; Lee, Lindquist, &
perienced as activating and pleasant (e.g., in the case Payne, in press; Lindquist & Barrett, 2008;
of pursuing a reward). All experiences have some Oosterwijk, Rotteveel, Fischer, & Hess, 2009;
core affective tone (Barrett & Bliss-Moreau, 2009; Oosterwijk et al., 2012), shifts physiology (i.e.,
Craig, 2009; Russell, 2003) including but not lim- whether someone is threatened versus challenged;
ited to the experience of emotion categories. For Jamieson et al., 2010; Kassam & Mendes, 2013;
instance, although fear is experienced as distinct Oosterwijk et al., 2009), and alters observed
from disgust, the TCE hypothesizes that each involves patterns of brain activity during emotions (e.g.,

similar core affect (e.g., feelings of high activation Lindquist et al., under review; Oosterwijk et al., 2012;
and unpleasantness). Properties of core affect can be Satpute, Shu, et al., 2013; Satpute, Wager, et al.,
construed as basic features of consciousness 2013; Satpute et al., 2016; for a meta-analysis, see
(Duncan & Barrett, 2007; Russell, 2005), and via Brooks et al., 2017). Finally, the TCE hypothesizes
reciprocal efferent and afferent projections between that specific core affective sensations and category
the brain and peripheral nervous system, core affect knowledge that are attended to and represented in any
can act as a barometer that allows an organism to given instance alter ongoing emotional experiences.
know whether it should approach or avoid some- The third “element” in emotion is executive
thing (Barrett & Bliss-Moreau, 2009; Russell, 2003). control. Executive control refers to attentional re-
The TCE predicts that the brain is always making sources that allow an individual to selectively
meaning of core affect—sensations that are them- enhance some information and suppress other

selves ambiguous (Barrett, 2017a; MacCormack & information (Mack & Rock, 1998). It is hypothe-
Lindquist, 2017). To do so, the brain relies on the sized that executive control helps a person select
ongoing context outside the body and prior experi- aspects of core affective representations, category
ences of which subjective experiences occurred in knowledge, or external sensory representations for
such contexts (Barrett, 2009, 2017a; Lindquist, 2013). conscious experience in a given instance and to
A person thus experiences a specific emotion when suppress other, less related representations. For
he or she automatically and unconsciously makes instance, executive control processes appear to be
meaning of (i.e., categorizes) their core affective sen- involved in selecting category knowledge during
sations in given contexts (e.g., while delivering a emotion (Brooks et al., 2017; Oosterwijk et al.,
speech) drawing on knowledge about specific emo- 2012). One hypothesis is that executive control
tion categories experienced in that context in the allows the brain to unite together representations
past (e.g., fear versus excitement). of core affect, category knowledge, and sensations
The second “element” in emotion is categorization. from external perceptions (e.g., vision) into a uni-
Categorization is the basic process(es) through fied experience of an emotion (see Lindquist, 2013
which the brain uses prior experiences (i.e., memo- for a discussion). Consistent with this hypothesis,
ries, semantic and concept knowledge) to make aspects of a brain network associated with execu-
predictions about the meaning of sensations in the tive control called the frontoparietal network show
present. Categorization is used to refine the meaning greater connectivity with the fusiform gyrus, an
of all sensory information, whether those sensations area involved in viewing faces, during intense anger
are external to the body (as in visual perception; experiences. These findings suggest that during

anger, participants may draw on prior experiences their functional neuroanatomy, appear to correspond
of anger that involve seeing the faces of their ene- to very basic psychological functions, many of
mies (Lindquist et al., under review). In such situ- which are predicted a priori by the TCE.
ations, regions associated with executive control Furthermore, these groups correspond to a set of
help to select these representations in the service of “intrinsic” networks that are formed by the brain’s
creating the experience of anger. structural architecture (Deco et al., 2011), develop
over infancy and early childhood (Gao, Alcauter,
Neural Bases of Emotions Smith, Gilmore, & Lin, 2015; Pendl et al., 2017),
Despite long-standing theoretical roots of psycho- are present across task domains (e.g., Habas et al.,
logical constructionist approaches to emotion, which 2009; Seeley et al., 2007; Vincent, Kahn, Snyder,
began in the 19th century (Dunlap, 1932; Harlow & Raichle, & Buckner, 2008), and exert constraints
Stagner, 1932, 1933; Spencer, 1855, 1894; Sully, on information processing during emotion and
1892; see Gendron & Barrett, 2009 for a historical cognition (Ciric, Nomi, Uddin, & Satpute, 2017;
review), the TCE is the first such approach to be Cohen, 2017; Krienen, Yeo, & Buckner, 2014; Yeo
applied to understanding neural bases of emotions et al., 2011; Yeo, Krienen, Chee, & Buckner 2014).
(Barrett & Satpute, 2013; Lindquist et al., 2012; The first group identified in our meta-analysis
Lindquist & Barrett, 2012; Touroutoglou et al., (Kober et al., 2008), referred to as the core limbic3
2015; for a neuroscience-based constructionist theory group, comprised the amygdala, hypothalamus,
of memory, see Schacter, Norman, & Koutstaal, ventral striatum, and periaqueductal gray, all re-
1998; Schacter, Addis, & Buckner, 2007; for a con- gions that contribute to visceromotor activation of
structionist theory of vision, see Bar, 2004). Indeed, the body via projections to the peripheral nervous
its historical predecessors were articulated before system (Barrett & Simmons, 2015; Buijs & Van
modern brain imaging—as described herein—was Eden, 2000). The second, the lateral paralimbic4
available. Neuroscience findings bolster and refine group, comprised the mid- and anterior insula and
behavioral and peripheral physiological work posterior orbitofrontal cortex (OFC), which receive
supporting the TCE. Rather than assuming that afferent information via brainstem nuclei from the
specific emotion categories, such as fear, map onto peripheral nervous system to represent visceromotor
singular neural mechanisms (e.g., anatomical regions changes in ongoing experience (i.e., interoception;
within the brain—Davis, 1992; or multivariate Craig, 2009; Kleckner et al., 2017). Together, this set
“fingerprints”—Saarimäki et al., 2015), the TCE of brain regions and their functional neuroanatomy
hypothesizes that neural networks supporting more correspond to the psychological element of core
basic psychological processes such as core affect, cat- affect. Interestingly, many of these same regions
egorization, and executive control contribute to constitute the intrinsic salience network (SN; Seeley
emotional experiences. et al., 2007; Yeo et al., 2011). Activity within the SN
There is growing evidence in the neuroimaging during rest predicts self-reported arousal to evocative
literature for the TCE hypotheses. As noted earlier, images (Touroutoglou, Hollenbeck, Dickerson, &
meta-analyses of neuroimaging studies on emotion Barrett, 2012), skin conductance responses (Kleckner
reveal that emotion categories such as anger, fear, et al., 2017), and reports of anxiety during scanning
sadness, disgust, and happiness do not correspond (Seeley et al., 2007). This suggests functional rele-
to specific anatomical regions (Lindquist et al., vance of this network to core affect.
2012; Vytal & Hamann, 2010). Critically, these The third group identified in our meta-analysis
meta-analyses reveal that during instances of emo- (Kober et al., 2008), referred to as the medial posterior
tion, there is activity within and across a set of group, consisted of the posterior cingulate cortex
common networks that also activate during other (PCC) extending into primary visual cortex, regions
psychological functions (e.g., memory, semantics, associated with self-referential processing and vision.
visual perception, etc.; see Barrett & Satpute, 2013; The fourth group was the medial PFC group, com-
Lindquist & Barrett, 2012). For instance, a meta- posed of the dorsal medial PFC (dmPFC), the
analysis using data-driven techniques to detect pat- pregenual anterior cingulate cortex (pgACC), and
terns of coactivation across neuroimaging studies of rostral dorsal ACC (rdACC). These regions are asso-
emotion revealed a set of six functional groups that ciated with self-referential processing (Lou et al.,
span both the subcortex and cortex (Kober et al., 2004; Moran et al., 2006) and representation of value
2008, see figure 7A–F). These functional groups did (Knutson, Taylor, Kaufman, Peterson, & Glover,
not correspond to specific emotions but, based on 2005; Levy & Glimcher, 2011). These regions often

coactivate together across studies, particularly studies and participants’ ratings of sadness additionally
of autobiographical memory and semantics (Binder, correlated with the degree of cohesion between

Desai, Graves, & Conant, 2009; Spreng, Mar, & these two networks. More recently, Raz and col-
Kim, 2009; Svoboda, McKinnon, & Levine, 2006), leagues (2016) extended these findings to examine
and are thought to collectively represent the brain’s internetwork connectivity differences across different
use of prior experiences to make meaning of internal discrete emotions including anger, fear, and sadness.
and external sensations in the moment (Bar, 2011). They examined connectivity within and between
Together, this set of brain regions and their func- the SN and the DMN. Greater connectivity between
tional neuroanatomy correspond to the psychological dorsal parts of the SN (dorsal anterior insula, dorsal
element of categorization. These same regions also ACC) and aspects of the DMN extending into the
constitute the intrinsic default mode network (DMN; subcortex (centromedial nucleus of the amygdala)
Spreng et al., 2009). Activity of the DMN during was associated with more intense ratings of emotion
rest predicts self-reflection (Northoff & Bermpohl, during the experience of most instances of emotion.
2004), emotion regulation (Wager, Davidson, These findings provide some of the first evidence
Hughes, Lindquist, & Ochsner 2008), and planning that networks associated with core affect and cate-
future behaviors (Spreng et al., 2009). Thus, this gorization interact during emotional experience.
network is involved in combining representations of If emotions emerge from dynamic functional
prior experiences for use in thinking about the self, coupling of intrinsic neural networks, then the novel
categorizing ongoing emotional experiences, and prediction of the TCE is that emotion dysregulation
projecting oneself into the future. in the context of psychopathology originates from
Finally, the fifth group, referred to as the cognitive/ perturbations in the domain-general networks that
motor group, included the right frontal operculum, contribute to emotions. Other recent accounts link
bilateral inferior frontal gyrus (IFG), presupple- psychopathology to dysregulation in intrinsic net-
mentary motor area (pre-SMA), and left middle works (e.g., Menon, 2011), but the TCE offers pre-
frontal gyrus. This set of brain regions and their dictions at both psychological and neural levels. In
functional neuroanatomy correspond to the psy- the case of anxiety, it predicts dysfunction in basic
chological element of executive control5 (Nee, psychological processes that support emotion expe-
Wager, & Jonides, 2007; Wager, Jonides, & Reading, rience, such as core affect, categorization, and exec-
2004). Notably, these regions constitute the intrinsic utive control, as manifested by dysfunction in the
executive control network known as the frontopari- neural networks that support these functions.
etal network (Corbetta & Shulman, 2002). This set Consistent with the TCE, preliminary evidence
of brain regions coactivate in response to top-down links anxiety disorders with alterations in func-
control that gates attention to sensory stimuli of po- tioning of the SN, DMN, and frontoparietal
tential behavioral significance (from the body, prior network, which are hypothesized to support core
experiences, or the world) in the moment (Aron, affect, categorization, and executive control, re-
Robbins, & Poldrack, 2004; Nee et al., 2007). spectively. Dysfunction in the anterior insula of
Activity of the frontoparietal network during rest the SN is thought to be a core feature of anxiety
predicts response inhibition (Nee et al., 2007), disorders (Paulus & Stein, 2006), suggesting an
action selection (Corbetta & Shulman, 2002), and impairment in core affective processing, and in
selection of semantic knowledge (Thompson-Schill, particular representation of afferent information
D’Esposito, Aguirre, & Farah, 1997). from the viscera. Hyperactivity of the anterior
The TCE suggests that networks mapping onto insula of the SN is observed in individuals high in
functions including core affect, categorization, and trait anxiety (Paulus & Stein, 2006; Stein et al.,
executive control functionally interact during the 2007) and individuals who score high on trait
experience of emotions. Growing evidence is con neuroticism (Feinstein, Stein, & Paulus, 2006).
sistent with this hypothesis. For instance, Raz et al. Neuroimaging work also shows decreased functional
(2012) used a network cohesion approach to examine connectivity between the dACC—a region of the
the inter- and intranetwork connectivity of the core SN implicated in processing negative affect, pain, and
limbic group observed in Kober et al. (2008) (roughly cognitive control (Shackman et al., 2011)—and
mapping onto aspects of the salience network) and the amygdala, a subregion of the SN (Touroutoglou
the mPFC (part of the default mode network). et al., 2012), among patients with generalized
There was increased functional connectivity between anxiety disorder at rest, relative to controls (Etkin,
these two networks during an instance of sadness Prater, Schatzberg, Menon, & Greicius, 2009).

This suggests impairment in processing salient and etwork and the amygdala, a region within the SN
n
potentially negatively valenced input. Furthermore, (Touroutoglou et al., 2012), are observed in patients
EEG studies report perturbed error-related brain with generalized anxiety disorder (Etkin et al.,
activity in highly anxious individuals, specifically 2009) and social anxiety disorder (Liao et al., 2010).
in the error-related negativity (ERN), a component Finally, patients with severe PTSD demonstrate
of the event-related potential (ERP) observed impairments in disengaging the DMN and engaging
following the commission of an error in reaction- the salience and frontoparietal networks during ex-
time tasks and linked to the ACC (Yeung, ecutive control tasks (Daniels et al., 2010). Together,
Botvinick, & Cohen, 2004). Studies demonstrate these findings suggest that disorder might be char-
enhanced ERN in tasks involving neutral, non- acterized by a relative imbalance in processes linked
emotional stimuli in patients with generalized to core affect versus conceptualization versus execu-
anxiety disorder (Weinberg, Olvet, & Hajcak,
tive control.
2010), obsessive-compulsive disorder (Xiao et al.,
2011), and subclinical anxiety (Hajcak, McDonald, & Future Directions
Simons, 2003). These findings are consistent with The TCE charts a path forward for future investiga-
increased functioning of the SN as a network im- tions into the brain bases of human emotion and
portant for detecting errors or conflict (Botvinick, emotion dysregulation. It offers predictions not of-
Braver, Barch, Carter, & Cohen, 2001; Carter, fered by traditional approaches. A first prediction is
Botvinick, & Cohen, 1999). that dysregulation will emerge from activity not
Other work links anxiety disorders with alterations only within intrinsic networks but also among
in the DMN. For instance, patients with anxiety these networks. The TCE predicts that anxiety may
relative to healthy controls show reductions in brain be more than a disorder circumscribed by an ana-
activation within the PCC and mPFC of the DMN tomically defined fear circuit, but perhaps more
while at rest, and while listening to emotionally related to abnormal variation within networks that
neutral and threat-related words (Zhao et al., 2007). support core affective, categorization, and executive
Critically, increased connectivity between parts of control processes. A second prediction is that dys-
the DMN (e.g., PCC) and the right amygdala, a regulation of intrinsic networks is transdiagnostic.
component of the SN, is associated with PTSD This prediction shares ideas in common with Insel
symptoms and predicts future PTSD (Lanius et al., et al. (2010) and Menon (2011). Here, we focused
2010). These findings could be evidence that indi- on anxiety disorders for illustration, and point out
viduals with PTSD are more likely to conceptualize that dysregulation of intrinsic networks spans not
core affective sensations (e.g., a beating heart) as only anxiety disorders but also other disorders. For
specific emotional experiences (e.g., fear) than healthy example, dysregulation of the salience network is
controls, who might experience these sensations as observed in major depressive disorder (Manoliu et al.,
transient bodily feelings and not emotional per se. 2014) and schizophrenia (Palaniyappan & Liddle,
Other evidence points to relative differences in the 2012). To understand how dysregulation in these
functional connectivity within the DMN (including networks occurs across disorders, we first need to
the ACC and mPFC) and SN (including the amyg- understand how much variation underlies “regu-
dala), with lesser functional connectivity in the lated” function of these networks. Evaluating these
DMN in PTSD but greater functional connectivity predictions relies not only on changing theoretical
within the SN (Sripada et al., 2012). frameworks for understanding emotions and
Finally, many with anxiety disorders show altered mental illness but also on relatively new analytic
function of the frontoparietal network and between techniques in neuroimaging.
this network and others. For instance, individuals
high in trait anxiety show weaker functional con- Examining Interplay of Networks
nectivity relative to controls between regions of the One new direction prompted by the TCE is to
SN (e.g., dACC) and the frontoparietal network evaluate neural networks that underlie regulated emo-
(e.g., dlPFC) in an emotionally neutral Stroop task tions and their interactions. As reviewed earlier,
(Basten, Stelzel, & Fiebach, 2011). These results evidence suggests that emotions emerge from interac-
point to a general (non-threat-related) impairment tive effects of broad-scale networks. Yet to date, very
of attentional control in individuals high in trait few studies have taken a network-based approach to
anxiety. Similarly, aberrant functional connectivity examining neural bases of emotions (although see
patterns between regions of the frontoparietal Lindquist et al., under review; Raz et al., 2012;

Raz et al., 2016; Touroutoglou et al., 2015). capture explanatory individual-level information
Neuroimaging is increasingly examining the function about behavior or cognitions (Mueller et al., 2013),
of intrinsic networks in psychopathology, but this and intersubject variability is often implicitly treated
research began as exploratory, and to our knowledge, as noise rather than biologically informative features
there is no unified effort to understand how within- of brain organization (Zilles & Amunts, 2013; see
network or between-network activity changes as a also Finn et al., 2015). The social and/or environ-
function of disorder and what the psychological im- mental context in which a phenomenon is taking
plications of these changes are. The TCE offers such place is rarely modeled or even considered (Guloksuz,
a framework. Of course, ongoing work must con- Pries, & van Os, 2017; Shankman & Gorka, 2015).
tinue to validate the approach and link psychologi- These practices can lead to the false interpretation
cal levels of analysis (e.g., core affect) to neural levels that a single process or set of processes is associated
of analysis (e.g., activity of the salience network). with a single emotion category, when in reality there
Novel statistical approaches are also necessary to may be different pathways to that emotion category
reach these aims. To study functional dynamics of across different people or even within the same
networks and how they change across different person across instances. Growing neuroimaging
emotional states (dynamic functional connectivity; research is consistent with the idea that there is
see Cohen, 2017), researchers must use advanced heterogeneity—and even degeneracy (Price &

multivariate statistics. For instance, functional con- Friston, 2002)—in the brain responses associated
nectivity examines how time series of activation with emotions between people and within people
within different brain areas covary with one another across contexts. Degeneracy refers to the biological
to form complex networks. Directed functional principle whereby different processes produce the
connectivity approaches (e.g., Gates & Molenaar, same outcome. As an example of degeneracy, different
2012; Gates, Molenaar, Iyer, Nigg, & Fair, 2014) brain patterns exist for the same emotion categories
further allow researchers to examine lagged and experienced across different contexts (e.g., Wilson-
contemporaneous correlations between these brain Mendenhall, Barrett, Simmons, & Barsalou, 2011).
area “hubs” and how these change across emotional Clinically, there is growing evidence that separate
states (e.g., anger versus fear). For instance, we can brain processes produce the same outcomes (e.g.,
examine how hubs of the salience network (e.g., anxiety symptoms; Fisher, 2015; Gates et al., 2014;
insula, amygdala, dACC) change in connectivity Price, Gates, Kraynak, Thase, & Siegle, 2017; Price,
with one another across anger and fear in healthy Lane, et al., 2017). Moving forward, we should
individuals. Similar approaches can be used to ex- recognize and model such sources of variation and
amine between-network covariation across different degeneracy if we are to better understand how varia-
emotional states. For example, we can examine how tion in brain processes leads to dysregulated emotions.
the salience network changes its connectivity with To study heterogeneity across categories (whether
the default mode network during fear versus anger. categories of regulated emotions such as fear and
By understanding these dynamics and how they sadness or diagnostic categories such as anxiety and
manifest among different healthy affective (and depression), researchers must use approaches that
even nonaffective) states, we can begin to under- model different pathways to the same outcomes.
stand regulated functions of the brain. Next, we can Network-based subgrouping approaches (e.g., Lane
systematically explore how these network dynamics & Gates, 2017) arrive at group-level network solu-
become dysregulated in mental illness. tions but also identify subgroups with different net-
work patterns. We can examine how hubs of the
Variability in Emotions and Diagnostic salience network (e.g., insula, amygdala, dACC) are
Categories connected differentially during fear in one context
A second new direction prompted by the TCE is to (e.g., social) versus another (e.g., threat). Similar ap-
examine and model variability underlying emotions, proaches can be used to examine between-network
both in regulated and in dysregulated forms across covariation across different emotional contexts (e.g.,
diagnostic groups. Most human imaging research how the salience network changes its connectivity
focuses on group-level mean brain activity without with the default mode network during social fear
considering individual differences in the circuitry versus threat). We can even examine how different
that is associated with emotions. Statistical brain maps network patterns predict similar degrees of reported
computed across groups of people often do not anxiety within a sample (e.g., Doyle et al., 2018).

Conclusion Bar, M. (Ed.). (2011). Predictions in the brain: Using our past to
generate a future. New York, NY: Oxford University Press.
In this chapter, we reviewed contemporary models
Barbas, H. (1995). Anatomic basis of cognitive-emotional
of emotion and their implications for what goes interactions in the primate prefrontal cortex. Neuroscience &
awry in the brain during emotion dysregulation. We Biobehavioral Reviews, 19, 499–510.
focused on neuroimaging approaches, which have Barrett, L. F. (2006a). Emotions as natural kinds? Perspectives on
promise for understanding emotion and emotion Psychological Science, 1, 28–58.
Barrett, L. F. (2006b). Solving the emotion paradox:
dysregulation in awake, emoting humans. After
Categorization and the experience of emotion. Personality
roughly 25 years of research, we have made substan- and Social Psychology Review, 10, 20–46.
tial discoveries. We look forward to future research Barrett, L. F. (2006c). Valence as a basic building block of
that uses sophisticated network-based approaches to emotional life. Journal of Research in Personality, 40, 35–55.
search for neural processes that contribute to both Barrett, L. F. (2009). The future of psychology: Connecting
mind to brain. Perspectives in Psychological Science, 4, 326–339.
healthy and dysregulated emotion.
Barrett, L. F. (2012). Emotions are real. Emotion, 12, 413–429.
Barrett, L. F. (2016). Navigating the science of emotion. In
Notes H. Meiselman (Ed.), Emotion measurement (pp. 31–63).
1. We note that these processes change developmentally and Cambridge, UK: Woodhead Publishing.
that there is important variation across the lifespan. We focus Barrett, L. F. (2017a). The theory of constructed emotion: An
herein on research from young, healthy adults with the caveat active inference account of interoception and categorization.
that there may be important differences in children and Social Cognitive and Affective Neuroscience, 12, 1–23.
adolescents, and in middle and older age. Barrett, L. F. (2017b). How emotions are made: The secret life of the
2. We recognize that the latest Diagnostic and Statistical brain. New York, NY: Houghton Mifflin Harcourt.
Manual of Mental Disorders (DSM-5) no longer classifies Barrett, L. F. (2017c). Functionalism cannot save the classical
PTSD as an anxiety disorder but instead as a “trauma- and view of emotion. Social Cognitive and Affective Neuroscience,
stressor-related disorder.” However, given the previous 12, 34–36.
scientific conceptualizations of PTSD as an anxiety-related Barrett, L. F., & Bar, M. (2009). See it with feeling: Affective
disorder and evidence for some shared neural circuitry predictions during object perception. Philosophical Transactions
between PTSD and anxiety (e.g., Etkin & Wager, 2007), we of the Royal Society B: Biological Sciences, 364, 1325–1334.
discuss PTSD throughout our chapter. Barrett, L. F., & Bliss-Moreau, E. (2009). Affect as a psychological
3. In Latin, the word “limbic” means “border.” Herein, when we primitive. Advances in Experimental Social Psychology, 41,
speak of a limbic group, we are referring to brain tissue 167–218.
primarily bordering or constituting the subcortex. Critically, Barrett, L. F., Lindquist, K., Bliss-Moreau, E., Duncan, S.,
we are not referring to notions of a limbic system, as outlined Gendron, M., Mize, J., & Brennan, L. (2007). Of mice and
in the triune brain concept. men: Natural kinds of emotion in the mammalian brain?
4. Paralimbic tissue is three-layer cortical tissue that abuts limbic Perspectives on Psychological Science, 2, 297–312.
tissue. Barrett, L. F., & Satpute, A. (2013). Large-scale brain networks in
5. We note that executive control processes are typically affective and social neuroscience: Towards an integrative
associated with several brain regions, not only the ones we architecture of the human brain. Current Opinion in
indicate here. In fact, regions from our cognitive/motor group Neurobiology, 23, 361–372.
emerged from data-driven methods and were labeled with the Barrett, L. F., & Satpute, A. B. (in press). Historical pitfalls and
network they best approximated. new directions in the neuroscience of emotion. Neuroscience
Letters. doi: 10.1016/j.neulet.2017.07.045
References Barrett, L. F., & Simmons, W. K. (2015). Interoceptive predictions
Adolphs, R. (1999). The human amygdala and emotion. The in the brain. Nature Reviews Neuroscience, 16, 419–429.
Neuroscientist, 5, 125–137. Barrett, L. F., & Wager, T. (2006). The structure of emotion:
Adolphs, R., Damasio, H., Tranel, D., & Damasio, A. R. (1996). Evidence from the neuroimaging of emotion. Current
Cortical systems for the recognition of emotion in facial Directions in Psychological Science, 15, 79–85.
expressions. Journal of Neuroscience, 16, 7678–7687. Basten, U., Stelzel, C., & Fiebach, C. J. (2011). Trait anxiety
Adolphs, R., Gosselin, F., Buchanan, T. W., Tranel, D., Schyns, modulates the neural efficiency of inhibitory control. Journal
P., & Damasio, A. R. (2005). A mechanism for impaired fear of Cognitive Neuroscience, 23, 3132–3145.
recognition after amygdala damage. Nature, 433, 68–72. Baumeister, R. F., DeWall, C. N., Vohs, K. D., & Alquist, J. L.
Adolphs, R., Tranel, D., Damasio, H., & Damasio, A. R. (1995). (2010). Does emotion cause behavior (apart from making
Fear and the human amygdala. Journal of Neuroscience, 15, people do stupid, destructive things)? In C. Agnew,
5879–5891. D. Carlston, W. Graziano, & J. Kelly (Eds.), Then a miracle
Amir, A., Lee, S. C., Headley, D. B., Herzallah, M. M., & Paré, occurs: Focusing on behavior in social psychological theory and
D. (2015). Amygdala signaling during foraging in a hazardous research (pp. 12–27). New York, NY: Oxford University
environment. Journal of Neuroscience, 35, 12994–13005. Press.
Aron, A. R., Robbins, T. W., & Poldrack, R. A. (2004). Baxter, M. G., & Murray, E. A. (2002). The amygdala and
Inhibition and the right inferior frontal cortex. Trends in reward. Nature Reviews Neuroscience, 3, 563–573.
Cognitive Sciences, 8, 170–177. Beauchaine, T. P. (2015a). Future directions in emotion
Bar, M. (2004). Visual objects in context. Nature Reviews dysregulation and youth psychopathology. Journal of Clinical
Neuroscience, 5, 617–629. Child and Adolescent Psychology, 44, 875–896.

Beauchaine, T. P. (2015b). Respiratory sinus arrhythmia: A Corbetta, M., & Shulman, G. L. (2002). Control of goal-directed
transdiagnostic biomarker of emotion dysregulation and and stimulus-driven attention in the brain. Nature Reviews
psychopathology. Current Opinion in Psychology, 3, 43–47. Neuroscience, 3, 201.
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion Craig, A. D. (2009). How do you feel—now? The anterior insula
regulation, and the latent structure of psychopathology: and human awareness. Nature Reviews Neuroscience, 10, 59–70.
An integrative and convergent historical perspective. Cunningham, W. A., & Brosch, T. (2012). Motivational salience:
International Journal of Psychophysiology, 119, 108–118. Amygdala tuning from traits, needs, values, and goals.
Berking, M., & Wupperman, P. (2012). Emotion regulation and Current Directions in Psychological Science, 21, 54–59.
mental health: Recent findings, current challenges, and Damasio, A. R., Grabowski, T. J., Bechara, A., Damasio, H.,
future directions. Current Opinion in Psychiatry, 25, 128–134. Ponto, L. L., Parvizi, J., & Hichwa, R. D. (2000). Subcortical
Binder, J. R., Desai, R. H., Graves, W. W., & Conant, L. L. and cortical brain activity during the feeling of self-generated
(2009). Where is the semantic system? A critical review and emotions. Nature Neuroscience, 3, 1049–1056.
meta-analysis of 120 functional neuroimaging studies. Daniels, J. K., McFarlane, A. C., Bluhm, R. L., Moores, K. A.,
Cerebral Cortex, 19, 2767–2796. Clark, C. R., Shaw, M. E., . . . Lanius, R. A. (2010). Switching
Birbaumer, N., Grodd, W., Diedrich, O., Klose, U., Erb, M., between executive and default mode networks in posttraumatic
Lotze, M., . . . Flor, H. (1998). fMRI reveals amygdala activation stress disorder: Alterations in functional connectivity. Journal
to human faces in social phobics. Neuroreport, 9, 1223–1226. of Psychiatry and Neuroscience, 35, 258–266.
Blanchard, D. C., & Blanchard, R. J. (1972). Innate and Davidson, R. J., & Irwin, W. (1999). The functional neuroanatomy
conditioned reactions to threat in rats with amygdaloid of emotion and affective style. Trends in Cognitive Sciences, 3,
lesions. Journal of Comparative and Physiological Psychology, 11–21.
81, 281–290. Davis, M. (1992). The role of the amygdala in fear and anxiety.
Botvinick, M. M., Braver, T. S., Barch, D. M., Carter, C. S., & Annual Review of Neuroscience, 15, 353–375.
Cohen, J. D. (2001). Conflict monitoring and cognitive Deco, G., Jirsa, V. K., & McIntosh, A. R. (2011). Emerging
control. Psychological Review, 108, 624–652. concepts for the dynamical organization of resting-state
Brooks, J. A., Shablack, H., Gendron, M., Satpute, A. B., activity in the brain. Nature Reviews Neuroscience, 12, 43–56.
Parrish, M. H., & Lindquist, K. A. (2017). The role of DeWall, C. N., Baumeister, R. F., Chester, D. S., & Bushman,
language in the experience and perception of emotion: B. J. (2016). How often does currently felt emotion predict
A neuroimaging meta-analysis. Social Cognitive and Affective social behavior and judgment? A meta-analytic test of two
Neuroscience, 12, 169–183. theories. Emotion Review, 8(2), 136–143.
Buhle, J. T., Silvers, J. A., Wager, T. D., Lopez, R., Onyemekwu, C., Diener, E., Larsen, R. J., Levine, S., & Emmons, R. A. (1985).
Kober, H., . . . Ochsner, K. N. (2014). Cognitive reappraisal Intensity and frequency: Dimensions underlying positive and
of emotion: A meta-analysis of human neuroimaging studies. negative affect. Journal of Personality and Social Psychology,
Cerebral Cortex, 24, 2981–2990. 48, 1253.
Buijs, R. M., & Van Eden, C. G. (2000). The integration of stress Doyle, C., Lane, S., Brooks, J., Wilkins, R., Gates, K., &
by the hypothalamus, amygdala and prefrontal cortex: Balance Lindquist, K. (2018). Degenerate neural pathways for
between the autonomic nervous system and the neuroendocrine emotion: An application of the subgrouping GIMME
system. Progress in Brain Research, 126, 117–132. algorithm. Manuscript in preparation.
Bylsma, L. M., Taylor-Clift, A., & Rottenberg, J. (2011). Duffy, E. (1941). An explanation of “emotional” phenomena
Emotional reactivity to daily events in major and minor without the use of the concept “emotion.” Journal of General
depression. Journal of Abnormal Psychology, 120, 155–167. Psychology, 25, 283–293.
Carter, C. S., Botvinick, M. M., & Cohen, J. D. (1999). The Duffy, E. (1957). The psychological significance of the
contribution of the anterior cingulate cortex to executive concept of “arousal” or “activation.” Psychological Review,
processes in cognition. Reviews in the Neurosciences, 10, 49–58. 64, 265–275.
Chanes, L., & Barrett, L. F. (2016). Redefining the role of limbic Duncan, S., & Barrett, L. F. (2007). Affect is a form of
areas in cortical processing. Trends in Cognitive Sciences, 20, cognition: A neurobiological analysis. Cognition and Emotion,
96–106. 21, 1184–1211.
Ciric, R., Nomi, J. S., Uddin, L. Q., & Satpute, A. B. (2017). Dunlap, K. (1932). Are emotions teleological constructs?
Contextual connectivity: A framework for understanding the American Journal of Psychology, 44, 572–576.
intrinsic dynamic architecture of large-scale functional brain Ekman, P. (1992). An argument for basic emotions. Cognition
networks. Scientific Reports, 7, 6537. and Emotion, 6, 169–200.
Clark, A. (2013). Whatever next? Predictive brains, situated Ekman, P., & Cordaro, D. (2011). What is meant by calling
agents, and the future of cognitive science. Behavioral and emotions basic. Emotion Review, 3, 364–370.
Brain Sciences, 36, 181–204. Etkin, A., Prater, K. E., Schatzberg, A. F., Menon, V., & Greicius,
Clark, D. A., & Beck, A. T. (2010). Cognitive theory and therapy M. D. (2009). Disrupted amygdalar subregion functional
of anxiety and depression: Convergence with neurobiological connectivity and evidence of a compensatory network in
findings. Trends in Cognitive Sciences, 14, 418–424. generalized anxiety disorder. Archives of General Psychiatry,
Clark-Polner, E., Johnson, T. D., & Barrett, L. F. (2016). 66, 1361–1372.
Multivoxel pattern analysis does not provide evidence to Etkin, A., & Wager, T. D. (2007). Functional neuroimaging of
support the existence of basic emotions. Cerebral Cortex, 27, anxiety: A meta-analysis of emotional processing in PTSD,
1944–1948. social anxiety disorder, and specific phobia. American Journal
Cohen, J. R. (2017). The behavioral and cognitive relevance of of Psychiatry, 164, 1476–1488.
time-varying, dynamic changes in functional connectivity. Falls, W. A., Miserendino, M. J., & Davis, M. (1992). Extinction
NeuroImage. doi: 10.1016/j.neuroimage.2017.09.036. of fear-potentiated startle: Blockade by infusion of an

NMDA antagonist into the amygdala. Journal of Neuroscience, Gross, J. J., & Thompson, R. A. (2007). Emotion regulation:
12, 854–863. Conceptual foundations. In J. J. Gross (Ed.), Handbook of
Fanselow, M. S. (1994). Neural organization of the defensive emotion regulation (pp. 3–24). New York, NY: Guilford
behavior system responsible for fear. Psychonomic Bulletin Press.
and Review, 1, 429–438. Guillory, S. A., & Bujarski, K. A. (2014). Exploring emotions
Feinstein, J. S., Adolphs, R., Damasio, A., & Tranel, D. (2011). using invasive methods: Review of 60 years of human
The human amygdala and the induction and experience of intracranial electrophysiology. Social Cognitive and Affective
fear. Current Biology, 21, 34–38. Neuroscience, 9, 1880–1889.
Feinstein, J. S., Buzza, C., Hurlemann, R., Follmer, R. L., Guloksuz, S., Pries, L. K., & Van Os, J. (2017). Application of
Dahdaleh, N. S., Coryell, W. H., . . . Wemmie, J. A. (2013). network methods for understanding mental disorders:
Fear and panic in humans with bilateral amygdala damage. Pitfalls and promise. Psychological Medicine, 47, 2743–2752.
Nature Neuroscience, 16, 270–272. Habas, C., Kamdar, N., Nguyen, D., Prater, K., Beckmann,
Feinstein, J. S., Stein, M. B., & Paulus, M. P. (2006). Anterior C. F., Menon, V., & Greicius, M. D. (2009). Distinct
insula reactivity during certain decisions is associated with cerebellar contributions to intrinsic connectivity networks.
neuroticism. Social Cognitive and Affective Neuroscience, 1, Journal of Neuroscience, 29, 8586–8594.
136–142. Hahn, A., Stein, P., Windischberger, C., Weissenbacher, A.,
Finn, E. S., Shen, X., Scheinost, D., Rosenberg, M. D., Huang, J., Spindelegger, C., Moser, E., .
.
.
Lanzenberger, R. (2011).
Chun, M. M., . . . Constable, R. T. (2015). Functional Reduced resting-state functional connectivity between
connectome fingerprinting: Identifying individuals using amygdala and orbitofrontal cortex in social anxiety disorder.
patterns of brain connectivity. Nature Neuroscience, 18, NeuroImage, 56, 881–889.
1664–1671. Hajcak, G., McDonald, N., & Simons, R. F. (2003). Anxiety and
Fisher, A. J. (2015). Toward a dynamic model of psychological error-related brain activity. Biological Psychology, 64, 77–90.
assessment: Implications for personalized care. Journal of Harlow, H. F., & Stagner, R. (1932). Psychology of feelings and
Consulting and Clinical Psychology, 83, 825–836. emotions. I. Theory of feelings. Psychological Review, 39,
Foland-Ross, L. C., Altshuler, L. L., Bookheimer, S. Y., 570–589.
Lieberman, M. D., Townsend, J., Penfold, C., . . . Rasser, P. E. Harlow, H. F., & Stagner, R. (1933). Psychology of feelings and
(2010). Amygdala reactivity in healthy adults is correlated emotions. II. Theory of emotions. Psychological Review, 40,
with prefrontal cortical thickness. Journal of Neuroscience, 30, 184–195.
16673–16678. Hayes, D. J., & Northoff, G. (2011). Identifying a network
Friston, K. (2010). The free-energy principle: A unified brain of brain regions involved in aversion-related processing:
theory? Nature Reviews Neuroscience, 11, 127–138. A cross-species translational investigation. Frontiers in
Furmark, T., Tillfors, M., Garpenstrand, H., Marteinsdottir, I., Integrative Neuroscience, 5, 49.
Långström, B., Oreland, L., & Fredrikson, M. (2004). Heller, A. S., & Casey, B. J. (2016). The neurodynamics of
Serotonin transporter polymorphism related to amygdala emotion: Delineating typical and atypical emotional processes
excitability and symptom severity in patients with social during adolescence. Developmental Science, 19, 3–18.
phobia. Neuroscience Letters, 362, 189–192. Hermundstad, A. M., Bassett, D. S., Brown, K. S., Aminoff,
Gao, W., Alcauter, S., Smith, J. K., Gilmore, J. H., & Lin, W. E. M., Clewett, D., Freeman, S., . . . Grafton, S. T. (2013).
(2015). Development of human brain cortical network Structural foundations of resting-state and task-based
architecture during infancy. Brain Structure and Function, functional connectivity in the human brain. Proceedings of
220, 1173–1186. the National Academy of Sciences, 110, 6169–6174.
Gates, K. M., & Molenaar, P. C. M. (2012). Group search Herry, C., Bach, D. R., Esposito, F., Di Salle, F., Perrig, W. J.,
algorithm recovers effective connectivity maps for individuals Scheffler, K., . . . Seifritz, E. (2007). Processing of temporal
in homogeneous and heterogeneous samples. NeuroImage, unpredictability in human and animal amygdala. Journal of
63, 310–319. Neuroscience, 27, 5958–5966.
Gates, K. M., Molenaar, P. C. M., Iyer, S. P., Nigg, J. T., & Fair, Hohwy, J. (2013). The predictive mind. New York, NY: Oxford
D. A. (2014). Organizing heterogeneous samples using University Press.
community detection of GIMME-derived resting state Hunt, W. A. (1941). Recent developments in the field of emotion.
functional networks. PLoS One, 9, e91322. Psychological Bulletin, 38, 249–276.
Gelman, S. A. (2009a). Learning from others: Children’s con Huth, A. G., Nishimoto, S., Vu, A. T., & Gallant, J. L. (2012).
struction of concepts. Annual Review of Psychology, 60, 115–140. A continuous semantic space describes the representation of
Gelman, S. A. (2009b). Essentialist reasoning about the thousands of object and action categories across the human
biological world. In A. Berthoz & Y. Christen (Eds.), brain. Neuron, 76, 1210–1224.
Neurobiology of “Umwelt” (pp. 7–16). Berlin, Heidelberg: Insel, T. R. (2014). The NIMH Research Domain Criteria
Springer. (RDoC) Project: Precision medicine for psychiatry. American
Gendron, M., & Barrett, L. F. (2009). Reconstructing the past: Journal of Psychiatry, 171, 395–397.
A century of ideas about emotion in psychology. Emotion Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D. S.,
Review, 1, 316–339. Quinn, K., . . . Wang, P. (2010). Research domain criteria
Gross, C. T., & Canteras, N. S. (2012). The many paths to fear. (RDoC): Toward a new classification framework for research
Nature Reviews Neuroscience, 13, 651–658. on mental disorders. American Journal of Psychiatry, 167,
Gross, J. J., & John, O. P. (2003). Individual differences in two 748–751.
emotion regulation processes: Implications for affect, Izard, C. (1992). Basic emotions, relations among emotions,
relationships, and well-being. Journal of Personality and Social and emotion-cognition relations. Psychological Review, 99,
Psychology, 85, 348. 561–565.

Jack, R. E., Garrod, O. G., Yu, H., Caldara, R., & Schyns, P. G. Kring, A. M. (2008). Emotion disturbances as transdiagnostic
(2012). Facial expressions of emotion are not culturally processes in psychopathology. In M. Lewis, J. M. Haviland-
universal. Proceedings of the National Academy of Sciences, 109, Jones, & L. F. Barrett (Eds.), Handbook of emotion (3rd ed.,
7241–7244. pp. 691–705). New York, NY: Guilford Press.
Jack, R. E., Sun, W., Delis, I., Garrod, O. G., & Schyns, P. G. Kring, A. M., & Mote, J. (2016). Emotion disturbances as
(2016). Four not six: Revealing culturally common facial transdiagnostic processes in psychopathology. In L. F.
expressions of emotion. Journal of Experimental Psychology: Barrett, M. Lewis, & J. M. Haviland-Jones (Eds.), Handbook
General, 145, 708–730. of emotion (4th ed., pp. 653–669). New York, NY: Guilford
James, W. (1890). The principles of psychology. New York, NY: Press.
Henry Holt and Company. Kuhn, T. (1961). The function of measurement in modern
Jamieson, J. P., Mendes, W. B., Blackstock, E., & Schmader, T. physical science. Isis, 52, 161–193.
(2010). Turning the knots in your stomach into bows: Kuhn, T. (1977). The essential tension. Chicago, IL: University of
Reappraising arousal improves performance on the GRE. Chicago Press.
Journal of Experimental Social Psychology, 46, 208–212. LaBar, K. S., LeDoux, J. E., Spencer, D. D., & Phelps, E. A.
Kashdan, T. B., & Steger, M. F. (2006). Expanding the topography (1995). Impaired fear conditioning following unilateral
of social anxiety: An experience-sampling assessment of temporal lobectomy in humans. Journal of Neuroscience, 15,
positive emotions, positive events, and emotion suppression. 6846–6855.
Psychological Science, 17, 120–128. Lane, S. T., & Gates, K. M. (2017). Automated selection of
Kassam, K. S., Markey, A. R., Cherkassky, V. L., Loewenstein, robust individual-level structural equation models for time
G., & Just, M. A. (2013). Identifying emotions on the basis series data. Structural Equation Modeling: A Multidisciplinary
of neural activation. PloS One, 8, e66032. Journal, 24, 768–782.
Kassam, K. S., & Mendes, W. B. (2013). The effects of measuring Lanius, R. A., Bluhm, R. L., Coupland, N. J., Hegadoren,
emotion: Physiological reactions to emotional situations K. M., Rowe, B., Theberge, J., . . . Brimson, M. (2010).
depend on whether someone is asking. PloS One, 8, e64959. Default mode network connectivity as a predictor of post-
Keltner, D., Ekman, P., Gonzaga, G. C., & Beer, J. (2003). traumatic stress disorder symptom severity in acutely
Facial expression of emotion. In R. J. Davidson, K. R. traumatized subjects. Acta Psychiatrica Scandinavica, 121,
Scherer, & H. H. Goldsmith (Eds.), Handbook of affective 33–40.
sciences (pp. 415–432). New York, NY: Oxford University Press. LeDoux, J. E. (1995). Emotion: Clues from the brain. Annual
Kim, M. J., Loucks, R. A., Palmer, A. L., Brown, A. C., Solomon, Review of Psychology, 46, 209–235.
K. M., Marchante, A. N., & Whalen, P. J. (2011). The LeDoux, J. (2007). The amygdala. Current Biology, 17,
structural and functional connectivity of the amygdala: From R868–R874.
normal emotion to pathological anxiety. Behavioural Brain LeDoux, J. E. (2012). Rethinking the emotional brain. Neuron,
Research, 223, 403–410. 73, 653–676.
Kirkland, T., & Cunningham, W. A. (2012). Mapping emotions LeDoux, J. E. (2013). The slippery slope of fear. Trends in
through time: How affective trajectories inform the language Cognitive Sciences, 17, 155–156.
of emotion. Emotion, 12, 268–282. LeDoux, J. E., Cicchetti, P., Xagoraris, A., & Romanski, L. M.
Kleckner, I. R., Zhang, J., Touroutoglou, A., Chanes, L., (1990). The lateral amygdaloid nucleus: Sensory interface of
Xia, Chengie, Simmons, W. K., . . . Barrett, L. F. (2017). the amygdala in fear conditioning. Journal of Neuroscience,
Evidence for a large-scale brain system supporting allostasis 10, 1062–1069.
and interoception in humans. Nature Human Behavior, 1, Lee, D. (2013). Decision making: From neuroscience to
0069. psychiatry. Neuron, 78, 233–248.
Klüver, H., & Bucy, P. C. (1937). “Psychic blindness” and other Lee, J. Y., Lindquist, K. A., & Nam, C. S. (2017). Emotional
symptoms following bilateral temporal lobectomy in Rhesus granularity effects on event-related brain potentials during
monkeys. American Journal of Physiology, 119, 352–353. affective picture processing. Frontiers in Human Neuroscience,
Knutson, B., Taylor, J., Kaufman, M., Peterson, R., & Glover, G. 11, 133.
(2005). Distributed neural representation of expected value. Lee, K., Lindquist, K. A., & Payne, B. K. (in press). Constructing
Journal of Neuroscience, 25, 4806–4812. bias: Conceptualization breaks the link between implicit bias
Kober, H., Barrett, L. F., Joseph, J., Bliss-Moreau, E., Lindquist, and fear of Black Americans. Emotion.
K., & Wager, T. D. (2008). Functional grouping and Levy, D. J., & Glimcher, P. W. (2011). Comparing apples and
cortical–subcortical interactions in emotion: A meta-analysis oranges: Using reward-specific and reward-general subjective
of neuroimaging studies. NeuroImage, 42, 998–1031. value representation in the brain. Journal of Neuroscience, 31,
Kolassa, I. T., & Elbert, T. (2007). Structural and functional 14693–14707.
neuroplasticity in relation to traumatic stress. Current Liao, W., Chen, H., Feng, Y., Mantini, D., Gentili, C.,
Directions in Psychological Science, 16, 321–325. Pan, Z., . . . Gong, Q. (2010). Selective aberrant functional
Kragel, P. A., & LaBar, K. S. (2015). Multivariate neural connectivity of resting state networks in social anxiety
biomarkers of emotional states are categorically distinct. disorder. NeuroImage, 52, 1549–1558.
Social Cognitive and Affective Neuroscience, 10, 1437–1448. Lin, D., Boyle, M. P., Dollar, P., Lee, H., Lein, E. S., Perona, P.,
Kreibig, S. D. (2010). Autonomic nervous system activity in & Anderson, D. J. (2011). Functional identification of an
emotion: A review. Biological Psychology, 84, 394–421. aggression locus in the mouse hypothalamus. Nature, 470,
Krienen, F. M., Yeo, B. T., & Buckner, R. L. (2014). 221–226.
Reconfigurable task-dependent functional coupling modes Lindquist, K. A. (2013). Emotions emerge from more
cluster around a core functional architecture. Philosophical basic psychological ingredients: A modern psychological
Transactions of the Royal Society B, 369, 20130526. constructionist model. Emotion Review, 5, 356–368.

Lindquist, K. A., & Barrett, L. F. (2008). Constructing emotion: distinct cognitive and affective components of self. Journal of
The experience of fear as a conceptual act. Psychological Cognitive Neuroscience, 18, 1586–1594.
Science, 19, 898–903. Motta, S. C., Goto, M., Gouveia, F. V., Baldo, M. V., Canteras,
Lindquist, K. A., & Barrett, L. F. (2012). A functional architecture N. S., & Swanson, L. W. (2009). Dissecting the brain’s fear
of the human brain: Insights from emotion. Trends in system reveals the hypothalamus is critical for responding in
Cognitive Sciences, 16, 533–540. subordinate conspecific intruders. Proceedings of the National
Lindquist, K. A., Gendron, M., Oosterwijk, S., & Barrett, L. F. Academy of Sciences, 106, 4870–4875.
(2013). Do people essentialize emotion? Individual differences Mueller, S., Wang, D., Fox, M. D., Yeo, B. T., Sepulcre, J.,
in emotional essentialism and consequences for emotional Sabuncu, M. R., . . . Liu, H. (2013). Individual variability in
complexity. Emotion, 13, 629–644. functional connectivity architecture of the human brain.
Lindquist, K. A., Pendl, S., Brooks, J. A., Wilkins, R. W., Kraft, Neuron, 77, 586–595.
R., & Gao, W. (2018). Dynamic functional connectivity of Myin-Germeys, I., Oorschot, M., Collip, D., Lataster, J.,
intrinsic networks during emotions. Manuscript submitted Delespaul, P., & van Os, J. (2009). Experience sampling
for publication. research in psychopathology: Opening the black box of daily
Lindquist, K. A., Satpute, A. B., Wager, T. D., Weber, J., & life. Psychological Medicine, 39, 1533–1547.
Barrett, L. F. (2016). The brain basis of positive and negative Nee, D. E., Wager, T. D., & Jonides, J. (2007). Interference
affect: Evidence from a meta-analysis of the human resolution: Insights from a meta-analysis of neuroimaging
neuroimaging literature. Cerebral Cortex, 5, 1910–1922. tasks. Cognitive, Affective, and Behavioral Neuroscience, 7, 1–17.
Lindquist, K. A., Siegel, E. H., Quigley, K. S., & Barrett, L. F. Northoff, G., & Bermpohl, F. (2004). Cortical midline structures
(2013). The hundred year emotion war: Are emotions natural and the self. Trends in Cognitive Sciences, 8, 102–107.
kinds or psychological constructions? Comment on Lench, Ochsner, K. N., & Gross, J. J. (2008). Cognitive emotion
Flores and Bench (2011). Psychological Bulletin, 139, 255–263. regulation: Insights from social cognitive and affective
Lindquist, K. A., Wager, T. D., Kober, H., Bliss-Moreau, E., & neuroscience. Current Directions in Psychological Science, 17,
Barrett, L. F. (2012). The brain basis of emotion: A meta- 153–158.
analytic review. Behavioral and Brain Sciences, 35, 121–143. Oosterwijk, S., Lindquist, K. A., Anderson, E., Dautoff, R.,
Logothetis, N. K. (2008). What we can do and what we cannot Moriguchi, Y., & Barrett, L. F. (2012). States of mind:
do with fMRI. Nature, 453, 869–878. Emotions, body feelings, and thoughts share distributed
Lou, H. C., Luber, B., Crupain, M., Keenan, J. P., Nowak, M., neural networks. NeuroImage, 62, 2110–2128.
Kjaer, T. W., . . . Lisanby, S. H. (2004). Parietal cortex and Oosterwijk, S., Rotteveel, M., Fischer, A. H., & Hess, U. (2009).
representation of the mental self. Proceedings of the National Embodied emotion concepts: How generating words about
Academy of Sciences, 101, 6827–6832. pride and disappointment influences posture. European
Lupyan, G., & Clark, A. (2015). Words and the world: Predictive Journal of Social Psychology, 39, 457–466.
coding and the language-perception-cognition interface. Ortony, A., Clore, G. L., & Collins, A. (1988). The cognitive
Current Directions in Psychological Science, 24, 279–284. structure of emotions. Cambridge, UK: Cambridge University
MacCormack, J. K., & Lindquist, K. A. (2017). Bodily Press.
contributions to emotion: Schachter’s legacy for a Palaniyappan, L., & Liddle, P. F. (2012). Does the salience
psychological constructionist view on emotion. Emotion network play a cardinal role in psychosis? An emerging
Review, 9, 36–45. hypothesis of insular dysfunction. Journal of Psychiatry and
Mack, A., & Rock, I. (1998). Inattentional blindness. Cambridge, Neuroscience, 37, 17–27.
MA: MIT Press. Panksepp, J. (1982). Toward a general psychobiological theory of
MacLean, P. D. (1949). Psychosomatic disease and the “visceral emotions. Behavioral and Brain Sciences, 5, 407–422.
brain”: Recent developments bearing on the Papez theory of Panksepp, J. (1998). Affective neuroscience: The foundations
emotion. Psychosomatic Medicine, 11, 338–353. of human and animal emotions. New York, NY: Oxford
Manoliu, A., Meng, C., Brandl, F., Doll, A., Tahmasian, M., University Press.
Scherr, M., . . . Riedl, V. (2014). Insular dysfunction within Panksepp, J. (2016). The psycho-neurology of cross-species
the salience network is associated with severity of symptoms affective/social neuroscience: Understanding animal affective
and aberrant inter-network connectivity in major depressive states as a guide to development of novel psychiatric treatments.
disorder. Frontiers in Human Neuroscience, 7, 930. Current Topics in Behavioral Neuroscience, 30, 109–125.
Martin, R. C., & Dahlen, E. R. (2005). Cognitive emotion Panksepp, J., & Watt, D. (2011). What is basic about basic
regulation in the prediction of depression, anxiety, stress, and emotions? Lasting lessons from affective neuroscience.
anger. Personality and Individual Differences, 39, 1249–1260. Emotion Review, 3, 387–396.
Menon, V. (2011). Large-scale brain networks and psychopathology: Paré, D., & Quirk, G. J. (2017). When scientific paradigms lead
A unifying triple network model. Trends in Cognitive Sciences, to tunnel vision: Lessons from the study of fear. NPJ Science
15, 483–506. of Learning, 2, 6–13.
Menon, V., & Uddin, L. Q. (2010). Saliency, switching, attention Paulus, M. P., & Stein, M. B. (2006). An insular view of anxiety.
and control: A network model of insula function. Brain Biological Psychiatry, 60, 383–387.
Structure and Function, 214, 655–667. Pendl, S., Salzwedel, A., Goldman, B., Barrett, L. F., Lin, W.,
Milad, M. R., Pitman, R. K., Ellis, C. B., Gold, A. L., Shin, Gilmore, J., & Gao W. (2017). Emergence of a hierarchical
L. M., Lasko, N. B., . . . Rauch, S. L. (2009). Neurobiological brain during infancy reflected by stepwise functional
basis of failure to recall extinction memory in posttraumatic connectivity. Human Brain Mapping, 38, 2666–2682.
stress disorder. Biological Psychiatry, 66, 1075–1082. Pernice, V., Staude, B., Cardanobile, S., & Rotter, S. (2011). How
Moran, J. M., Macrae, C. N., Heatherton, T. F., Wyland, C. L., structure determines correlations in neuronal networks.
& Kelley, W. M. (2006). Neuroanatomical evidence for PLoS Computational Biology, 7, e1002059.

Pessoa, L. (2008). On the relationship between emotion and of discrete functional subregions of the human periaqueductal
cognition. Nature Reviews Neuroscience, 9, 148–158. gray. Proceedings of the National Academy of Sciences, 110,
Phan, K. L., Fitzgerald, D. A., Nathan, P. J., & Tancer, M. E. 17101–17106.
(2006). Association between amygdala hyperactivity to harsh Schachter, S., & Singer, J. (1962). Cognitive, social, and
faces and severity of social anxiety in generalized social physiological determinants of emotional state. Psychological
phobia. Biological Psychiatry, 59, 424–429. Review, 69, 379.
Phelps, E. A., & LeDoux, J. E. (2005). Contributions of the Schacter, D. L., Addis, D. R., & Buckner, R. L. (2007).
amygdala to emotion processing: From animal models to Remembering the past to imagine the future: The prospective
human behavior. Neuron, 48, 175–187. brain. Nature Reviews Neuroscience, 8, 657–661.
Poyo Solanas, M., Zhan, M., Vaessen, M., Hortensius, R., Schacter, D. L., Norman, K. A., & Koutstaal, W. (1998). The
Engelen, T., & de Gelder, B. (2017). Looking at the face and cognitive neuroscience of constructive memory. Annual
seeing the whole body. Neural basis of combined face and Review of Psychology, 49, 289–318.
body expressions. Social Cognitive and Affective Neuroscience, Seeley, W. W., Menon, V., Schatzberg, A. F., Keller, J., Glover,
13, 135–144. G. H., Kenna, H., . . . Greicius, M. D. (2007). Dissociable
Price, C. J., & Friston, K. J. (2002). Degeneracy and cognitive intrinsic connectivity networks for salience processing and
anatomy. Trends in Cognitive Sciences, 6, 416–421. executive control. Journal of Neuroscience, 27, 2349–2356.
Price, R. B., Gates, K., Kraynak, T. E., Thase, M. E., & Siegle, Sehlmeyer, C., Schöning, S., Zwitserlood, P., Pfleiderer, B.,
G. J. (2017). Data-driven subgroups in depression derived Kircher, T., Arolt, V., & Konrad, C. (2009). Human fear
from directed functional connectivity paths at rest. conditioning and extinction in neuroimaging: A systematic
Neuropsychopharmacology, 42, 2623–2632. review. PloS One, 4, e5865.
Price, R. B., Lane, S., Gates, K., Kraynak, T. E., Horner, M. S., Shackman, A. J., Salomons, T. V., Slagter, H. A., Fox, A. S.,
Thase, M. E., & Siegle, G. J. (2017). Parsing heterogeneity in Winter, J. J., & Davidson, R. J. (2011). The integration of
the brain connectivity of depressed and healthy adults during negative affect, pain and cognitive control in the cingulate
positive mood. Biological Psychiatry, 81, 347–357. cortex. Nature Reviews Neuroscience, 12, 154–167.
Rauch, S. L., Whalen, P. J., Shin, L. M., McInerney, S. C., Shankman, S. A., & Gorka, S. M. (2015). Psychopathology
Macklin, M. L., Lasko, N. B., . . . Pitman, R. K. (2000). research in the RDoC era: Unanswered questions and the
Exaggerated amygdala response to masked facial stimuli in importance of the psychophysiological unit of analysis.
posttraumatic stress disorder: A functional MRI study. International Journal of Psychophysiology, 98, 330–337.
Biological Psychiatry, 47, 769–776. Sharp, C., Monterosso, J., & Montague, P. R. (2012).
Raz, G., Touroutoglou, T., Wilson-Mendenhall, C., Gilam, G., Neuroeconomics: A bridge for translational research.
Lin, T., Gonen, T., . . . Barrett, L. F. (2016). Functional Biological Psychiatry, 72, 87–92.
connectivity dynamics during film viewing reveal common Shin, L. M., Rauch, S. L., & Pitman, R. K. (2006). Amygdala,
networks for different emotional experiences. Cognitive, medial prefrontal cortex, and hippocampal function in
Affective, and Behavioral Neuroscience, 16, 709–723. PTSD. Annals of the New York Academy of Sciences, 1071,
Raz, G., Winetraub, Y., Jacob, Y., Kinreich, S., Maron-Katz, A., 67–79.
Shaham, G., . . . Hendler, T. (2012). Portraying emotions at Siegel, E. H., Sands, M. K., Van den Noortgate, W., Condon, P.,
their unfolding: A multilayered approach for probing Chang, Y., Dy, J., . . . Barrett, L. F. (2018). Emotion fingerprints
dynamics of neural networks. NeuroImage, 60, 1448–1461. or emotion populations? A meta analytic investigation of
Ross, L., & Ward, A. (1996). Naive realism in everyday life: autonomic features of emotion categories. Psychological
Implications for social conflict and misunderstanding. In Bulletin, 144, 343–393.
E. S. Reed, E. Turiel, & T. Brown (Eds.), Values and Spencer, H. (1855). Principals of psychology. London, UK:
Knowledge (pp. 103–135). Hillsdale, NJ: Lawrence Erlbaum Longman, Brown, Green & Longmans.
Associates. Spencer, H. (1894). Principals of psychology. New York, NY:
Russell, J. A. (2003). Core affect and the psychological D. Appelton & Company.
construction of emotion. Psychological Review, 110, 145–172. Spreng, R. N., Mar, R. A., & Kim, A. S. (2009). The common
Russell, J. A. (2005). Emotion in human consciousness is built neural basis of autobiographical memory, prospection,
on core affect. Journal of Consciousness Studies, 12, 26–42. navigation theory of mind, and the default mode:
Russell, J. A. (2009). Emotion, core affect, and psychological A quantitative meta-analysis. Journal of Cognitive Neuroscience,
construction. Cognition and Emotion, 23, 1259–1283. 21, 489–510.
Saarimäki, H., Gotsopoulos, A., Jääskeläinen, I. P., Lampinen, J., Sprooten, E., Rasgon, A., Goodman, M., Carlin, A., Leibu, E.,
Vuilleumier, P., Hari, R., .
. .
Nummenmaa, L. (2015). Lee, W. H., & Frangou, S. (2017). Addressing reverse
Discrete neural signatures of basic emotions. Cerebral Cortex, inference in psychiatric neuroimaging: Meta-analyses of task-
26, 2563–2573. related brain activation in common mental disorders. Human
Satpute, A. B., Nook, E. C., Narayanan, S., Shu, J., Weber, J., & Brain Mapping, 38, 1846–1864.
Ochsner, K. N. (2016). Emotions in “black and white” or Sripada, R. K., King, A. P., Welsh, R. C., Garfinkel, S. N., Wang,
shades of gray? How we think about emotion shapes our X., Sripada, C. S., & Liberzon, I. (2012). Neural dysregulation
perception and neural representation of emotion. in posttraumatic stress disorder: Evidence for disrupted
Psychological Science, 27, 1428–1442. equilibrium between salience and default mode brain
Satpute, A. B., Shu, J., Weber, J., Roy, M., & Ochsner, K. N. networks. Psychosomatic Medicine, 74, 904–911.
(2013). The functional neural architecture of self-reports of Stein, M. B., Goldin, P. R., Sareen, J., Zorrilla, L. T. E., &
affective experience. Biological Psychiatry, 73, 631–638. Brown, G. G. (2002). Increased amygdala activation to
Satpute, A. B., Wager, T. D., Cohen-Adad, J., Bianciardi, M., angry and contemptuous faces in generalized social phobia.
Choi, J. K., Buhle, J. T., . . . Barrett, L. F. (2013). Identification Archives of General Psychiatry, 59, 1027–1034.

Stein, M. B., Simmons, A. N., Feinstein, J. S., & Paulus, M. P. pathways mediating successful emotion regulation. Neuron,
(2007). Increased amygdala and insula activation during 59, 1037–1050.
emotion processing in anxiety-prone subjects. American Wager, T. D., Jonides, J., & Reading, S. (2004). Neuroimaging
Journal of Psychiatry, 164, 318–327. studies of shifting attention: A meta-analysis. NeuroImage, 4,
Striedter, G. F. (2005). Principles of brain evolution. Sunderland, 1679–1693.
MA: Sinauer Associates. Wager, T. D., Kang, J., Johnson, T. D., Nichols, T. E., Satpute,
Sully, J. (1892). The human mind (Vol. 2). London, UK: Longmans, A. B., & Barrett, L. F. (2015). A Bayesian model of category-
Green, & Company. specific emotional brain responses. PLoS Computational
Svoboda, E., McKinnon, M. C., & Levine, B. (2006). Biology, 11, e1004066.
The functional neuroanatomy of autobiographical memory: Watson, D., & Tellegen, A. (1985). Toward a consensual structure
A meta-analysis. Neuropsychologia, 44, 2189–2208. of mood. Psychological Bulletin, 98, 219.
Thompson-Schill, S. L., D’Esposito, M., Aguirre, G. K., & Waugh, C. E., Hamilton, J. P., & Gotlib, I. H. (2010). The
Farah, M. J. (1997). Role of left inferior prefrontal cortex in neural temporal dynamics of the intensity of emotional
retrieval of semantic knowledge: A reevaluation. Proceedings experience. NeuroImage, 49, 1699–1707.
of the National Academy of Sciences, 94, 14792–14797. Weinberg, A., Olvet, D. M., & Hajcak, G. (2010). Increased
Touroutoglou, A., Bliss-Moreau, E., Zhang, J., Mantini, D., error-related brain activity in generalized anxiety disorder.
Vanduffel, W., Dickerson, B., & Barrett, L. F. (2016). A Biological Psychology, 85, 472–480.
ventral salience network in the Macaque brain. NeuroImage, Wilson-Mendenhall, C. D., Barrett, L. F., & Barsalou, L. W.
132, 190–197. (2013a). Neural evidence that human emotions share core
Touroutoglou, A., Hollenbeck, M., Dickerson, B. C., & Barrett, affective properties. Psychological Science, 24, 947–956.
L. F. (2012). Dissociable large-scale networks anchored in the Wilson-Mendenhall, C. D., Barrett, L. F., & Barsalou, L. W.
right anterior insula subserve affective experience and (2013b). Situating emotional experience. Frontiers in Human
attention. NeuroImage, 60, 1947–1958. Neuroscience, 7, 1–16.
Touroutoglou, A., Lindquist, K. A., Dickerson, B. C., & Barrett, Wilson-Mendenhall, C. D., Barrett, L. F., & Barsalou, L. W.
L. F. (2015). Intrinsic connectivity in the human brain does (2014). Variety in emotional life: Within-category typicality
not reveal networks for “basic” emotions. Social Cognitive of emotional experiences is associated with neural activity in
and Affective Neuroscience, 10, 1257–1265. large-scale brain networks. Social Cognitive and Affective
Tovote, P., Fadok, J. P., & Lüthi, A. (2015). Neuronal circuits for Neuroscience, 10, 62–71.
fear and anxiety. Nature Reviews Neuroscience, 16, 317–331. Wilson-Mendenhall, C. D., Barrett, L. F., Simmons, W. K., &
Tracy, J. L., & Randles, D. (2011). Four models of basic emotions: Barsalou, L. W. (2011). Grounding emotion in situated
A review of Ekman and Cordaro, Izard, Levenson, and conceptualization. Neuropsychologia, 49, 1105–1127.
Panksepp and Watt. Emotion Review, 3, 397–405. Wundt, W. (1998). Outlines of psychology (C. H. Judd, Trans.).
van Den Heuvel, M. P., Mandl, R. C., Kahn, R. S., Pol, H., & Bristol, UK: Thoemmes Press. (Original work published 1897.)
Hilleke, E. (2009). Functionally linked resting-state networks Xiao, Z., Wang, J., Zhang, M., Li, H., Tang, Y., Wang, Y., . . . &
reflect the underlying structural connectivity architecture of Fromson, J. A. (2011). Error-related negativity abnormalities
the human brain. Human Brain Mapping, 30, 3127–3141. in generalized anxiety disorder and obsessive–compulsive
Vazdarjanova, A., & McGaugh, J. L. (1998). Basolateral amygdala disorder. Progress in Neuro-Psychopharmacology and Biological
is not critical for cognitive memory of contextual fear Psychiatry, 35, 265–272.
conditioning. Proceedings of the National Academy of Sciences, Yeo, B. T., Krienen, F. M., Chee, M. W., & Buckner, R. L.
95, 15003–15007. (2014). Estimates of segregation and overlap of functional
Vincent, J. L., Kahn, I., Snyder, A. Z., Raichle, M. E., & connectivity networks in the human cerebral cortex.
Buckner, R. L. (2008). Evidence for a frontoparietal control NeuroImage, 88, 212–227.
system revealed by intrinsic functional connectivity. Journal Yeo, B. T., Krienen, F. M., Sepulcre, J., Sabuncu, M. R., Lashkari,
of Neurophysiology, 100, 3328–3342. D., Hollinshead, M., . . . Fischl, B. (2011). The organization
Vytal, K., & Hamann, S. (2010). Neuroimaging support of the human cerebral cortex estimated by intrinsic functional
for discrete neural correlates of basic emotions: A voxel- connectivity. Journal of Neurophysiology, 106, 1125–1165.
based meta-analysis. Journal of Cognitive Neuroscience, 22, Yeung, N., Botvinick, M. M., & Cohen, J. D. (2004). The
2864–2885. neural basis of error detection: Conflict monitoring and the
Wager, T. D., Barrett, L. F., Bliss-Moreau, E., Lindquist, K., error-related negativity. Psychological Review, 111, 931–959.
Duncan, S., Kober, H., . . . Mize, J. (2008). The neuroimaging Zhao, X. H., Wang, P. J., Li, C. B., Hu, Z. H., Xi, Q., Wu, W. Y.,
of emotion. In M. Lewis, J. M. Haviland-Jones, & L. F. & Tang, X. W. (2007). Altered default mode network activity
Barrett (Eds.), Handbook of emotion (3rd ed., pp. 249–271). in patient with anxiety disorders: An fMRI study. European
New York, NY: Guilford Press. Journal of Radiology, 63, 373–378.
Wager, T. D., Davidson, M. L., Hughes, B. L., Lindquist, Zilles, K., & Amunts, K. (2013). Individual variability is not
M. A., & Ochsner, K. N. (2008). Prefrontal-subcortical noise. Trends in Cognitive Sciences, 17, 153–155.

CH A PT E R
Behavioral and Molecular Genetics
15 of Emotion Dysregulation
Lance M. Rappaport, Sage E. Hawn, Cassie Overstreet, and Ananda B. Amstadter
Abstract
Given the critical role that emotion dysregulation plays in many psychiatric disorders, there is a need
to understand the biological underpinnings of emotion regulation deficits. This chapter opens with a
brief overview of emotion regulation and constructs that fall under its broad umbrella. Next, it provides
a brief primer of behavioral genetic research methods, summarizes existing literature regarding the
heritability of emotional dysregulation, provides an overview of molecular genetic research methods,
and reviews extant molecular genetic literature on emotion regulation. Finally, the chapter reviews the
limitations of existing research and identifies promising areas of future inquiry that may clarify the
underlying structure of emotion dysregulation and identify the role of common genetic loci in associations
between emotion dysregulation and psychopathology.
Keywords: genetics, gene, emotion regulation, twin, heritability
Affective experiences characterize much of human Wirtz, Svaldi, & Hofmann, 2014; Bylsma, Morris,
life and influence behavior. Memorable events are & Rottenberg, 2008; Mennin, Heimberg, Turk, &
characterized by particularly significant shifts in Fresco, 2002; Tull & Roemer, 2007) and external-
affect (e.g., a wedding, death of a loved one). izing conditions (see Mullin & Hinshaw, 2007;
Moreover, the effects of emotionally charged events Shader et al., 2017). Moreover, emotion regulatory
are felt and expressed after the events (e.g., the hon- deficits clarify points of convergence and distinction
eymoon, loss of a loved one). Notably, altered affective between highly comorbid conditions (e.g., Mennin,
experiences characterize most psychiatric conditions Holaway, Fresco, Moore, & Heimberg, 2007;
(American Psychiatric Association, 2013) and confer Mennin, McLaughlin, & Flanagan, 2009; Rappaport,
risk for clinically relevant behaviors. For example, Moskowitz, & D’Antono, 2014, 2017). Such findings
influential conceptualizations of substance use highlight the importance of understanding influences
(Khantzian, 1985; Wills, Pokhrel, Morehouse, & on emotion regulation, both genetic and environ-
Fenster, 2011), alcohol use (Bolton, Robinson, & mental in nature.
Sareen, 2009), nonsuicidal self-injury (e.g., Klonsky Given the centrality of emotion to psychiatric
& Muehlenkamp, 2007), suicide (Johnston et al., disorders, theories regarding the nature of affective
2017), aggression (Davidson, Putnam, & Larson, experiences and resulting efforts at modulating
2000), and disordered eating behavior (Harrison, them have been a central focus of psychology since
Sullivan, Tchanturia, & Treasure, 2010) emphasize its
inception. As summarized in Gross (1998),
the role of coping with negative affect or augmenting early psychoanalytic theory discussed conscious
positive affect, broadly termed emotion regulation. and unconscious attempts to regulate anxiety or
In fact, emotion regulatory deficits have been asso- general distress conferred by interactions among
ciated with numerous internalizing (e.g., Aldao, the id, ego, and superego (Freud, 1926). As the field
Nolen-Hoeksema, & Schweizer, 2010; Berking, has evolved, so have theories of emotion regulation.
203
In the contemporary adult literature, emotion underpinnings of emotion regulation is important
regulation is often viewed through cognitive and (Beauchaine, 2015b). Although the literature on
behavioral formulations wherein research examines emotion regulation is vast, much remains to be
individual differences in coping behaviors and learned about genetic influences. In this chapter, we
their efficacy (Lazarus, 2000) or cognitive-behavioral use broad definitions of emotion regulation and
approaches to more efficiently downregulate nega- dysregulation, referring to the host of processes—
tive affect (e.g., Linehan, 1993). Child and adolescent conscious, voluntary, or not—through which indi-
researchers often view emotion regulation more viduals influence what emotions they experience,
broadly, defining it as the set processes through when their emotions occur, and how they are ex-
which individuals alter their emotional experience pressed (see, e.g., Cole et al., 2004; Gross, 1998;
and/or expression to achieve goal-directed behaviors Thompson, 1990). Given scant research on the
(e.g., Beauchaine, 2015a; Thompson, 1990). This genetics of emotion regulation, we adopt a broad
definition acknowledges both effortful and auto- interpretation of this definition to select studies for
mated emotion regulation processes (see Cole, review and to provide readers with as complete a
Martin, & Dennis, 2004). basis as possible for understanding this literature.
Gross and colleagues provide an influential Our aims are to (1) provide readers with an overview
framework based on processes of emotional experi- of behavioral and molecular genetic research
ences from an evocative event through attempts to methods, (2) review existing research on genetic
modulate one’s emotional responses (Gross, 1998; and environmental contributions to emotion dys-
Gross & Muñoz, 1995; Gross & Thompson, 2007). regulation, and (3) discuss limitations of the exist-
Their so-called process model of emotion regulation ing literature and propose a framework to guide
describes a sequence of events with potential points future research.
where an individual might intervene to alter his or
her experience (see Figure 4 in Gross, 1998, p. 282). Twin and Family Studies of
For example, one might select or modify a situation Emotion Regulation
to avoid events that evoke negative affect (e.g., in- Overview of Twin and Family Studies
terpersonal conflict) or foster events that evoke Twin and family designs allow researchers to disen-
positive affect (e.g., social interaction with friends). tangle the roles of unique and shared environmental
Additionally, following a positive or negative influences from genetic (i.e., heritable) influences
event, one might attempt to modulate his or her on individual differences (measurable traits), which
physiological-affective response, such as through are referred to as phenotypes. For example, in a sample
shifting attention (e.g., Hakamata et al., 2010) or by of monozygotic twins, dizygotic twins, and/or other
altering his or her cognitive appraisal of the event siblings, between-person variance in emotion regu-
(e.g., Beck, Rush, Shaw, & Emery, 1979). Alternatively, lation can be decomposed into that shared within
one might engage in behavioral strategies to modu- families, which is represented by the correlation
late resulting emotions (e.g., Carver, Scheier, & between twins/siblings/relatives, and residual vari-
Weintraub, 1989). This framework also identifies ance. This phenomenon is, more broadly, referred
possible deficits in successful regulation of emo- to as nonindependence in many other areas of
tional experience. For example, increased reactivity research (see Kenny, Kashy, & Cook, 2006 for

to stress might result from heightened physiological review). To the extent that the trait is heritable, the
sensitivity, impaired attention deployment, or im- correlation between monozygotic twins, who share
paired cognitive reappraisal. Furthermore, difficulties 100% of segregating genes, ought to be larger than
downregulating negative affect may result from im- the correlation between dizygotic twins or siblings,
pairment in initiating emotion regulatory behaviors who share, on average, 50% of segregating genes
or from choosing ineffective regulatory behaviors (Mather, 1949; Mather & Jinks, 1971). Similarly,
(e.g., Berking & Wupperman, 2012; Houben, Van monozygotic twins, dizygotic twins, and siblings
Den Noortgate, & Kuppens, 2015; Kuppens, Allen, share environmental experiences that influence the
& Sheeber, 2010). family (e.g., socioeconomic status, parenting; Jinks
& Fulker, 1970). Therefore, by comparing the corre-
Chapter Aims lation between mono- and dizygotic twins to each
Given the central role that emotion and processes other and to zero, the biometrical model, which is also
involved in emotion regulation play in numerous known as the twin model, can distinguish the pro-
forms of psychopathology, understanding etiologic portion of variance in a phenotype due to heritable
204 Genetics of Emotion Dysregul ation

factors and shared environmental factors (e.g., factors, which may indicate the potential for inter-
Fulker, 1981). Remaining, or residual, variance, which vention (McRae et al., 2017).
is specific to each individual, is attributed to unique Other twin studies have incorporated behavioral
environmental factors (e.g., stressful life events, peer measures of emotion dysregulation. In one such
relations) and measurement error. This model has study, the heritability coefficient was .43 for indi-
been extended to include other familial relationships vidual differences in observational ratings of toddlers’
(Eaves, 1976), including adopted children who behavior (Wang & Saudino, 2013). Kanakam and
share different environmental experiences (Heath, colleagues reported greater within-pair similarity
Kendler, Eaves, & Markell, 1985), and more recently among monozygotic twins than dizygotic twins for
to incorporate known genetic similarity based emotion recognition and social attention processing
on genetic relatedness between nonfamilial pairs tasks, but not for self-reported emotion dysregula-
(Kirkpatrick & Neale, 2015). tion (Kanakam, Krug, Raoult, Collier, & Treasure,
2013). Thus, consistent with reviews cited previously,
Review of Twin and Family Studies there may be a stronger influence of environmental
of Emotion Regulation factors on emotion regulation relative to other
The twin literature regarding emotion regulation is emotional processes.
broad and heterogeneous; however, there is evidence More recently, Weinberg and colleagues demon-
that emotion regulation is moderately heritable, strated moderate heritability (.45 to .55) for brain
with genetic factors accounting for approximately activation patterns during periods when emotion
40% of individual differences in emotion regulation regulation may occur (i.e., while viewing pleasant,
constructs (for reviews see Canli, Ferri, & Duman, neutral, and unpleasant pictures from the
2009; Goldsmith, Pollak, & Davidson, 2008; International Affective Picture System; Weinberg,
Hawn, Overstreet, Stewart, & Amstadter, 2015). Venables, Proudfit, & Patrick, 2015). In summary,
However, heritability coefficients fall within the despite inconsistencies in operationalization and
wide range of .25 to .55 due to a significant degree assessment, the twin literature suggests moderate
of definitional and methodological variability across heritabilities across multiple methods and concep-
the literature. tualizations of emotion regulation.
To date, numerous twin studies of emotion
regulation have focused on associated traits such as General Limitations of Twin and Family
personality. For example, emotion dysregulation is Studies
often conceptualized as a component of neuroti- Although the biometrical model permits disaggre-
cism, which is heritable (e.g., Jang, Livesley, & gating of phenotypic variance due to heritable and
Vemon, 1996) and influenced by genetic factors environmental contributions, findings of moderate
that also influence associated internalizing psycho- heritability must be considered in light of several
pathology (Hettema, Neale, Myers, Prescott, & limitations. For example, heritable contributions to
Kendler, 2006). Additionally, several twin studies any phenotype are estimated as the proportion of
examine heritability of emotion regulation based genetic variance to overall phenotypic variance
on self-report measures. For example, Coccaro and (Visscher, Hill, & Wray, 2008). In practical research
colleagues used self-report measures (Affect Lability applications, overall phenotypic variance is esti-
Scale, Affect Intensity Measure) to estimate herita- mated from a sample. When other unaccounted for
bility at .40 for affective liability and intensity of individual differences (e.g., age, sex) influence the
emotional experiences (Coccaro, Ong, Seroczynski, phenotype, overall phenotypic variance is inflated,
& Bergeman, 2012). Others have found that heri- which biases heritability estimates downward. In
tabilities of mean level and intraindividual variation addition, heritable and phenotypic variance may
in negative affect are lower among older partici- occur across samples, which can bias heritability
pants (i.e., ages 25 to 74), which the authors estimates in either direction. For example, peer

suggest may be due to acquisition of emotion regu- victimization may decrease with age (Ladd, Ettekal,
lation skills over time (Neiss & Almeida, 2004). & Kochenderfer-Ladd, 2017), thereby reducing
Finally, evidence suggests that different aspects of phenotypic variance in older samples. Such reduc-
emotional processing (i.e., cognitive reappraisal,
tions in phenotypic variance may increase heritabil-
neuroticism) and emotion regulatory strategies
ity estimates since genetic variance becomes a larger
(i.e., expressive suppression) may be differentially proportion of total variance. In other instances, en-
heritable and influenced heavily by environmental vironmental factors may impede development of a
Rappaport, Hawn, Overstreet, and Amstadter 205

heritable trait. For example, as children age, increased dysregulation—both is heritable and accounts for
access to alcohol yields increasing heritability coeffi- common variance among internalizing and exter-
cients for alcohol use (e.g., Edwards & Kendler, 2013). nalizing disorders (see, e.g., Tackett et al., 2013).
At younger ages, children are not exposed to alcohol,
so heritability cannot be accurately assessed. Finally, Future Directions of Twin and Family
heritability coefficients provide no information about Studies of Emotion Regulation
specific genes that influence a given trait (see, e.g., There are a number of important areas for the devel-
Beauchaine, Gatzke-Kopp, & Gizer, 2017). Thus, opment of future biometric studies of emotion reg-
molecular genetic studies are needed to identify ulation. For example, the biometrical model, which
specific genetic variants (i.e., alleles). has been used to study multiple phenotypes (see
Table 15.1), could be applied to emotion regulation
Limitations of Twin and Family Studies to address questions regarding genetic contributions
of Emotion Regulation to specific correlations between emotion regulatory
Across diverse research methods, heritability coeffi- deficits and related traits. It could also be used to
cients for emotion regulation and associated traits understand the underlying latent structure of
are modest. However, relatively small sample sizes multiple emotion regulatory deficits. Using this ap-
mean that confidence intervals vary widely. In some proach, correlations among multiple phenotypes
cases, meta-analysis can be used to refine the preci- are decomposed to identify contributions of herit-
sion of heritability estimates (e.g., Hunter, Schmidt, able and environmental influences on each pheno-
& Jackson, 1982), yet diversity in methods used to type, and the correlation between them (e.g., Burt,
measure emotion regulation (e.g., self-report, be- Krueger, McGue, & Iacono, 2001; Fulker, 1977).
havioral studies, functional magnetic resonance im- This modeling framework has been used in the psy-
aging paradigms) precludes any comprehensive chopathology literature by Kendler and colleagues,
meta-analysis. Moreover, with few exceptions, exist- who identified four underlying factors that describe
ing research has not evaluated the influence of sex, the contribution of genetic risk to psychopathology
age, or ethnicity on genetic contributions to emotion (Kendler et al., 2011). Specifically, one extension of
regulation (e.g., Rice, Harold, & Thapar, 2002). As the biometric model, the common pathway model,
discussed in detail later and articulated elsewhere evaluates whether correlated genetic and environ-
(e.g., Beauchaine, 2015a; Cole et al., 2004), multi- mental influences on a set of phenotypes are due to
method research is needed to disentangle the under- one or more latent phenotypic factors (e.g., Karkowski,
lying structure of multiple components of emotion Prescott, & Kendler, 2000).
dysregulation. Furthermore, longitudinal research As applied to the study of emotion regulation,
is needed to clarify the developmental course of biometric twin and family research might clarify the
emotion regulation; prior research has examined latent structure of emotion regulation to determine
emotion regulation. Notably, limited developmental whether it is composed of a single or multiple un-
research conducted to date suggests that physiologi- derlying factors with different genetic architecture.
cal markers of emotion dysregulation emerge over Once the underlying latent structure of emotion
time during childhood and adolescence among regulation is clarified, future molecular genetic
both internalizing and externalizing samples (e.g., studies, discussed later, could be conducted to fur-
Beauchaine, Gatzke-Kopp, & Mead, 2007; Koenig, ther our understanding of etiology. Finally, twin
Kemp, Beauchaine, Thayer, & Kaess, 2016). Finally, and family studies could clarify the contribution of
although research has examined different compo- common heritable and environmental influences on
nents of emotion dysregulation, future research is associations of specific emotion regulatory deficits
needed to estimate the heritable contributions to with specific psychiatric conditions. Specific emo-
emotion dysregulation in psychopathology. For ex- tion regulatory deficits may manifest in multiple,
ample, given evidence that internalizing (Hettema comorbid disorders (e.g., Mennin et al., 2007).
et al., 2006; Sullivan, Neale, & Kendler, 2000) and Clarifying the structure and heritability of emotion
externalizing disorders are moderately heritable regulatory deficits may therefore elucidate a common
(Kendler et al., 2011), future research might clarify pathway to multiple disorders, which could help
the degree of genetic overlap between emotion dys- explain both genetic pleiotropy (common genetic
regulation and internalizing disorders. As noted correlates among multiple disorders) and high
previously, research conducted to date suggests that rates of psychiatric comorbidity (Beauchaine &
neuroticism—a construct with clear links to emotion Constantino, 2017; Miller & Rockstroh, 2013).

Table 15.1 Example Genetic Research Methodologies
Research Methodology Distinguishing Features Example Empirical Question(s)
Biometrical Twin and Genetic and environmental contributions to What is the contribution of genetic
Family Models (Single one phenotype are estimated based on known influences (i.e., heritability) to a specific
Phenotype) genetic relatedness (based on gene segregation emotion regulatory deficit (e.g.,
and recombination) and environmental heightened affective intensity)?
relatedness (based on rearing history). What is the contribution, to a specific
emotion regulatory deficit, of
environmental factors within a family?
Biometrical Twin and Known genetic relatedness and/or What is the contribution of common
Family Models environmental relatedness are used to estimate genetic loci to the association of a specific
(Multiple Phenotypes) the magnitude and structure of genetic and emotion regulatory deficit with
environmental contributions to multiple psychopathology?
phenotypes. What is the underlying latent structure of
multiple emotion regulatory deficits based
on common genetic and environmental
influences?
Candidate Gene Genetic information is limited to specific Does this specific genetic allele contribute
Methodology target alleles identified a priori. to a specific emotion regulatory deficit?
Genome-Wide Many alleles across the genome are examined Which genetic alleles contribute to a
Association Study without a priori hypotheses. specific emotion regulatory deficit?
(GWAS)
Polygenic Risk Score Overall genetic liability to a phenotype is What is the aggregate contribution of all
(PRS) estimated by aggregating effects of multiple genetic loci to a specific emotion
genetic loci. regulatory deficit?
What is the overlap in genetic loci
between multiple phenotypes (e.g.,
between a specific emotion regulatory
deficit and psychiatric disorder)?
Linkage Disequilibrium Estimate heritability from the aggregate What is the heritability of a specific
(LD) Score Regression influence of multiple polymorphisms while emotion regulatory deficit?
accounting for LD between multiple
polymorphisms. Estimation is based on
summary statistics rather than raw data.
Univariate Genetic relatedness of participants is What is the contribution of genetic
Genome-Wide estimated based on allelic data across the influences (i.e., heritability) to a specific
Complex Trait genome. Genetic relatedness is used to emotion regulatory deficit (e.g.,
Analysis (GCTA) estimate heritability of a single phenotype. heightened affective intensity)?
Bivariate/Multivariate Similar to univariate GCTA, genetic What is the contribution of common
GCTA relatedness of participants is estimated based genetic loci to the association of a specific
on allelic data across the genome. However, emotion regulatory deficit with
genetic relatedness is used to estimate psychopathology?
heritability of multiple phenotypes and the What is the underlying latent structure of
contribution of common genetic loci to the multiple emotion regulatory deficits based
correlation between phenotypes. on common genetic and environmental
influences?
Molecular Genetic Studies of Emotion 2000), only molecular genetic studies can identify
Regulation specific genetic variants (alleles) that account for
Overview of Molecular Genetics heritable risk. Before reviewing the relevant litera-
Although twin and family studies can determine the ture, we provide a very brief introduction to the rel-
heritability of a phenotype (e.g., Sullivan et al., evant terminology in molecular genetic research.

Deoxyribonucleic acid (DNA) is composed of acetylation (bonding of an acetyl group), which can
four chemical bases (adenine [A], guanine [G], impede or facilitate gene transcription without
cytosine [C], and thymine [T]), which, when altering the genetic sequence. Additionally, emerging
transcribed into ribonucleic acid (RNA), code for evidence suggests that some epigenetic modifications
production of specific protein chains. Between-person to the genome are transmitted through reproduction,
variation in observed phenotypes arises, in part, thereby complicating the study of genetic inheritance.
from variation in the specific composition of DNA, However, a detailed discussion of this literature is
referred to as polymorphisms, which can alter result- outside the scope of the present chapter (for further
ing proteins. Different combinations of base pairs, discussion see Kendler, Jaffee, & Romer, 2011).
called alleles, are nested within genetic regions,
called genes, where they code for protein chains. Review of Molecular Genetic Studies of
This combination of base pairs (i.e., alleles) at a Emotion Regulation
given site is called a genotype, which describes the Compared to the literature on the heritability of
function of that site within the genetic region (i.e., emotion regulation, the literature addressing specific
gene). Many allelic variations produce no discernible genetic variation associated with emotion regulation
effect on resulting protein chains, which are there- is more plentiful, with approximately 25 studies
fore referred to as nonfunctional polymorphisms. In published to date. However, as discussed in more
contrast, other points of allelic variation affect re- detail later, this literature has focused primarily on a
sulting products, and are referred to as functional small number of candidate polymorphisms.
polymorphisms. For example, specific alleles might Among the most often studied candidate poly-
code for an early break in the protein chain, called a morphisms is the serotonin transporter-linked
stop codon, whereas other alleles might code for a polymorphism (5-HTTLPR). Following evidence
higher frequency of transcription, thereby produc- implicating the serotonin system in internalizing
ing more of the resulting protein. disorders (Owens & Nemeroff, 1994) and genetic
Most allelic variation is categorized into two forms: variants of the serotonin system in neuroticism
single nucleotide polymorphisms (SNPs [“snips”], (Lesch et al., 1994, 1996), candidate gene research has
identified by reference sequence [rs] numbers) and explored the interplay of emotion regulation and
variable number tandem repeats (VNTRs). The polymorphisms within the serotonin system includ-
former describes the change of a single base pair ing 5-HTTLPR-associated genetic risk (Canli &
(e.g., from G to A), whereas the latter describes a Lesch, 2007) and genes that affect serotonin expres-
repeated copy of a specific genetic sequence. There sion (Waider, Araragi, Gutknecht, & Lesch, 2011).
are many points of allelic variation across the human The low transcribing 5-HTT allele confers vulnera-
genome and within each gene. However, candidate bility to a number of possible emotion dysregulation
gene studies are generally limited to a small, prede- facets, including attentional biases (positive biases,
termined set of putative sites. Existing candidate Beevers et al., 2011; negative biases, Pergamin-Hight,
gene research of emotion dysregulation has exam- Bakermans-Kranenburg, van IJzendoorn, & Bar-
ined both SNPs and VNTRs, such as an SNP on Haim, 2012), distress tolerance (Amstadter et al.,
the catechol-0-methyltransferase gene (COMT) 2012), inappropriate affective display/lack of emo-
that produces a Met group instead of Val (i.e., tional self-awareness (Viddal, Berg-Nielsen, Belsky,
COMT Val158Met) and a VNTR in the promoter & Wichstrøm, 2017), physiological reactivity to
region of the serotonin transporter gene (5-HTTLPR). emotional stimuli (Plieger et al., 2017), and self-
Although research on genetic polymorphisms reported emotional responses and facial expressions
investigates variants in the sequence of DNA (i.e., during emotion induction (Gilman et al., 2015).
ordering of base pairs), DNA transcription is also However, the association between 5-HTT and
influenced by modifications that are potentially emotion regulation is not consistent throughout the
heritable but also reversible (Bell & Spector, 2011). literature and may be influenced by lack of stand-
These epigenetic effects alter DNA structure (i.e., ardization in research methods (e.g., self-report
molecular composition of base pairs), with implica- vs. behavioral vs. neuroimaging methods). For exam-
tions for emotion regulation and psychopathology ple, in a study using a behavioral task—the Face-
(e.g., Mill & Petronis, 2007; Turecki & Meaney, Word Emotion Conflict Task—no evidence of a 5-
2016). For example, considerable research has ex- HTT gene effect was found (Waring, Etkin,
amined histone modification of DNA, including Hallmayer, & O’Hara, 2014). It is important to
DNA methylation (bonding of a methyl group) and note, however, that an absence of main effects does

not mean that serotonergic vulnerability is irrelevant which show increased anxiety-like behaviors when
to understanding emotion dysregulation. Rather, se- TPH2 is knocked out (see Waider et al., 2011 for
rotonergic expression may interact with other genes review). Additionally, associations have been reported
and environmental risk exposures to eventuate in between emotion dysregulation and the 66Met allele
poor emotion regulation. For example, Crowell et al. of the brain-derived neurotrophic factor gene
(2008) found that adolescents’ serotonergic function (BDNF), which is associated with reduced amygdala
interacted with family negativity and conflict to ex- habituation to emotional stimuli during functional
plain 64% of the variance in self-injury episodes in magnetic resonance imaging (fMRI; Perez-
a self-harming sample. Self-injury is considered by Rodriguez et al., 2017). Notably, the Met allele may
most to be an extreme expression of emotion dys- interact with child maltreatment to predict an im-
regulation. Furthermore, Surguladze and colleagues paired ability to downregulate negative affect (Miu
found that an interaction between the 5-HTTLPR et al., 2017). Met carriers with a history of maltreat-
low transcribing allele and Met alleles is associated ment report the lowest levels of cognitive reappraisal,
with reduced connectivity in various brain regions whereas Met carriers with no history of maltreatment
associated with emotion dysregulation (Surguladze report the highest levels.
et al., 2012). However, they report no evidence of Additional genes have been implicated in emo-
any main effects of 5-HTTLPR polymorphisms. tion regulation. For example, low expression of
Another frequently studied polymorphism in the neuropeptide Y (NPY) may be associated with
emotion regulation literature is the Val158Met SNP increased medial prefrontal cortical reactivity to
found in the COMT gene. The COMT Val allele has negative stimuli following exposure to negative

been associated with emotion dysregulation across a valence words (Mickey et al., 2011). Similarly, the
variety of contexts, including self-reported distress neuropeptide S gene (NPS) may predict altered
tolerance (Amstadter et al., 2012), self-reported hemoglobin concentration in the prefrontal cortex
ability to efficiently regulate one’s emotions (Weiss in response to negative emotional pictures (Guhn
et al., 2014), emotion management and regulation et al., 2015). In addition, Pagliaccio and colleagues
(Lin et al., 2013), and amygdala activity in response report that greater genetic profile risk scores summed
to fearful/angry stimuli (Domschke et al., 2012). across 10 SNPs within four integral hypothalamic-
Similar to research on 5-HTTLPR, studies investi- pituitary-adrenal (HPA) axis genes (i.e., CRHR1,
gating associations between COMT and emotion NR3C2, NR3C1, and FKBP5) predict weaker con-
regulation have produced inconsistent results. For nectivity of the left amygdala with the putamen
example, Lonsdorf et al. (2011) report that the COMT and enhanced connectivity with the postcentral
Met allele was associated with increased left amygdala gyrus (Pagliaccio et al., 2015). Moreover, the inter-
reactivity to angry stimuli, in contrast with previ- action of genetic risk scores and early life stress was
ously discussed evidence supporting a positive asso- associated with weakened connectivity of the amyg-
ciation between emotion regulation and the Val dala with the parahippocampal gyrus, caudate, and
allele. Similarly, Swart et al. (2011) described a posi- inferior and middle frontal gyri. Children with the
tive relation between Met homozygosity and diffi- highest genetic risk scores who experienced early
culty verbalizing feelings, as well as an association life stress showed the weakest connectivity. In an-
between the Met allele and attenuated brain activa- other study, the FKBP5 polymorphism rs1360780
tion in the posterior cingulate gyrus and precuneus was associated with increased left amygdala reactiv-
during evaluation of affective valence. ity and increased coupling with the left hippocam-
Despite intense focus on 5-HTTLPR and COMT, pus and orbitofrontal cortex during emotional
other genes may be associated with emotion regula- face-matching—which were in turn associated with
tory processes. However, studies on other genetic depressive symptoms (Holz et al., 2015). Finally,
variants are characterized by definitional and meth- a polymorphism on the oxytocin receptor gene
odological heterogeneity. For example, different (OXTR) may interact with culture to predict spe-
forms of the tryptophan hydroxylase-2 (TPH2) cific facets of emotion regulation, such as emotion
gene may influence the ability to process fearful/ suppression (Kim et al., 2011).
angry faces and cope with negative stimuli through
both behavioral (Waider et al., 2011) and self-report General Limitations of Molecular
measures (Szily & Kéri, 2012). Evidence of an Genetic Studies
association between the TPH2 gene and emotion Findings from candidate gene research, similar
regulation has also been demonstrated among mice, to other methods, must be considered in light of

several limitations. First, evidence of significant Limitations of Molecular Genetic Studies
effects for specific genetic loci are often inconsist- of Emotion Regulation
ent across studies, and studies vary on selection of Similar to the state of affairs in research using the
specific SNPs and coverage of common variation twin and family designs, most molecular genetic
(Karg, Burmeister, Shedden, & Sen, 2011; Munafò, studies have examined a single component of emo-
Durrant, Lewis, & Flint, 2009; Risch et al., tion dysregulation. In addition, selection of candi-
2009). Second, almost no studies of rare genetic date genes has been guided by prior evidence that
variation (e.g., copy number variants [CNVs], the chosen polymorphism (e.g., 5-HTT) associates
rare de novo mutations) have been conducted, with a related psychiatric disorder (e.g., depression),
even though they are known contributors to psy- or indications that an associated biological system is
chopathology (see, e.g., Girirajan, Campbell, & implicated in emotional processing (e.g., genetic
Eichle, 2011). Third, considerable heterogeneity polymorphisms that contribute to the HPA axis
exists in study design and sample demographics. leading to the inclusion of the FKPB5 variation for
Participants from different ancestral groups differ candidate gene studies of emotion regulation). This
in genetic composition. This phenomenon—re- limitation may impede discovery of genetic overlap
ferred to as population stratification—can be an of emotion regulation with the range of genetic
important confound when a trait of interest is as- loci identified in genome-wide association studies
sociated with third variables that differ by ethnic (GWASs; see later) of psychopathology (e.g., Lee
group (e.g., sociocultural experiences). Although et al., 2013). Finally, type I and type II error rates may
methods exist to adjust for population stratifica- be high, with substantial variation in effect sizes.
tion (e.g., Price et al., 2006; Price, Zaitlen, Reich,
& Patterson, 2010), application of such methods Future Directions of Molecular Genetic
is inconsistent (Freedman et al., 2004). At the Studies of Emotion Regulation
expense of broader generalizability, genetic research To date, genetic research on emotion regulation and
should either limit samples to participants from dysregulation has been conducted using a candidate
few (even one) ancestral groups or recruit larger gene design. Although this approach suggests a
samples in which stratification can be assessed number of loci that may be related to emotion regu-
directly (Cai et al., 2015; Flint, Chen, Shi, & lation, some of which have replicated, this approach
Kendler, 2012). suffers several notable limitations (see earlier; Dick
Additional limitations of candidate gene re- et al., 2011). Whereas candidate gene research re-
search include small sample sizes and small effect quires a priori selection of genetic targets, GWASs
sizes, which present the possibility of type II errors, are agnostic to specific loci, and rather scan the
and a lack of clarity regarding possible biological entire genome for polymorphisms that are associ-
mechanisms that explain mechanisms through ated with specific phenotypes (see Table 15.1).
which allelic variation yields complex traits (Dick, GWASs permit discovery of—along the entire
Latendresse, & Riley, 2011). Candidate gene re- genome or within specific chromosomal regions—
search also risks increasing type II error rates in genetic correlates not previously considered in can-
two ways, which may be compounded when past didate gene research (e.g., Ripke et al., 2014).
findings are used to select candidate polymor- However, the large number of alleles evaluated
phisms. First, using this approach, candidate gene yields a vastly inflated type I error rate, which must
studies are necessarily restricted in the number of be corrected by setting stringent test-wise alpha
genetic variants considered, so noncandidates are levels (Bland & Altman, 1995). Although several
not assessed. Second, although large sample sizes procedures exist to adjust experiment-wise false dis-
are needed to demonstrate statistical significance covery rates (Benjamini & Yekutieli, 2001; Storey,
for small effects (e.g., Burmeister, McInnis, & 2003), all yield increased type II error rates. To bal-
Zöllner, 2008), most candidate gene studies are ance this tradeoff between type I and type II errors,
relatively small in size. Therefore, potentially enormous samples by traditional standards are
promising genetic correlates are unexplored based needed. This dynamic led to the development of
on low statistical power. This limitation can also be psychiatric genomic consortia in which samples are
addressed through meta-analysis (Hedges & pooled for analysis (Geschwind & Flint, 2015;
Pigott, 2001) if research methods are standardized Lehner, Senthil, & Addington, 2015). Analyses
to facilitate aggregating data. of data from genomics consortia have identified

significant and potentially meaningful loci for indexes overall genetic burden for a trait. Other
several psychiatric disorders (e.g., Lee et al., 2013; traits can be regressed onto the PRS to estimate the
Ripke et al., 2014) and have demonstrated the degree of genetic overlap. For example, based on
importance of large sample sizes (Levinson et al., published GWAS results, Duncan et al. (2017)
2014). In fact, sufficient power in GWASs requires computed the PRS and used related linkage disequi-
increasingly large samples, sometimes on the order librium (LD; nonrandom allelic association across
of 125,000 participants (e.g., Ripke et al., 2014). By loci) score regression to identify cross-disorder genetic
identifying candidate emotion regulatory deficits overlap for posttraumatic stress disorder, schizo-
from biometric studies and refining measurement of phrenia, and bipolar disorder. In a GWAS of emo-
these constructs with prioritization of phenotypic tion dysregulation, PRS and LD score regression
harmonization, future molecular genetic efforts that might identify aggregate influences of multiple ge-
include aggregation across studies will be facilitated. netic variants (see Table 15.1). As noted previously,
This type of collaborative effort could produce a however, GWASs require samples larger than might
large-scale consortium that may be powered to be feasible, with more intensive methods required
identify variants associated with emotion regulation to assess emotion dysregulation. Instead, an exten-
and dysregulation. sion of PRS and related LD score regression might
GWAS research has been expanded to examine clarify associations between emotion dysregulation
interactions between putative genetic vulnerability and specific psychiatric disorders. Such research might
loci and environmental risk factors (e.g., Winkler assess a variety of promising emotion dysregulation
et al., 2015). Although statistical power is further markers and genotyped SNPs that have been assessed
limited when evaluating interactions (McClelland in GWASs of psychopathology. Then, PRS score
& Judd, 1993), recent findings in the neuroscience and LD score regression facilitates estimating each
literature indicate promise for genome-wide inter- participant’s genetic liability, onto which one could
action studies. For example, the Alzheimer’s Disease regress emotion regulatory deficits to identify the
Neuroimaging Initiative recently reported an inter- contribution, to a specific deficit, of genetic loci un-
β-amyloid deposition on cognitive impairment

action between genetic loci in the IAPP gene and derlying risk for specific psychiatric disorders. For
example, French et al. (2015) estimated a polygenic
(Roostaei et al., 2017). Critical Gene × Environment risk for schizophrenia based on prior GWAS results.
interactions may also be relevant for the study of They then demonstrated an interaction between ge-
emotion dysregulation. For example, emotion regu- netic risk and cannabis use on cortical thickness.
latory deficits are affected by exposure to specific Finally, recent developments in statistical methods
environmental risk factors, including adverse family have allowed for SNP-based heritability estimates to
environments and early life trauma exposure (e.g., be computed in samples of unrelated participants.
Crowell et al., 2017; Kim & Cicchetti, 2009). These For example, univariate genome-wide complex trait
may interact with genetic loci that confer vulnera- analysis (GCTA) leverages the genetic relatedness of
bility to emotion dysregulation (e.g., Crowell et al., many individuals to estimate the SNP-based herita-
2008). bility of traits based on their correlations with em-
With the decreasing cost of GWAS arrays, such pirical genetic relatedness in the sample (Manolio
research has become more common. Furthermore, et al., 2009; Yang et al., 2010). Univariate GCTA
novel statistical innovations provide for aggregating could clarify the overall heritability of a specific
genetic risk in sophisticated ways. This is important, emotion regulatory deficit from GWAS data (see
as the nature of psychiatric and psychological traits Table 15.1). By extension, bivariate GCTA uses ge-
is complex, with single genetic variants accounting netic relatedness among individuals to estimate the
for small proportions of heritable traits (Burmeister SNP-based heritability of each trait and the contri-
et al., 2008; Cohen, 2016). Instead, complex genetic bution of similar genetic loci to covariances among
architecture requires us to examine the aggregate traits, akin to multivariate biometric models. For
and interactive effects of multiple alleles (Iacono, example, Plomin and colleagues used bivariate
Malone, & Vrieze, 2017; Manolio et al., 2009; GCTA to demonstrate correlated genetic influences
Plomin & Simpson, 2013). In GWAS research, to different components of intelligence (Plomin
small associations of a given trait with many alleles et al., 2013; Trzaskowski, Davis, et al., 2013;
across the human genome can be aggregated to Trzaskowski, Shakeshaft, & Plomin, 2013). Similar
form an overall polygenic risk score (PRS), which research on components of emotion regulation

might clarify the structure of multiple types of c onceptualizations. For example, evidence of specific
deficits that have thus far been examined individually. emotion regulation deficits within anxiety and de-
Moreover, bivariate GCTA may inform the role of pressive disorders agrees with the tripartite model
common genetic influences on associations between (Clark & Watson, 1991; Watson et al., 1995); certain
emotion dysregulation and psychiatric disorders. deficits correlate with both anxiety and depressive
symptoms, whereas other deficits suggest points of
Recommendations and Future Directions divergence (e.g., Mennin et al., 2007). Recommended
As described previously, developments in genetic future directions that follow describe how genetic
methods may clarify the contribution of genetic research might evaluate specific emotion regulatory
variation to emotion dysregulation. Advances in deficits as potential endophenotypes and mechanisms
biometrical twin and family research may inform in the development of specific psychiatric disorders.
the structure of emotion dysregulation, including We provide a brief overview of criteria to detect psy-
its associations with specific disorders, and indicate chiatric endophenotypes and then propose that
putative deficits for further study. Similarly, devel- future research mine the rich set of known deficits
opments in molecular genetic methods will likely in emotion dysregulation to identify potential en-
elucidate the polygenic architecture of emotion dys- dophenotypes. More specifically, we propose that
regulation, including shared loci with specific forms future research (1) clarify the nature of emotion reg-
of psychopathology. Both approaches will clarify ulation deficits and refine their assessment, (2) clar-
the etiology of emotion dysregulation and its role in ify the structure of emotion dysregulation based on
the development of psychopathology. Such research the structure of genetic and environmental contri-
is consistent with the recent Research Domain butions to its etiology, and (3) conduct longitudinal
Criteria (RDoC) initiative of the National Institute studies to inform our understanding of the role of
of Mental Health, which addresses liability to psy- emotion dysregulation in the onset and course of
chopathology across levels of analysis spanning psychopathology.
genes to environments (see Insel et al., 2010). RDoC
emphasizes identification of putative psychiatric en- Evaluate a Psychiatric Endophenotype
dophenotypes (National Advisory Mental Health Traditionally, to qualify as an endophenotype, a
Council Workgroup on Tasks and Measures for biomarker or other phenotype must (1) be corre-
RDoC, 2016)—potential psychobiological compo- lated with at least one psychiatric condition, (2) be
nents of psychiatric conditions with less complex heritable, (3) be state independent (therefore mani-
etiology (see Gottesman & Gould, 2003). To the festing among affected individuals both inside and
extent that a potential endophenotype is associated outside acute illness episodes), and (4) cosegregate
with multiple conditions, it may clarify the role of with related psychiatric conditions within families
genetic and environmental influences in the comor- (Gottesman & Gould, 2003). However, this formu-
bidity between conditions. For example, high rates lation was recently expanded to recognize that puta-
of genetic pleiotropy (Kendler et al., 2011; Lee et al., tive endophenotypes may relate to more than one
2013) may occur when overlapping genes are associ- disorder (Beauchaine & Constantino, 2017; Iacono,
ated with an endophenotype that contributes to the Malone, & Vrieze, 2017). Several expanded criteria
development of multiple conditions. For example, include that multiple processes influence the mani-
Lee et al. reported a moderate genetic correlation festation of a disorder and that the candidate deficit
between bipolar disorder and major depressive (1) can be assessed at multiple levels of analysis,
disorder. If both conditions are influenced by a (2) correlates with genetically correlated conditions
common endophenotype (e.g., few skills to reduce (e.g., Hettema, Prescott, Myers, Neale, & Kendler,
negative affect; Radkovsky, McArdle, Bockting, & 2005; Kendler, Neale, Kessler, Heath, & Eaves,
Berking, 2014; Van Rheenen, Murray, & Rossell, 1992), and (3) is associated with causes rather than
2015), then genes that influence the endophenotype sequelae of the condition (Cannon & Keller, 2006).
likely confer vulnerability to both disorders. Specific to the last point, Cannon and Keller (2006)
The case has been made for emotion dysregulation clarify that circular and circuitous associations
as a transdiagnostic endophenotype (Beauchaine, might unfold over time, wherein consequences of
2015b; Beauchaine & Thayer, 2015). As described one condition increase the risk for a subsequent
earlier, specific emotion regulatory deficits clarify condition (Kessler et al., 2008). However, endophe-
convergence and divergence between many psychi- notypes should be distinct from the consequences
atric disorders in accordance with theoretical of associated disorders.

Improved Precision in Phenotype Assessment increased intraindividual variability, in multiple
Most existing research on emotion regulation has psychiatric disorders (aan het Rot, Hogenelst, &
focused on self-reports and responses to laboratory- Schoevers, 2012; Ebner-Priemer & Trull, 2009;
based tasks. Factor analysis of multiple self-report Houben et al., 2015; Kopala-Sibley, Rappaport,
emotion regulation measures, such as the Difficulties Sutton, Moskowitz, & Zuroff, 2013; Odgers et al.,
in Emotion Regulation Scale (DERS; Gratz & 2009; Russell, Moskowitz, Zuroff, Sookman, &
Roemer, 2004), largely recovers similar components Paris, 2007; Trull et al., 2008; Walz, Nauta, & aan
(e.g., poor understanding, maladaptive manage- het Rot, 2014), as a marker of acute psychiatric risk
ment) along with an overarching factor that repre- (e.g., van de Leemput et al., 2014) and as a genera-
sents general emotion dysregulation (Mennin et al., tor of interpersonal distress (Côté, Moskowitz, &
2007). Self-reports of emotion regulation deficits Zuroff, 2012; Erickson, Newman, & Pincus, 2009;
provided early evidence that specific deficits may Sadikaj et al., 2015; Tracey & Rohlfing, 2010).
distinguish among psychiatric disorders (e.g., Following from the previous paragraphs, multi-
Mennin et al., 2009; Tull & Roemer, 2007). method research is needed to leverage the strengths
Similarly, in laboratory-based research, emotion and weaknesses of various approaches (Campbell &
dysregulation is assessed based on performance on Fiske, 1959). Converging evidence across multiple
standardized cognitive measures, such as emotion methods suggests that we refine our selection
processing (e.g., the Emotional Stroop task; Kanakam of candidate emotion regulation deficits for fur-
et al., 2013), and participant responses to well- ther genetic study. For example, using ecological
documented, standardized stressors. However, momentary assessment (EMA), Kuppens and

laboratory-based assessments pose different limita- colleagues demonstrated increased emotional inertia,
tions to those inherent in retrospective self-reports. which describes stronger lagged effects of negative
Along with limited generalizability to naturalistic affect over time (Kuppens et al., 2010, 2012). This is
settings, laboratory-based tasks are limited to assessing consistent with laboratory evidence that major de-
select components of the emotion regulatory pro- pressive disorder may be associated with reduced
cesses. For example, attentional biases (e.g., Beevers emotional reactivity (see Bylsma et al., 2008 for
et al., 2011; Pergamin-Hight et al., 2012) and dis- review; Bylsma, Taylor-Clift, & Rottenberg, 2011).
tress tolerance (e.g., Amstadter et al., 2012; Leyro, Similarly, laboratory-based research suggests that
Zvolensky, & Bernstein, 2010) relate to important, major depressive disorder, and its attendant symp-
distinct aspects of emotion regulation. However, in toms, may be associated with impairment in initiating
laboratory-based assessment, each deficit is assessed emotion regulatory behavior (Berking et al., 2014;
in a different method. Therefore, clarifying the un- Berking & Wupperman, 2012; Radkovsky et al.,
derlying structure of multiple emotion regulatory 2014). This is further supported by evidence, from
deficits can become confounded with task-specific EMA research, that individuals who report elevated
error. Additionally, unrelated facets of specific psy- depression symptoms demonstrate reduced mo-
chiatric disorders may interfere with performance on mentary behavioral reactivity to social (Zuroff,
laboratory tasks and introduce task-specific noise. Fournier, & Moskowitz, 2007) and emotional cues
For example, psychomotor retardation may impair (Rappaport et al., 2017). In conclusion, to improve
task performance in a sample of individuals diag- assessment of emotion dysregulation, future re-
nosed with major depressive disorder (American search would benefit from multimethod designs
Psychiatric Association, 2013). that identify novel deficits in emotion regulation
In addition, laboratory-based methods cannot and leverage the strengths and weaknesses of each
detect dynamics in affect over the course of hours, approach to refine the selection of potential deficits
days, and so forth, which may index novel compo- for further genetic study.
nents of emotion dysregulation (Boker & Nesselroade,
2002; Moskowitz & Sadikaj, 2011; Trull & Ebner- Conduct More Longitudinal Research
Priemer, 2013). For example, Boker and colleagues While longitudinal research documents the devel-
identified regular oscillations in substance use opment of emotion dysregulation and implications
(Boker & Graham, 1998) and emotion (Bisconti, for psychopathology (e.g., Kim-Spoon, Cicchetti, &
Bergeman, & Boker, 2004; Boker & Laurenceau, Rogosch, 2013; Vasilev, Crowell, Beauchaine, Mead,
2006; Chow, Ram, Boker, Fujita, & Clore, 2005) & Gatzke-Kopp, 2009), most prior genetic studies
across hours and days. Evidence also points toward of emotion regulation have been cross-sectional. It
the importance of affective dynamics, such as is well known that adolescence and early adulthood

represent significant periods of increased risk for to answer key questions with regard to heritability
many psychiatric disorders associated with emotion and overlap with related traits including psychiat-
dysregulation (Merikangas et al., 2010), which sub- ric disorders. Such studies would be more power-
sequently influence psychopathology in adulthood ful if conducted through genomics consortia.
(Feng et al., 2009; Hatzenbuehler, McLaughlin, & Additionally, molecular genetic research of emotion
Nolen-Hoeksema, 2008; Nelemans et al., 2014). regulatory deficits may leverage gene-finding efforts
Several studies have examined genetic contributions for psychiatric conditions (e.g., Logue et al., 2015;
to emotion dysregulation in children (e.g., Goldsmith Otowa et al., 2016) to clarify specific points of
et al., 2008; Wang & Saudino, 2013). However, genetic overlap between components of emotion
physiological correlates of emotion dysregulation dysregulation and psychopathology. Finally, mul-
follow protracted developmental courses among timethod research, particularly research that
children and adolescents with both internalizing incorporates recent developments in EMA, is

and externalizing disorders (see Beauchaine et al., poised to identify novel emotion regulation deficits,
2007; Koenig et al., 2016; Pine & Fox, 2015). clarify selection and assessment of promising
Therefore, studies are needed to understand devel- candidate emotion regulation–related endopheno-
opmental changes in emotion dysregulation, genetic types, inform the structure of emotion regulation
contributions to the development of emotion dys- deficits, and evaluate the longitudinal role of emo-
regulation, and subsequent influences on the devel- tion dysregulation as risk factors or mechanisms in
opment of psychopathology. Statistically, Maxwell the development, onset, and course of psychopa-
and colleagues recommend longitudinal research to thology from childhood through adulthood.
evaluate statistical mediation, such as the temporal
patterning of processes in child development (Cole Funding Acknowledgments
& Maxwell, 2003; Maxwell & Cole, 2007; Maxwell, Dr. Rappaport is supported by NIH T32MH020030. Ms. Hawn
Cole, & Mitchell, 2011; Shrout, Keyes, & Ornstein, is supported by NIH F31AA025820. Ms. Overstreet is supported
by NIH F31DA038912. Dr. Amstadter is supported by BBRF
2011). Genetic research might also inform examina- 20066 and NIH grants R01AA020179, K02AA023239,
tion of causal influence (e.g., De Moor, Boomsma, R01MH101518, and P60MD002256.
Stubbe, Willemsen, & de Geus, 2008; Duffy &
Martin, 1994), particularly within a longitudinal References
design. Longitudinal, developmental research using aan het Rot, M., Hogenelst, K., & Schoevers, R. A. (2012).
Mood disorders in everyday life: A systematic review of
genetically informative samples (biometrical twin
experience sampling and ecological momentary assessment
and family designs) might provide important in- studies. Clinical Psychology Review, 32, 510–523.
sights into the development of emotion regulation Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
deficits and their role in psychopathology. Emotion-regulation strategies across psychopathology: A meta-
analytic review. Clinical Psychology Review, 30, 217–237.
American Psychiatric Association. (2013). Diagnostic and
Conclusion
statistical manual of mental disorders (5th ed.). Arlington, VA:
Twin research suggests that emotion regulation is Author.
moderately heritable (~.25 to .55), estimates that Amstadter, A. B., Daughters, S. B., MacPherson, L., Reynolds,
are consistent with related psychiatric conditions E. K., Danielson, C. K., Wang, F., . . . Lejuez, C. W. (2012).
(Sullivan et al., 2000) and personality traits (e.g., Genetic associations with performance on a behavioral
measure of distress intolerance. Journal of Psychiatric Research,
neuroticism; Hettema et al., 2006; Khan, Jacobson,
46, 87–94.
Gardner, Prescott, & Kendler, 2005). Candidate gene Beauchaine, T. P. (2015a). Future directions in emotion
studies have attempted to identify genetic variants dysregulation and youth psychopathology. Journal of Clinical
that account for heritability of emotion regulation, Child and Adolescent Psychology, 44, 875–896.
with some replicated effects and some nonreplica- Beauchaine, T. P. (2015b). Respiratory sinus arrhythmia:
A transdiagnostic biomarker of emotion dysregulation and
tions. No GWAS research has been conducted to
psychopathology. Current Opinion in Psychology, 3, 43–47.
date—a critical shortcoming as we seek to identify Beauchaine, T. P., & Constantino, J. N. (2017). Redefining the
genetic contributions to emotion dysregulation. It endophenotype concept to accommodate transdiagnostic
will be critical for the field to standardize emotion vulnerabilities and etiological complexity. Biomarkers in
regulation phenotypes so investigators can pool data Medicine, 11, 769–780.
Beauchaine, T. P., Gatzke-Kopp, L. M., & Gizer, I. R. (2017).
across studies for large-scale, well-powered, molecu-
Genetic, environmental, and epigenetic influences on
lar genetic studies. Methodological and statistical behavior. In T. P. Beauchaine & S. P. Hinshaw (Eds.), Child
developments in genetic research (e.g., PRS) can be and adolescent psychopathology (3rd ed., pp. 68–109).
applied to GWASs in emotion dysregulation studies Hoboken, NJ: Wiley.

Beauchaine, T. P., Gatzke-Kopp, L., & Mead, H. K. (2007). identifies two loci for major depressive disorder. Nature, 523,
Polyvagal theory and developmental psychopathology: 588–591.
Emotion dysregulation and conduct problems from Campbell, D. T., & Fiske, D. W. (1959). Convergent and
preschool to adolescence. Biological Psychology, 74, 174–184. discriminant validation by the multitrait-multimethod
Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as matrix. Psychological Bulletin, 56, 81.
a transdiagnostic biomarker of psychopathology. International Canli, T., Ferri, J., & Duman, E. A. (2009). Genetics of emotion
Journal of Psychophysiology, 98, 338–350. regulation. Neuroscience, 164, 43–54.
Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Canli, T., & Lesch, K.-P. (2007). Long story short: The serotonin
Cognitive therapy of depression. New York, NY: Guilford Press. transporter in emotion regulation and social cognition.
Beevers, C. G., Marti, C. N., Lee, H.-J., Stote, D. L., Ferrell, R. E., Nature Neuroscience, 10, 1103–1109.
Hariri, A. R., & Telch, M. J. (2011). Associations between Cannon, T. D., & Keller, M. C. (2006). Endophenotypes in the
serotonin transporter gene promoter region (5-HTTLPR) genetic analyses of mental disorders. Annual Review of
polymorphism and gaze bias for emotional information. Clinical Psychology, 2, 267–290.
Journal of Abnormal Psychology, 120, 187–197. Carver, C. S., Scheier, M. F., & Weintraub, J. K. (1989). Assessing
Bell, J. T., & Spector, T. D. (2011). A twin approach to unraveling coping strategies: A theoretically based approach. Journal of
epigenetics. Trends in Genetics, 27, 116–125. Personality and Social Psychology, 56, 267–283.
Benjamini, Y., & Yekutieli, D. (2001). The control of the false Chow, S.-M., Ram, N., Boker, S. M., Fujita, F., & Clore, G.
discovery rate in multiple testing under dependency. Annals (2005). Emotion as a thermostat: Representing emotion
of Statistics, 29, 1165–1188. regulation using a damped oscillator model. Emotion, 5,
Berking, M., Wirtz, C. M., Svaldi, J., & Hofmann, S. G. (2014). 208–225.
Emotion regulation predicts symptoms of depression over Clark, L. A., & Watson, D. (1991). Tripartite model of anxiety
five years. Behaviour Research and Therapy, 57, 13–20. and depression: Psychometric evidence and taxonomic
Berking, M., & Wupperman, P. (2012). Emotion regulation and implications. Journal of Abnormal Psychology, 100, 316–336.
mental health: Recent findings, current challenges, and Coccaro, E. F., Ong, A. D., Seroczynski, A. D., & Bergeman,
future directions. Current Opinion in Psychiatry, 25, 128–134. C. S. (2012). Affective intensity and lability: Heritability
Bisconti, T. L., Bergeman, C. S., & Boker, S. M. (2004). Emotional in adult male twins. Journal of Affective Disorders, 136,
well-being in recently bereaved widows: A dynamical systems 1011–1016.
approach. The Journals of Gerontology Series B: Psychological Cohen, B. M. (2016). Embracing complexity in psychiatric
Sciences and Social Sciences, 59, P158–P167. diagnosis, treatment, and research. JAMA Psychiatry, 73,
Bland, J. M., & Altman, D. G. (1995). Multiple significance 1211–1212.
tests: The Bonferroni method. BMJ, 310, 170. Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion
Boker, S. M., & Graham, J. (1998). A dynamical systems analysis regulation as a scientific construct: Methodological challenges
of adolescent substance abuse. Multivariate Behavioral and directions for child development research. Child
Research, 33, 479–507. Development, 75, 317–333.
Boker, S. M., & Laurenceau, J.-P. (2006). Dynamical systems Cole, D. A., & Maxwell, S. E. (2003). Testing mediational
modeling: An application to the regulation of intimacy and models with longitudinal data: Questions and tips in the use
disclosure in marriage. In T. A. Walls & J. L. Schafer (Eds.), of structural equation modeling. Journal of Abnormal
Models for intensive longitudinal data (pp. 195–218). New York, Psychology, 112, 558–577.
NY: Oxford University Press. Côté, S., Moskowitz, D. S., & Zuroff, D. C. (2012). Social
Boker, S. M., & Nesselroade, J. R. (2002). A method for modeling relationships and intraindividual variability in interpersonal
the intrinsic dynamics of intraindividual variability: Recovering behavior: Correlates of interpersonal spin. Journal of
the parameters of simulated oscillators in multi-wave panel Personality and Social Psychology, 102, 646–659.
data. Multivariate Behavioral Research, 37, 127–160. Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C. J.,
Bolton, J. M., Robinson, J., & Sareen, J. (2009). Self-medication Vasilev, C. A., & Stevens, A. L. (2008). Parent-child
of mood disorders with alcohol and drugs in the National interactions, peripheral serotonin, and self-inflicted injury in
Epidemiologic Survey on Alcohol and Related Conditions. adolescents. Journal of Consulting and Clinical Psychology, 76,
Journal of Affective Disorders, 115, 367–375. 15–21.
Burmeister, M., McInnis, M. G., & Zöllner, S. (2008). Crowell, S. E., Butner, J., Wiltshire, T. J., Munion, A. K.,
Psychiatric genetics: Progress amid controversy. Nature Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating
Reviews Genetics, 9, 527–540. emotional and biological sensitivity to maternal behavior
Burt, S. A., Krueger, R. F., McGue, M., & Iacono, W. G. (2001). among depressed and self-injuring adolescent girls
Sources of covariation among attention-deficit/hyperactivity using nonlinear dynamics. Clinical Psychological Science, 5,
disorder, oppositional defiant disorder, and conduct disorder: 272–285.
The importance of shared environment. Journal of Abnormal Davidson, R. J., Putnam, K. M., & Larson, C. L. (2000).
Psychology, 110, 516–525. Dysfunction in the neural circuitry of emotion regulation—A
Bylsma, L. M., Morris, B. H., & Rottenberg, J. (2008). A meta- possible prelude to violence. Science, 289, 591–594.
analysis of emotional reactivity in major depressive disorder. De Moor, M. H., Boomsma, D. I., Stubbe, J. H., Willemsen, G.,
Clinical Psychology Review, 28, 676–691. & de Geus, E. J. (2008). Testing causality in the association
Bylsma, L. M., Taylor-Clift, A., & Rottenberg, J. (2011). between regular exercise and symptoms of anxiety and
Emotional reactivity to daily events in major and minor depression. Archives of General Psychiatry, 65, 897–905.
depression. Journal of Abnormal Psychology, 120, 155–167. Dick, D. M., Latendresse, S. J., & Riley, B. (2011). Incorporating
Cai, N., Bigdeli, T. B., Kretzschmar, W., Li, Y., Liang, J., Song, genetics into your studies: A guide for social scientists.
L., .
.
.
Flint, J. (2015). Sparse whole-genome sequencing Frontiers in Psychiatry, 2, 17.

Domschke, K., Baune, B. T., Havlik, L., Stuhrmann, A., Suslow, T., Gottesman, I. I., & Gould, T. D. (2003). The endophenotype
Kugel, H., . . . Dannlowski, U. (2012). Catechol-O- concept in psychiatry: Etymology and strategic intentions.
methyltransferase gene variation: Impact on amygdala American Journal of Psychiatry, 160, 636–645.
response to aversive stimuli. NeuroImage, 60, 2222–2229. Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment
Duffy, D. L., & Martin, N. G. (1994). Inferring the direction of emotion regulation and dysregulation: Development,
of causation in cross-sectional twin data: Theoretical factor structure, and initial validation of the difficulties in
and empirical considerations. Genetic Epidemiology, 11, emotion regulation scale. Journal of Psychopathology and
483–502. Behavioral Assessment, 26, 41–54.
Duncan, L. E., Ratanatharathorn, A., Aiello, A. E., Almli, L. M., Gross, J. J. (1998). The emerging field of emotion regulation:
Amstadter, A. B., Ashley-Koch, A. E., . . . Koenen, K. C. An integrative review. Review of General Psychology, 2,
(2017). Largest GWAS of PTSD (N=20070) yields genetic 271–299.
overlap with schizophrenia and sex differences in heritability. Gross, J. J., & Muñoz, R. F. (1995). Emotion regulation and
Molecular Psychiatry, 23, 666–673. mental health. Clinical Psychology: Science and Practice, 2,
Eaves, L. J. (1976). A model for sibling effects in man. Heredity, 151–164.
36(2), 205–214. Gross, J. J., & Thompson, R. A. (2007). Emotion regulation:
Ebner-Priemer, U. W., & Trull, T. J. (2009). Ecological Conceptual foundations. In J. J. Gross (Ed.), Handbook of
momentary assessment of mood disorders and mood emotion regulation (pp. 3–24). New York, NY: Guilford
dysregulation. Psychological Assessment, 21, 463–475. Press.
Edwards, A. C., & Kendler, K. S. (2013). Alcohol consumption Guhn, A., Domschke, K., Müller, L. D., Dresler, T., Eff, F., Kopf,
in men is influenced by qualitatively different genetic factors J., . . . Herrmann, M. J. (2015). Neuropeptide S receptor gene
in adolescence and adulthood. Psychological Medicine, 43, variation and neural correlates of cognitive emotion
1857–1868. regulation. Social Cognitive and Affective Neuroscience, 10,
Erickson, T. M., Newman, M. G., & Pincus, A. L. (2009). 1730–1737.
Predicting unpredictability: Do measures of interpersonal Hakamata, Y., Lissek, S., Bar-Haim, Y., Britton, J. C., Fox,
rigidity/flexibility and distress predict intraindividual N. A., Leibenluft, E., . . . Pine, D. S. (2010). Attention bias
variability in social perceptions and behavior? Journal of modification treatment: A meta-analysis toward the
Personality and Social Psychology, 97, 893–912. establishment of novel treatment for anxiety. Biological
Feng, X., Keenan, K., Hipwell, A. E., Henneberger, A. K., Psychiatry, 68, 982–990.
Rischall, M. S., Butch, J., . . . Babinski, D. E. (2009). Harrison, A., Sullivan, S., Tchanturia, K., & Treasure, J. (2010).
Longitudinal associations between emotion regulation Emotional functioning in eating disorders: Attentional bias,
and depression in preadolescent girls: Moderation by emotion recognition and emotion regulation. Psychological
the caregiving environment. Developmental Psychology, 45, Medicine, 40, 1887–1897.
798–808. Hatzenbuehler, M. L., McLaughlin, K. A., & Nolen-Hoeksema,
Flint, J., Chen, Y., Shi, S., & Kendler, K. S. (2012). Epilogue: S. (2008). Emotion regulation and internalizing symptoms
Lessons from the CONVERGE study of major depressive in a longitudinal study of sexual minority and heterosexual
disorder in China. Journal of Affective Disorders, 140, 1–5. adolescents. Journal of Child Psychology and Psychiatry, 49,
Freedman, M. L., Reich, D., Penney, K. L., McDonald, G. J., 1270–1278.
Mignault, A. A., Patterson, N., . . . Altshuler, D. (2004). Hawn, S. E., Overstreet, C., Stewart, K. E., & Amstadter, A. B.
Assessing the impact of population stratification on genetic (2015). Recent advances in the genetics of emotion regulation:
association studies. Nature Genetics, 36, 388–393. A review. Current Opinion in Psychology, 3, 108–116.
French, L., Gray, C., Leonard, G., Perron, M., Pike, G. B., Heath, A. C., Kendler, K. S., Eaves, L. J., & Markell, D. (1985).
Richer, L., . . . Paus, T. (2015). Early cannabis use, polygenic The resolution of cultural and bio-logical inheritance:
risk score for schizophrenia, and brain maturation in Informativeness of different relationships. Behavior Genetics,
adolescence. JAMA Psychiatry, 72, 1002–1011. 15, 439–465.
Freud, S. (1926). Inhibitions, symptoms, anxiety (J. Strachey, Ed., Hedges, L. V., & Pigott, T. D. (2001). The power of statistical
A. Strachey, Trans.). New York, NY: Norton. tests in meta-analysis. Psychological Methods, 6, 203–217.
Fulker, D. W. (1977). Multivariate extensions of a biometrical Hettema, J. M., Neale, M. C., Myers, J. M., Prescott, C. A., &
model of twin data. Progress in Clinical and Biological Kendler, K. S. (2006). A population-based twin study of
Research, 24, 217–236. the relationship between neuroticism and internalizing
Fulker, D. W. (1981). Biometrical genetics and individual disorders. American Journal of Psychiatry, 163, 857–864.
differences. British Medical Bulletin, 37, 115–120. Hettema, J. M., Prescott, C. A., Myers, J. M., Neale, M. C., &
Geschwind, D. H., & Flint, J. (2015). Genetics and genomics of Kendler, K. S. (2005). The structure of genetic and
psychiatric disease. Science, 349, 1489–1494. environmental risk factors for anxiety disorders in men and
Gilman, T. L., Latsko, M., Matt, L., Flynn, J., de la Cruz women. Archives of General Psychiatry, 62, 182–189.
Cabrera, O., Douglas, D., . . . Coifman, K. G. (2015). Variation Holz, N. E., Buchmann, A. F., Boecker, R., Blomeyer, D.,
of 5-HTTLPR and deficits in emotion regulation: A pathway Baumeister, S., Wolf, I., . . . Laucht, M. (2015). Role of
to risk? Psychology and Neuroscience, 8, 397–413. FKBP5 in emotion processing: Results on amygdala activity,
Girirajan, S., Campbell, C. D., & Eichle, E. E. (2011). Human connectivity and volume. Brain Structure and Function, 220,
copy number variation and complex genetic disease. Annual 1355–1368.
Review of Genetics, 45, 203–226. Houben, M., Van Den Noortgate, W., & Kuppens, P. (2015).
Goldsmith, H. H., Pollak, S. D., & Davidson, R. J. (2008). The relation between short-term emotion dynamics and
Developmental neuroscience perspectives on emotion psychological well-being: A meta-analysis. Psychological
regulation. Child Development Perspectives, 2, 132–140. Bulletin, 141, 901–930.

Hunter, J. E., Schmidt, F. L., & Jackson, G. B. (1982). Meta- emotion regulation. Social Psychological and Personality
analysis: Cumulating research findings across studies. Beverly Science, 2, 665–672.
Hills, CA: Sage. Kim, J., & Cicchetti, D. (2009). Longitudinal pathways linking
Iacono, W. G., Malone, S. M., & Vrieze, S. I. (2017). child maltreatment, emotion regulation, peer relations, and
Endophenotype best practices. International Journal of psychopathology. Journal of Child Psychology and Psychiatry,
Psychophysiology, 111, 115–144. 51, 706–716.
Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D. S., Kim-Spoon, J., Cicchetti, D., & Rogosch, F. A. (2013). A
Quinn, K., . . . Wang, P. (2010). Research domain criteria longitudinal study of emotion regulation, emotion lability-
(RDoC): Toward a new classification framework for research negativity, and internalizing symptomatology in maltreated
on mental disorders. American Journal of Psychiatry, 167, and nonmaltreated children. Child Development, 84, 512–527.
748–751. Kirkpatrick, R. M., & Neale, M. C. (2015). Combining
Jang, K. L., Livesley, W. J., & Vemon, P. A. (1996). Heritability genomic-relatedness-matrix restricted maximum likelihood
of the big five personality dimensions and their facets: A twin (greml) with structural equation modeling in openmx.
study. Journal of Personality, 64, 577–592. Behavior Genetics, 45, 665.
Jinks, J. L., & Fulker, D. W. (1970). Comparison of the Klonsky, E. D., & Muehlenkamp, J. J. (2007). Self-injury: A
biometrical genetical, MAVA, and classical approaches to the research review for the practitioner. Journal of Clinical
analysis of human behavior. Psychological Bulletin, 73, 311–349. Psychology, 63, 1045–1056.
Johnston, J. A., Wang, F., Liu, J., Blond, B. N., Wallace, A., Liu, Koenig, J., Kemp, A., Beauchaine, T. P., Thayer, J. F., & Kaess,
J., . . . Blumberg, H. P. (2017). Multimodal neuroimaging of M. (2016). Depression and resting state heart rate variability
frontolimbic structure and function associated with suicide in children and adolescents: A systematic review and meta-
attempts in adolescents and young adults with bipolar analysis. Clinical Psychology Review, 46, 136–150.
disorder. American Journal of Psychiatry, 174, 667–675. Kopala-Sibley, D. C., Rappaport, L. M., Sutton, R., Moskowitz,
Kanakam, N., Krug, I., Raoult, C., Collier, D., & Treasure, J. D. S., & Zuroff, D. C. (2013). Self-criticism, neediness,
(2013). Social and emotional processing as a behavioural and connectedness as predictors of interpersonal behavioral
endophenotype in eating disorders: A pilot investigation in variability. Journal of Social and Clinical Psychology, 32,
twins. European Eating Disorders Review, 21, 294–307. 770–790.
Karg, K., Burmeister, M., Shedden, K., & Sen, S. (2011). The Kuppens, P., Allen, N. B., & Sheeber, L. B. (2010). Emotional
serotonin transporter promoter variant (5-HTTLPR), stress, inertia and psychological maladjustment. Psychological
and depression meta-analysis revisited: Evidence of genetic Science, 21, 984–991.
moderation. Archives of General Psychiatry, 68, 444–454. Kuppens, P., Sheeber, L. B., Yap, M. B. H., Whittle, S., Simmons,
Karkowski, L. M., Prescott, C. A., & Kendler, K. S. (2000). J. G., & Allen, N. B. (2012). Emotional inertia prospectively
Multivariate assessment of factors influencing illicit substance predicts the onset of depressive disorder in adolescence.
use in twins from female-female pairs. American Journal of Emotion, 12, 283–289.
Medical Genetics Part A, 96, 665–670. Ladd, G. W., Ettekal, I., & Kochenderfer-Ladd, B. (2017). Peer
Kendler, K. S., Aggen, S. H., Knudsen, G. P., Røysamb, E., victimization trajectories from kindergarten through high
Neale, M. C., & Reichborn-Kjennerud, T. (2011). The school: Differential pathways for children’s school engagement
structure of genetic and environmental risk factors for and achievement? Journal of Educational Psychology, 109,
syndromal and subsydromal common DSM-IV axis I and 826–841.
axis II disorders. American Journal of Psychiatry, 168, 29–39. Lazarus, R. S. (2000). Toward better research on stress and
Kendler, K. S., Jaffee, S. R., & Romer, D. (2011). The dynamic coping. American Psychologist, 55, 665–673.
genome and mental health. New York, NY: Oxford University Lee, S. H., Ripke, S., Neale, B. M., Faraone, S. V., Purcell, S. M.,
Press. Perlis, R. H., . . . Wray, N. R. (2013). Genetic relationship
Kendler, K. S., Neale, M. C., Kessler, R. C., Heath, A. C., & between five psychiatric disorders estimated from genome-
Eaves, L. J. (1992). Major depression and generalized anxiety wide SNPs. Nature Genetics, 45, 984–994.
disorder: Same genes, (partly) different environments? Lehner, T., Senthil, G., & Addington, A. M. (2015). Convergence
Archives of General Psychiatry, 49, 716–722. of advances in genomics, team science, and repositories as
Kenny, D. A., Kashy, D. A., & Cook, W. L. (2006). Dyadic data drivers of progress in psychiatric genomics. Biological
analysis. New York, NY: Guilford Press. Psychiatry, 77, 6–14.
Kessler, R. C., Gruber, M., Hettema, J. M., Hwang, I., Sampson, Lesch, K.-P., Balling, U., Gross, J., Strauss, K., Wolozin, B. L.,
N., & Yonkers, K. A. (2008). Co-morbid major depression Murphy, D. L., & Riederer, P. (1994). Organization of the
and generalized anxiety disorders in the National human serotonin transporter gene. Journal of Neural
Comorbidity Survey follow-up. Psychological Medicine, 38, Transmission/General Section JNT, 95, 157–162.
365–374. Lesch, K.-P., Bengel, D., Heils, A., Sabol, S. Z., Greenberg,
Khan, A. A., Jacobson, K. C., Gardner, C. O., Prescott, C. A., & B. D., Petri, . . . Murphy, D. L. (1996). Association of anxiety-
Kendler, K. S. (2005). Personality and comorbidity of related traits with a polymorphism in the serotonin
common psychiatric disorders. British Journal of Psychiatry, transporter gene regulatory region. Science, 274, 1527–1531.
186, 190–196. Levinson, D. F., Mostafavi, S., Milaneschi, Y., Rivera, M., Ripke,
Khantzian, E. J. (1985). The self-medication hypothesis of S., Wray, N. R., & Sullivan, P. F. (2014). Genetic studies of
addictive disorders: Focus on heroin and cocaine dependence. major depressive disorder: Why are there no genome-wide
American Journal of Psychiatry, 142, 1259–1264. association study findings and what can we do about it?
Kim, H. S., Sherman, D. K., Mojaverian, T., Sasaki, J. Y., Park, Biological Psychiatry, 76, 510–512.
J., Suh, E. M., & Taylor, S. E. (2011). Gene-culture Leyro, T. M., Zvolensky, M. J., & Bernstein, A. (2010). Distress
interaction: Oxytocin receptor polymorphism (OXTR) and tolerance and psychopathological symptoms and disorders:

A review of the empirical literature among adults. Mill, J., & Petronis, A. (2007). Molecular studies of major
Psychological Bulletin, 136, 576–600. depressive disorder: The epigenetic perspective. Molecular
Lin, C.-H., Tseng, Y.-L., Huang, C.-L., Chang, Y.-C., Tsai, Psychiatry, 12, 799–814.
G. E., & Lane, H.-Y. (2013). Synergistic effects of COMT Miller, G. A., & Rockstroh, B. (2013). Endophenotypes in
and TPH2 on social cognition. Psychiatry: Interpersonal and psychopathology research: Where do we stand? Annual
Biological Processes, 76, 273–294. Review of Clinical Psychology, 9, 177–213.
Linehan, M. M. (1993). Cognitive-behavioral treatment of Miu, A. C., Carnuta, M., Vulturar, R., Szekely-Copîndean,
borderline personality disorder. New York, NY: Guilford Press. R. D., Bîlc, M. I., Chis, A., . . . Gross, J. J. (2017). BDNF
Logue, M. W., Amstadter, A. B., Baker, D. G., Duncan, L., Val66Met polymorphism moderates the link between child
Koenen, K. C., Liberzon, I., . . . Uddin, M. (2015). The maltreatment and reappraisal ability: BDNF Val66Met, child
Psychiatric Genomics Consortium Posttraumatic Stress maltreatment and reappraisal. Genes, Brain and Behavior,
Disorder Workgroup: Posttraumatic stress disorder enters 16(4), 419–426.
the age of large-scale genomic collaboration. Neuropsycho Moskowitz, D. S., & Sadikaj, G. (2011). Event-contingent
pharmacology, 40, 2287–2297. sampling. In T. Mehl & T. Conner (Eds.), Handbook of
Lonsdorf, T. B., Golkar, A., Lindstöm, K. M., Fransson, P., research methods for studying daily life (pp. 160–175).
Schalling, M., Öhman, A., & Ingvar, M. (2011). 5-HTTLPR New York, NY: Guilford Press.
and COMTval158met genotype gate amygdala reactivity and Mullin, B. C., & Hinshaw, S. P. (2007). Emotion regulation and
habituation. Biological Psychology, 87, 106–112. externalizing disorders in children and adolescents. In
Manolio, T. A., Collins, F. S., Cox, N. J., Goldstein, D. B., J. J. Gross (Ed.), Handbook of emotion regulation (pp. 523–541).
Hindorff, L. A., Hunter, D. J., . . . Visscher, P. M. (2009). New York, NY: Guilford Press.
Finding the missing heritability of complex diseases. Nature, Munafò, M. R., Durrant, C., Lewis, G., & Flint, J. (2009). Gene
461, 747–753. × Environment interactions at the serotonin transporter
Mather, K. (1949). Biometrical genetics. London, UK: Methuen locus. Biological Psychiatry, 65, 211–219.
& Co. National Advisory Mental Health Council Workgroup on Tasks
Mather, K., & Jinks, J. L. (1971). Biometrical genetics: The study of and Measures for Research Domain Criteria. (2016).
continuous variation. London, UK: Chapman and Hall. Behavioral assessment methods for RDoC constructs. Bethesda,
Maxwell, S. E., & Cole, D. A. (2007). Bias in cross-sectional MD: National Institute of Mental Health.
analyses of longitudinal mediation. Psychological Methods, 12, Neiss, M., & Almeida, D. M. (2004). Age differences in the
23–44. heritability of mean and intraindividual variation of
Maxwell, S. E., Cole, D. A., & Mitchell, M. A. (2011). Bias in psychological distress. Gerontology, 50, 22–27.
cross-sectional analyses of longitudinal mediation: Partial Nelemans, S. A., Hale, W. W., Branje, S. J. T., Raaijmakers,
and complete mediation under an autoregressive model. Q. A. W., Frijns, T., van Lier, P. A. C., & Meeus, W. H. J.
Multivariate Behavioral Research, 46, 816–841. (2014). Heterogeneity in development of adolescent anxiety
McClelland, G. H., & Judd, C. M. (1993). Statistical difficulties disorder symptoms in an 8-year longitudinal community
of detecting interactions and moderator effects. Psychological study. Development and Psychopathology, 26, 181–202.
Bulletin, 114, 376–390. Odgers, C. L., Mulvey, E. P., Skeem, J. L., Gardner, W., Lidz,
McRae, K., Rhee, S. H., Gatt, J. M., Godinez, D., Williams, C. W., & Schubert, C. (2009). Capturing the ebb and flow
L. M., & Gross, J. J. (2017). Genetic and environmental of psychiatric symptoms with dynamical systems models.
influences on emotion regulation: A twin study of cognitive American Journal of Psychiatry, 166, 575–582.
reappraisal and expressive suppression. Emotion, 17, 772–777. Otowa, T., Hek, K., Lee, M., Byrne, E. M., Mirza, S. S., Nivard,
Mennin, D. S., Heimberg, R. G., Turk, C. L., & Fresco, D. M. M. G., . . . Hettema, J. M. (2016). Meta-analysis of genome-
(2002). Applying an emotion regulation framework to wide association studies of anxiety disorders. Molecular
integrative approaches to generalized anxiety disorder. Psychiatry, 21, 1391–1399.
Clinical Psychology: Science and Practice, 9, 85–90. Owens, M. J., & Nemeroff, C. B. (1994). Role of serotonin in
Mennin, D. S., Holaway, R. M., Fresco, D. M., Moore, M. T., & the pathophysiology of depression: Focus on the serotonin
Heimberg, R. G. (2007). Delineating components of transporter. Clinical Chemistry, 40, 288–295.
emotion and its dysregulation in anxiety and mood Pagliaccio, D., Luby, J. L., Bogdan, R., Agrawal, A., Gaffrey,
pathology. Behavior Therapy, 38, 284–302. M. S., Belden, A. C., . . . Barch, D. M. (2015). Amygdala
Mennin, D. S., McLaughlin, K. A., & Flanagan, T. J. (2009). functional connectivity, HPA axis genetic variation, and life
Emotion regulation deficits in generalized anxiety disorders, stress in children and relations to anxiety and emotion
social anxiety disorder, and their co-occurrence. Journal of regulation. Journal of Abnormal Psychology, 124, 817–833.
Anxiety Disorders, 23, 866–871. Perez-Rodriguez, M. M., New, A. S., Goldstein, K. E., Rosell, D.,
Merikangas, K. R., He, J., Burstein, M., Swanson, S. A., Avenevoli, Yuan, Q., Zhou, Z., . . . Hazlett, E. A. (2017). Brain-derived
S., Cui, L., . . . Swendsen, J. (2010). Lifetime prevalence of neurotrophic factor Val66Met genotype modulates amygdala
mental disorders in U.S. adolescents: Results from the habituation. Psychiatry Research: Neuroimaging, 263, 85–92.
National Comorbidity Survey Replication–Adolescent Pergamin-Hight, L., Bakermans-Kranenburg, M. J., van
Supplement (NCS-A). Journal of the American Academy of IJzendoorn, M. H., & Bar-Haim, Y. (2012). Variations in the
Child and Adolescent Psychiatry, 49, 980–989. promoter region of the serotonin transporter gene and biased
Mickey, B. J., Zhou, Z., Heitzeg, M. M., Heinz, E., Hodgkinson, attention for emotional information: A meta-analysis.
C. A., Hsu, D. T., .
.
.
Zubieta, J. K. (2011). Emotion Biological Psychiatry, 71, 373–379.
processing, major depression, and functional genetic Pine, D. S., & Fox, N. A. (2015). Childhood antecedents and
variation of neuropeptide Y. Archives of General Psychiatry, risk for adult mental disorders. Annual Review of Psychology,
68, 158–166. 66, 459–485.

Plieger, T., Melchers, M., Vetterlein, A., Görtz, J., Kuhn, S., Quantifying respiratory sinus arrhythmia: Effects of
Ruppel, M., & Reuter, M. (2017). The serotonin transporter misspecifying breathing frequencies across development.
polymorphism (5-HTTLPR) and coping strategies influence Development and Psychopathology, 30, 351–366.
successful emotion regulation in an acute stress situation: Shrout, P. E., Keyes, K., & Ornstein, K. (Eds.). (2011). Causality
Physiological evidence. International Journal of Psychophysiology, and psychopathology: Finding the determinants of disorders and
114, 31–37. their cures. New York, NY: Oxford University Press.
Plomin, R., Haworth, C. M. A., Meaburn, E. L., Price, T. S., Storey, J. D. (2003). The positive false discovery rate: A
Wellcome Trust Case Control Consortium 2, & Davis, Bayesian interpretation and the q-value. Annals of Statistics,
O. S. P. (2013). Common DNA markers can account for 31, 2013–2035.
more than half of the genetic influence on cognitive abilities. Sullivan, P. F., Neale, M. C., & Kendler, K. S. (2000). Genetic
Psychological Science, 24, 562–568. epidemiology of major depression: Review and meta-
Plomin, R., & Simpson, M. A. (2013). The future of genomics analysis. American Journal of Psychiatry, 157, 1552–1562.
for developmentalists. Development and Psychopathology, 25, Surguladze, S. A., Radua, J., El-Hage, W., Gohier, B., Sato, J. R.,
1263–1278. Kronhaus, D. M., . . . Phillips, M. L. (2012). Interaction of
Price, A. L., Patterson, N. J., Plenge, R. M., Weinblatt, M. E., catechol-O-methyltransferase and serotonin transporter
Shadick, N. A., & Reich, D. (2006). Principal components genes modulates effective connectivity in a facial emotion-
analysis corrects for stratification in genome-wide association processing circuitry. Translational Psychiatry, 2, e70.
studies. Nature Genetics, 38, 904–909. Swart, M., Bruggeman, R., Larøi, F., Alizadeh, B. Z., Kema, I.,
Price, A. L., Zaitlen, N. A., Reich, D., & Patterson, N. (2010). Kortekaas, R., . . . Aleman, A. (2011). COMT Val158Met
New approaches to population stratification in genome-wide polymorphism, verbalizing of emotion and activation of
association studies. Nature Reviews Genetics, 11, 459–463. affective brain systems. NeuroImage, 55(1), 338–344.
Radkovsky, A., McArdle, J. J., Bockting, C. L. H., & Berking, Szily, E., & Kéri, S. (2012). Emotion appraisal and the tryptophan
M. (2014). Successful emotion regulation skills application hydroxylase 2 (TPH2) gene. Journal of Neural Transmission,
predicts subsequent reduction of symptom severity during 119, 1261–1265.
treatment of major depressive disorder. Journal of Consulting Tackett, J. L., Lahey, B. B., van Hulle, C., Waldman, I., Krueger,
and Clinical Psychology, 82, 248–262. R. F., & Rathouz, P. J. (2013). Common genetic influences
Rappaport, L. M., Moskowitz, D. S., & D’Antono, B. (2014). on negative emotionality and a general psychopathology
Naturalistic interpersonal behavior patterns differentiate factor in childhood and adolescence. Journal of Abnormal
depression and anxiety symptoms in the community. Journal Psychology, 122, 1142–1153.
of Counseling Psychology, 61, 253–263. Thompson, R. A. (1990). Emotion and self-regulation. In
Rappaport, L. M., Moskowitz, D. S., & D’Antono, B. (2017). R. A. Thompson (Ed.), Nebraska Symposium on Motivation:
Depression symptoms moderate the association between Vol. 36. Socioemotional development (pp. 383–483). Lincoln,
emotion and communal behavior. Journal of Counseling NE: University of Nebraska Press.
Psychology, 64, 269–279. Tracey, T. J. G., & Rohlfing, J. E. (2010). Variations in the
Rice, F., Harold, G. T., & Thapar, A. (2002). Assessing the effects understanding of interpersonal behavior: Adherence to the
of age, sex, and shared environment on the genetic aetiology interpersonal circle as a moderator of the rigidity-psychological
of depression in childhood and adolescence. Journal of Child well-being relation. Journal of Personality, 78, 711–746.
Psychology and Psychiatry, 43, 1039–1051. Trull, T. J., & Ebner-Priemer, U. (2013). Ambulatory assessment.
Ripke, S., Neale, B. M., Corvin, A., Walters, J. T. R., Farh, K.- Annual Review of Clinical Psychology, 9, 151–176.
H., Holmans, P. A., . . . O’Donovan, M. C. (2014). Biological Trull, T. J., Solhan, M. B., Tragesser, S. L., Jahng, S., Wood,
insights from 108 schizophrenia-associated genetic loci. P. K., Piasecki, T. M., & Watson, D. (2008). Affective
Nature, 511, 421–427. instability: Measuring a core feature of borderline personality
Risch, N., Herrell, R., Lehner, T., Liang, K.-Y., Eaves, L., disorder with ecological momentary assessment. Journal of
Hoh, J., . . . Merikangas, K. R. (2009). Interaction between Abnormal Psychology, 117, 647–661.
the serotonin transporter gene (5-HTTLPR), stressful life Trzaskowski, M., Davis, O. S. P., DeFries, J. C., Yang, J.,
events, and risk of depression: A meta-analysis. JAMA, 301, Visscher, P. M., & Plomin, R. (2013). DNA evidence for
2462–2471. strong genome-wide pleiotropy of cognitive and learning
Roostaei, T., Nazeri, A., Felsky, D., De Jager, P. L., Schneider, abilities. Behavior Genetics, 43, 267–273.
J. A., Pollock, B. G., . . . Voineskos, A. N. (2017). Genome- Trzaskowski, M., Shakeshaft, N. G., & Plomin, R. (2013).
wide interaction study of brain beta-amyloid burden and Intelligence indexes generalist genes for cognitive abilities.
cognitive impairment in Alzheimer’s disease. Molecular Intelligence, 41, 560–565.
Psychiatry, 22, 287–295. Tull, M. T., & Roemer, L. (2007). Emotion regulation
Russell, J. J., Moskowitz, D. S., Zuroff, D. C., Sookman, D., & difficulties associated with the experience of uncued panic
Paris, J. (2007). Stability and variability of affective experience attacks: Evidence of experiential avoidance, emotional
and interpersonal behavior in borderline personality disorder. nonacceptance, and decreased emotional clarity. Behavior
Journal of Abnormal Psychology, 116, 578–588. Therapy, 38, 378–391.
Sadikaj, G., Rappaport, L. M., Moskowitz, D. S., Zuroff, D. C., Turecki, G., & Meaney, M. J. (2016). Effects of the social
Koestner, R., & Powers, T. (2015). Consequences of environment and stress on gluco-corticoid receptor gene
interpersonal spin on couple-relevant goal progress and methylation: A systematic review. Biological Psychiatry, 79,
relationship satisfaction in romantic relationships. Journal of 87–96.
Personality and Social Psychology, 109, 722–737. van de Leemput, I. A., Wichers, M., Cramer, A. O. J., Borsboom,
Shader, T. M., Gatzke-Kopp, L. M., Crowell, S. E., Reid, M. J., D., Tuerlinckx, F., Kuppens, P., . .
.
Scheffer, M. (2014).
Thayer, J. F., Vasey, M. W., . . . Beauchaine, T. P. (2017). Critical slowing down as early warning for the onset and

termination of depression. Proceedings of the National investigation. American Journal of Geriatric Psychiatry, 22,
Academy of Sciences, 111, 87–92. 946–950.
Van Rheenen, T. E., Murray, G., & Rossell, S. L. (2015). Emotion Watson, D., Weber, K., Assenheimer, J. S., Clark, L. A., Strauss,
regulation in bipolar disorder: Profile and utility in predicting M. E., & McCormick, R. A. (1995). Testing a tripartite
trait mania and depression propensity. Psychiatry Research, model: I. Evaluating the convergent and discriminant
225, 425–432. validity of anxiety and depression symptom scales. Journal of
Vasilev, C. A., Crowell, S. E., Beauchaine, T. P., Mead, H. K., & Abnormal Psychology, 104, 3–14.
Gatzke-Kopp, L. M. (2009). Correspondence between Weinberg, A., Venables, N. C., Proudfit, G. H., & Patrick, C. J.
physiological and self-report measures of emotion (2015). Heritability of the neural response to emotional
dysregulation: A longitudinal investigation of youth with pictures: Evidence from ERPs in an adult twin sample. Social
and without psychopathology. Journal of Child Psychology Cognitive and Affective Neuroscience, 10, 424–434.
and Psychiatry, 50, 1357–1364. Weiss, E. M., Freudenthaler, H. H., Fink, A., Reiser, E. M.,
Viddal, K. R., Berg-Nielsen, T. S., Belsky, J., & Wichstrøm, L. Niederstätter, H., Nagl, S., . . . Papousek, I. (2014). Differential
(2017). Change in attachment predicts change in emotion influence of 5-HTTLPR—Polymorphism and COMT
regulation particularly among 5-HTTLPR short-allele Val158Met polymorphism on emotion perception and
homozygotes. Developmental Psychology, 53, 1316–1329. regulation in healthy women. Journal of the International
Visscher, P. M., Hill, W. G., & Wray, N. R. (2008). Heritability Neuropsychological Society, 20, 516–524.
in the genomics era—Concepts and misconceptions. Nature Wills, T. A., Pokhrel, P., Morehouse, E., & Fenster, B. (2011).
Reviews Genetics, 9, 255–266. Behavioral and emotional regulation and adolescent substance
Waider, J., Araragi, N., Gutknecht, L., & Lesch, K.-P. (2011). use problems: A test of moderation effects in a dual-process
Tryptophan hydroxylase-2 (TPH2) in disorders of model. Psychology of Addictive Behaviors, 25, 279–292.
cognitive control and emotion regulation: A perspective. Winkler, T. W., Justice, A. E., Graff, M., Barata, L., Feitosa,
Psychoneuroendocrinology, 36, 393–405. M. F., Chu, S., . . . Loos, R. J. F. (2015). The influence of age
Walz, L. C., Nauta, M. H., & aan het Rot, M. (2014). Experience and sex on genetic associations with adult body size and
sampling and ecological momentary assessment for studying shape: A large-scale genome-wide interaction study. PLOS
the daily lives of patients with anxiety disorders: A systematic Genetics, 11, e1005378.
review. Journal of Anxiety Disorders, 28, 925–937. Yang, J., Benyamin, B., McEvoy, B. P., Gordon, S., Henders,
Wang, M., & Saudino, K. J. (2013). Genetic and environmental A. K., Nyholt, D. R., . . . Visscher, P. M. (2010). Common
influences on individual differences in emotion regulation SNPs explain a large proportion of the heritability for human
and its relation to working memory in toddlerhood. Emotion, height. Nature Genetics, 42, 565–569.
13, 1055–1067. Zuroff, D. C., Fournier, M. A., & Moskowitz, D. S. (2007).
Waring, J. D., Etkin, A., Hallmayer, J. F., & O’Hara, R. (2014). Depression, perceived inferiority, and interpersonal behavior:
Connectivity underlying emotion conflict regulation in Evidence for the involuntary defeat strategy. Journal of Social
older adults with 5-HTTLPR short allele: A preliminary and Clinical Psychology, 26, 751–778.

CH A PTE R
Epigenetic Foundations of Emotion
16 Dysregulation
Mindy Brown, Elisabeth Conradt, and Sheila E. Crowell
Abstract
Emotion dysregulation is a pervasive clinical problem that likely emerges from complex Gene ×
Environment interactions across development. Epigenetic processes provide a molecular basis by
which genotype interacts with the environment across the lifespan to produce phenotype.
Epigenetics is defined by molecular processes occurring on and around the genome that regulate
gene activity without changing DNA sequence. This chapter describes how epigenetic mechanisms
are assessed and provides a brief review of current research on epigenetics, emotion dysregulation,
and associated disorders. It then highlights four biological pathways of interest, the serotonin,
dopamine, and norepinephrine systems and the limbic-hypothalamic pituitary adrenal (L-HPA) axis,
and argues that, to advance understanding of the pathophysiology of emotion dysregulation,
biological pathways rather than single genes must be measured. The chapter describes challenges for
the field of epigenetics and how novel methods could be leveraged to overcome those challenges.
Keywords: emotion dysregulation, epigenetics, biological pathways, serotonin, dopamine, borderline

personality disorder
Introduction disorder, and schizophrenia (see Mill & Petronis,

In the last century in psychological science, there has 2007, 2008; Petronis, 2003, 2004; Poulter et al.,
been a gradual dissolution of boundaries between 2008; Schanen, 2006; Smith et al., 2011). However,
genes and environments. Most recently, this disso- this focus on discrete psychiatric outcomes conflicts
lution follows from the discovery that epig enetic with a more recent understanding that many of these
processes—defined as modifications to DNA struc- outcomes result from common pathways that have
ture that do not alter DNA sequence—provide shared genetic underpinnings and biological cor-
molecular bases through which genes and environ- relates that originate early in life (Insel, 2014).
ments interact to affect behavioral development Emotion dysregulation is a trait that appears to
(Bird, 2007). Epigenetic processes provide mecha- predate the emergence of many psychiatric disor-
nistic links between environmental influences and ders. Emotion dysregulation often emerges early in
gene expression (Boyce & Kobor, 2015). The science childhood, has measurable biological correlates, and
of epigenetics, especially as it applies to the etiology is often transmitted across generations (Beauchaine,
of psychopathology, has garnered considerable Crowell, & Hsiao, 2015; Buckholdt, Parra, & Jobe-
interest in recent years due to the possibility that Shields, 2014). We argue that studying the epig e
epigenetic processes may contribute to etiopatho- netic foundations of emotion dysregulation will
physiologies of psychiatric disorders including illuminate measurable and potentially malleable
addiction, attention-deficit/hyperactivity disorder pathways that can be targeted for intervention. By
(ADHD), autism spectrum disorder (ASD), bipolar focusing on epigenetic pathways rather than single
disorder, major depression, posttraumatic stress genes, we may be able to reduce disease burden for
221
a wide range of psychiatric conditions for which Histone modification occurs when histone proteins
emotion dysregulation is a central feature. Here we bind to molecules in the cell, which causes the DNA
examine a subset of biological pathways that give to uncoil, creating an open chromatin structure
rise to physiological dysregulation among individu- (Moore, 2015). Transcription factors are proteins
als who exhibit emotion dysregulation. Currently, that translate genetic information gathered from the
there are two common methods for studying epige DNA itself (A, C, T, G) to messenger RNA. This
netic associations with psychological constructs: process is called transcription and is the first step in
candidate epigenetic and epigenome-wide associa- transformation of genes to proteins. Transcription
tion studies. We briefly discuss the merits and limi- factors are critical links for understanding how
tations of these approaches and suggest a more epigenetic processes affect phenotypes. A central hy-
novel pathway-oriented method for analyzing epi pothesis of epigenetic research is that transcription
genetic bases of emotion dysregulation. We focus factor binding sites on a gene, which tend to be in
specifically on the dopamine system, the serotonin areas of the gene where many cytosines and gua-
system, and the limbic-hypothalamic-pituitary- nines cluster together, are critical for uncovering
adrenal (L-HPA) axis—all of which are implicated how environmental events induce (i.e., “regulate,”
in emotion dysregulation. When relevant, we also “activate,” “turn on,” “silence”) gene expression. When
discuss other neurotransmitter systems. DNA uncoils, transcription factors become more
accessible, thereby increasing expression of the gene
Epigenetics (Jones, 2012). Histone modification is unstable and
Epigenetic processes are studied by extracting seems to fluctuate randomly (Wang et al., 2012).
DNA and examining chemical modifications that These modifications are difficult to study in humans
reside “above” (epi) the DNA itself (genetic). because of this instability, so they are not examined
Nuclei of all cells contain chromosomes composed often in human behavioral epigenetic research.
of DNA. DNA sequence is set at conception and, Genomic imprinting is a regulatory mechanism
in the absence of an extreme environmental event that leads to imbalanced expression of one or more
(e.g., radiation exposure), does not change. DNA among about 400 genes (Baran et al., 2015). In this
comprises a sugar and phosphate molecule and case, rather than epigenetics acting as an environ-
four nucleotides: adenine, thymine, cytosine, and mentally induced alteration of gene structure, the
guanine (A, T, C, G). These are arranged in base alteration is inherited. In both cases, molecular in-
pairs (e.g., TA, GC), which form rungs of the formation is telling the DNA information to act
DNA double helix. Single nucleotide polymor- differently depending on the cell type in which it is
phisms (SNPs) are DNA sequence variations that manifest (Greally, 2018). Modification occurs in
occur when nucleotide base pairs differ between either DNA or histones of one parental gamete
members of a species (see Figure 16.1). Active genes (maternal or paternal), which results in the opposite
code for expression of different proteins, which parental gene copy being expressed (Barlow &
affects structural and functional outputs of diverse Bartolomei, 2014). In some cases, the extent of ex-
body systems. These structural and functional pression depends on the gene’s parental origin. For
outputs (e.g., height, mood, personality) make up example, a gene inherited from the mother may be
observable phenotypes. Thus, DNA is an instruction fully expressed, but when the same gene is inherited
manual for our bodies. from the father, it is partly expressed (Flint, 1992).
If extended, DNA from a single human cell Disease severity may therefore vary, depending on
(double helix) would be about three meters long— which parent the gene is inherited from. For exam-
the length of a car. For DNA to fit within each ple, when an individual inherits Huntington’s dis-
nucleus, it is wound tightly around proteins called ease from his or her father, age of onset is much
histones (Carey, 2013). This complex of DNA and earlier than when inherited from his or her mother
histone proteins makes up chromatin (Moore, 2015). (Bird, Caro, & Pilling, 1974; Boehnke, Conneally,
A change in chromatin structure, called chromatin & Lange, 1983; Myers, Madden, Teague, & Falek,
remodeling, forms the basis for a wide range of epi- 1982; Newcombe, Walker, & Harper, 1981). In
genetic mechanisms, the three most common being many genes, chromosomes that come from the
histone modification, genomic imprinting, and DNA mother or the father are indistinguishable. However,
methylation (Lester, Marsit, Conradt, Bromer, & there are cases where epigenetic marks distinguish
Padbury, 2012). chromosomes as coming from a female or a male.
222 Epigenetic Foundations of Emotion Dysregul ation

Figure 16.1 Illustration of a single nucleotide polymorphism (SNP) within the DNA double helix. A = adenine, T = thymine,
C = cytosine, G = guanine.
Ayday, E., De Cristofaro, E., Hubaux, J-P., & Tsudik, G. (2013). The chills and thrills of whole genome sequencing. Computer.
doi:10.1109/MC.2013.333.
These chromosomes do not function in the same promoter region of a gene, where gene expression
way. For example, the first developmental disorder is controlled. The promoter is a region of DNA
to be recognized as fundamentally epigenetic was that is involved in transcription, and it is marked
Prader-Willi syndrome, which is conferred through by a particular sequence of nucleotides. Cytosine
a missing segment on the 15th paternal chromo- and guanine clusters are called CpG sites (for
some. This area normally produces important small cytosine–phosphate–guanine). Regions on the gene
nuclear RNAs (snRNAs), and without this section, with several clusters of CpG sites are called CpG
these snRNAs are not produced. In typically devel- islands. DNA methylation occurs when a methyl
oping individuals, the corresponding segment on group attaches to a cytosine that is part of this
the maternal chromosome is imprinted and, thus, CpG site. Consequently, addition of this methyl
not expressed. When the paternal gene is not pres- group in the context of a CpG island usually blocks
ent, the maternal gene is unavailable to compensate gene transcription, thereby inhibiting activity of the
for the missing paternal one (Moore, 2015). Histone gene (Charney, 2012). It is important to note that
modification and genomic imprinting are important DNA methylation does not always lead to “gene
epigenetic mechanisms that have been understudied silencing.” When DNA methylation takes place on
in the behavioral epigenetics literature relative to regions other than the promoter, such as the gene
DNA methylation. body, gene expression may be stimulated.
To understand DNA methylation, it is important The assumption that DNA methylation results
to note that nucleotides (A, T, C, G) do not cluster in durable changes to human behavior is tenuous.
randomly on a gene. Rather, C tends to precede G In fact, we do not expect that individual differences
in repetitive patterns that typically occur in the in DNA methylation in one or even 20 CpG sites
Brown, Conradt, and Crowell 223

will “cause” or “promote” development of complex early experiences (Meaney, 2004; Moore, 2015;
behavioral phenotypes such as emotion dysregulation. Weaver et al., 2004). These and other studies using
In many studies of associations between DNA diverse stress paradigms demonstrated that rat pups
methylation and behavior, the particular methylation exposed to stress either in utero or early in life
site is in an area nowhere near a transcription factor exhibited epigenetically induced alterations in do-
binding site (Boyce & Kobor, 2015). How, then, pamine D2 and D3 receptor availability, serotonin
could DNA methylation inhibit gene expression 5-HT1A messenger RNA levels, 5-HT1A receptor
and protein production? In many instances, DNA binding, and nerve growth factor NGF1-A transcrip-
methylation has little functional importance. tion binding, among other effects (see Beauchaine,
Nevertheless, it is plausible that when DNA meth- Neuhaus, Zalewski, Crowell, & Potapova, 2011).
ylation occurs in a set of genes regulating biological The first authors to partially translate such
pathways, these biological pathways are altered, which research to humans were Oberlander et al. (2008).
in turn may affect susceptibility to disease in partic- They found that pregnant women who experienced
ular environmental contexts. This hypothesis—that more stress in their third trimester of pregnancy had
functional epigenetic pathways contribute to complex infants with increased methylation of NR3c1. This
behavioral outcomes—capitalizes on advantages of increased methylation was associated with height-
both candidate epigenetic and epigenome-wide ened salivary cortisol stress responses from infants at
association research (Conradt, Adkins, Crowell,
age three months (Oberlander et al., 2008). This
Kobor, & Monk, 2018). landmark study stimulated much interest for fur-
ther investigations into epigenetic mechanisms of
Behavioral Epigenetics: History of the Field behavior. The science of epigenetics as it relates to
In the 1940s, Waddington introduced the term human behavior has evolved considerably since.
epigenetics to describe interactions between genes
and their products (a protein or RNA), which give Behavioral Epigenetics: Current State
rise to phenotypes. He argued that genes must be of the Field
expressed differently depending on environmental Two common methods of studying epigenetic
conditions. This interpretation was important be- processes include candidate epigenetic studies and
cause he connected genetic expression to environ- epigenome-wide association studies (EWASs). To
mental influences, which then determine individual date, a majority of studies in the human literature
features (Moore, 2015). A reinterpretation of this are candidate epigenetic (Lester, Conradt, & Marsit,
definition by D. L. Nanney in the 1950s was the 2016). This method focuses on one or two genes
first to associate epigenetics with cellular memory. It that are theorized to be associated with a certain
was this interpretation that Arthur Riggs and Robin mechanism or outcome. Such studies begin with a
Holliday referred to in the 1970s as they examined priori hypotheses about environmental influences
DNA methylation following cell replication (Greally, and how these environmental influences and gene
2018). Early understanding of epigenetic mechanisms function may affect later behavior (Keating, 2016).
was focused on cell differentiation or specialization. For example, because the glucocorticoid system is
Specifically, all cells contain DNA that is virtually (1) intricately involved in human stress responding
identical, and epigenetic processes determine that and (2) functionally affected by stress exposure,
cells in skin become skin cells rather than lung glucocorticoid genes are reasonable candidates for
tissue cells (Carey, 2013). epigenetic study (e.g., Reul et al., 2015).
Early experimental work on epigenetics was Accordingly, one of the most widely studied can-
conducted primarily with rats. For example, Meaney didate genes in epigenetics research is NR3c1, the
and colleagues (e.g., Champagne, Francis, Mar, & glucocorticoid receptor gene. The glucocorticoid re-
Meaney, 2003; Liu et al., 1997) examined effects of ceptor is expressed in almost every cell in the body
early experience on later stress reactivity. They and is involved in L-HPA axis regulation. This recep-
noticed that some rat mothers spend more time tor gene binds to cortisol, a stress hormone. When
licking, grooming, and arch-backed nursing their NR3c1 is methylated, it blocks receptor binding,
pups, and that pups exposed to low levels of lick- resulting in more circulating cortisol in the blood-
ing, grooming, and nursing in the first 10 days of stream. Increased methylation of NR3c1 is implicated
life did not tolerate stressors as well as pups that in a variety of disorders associated with emotion
were raised by mothers who engaged in higher rates dysregulation, although findings are inconsistent.
of these behaviors. Thus, rat behavior is affected by For example, increased (Nantharat, Wanitchanon,

Amesbutr, Tammachote, & Praphanphoj, 2015) norepinephrine, serotonin, and dopamine systems,
and decreased (Na et al., 2014) methylation of given their relevance to behavior and emotion dys-
NR3c1 are reported among adults with depression, regulation—especially in contexts of environmental
and other studies find no association (Melas et al., adversity (see, e.g., Beauchaine, Klein, Crowell,
2013). Increased methylation of NR3c1 is also asso- Derbidge, & Gatzke-Kopp, 2009; Beauchaine et al.,
ciated with borderline personality disorder among 2011; Crowell, Beauchaine, & Linehan, 2009).
those who were sexually abused in childhood Emotion dysregulation is a core feature of
(Schwarze, Hellhammer, Frieling, Mobascher, & borderline personality disorder (BPD) and other
Lieb, 2017). personality disorders (Linehan, 1987). In a large
Researchers who take a candidate epigenetic sample of treatment-seeking outpatients, Dimaggio
approach can examine specific genes thought to be and colleagues (2017) found that emotion dysregu-
implicated in the pathophysiology of a disorder of lation was a key feature of many personality disor-
interest. Yet virtually all psychiatric disorders are ders and may serve as a transdiagnostic treatment
genetically complex and multifactorial. Thus, bio- target (Dimaggio et al., 2017). Crowell and colleagues
logical pathways to disorders involve dozens and (Beauchaine et al., 2009; Crowell et al., 2009)
even hundreds of genes. Although candidate gene reviewed biological vulnerabilities to and environ-
studies can find relatively small effects, they are un- mental risk factors for development of emotion
derpowered for identifying polygenic influences dysregulation, a core dysfunction among those with
on psychopathology (see, e.g., Dick et al., 2015). BPD. Key among these biological vulnerabilities are
Candidate gene and candidate epigenetic studies abnormal responding in monoamine neurotrans-
therefore oversimplify complex determinants of mitter systems, including serotonin, dopamine, and
psychopathology—a primary motivation for the norepinephrine, as well as HPA-axis responding.
emergence of genome-wide association studies Next, we will illustrate how psychopathology is
(GWAS) and EWASs. linked to these specific biological pathways.
With EWASs, DNA methylation markers
are analyzed across over 800,000 CpG sites. This Neurotransmitter Systems
“bottom-up” method is useful for generating theo- Serotonin
ries, as the experimenter has access to a large amount Serotonin (5-HT) neurotransmission is implicated
of data and is able to examine correlations between in diverse body functions, including cognition,
experimental manipulations and the entire epig- emotion, sensory processing, motor activity, diges-
enome, sometimes described as the “methylome.” tion, and reproduction (Jacobs & Azmitia, 1992). It
However, there are limitations associated with this is found throughout the central nervous system,
technique. Because of the vast array, EWASs are and in peripheral tissues. It is expressed heavily in
generally not theory driven, and are often used to the amygdala, hypothalamus, and pituitary adrenal
explore rather than test hypotheses. When con- gland—all of which are involved in mood regula-
ducting EWASs, hundreds of thousands of association (Hood et al., 2006). Serotonin plays a major
tions are examined, which increases the likelihood role in modulating emotional states and is often im-
of false positives (Birney, Smith, & Greally, 2016). plicated in risk for emotion dysregulation. Adults
Family-wise alpha error corrections also result in with mood and anxiety disorders exhibit abnormal-
false negatives. Moreover, because of the expertise ities in serotoninergic function, and serotonin is a
needed to analyze data, EWASs may necessitate large primary target for drugs used in treating these disor-
cooperative teams of analysts (Flanagan, 2015). ders (Hariri & Holmes, 2006). Functional deficits
Nevertheless, it is currently the gold standard tech- in the central 5-HT system are related to impulsive
nique used in the behavioral epigenetic literature aggression, affective instability, and mood disorders
given the possibility of detecting newfound asso- (e.g., Kamali, Oquendo, & Mann, 2001).
ciations between phenotypes and multiple epigenetic Considerable evidence implicates 5-HT function
effects. in mood disorders, suicidal and nonsuicidal self-
We argue that the optimal way to progress with injury, and aggression. Lower levels of serotonin are
epigenetic studies of emotion dysregulation is to ex- related to higher stress reactivity in girls, which
amine a theory-driven network of epigenetic mark- could increase susceptibility to depression when
ers associated with one or more biological pathways stressful life events occur (Gotlib, Joorman, Minor,
of interest. Thus, we consider examining epigenetic & Hallmayer, 2008). Individuals with borderline
bases for functional alterations to the L-HPA axis, personality disorder and related conditions such as

suicidal and nonsuicidal self-injury show reduced imbue diminished capacity to regulate negative
5-HT expression (see Crowell et al., 2009). Direct emotions (van Roekel et al., 2017). Next, we out-
experiments with individuals diagnosed with BPD line the importance of studying epigenetic bases of
also reveal deficits in 5-HT (Coccaro, Kavoussi, 5-HT expression, and possible links to emotion
Cooper, & Hauger, 1997). Reduced central 5-HT is dysregulation.
also observed in many personality disorders charac-
terized by impulsive aggression and emotional in- DNA Methylation of the Serotonin
stability, such as borderline personality disorder Transporter Gene and Emotion
(Gurvits, Koenigsberg, & Siever, 2000). Dysregulation
Two relevant genes for the present discussion In the absence of existing data examining possible
include HTR2A and SLC6A4. HTR2A is expressed epigenetic bases for emotion dysregulation, we focus
in the placenta and encodes a serotonin receptor on pathologies for which emotion dysregulation is
subtype. Serotonin expression affects fetal develop- a core feature, such as mood disorders and BPD.
ment even before birth. Fetuses rely on maternal High methylation of SLC6A4 is associated with
and placental-derived 5-HT during early develop- reduced activity of SLC6A4 (Olsson et al., 2010;
ment, before they produce their own, thus making Philibert et al., 2008). Thus, production of 5-HT
it particularly susceptible to prenatal serotonin should be reduced. In a recent systematic review,
exposure (Paquette et al., 2013). Low levels of
Provenzi, Giorda, Beri, and Montirosso (2016)
placental serotonin are related to lower levels of found that, in 17 of the 19 studies reviewed, exposure
serotonin in the fetal forebrain (Sato, 2013). Later to early life stress such as trauma and maternal de-
in life, HTR2A expression is implicated in suicide. pression was associated with greater methylation
Furthermore, a specific polymorphism (C102T) of of SLC6A4. In the majority of studies, higher
HTR2A may be involved in susceptibility to stress- SLC6A4 methylation was related to poorer social
ful life events and suicide (Ghasemi, Seifi, Baybordi, and emotional outcomes. For example, methyla-
Danaei, & Rad, 2018). tion in children born preterm was associated with
The SLC6A4 gene encodes for the serotonin problem behavior at age seven (Chau et al., 2014).
transporter 5-HTT. 5-HTT removes 5-HT from Among adolescents, SLC6A4 methylation was
the synaptic cleft. SLC6A4 is regulated by the associated with adverse life events (van der Knaap
5-HTTLPR polymorphism (Canli & Lesch, 2007). et al., 2015). In a study of adults exposed to early
5-HTTLPR is expressed in long (l) and short (s) childhood traumatic life events, SLC6A4 methyl-
alleles, which affect individual differences in 5-HTT ation was associated with childhood abuse (Booij
expression. This polymorphism is one of the most et al., 2015).
intensely studied genetic factors in depression (van Notably, however, not all studies find associa-
Roekel, Verhagen, Engels, & Kuppens, 2017). The tions between SLC6A4 methylation and psychiatric
s allele is associated with lower 5-HTT activity and outcomes associated with emotion dysregulation.
thus faster reuptake of 5-HT compared to the l For example, null outcomes are reported between
allele. Decades of research indicate that individuals SLC6A4 methylation and anxiety and depression
with the s allele (particularly s/s homozygotes) are among adults (Booij et al., 2015; Chagnon, Potvin,
vulnerable to anxiety and depression in adulthood Hudon, & Preville, 2015), and in one study, expo-
(Caspi et al., 2003; Hariri et al., 2002; Kendler, sure to prenatal depression resulted in decreased
Kuhn, Vittum, Prescott, & Riley, 2005; Suomi, SLC6A4 methylation (Devlin, Brain, Austin, &
2006). While processing emotional stimuli, s allele Oberlander, 2010). There may be important mod-
carriers show more negative emotion expression erators that explain associations between SLC6A4
(Canli & Lesch, 2007). Short allele carriers also show methylation and emotion dysregulation, notably
(1) increased electrodermal responding while the serotonin transporter-linked polymorphism
watching aversive stimuli (Plieger et al., 2017) and 5-HTTLPR (Palma-Gudiel & Fananas, 2017).
(2) deficiencies in emotion regulation (Pezawas As reviewed previously, individuals with the
et al., 2005). Individuals at risk for depression are 5-HTTLPR s allele may be vulnerable to emotion
more likely to be s allele carriers, which is associated dysregulation. Therefore, genetic and epigenetic
with hypercortisolism (chronically high cortisol contributions are important for predicting variability
levels). Thus, the s allele, through its effects on tran- in serotonin expression (Palma-Gudiel & Fananas,
scription, expression, and function of the serotonin 2017). Greater methylation of SLC6A4 in response to
transporter (Hariri & Holmes, 2006), appears to stress is associated with vulnerability to psychiatric

disorders such as major depressive disorder, occurs upon presentation of reward cues—prior to
posttraumatic stress disorder, bipolar disorder, sui- reward delivery (see Schultz, 2010). Thus, DA sig-
cidal behaviors, and alcohol dependence, but in nals are essential for associative learning and other
many cases, only in carriers of the s allele (Palma- stimulus-response contingencies (e.g., Berridge &
Gudiel & Fananas, 2017). In a longitudinal study of Robinson, 1998; Wise, 2004). Despite partly disso-
adults who were adopted domestically into middle- ciable functions, the mesolimbic and mesocortical
class families as children, the s allele, combined with systems are sometimes referred to collectively as the
low levels of methylation of 5-HTTLPR, predicted mesocorticolimbic pathway.
unresolved loss/trauma symptoms. In contrast, the s Given its role in generating approach-related
allele, combined with high levels of methylation emotions, DA plays an important role in mood
of 5-HTTLPR, was associated with low levels of regulation and affective responding. Low tonic DA
unresolved loss/trauma (van Ijzendoorn, Caspers, in striatal structure activity is associated with negative
Bakermans-Kranenburg, Beach, & Philibert, 2010). affect and trait irritability (Laakso et al., 2003).
It is important to emphasize that we cannot infer Decreased phasic DA responding in striatal regions
direction of effect from this literature. It is therefore is associated with anhedonia—a hallmark of
unclear whether SLC6A4 methylation is associated depression—and a symptom of several other psy-
etiologically with emotion dysregulation or is chiatric disorders (Forbes & Dahl, 2012; Zisner &
a sequel of emotion dysregulation. Studies exam- Beauchaine, 2016). In contrast, increased dopamine
ining DNA methylation pre- and posttreatment has been associated with mania (Park & Kang,
in responders and nonresponders are warranted. 2013). Disruptions in DA modulation may elicit
Furthermore, given the complexity of the emotion other mood-related pathologies, including schizo-
dysregulation phenotype, it is critical that we inter- phrenia (Grace, 2016). Impaired functioning of
rogate additional biological systems associated with neural circuits involved in motivation and positive
its etiology, including the dopamine (DA) system. behavior reinforcement may also lead to emotion
dysregulation (Friedel, 2004). Beauchaine and col-
Dopamine leagues (2017) have reviewed compelling evidence
DA is also implicated in emotion dysregulation of an association between deficient mesolimbic
(Crowell et al., 2009). The brain contains several dopamine responding and vulnerability to all

DA pathways, including the nigrostriatal, the meso- externalizing behaviors, such as attention-deficit/
limbic, the mesocortical, and the tuberoinfundibu- hyperactivity disorder, antisocial personality disorder,
lar (Kopinathan, Scammells, Lane, & Capuano, conduct disorder, oppositional defiant disorder, and
2016). These pathways are involved in diverse and substance use disorder. They argue that deficient
often overlapping functions ranging from executive mesolimbic dopamine responding leads to psycho-
control and attention to movement, speech, logical states such as irritability and discontentment,
emotional responding, and reward processing.
which give rise to hyperactivity and impulsivity as a
Dopamine pathways that underlie reward processing means of behaviorally upregulating an aversive
and associated approach emotions (e.g., wanting, emotional state. The combination of these emo-
seeking, enthusiasm) include the mesolimbic and tional states and behaviors with environmental risk
mesocortical DA systems. The mesolimbic system, factors and socialization processes serves to increase
including projections from the ventral tegmental the probability of emotion dysregulation through-
area to the nucleus accumbens and other parts of out development (Beauchaine et al., 2017).
the ventral striatum, is often referred to as the pri- One of the most studied genes in connection
mary reward pathway. Mesolimbic DA neurons fire with psychiatric disorders is DRD4, a dopamine
in response to natural reinforcers and virtually all receptor. It influences the postsynaptic action of
drugs of abuse (see Koob, Arends, & Le Moal, dopamine and is involved in several neurological
2014). This system projects forward to the mesocor- processes. It confers vulnerability to several psychi-
tical system (Russo & Nestler, 2013), which plays an atric conditions, including schizophrenia, bipolar
important role in valuing reward magnitudes, and in disorder, ADHD, addiction, and anorexia (Ptáček,
exerting top-down executive control over approach- Kuželová, & Stefano, 2011). The SLC6A3 gene en-
related emotions (see Beauchaine & Thayer, 2015). codes for a dopamine transporter (DAT1). The
The mesolimbic system exhibits phasic DA neural 9-repeat allele polymorphism of DAT1 is also asso-
responding to novel reinforcers; however, once rein- ciated with depression among adults diagnosed with
forcement contingencies are learned, DA release BPD across two independent samples (Joyce et al.,

2006). This same polymorphism has been linked to or perceived—hypophysiotrophic neurons secrete
other externalizing behavior including alcohol abuse corticotropin-releasing factor (CRF), the primary
and conduct disorder (Bau et al., 2001). Notably, regulator in the L-HPA axis. CRF binds to receptors
several other genes that affect DA neurotransmis- on the anterior pituitary gland, triggering release of
sion confer vulnerability to externalizing disorders adrenocorticotrophic hormone (ACTH; Smith &
(e.g., other DA receptors, monoamine oxidase A), Vale, 2006). This, in turn, stimulates the synthesis
which are often characterized by emotion dysregula- and release of cortisol, which indexes physiological
tion (Gizer, Otto, & Ellingson, 2016). responses that facilitate coping with, reactions to,
and recovery from the stressful situation (McEwen,
Epigenetic Bases of Dopamine and 2004). Downstream effects of cortisol release in-
Emotion Dysregulation clude anti-inflammatory and immunosuppressive
It is likely that epigenetic alterations in DA gene responses (Oakley & Cidlowski, 2011), coordina-
expression affect reward processing (Russo & Nestler, tion of the sleep–wake cycle, and enhanced learning
2013). One candidate is DRD4, a dopamine recep- and memory processing (Watson & Mackin, 2006).
tor gene associated with novelty seeking (Kluger, However, repeated activation of the L-HPA axis in-
Siegfried, & Ebstein, 2002) and executive function duces strain on biological systems, resulting in in-
(Froehlich et al., 2007; Gilsbach et al., 2012). It is creased likelihood of disease, lowered cognitive
also implicated in disorders in which emotion function, and psychopathology (Juster et al., 2011;
dysregulation is common, including schizophrenia, Koss & Gunnar, 2018; Suor, Sturge-Apple, Davies,
bipolar disorder, externalizing disorders, and addic- Cicchetti, & Manning, 2015).
tive behaviors (e.g., Gizer et al., 2016). In theory, Ordinarily, the L-HPA axis operates within
DRD4 methylation should be associated with fewer homeostatically defined bounds. However, repeated
DA receptors and, in turn, more DA in the ventral overactivation alters homeostatic set-points, result-
tegmental area, nucleus accumbens, and prefrontal ing in new, allostatically defined operating ranges
cortex. (McEwen, 2017). This process—often referred to as
Much of the literature on epigenetic regulation allostatic load—is observed among those who incur
of DRD4 is focused on children with ADHD. In a child maltreatment and other forms of early life ad-
relatively large (N = 426) sample of children in the versity (Koss & Gunnar, 2018; Suor et al., 2015).
Netherlands, decreased methylation of DRD4 at These children often show blunted cortisol responses
birth was related to symptoms of ADHD (van Mil well into adulthood. In contrast, other psychiatric
et al., 2014). On the other hand, in a sample of 330 disorders are characterized by elevated L-HPA axis
children, increased DRD4 methylation was related reactivity (Keller et al., 2017; Watson & Mackin,
to greater cognitive/attentional problems in chil- 2006). Moreover, higher levels of corticotropin-
dren with ADHD (Dadds, Schollar-Root, Lenroot, releasing hormone (CRH) are found in hypothal-
Moul, & Hawes, 2016). Less methylation of DAT1, ami of patients with mood disorders. L-HPA axis
or SLC6A3, a dopamine transporter, was related to dysfunction is observed in major depressive disorder,
improvements in pharmacological (methylpheni- obesity, bipolar disorder, chronic fatigue syndrome,
date) treatment response in children with ADHD self-injury, and suicide (Beauchaine, Crowell, &
(Ding et al., 2017). Thus, children with ADHD and Hsiao, 2015; Coryell & Schlesser, 2001; Watson &
low DAT1 methylation levels responded better to Mackin, 2006).
methylphenidate. No associations between DRD4
methylation and treatment response were found, Epigenetic Bases of Limbic-Hypothalamic
although other studies have been mixed regarding Pituitary Adrenal Axis Function and
associations between DRD4 and ADHD. Emotion Dysregulation
There are a number of genes implicated in L-HPA
Limbic-Hypothalamic Pituitary axis function. Three candidate genes have been
Adrenal Axis studied in the emotion dysregulation literature. The
The L-HPA axis is a collection of functionally inter- NR3c1 gene codes for the glucocorticoid receptor.
connected structures including the hypothalamus, High levels of DNA methylation of NR3c1 result in
paraventricular nucleus, adrenal pituitary, and fewer glucocorticoid receptors in the hippocampus.
adrenal glands. The L-HPA axis serves to coordinate Because binding of cortisol to these receptors helps
and regulate stress responding (Smith & Vale, “turn off” the L-HPA axis, fewer glucocorticoid re-
2006). When stress is detected—whether real ceptors results in greater circulating cortisol and

greater cortisol reactivity (Turecki & Meaney, 2016). that interact with environmental risk and adversity
Increased methylation of NR3c1 in infants at birth is across development. This applies to behaviors
associated with increased salivary cortisol at three including anger, frustration, conduct prob-

months (Oberlander et al., 2008) and five months lems, aggression, delinquency, and oppositional-
(Conradt et al., 2015). Among humans, hypermeth- ity (Beauchaine et al., 2017; Deater-Deckard,
ylation of NR3c1 is associated with impaired L-HPA Petrill, & Thompson, 2007).
axis function, which may increase vulnerability to After reviewing the literature and current theory
major depression, borderline personality disorder, to identify biological pathways of interest, the next
and other psychiatric conditions (Palma-Gudiel, step is to generate a list of all possible genes, epig e
Cordova-Palomera, Leza, & Fananas, 2015). netic markers, and neurotransmitter systems in-
An important modulator of glucocorticoid activity volved. This can be accomplished through PubMed
is FKBP5. The FKBP5 gene is regulated through searches and should include any regulatory regions
interactions between environmental stressors and of genes that are expected to be involved in gene
epigenetic modifications to genomic sites that are expression, including promoters and enhancers.
glucocorticoid responsive (Zannas, Wiechmann, There are also databases that can be interrogated to
Gassen, & Binder, 2016). In a study of the victims investigate genes that regulate the expression of
of the World Trade Center attacks, Yehuda and other genes, such as GeneMania (Warde-Farley et al.,
colleagues (2009) found that FKBP5 expression is 2010). Next, EWAS is conducted, providing a longer
reduced among those with posttraumatic stress list of every site that shows an association with the
disorder (PTSD). They also found increased meth- targeted neural system/pathway. From there, a
ylation of FKBP5 in Holocaust victims compared shorter list can be generated using machine learning
to controls. However, interestingly, offspring of techniques that can best predict function of the
Holocaust survivors exhibited less methylation than targeted biological pathway. Machine learning

controls. Victims and the victims’ offspring’s meth- techniques allow preliminary gene selections to be
ylation levels were correlated, suggesting potential supplemented with other regions that are associated
intergenerational epigenetic transmission in the with the pathway of interest. Once this list is com-
children of highly traumatized victims. plete, bioinformatics approaches can be used to ex-
Prenatal exposure to maternal mood disorders amine associations between epigenetic regulation of
(e.g., anxiety and depression) is associated with ele- the neural systems and expression of emotion dys-
vated methylation of 11-beta hydroxysteroid dehy- regulation (Conradt et al., 2018).
drogenase type 2 (11β-HSD2; Glover, 2014). DNA It is important to take a new, innovative ap-
methylation is believed to suppress the activity of proach to studying epigenetics (Lee & Sawa, 2014).
this gene (Seckl & Holmes, 2007). 11β-HSD2 con- As this field is in an emergent stage, so is the ap-
verts maternal cortisol to inert cortisone once ma- proach to analysis. Studying these systems using a
ternal cortisol passes through the placenta. An im- pathway-focused approach is both novel and im-
portant function is to regulate the amount of portant. It involves taking the strengths of both the
cortisol to which fetuses are exposed (Glover, 2014). candidate genetics and EWAS approaches and com-
With less of this enzyme to provide a barrier, fetuses bining them into a hybrid: a new way of studying
are exposed to higher levels of maternal cortisol, epigenetics that is driven by theory while capitaliz-
even if maternal cortisol levels remain constant. ing on advances in the field. Associations between
emotion dysregulation and gene expression will not
A Pathway Approach to Epigenetics be simple (i.e., attributable to one gene or even a
of Emotion Dysregulation cluster of genes). Rather, epigenetic changes to
Most epigenetic studies of genes associated with DA functionally interdependent biological pathways
and 5-HT neurotransmission focus on candidate ef- will underlie emotion dysregulation. To move the
fects. As noted previously, development of emotion field forward, we need to focus on specific gene net-
dysregulation and related traits is complex and most works and their functional interactions.
likely does not originate from a single CpG site or To be clear, epigenetic effects are unlikely to
set of sites. Our proposed method of studying explain all of emotion dysregulation. For example,
epigenetics of emotion dysregulation is based on some variance in emotion dysregulation may be
theory and evidence of related biological pathways simply attributable to genetic code. Even if epig enetic
(Allen et al., 2010). Research suggests that emotion studies identify a strong connection between a bio-
dysregulation stems from genetic vulnerabilities logical pathway and a disorder related to emotion

dysregulation, we must acknowledge that this will with oxygen transport. We now have statistical
not explain everything about the disorder. In addi- methods to control for cell type in blood, buccal,
tion, Genetic × Epigenetic interactions may help to and placental samples (Houseman et al., 2012), but
explain variation in emotion dysregulation. this control is rarely used in behavioral epigenetic
research. Some studies do examine DNA methyla-
Unresolved Controversies and Challenges tion differences in the brains of deceased adults
to the Study of Epigenetics (McGowan et al., 2009). These postmortem studies,
Leveraging the science of epigenetics to study devel- however, are also impacted by the cell type concern
opment of emotion dysregulation can yield fruitful since the brain consists of a mixture of cell types in-
results, but there are inherent challenges. These including astrocytes, oligodendrocytes, and microglia.
clude the need for: normative developmental studies, Some evidence suggests that we can reliably index
justification for tissue type sampled, recognition of methylation changes system-wide (Szyf & Bick,
genetic variability, independent replication, and re- 2013). Studies demonstrate similar methylation pat-
search designs that come closer to inferring causality. terns across tissues systems: across brain and blood
(Auta et al., 2013) and across blood and saliva (Rosas
Need for Normative Developmental Studies et al., 2001). However, other researchers find small
DNA methylation accrues naturally over time. In a or nonsignificant correlations in CpG sites within
formative study, Fraga et al. (2005) examined changes candidate genes that were relevant to the experi-
in DNA methylation among monozygotic twins in ment (Smith et al., 2014). Similarly, Walton and
a cohort ranging in age from 3 to 74 years. In early colleagues (2016) demonstrated a .08 correlation of
life, the methylomes of each twin pair were almost methylated CpG sites between blood and brain
indistinguishable, but as the pairs aged, there were cells, which was a significant amount (more than a
greater differences in DNA methylation and histone chance expectation). However, this is not a large
acetylation, which in turn affected gene expression enough correlation that blood methylation could be
(Fraga et al., 2005). This was a cross-sectional cohort, used to reliably predict brain methylation (Walton
and because of the dearth of longitudinal studies, et al., 2016).
we still know very little about the typical trajectory In spite of these limitations, progress continues.
of DNA methylation. For example, little is known Recent improvements in DNA methylation profil-
about normative epigenetic changes across the ing technology show promising results. Forest and
lifespan: it would be especially helpful to identify colleagues (2018) obtained data from two studies, at
potential sensitive developmental periods. Rodent multiple time points, and across three tissue types
studies have shown that experiences during certain (buccal epithelial cells, whole blood, and finger-
sensitive windows of time have influenced patterns prick dried blood spots). Using EWASs and the
of development, which can lead to certain behavioral Illumina 450 K array, they found significant stabil-
outcomes (Roth & Sweatt, 2011). These studies have ity across these tissue types. Smith and colleagues
yet to be replicated with human subjects. Identifying conducted research examining differences between
these normative patterns is important if we are to tissue types and interindividual variation in gene
recognize patterns associated with psychopathology regulation. They emphasize the need for further ex-
or stressful life trajectories. ploration and characterization of the genome as far
as biomarker development to facilitate population-
Tissue Type based studies of disease (Smith, Hanson, Norton,
To date, most epigenetic studies with humans have Hollingshaus, & Mineau, 2014). They conclude
inferred that epigenetic processes were occurring in that although methylation is often tissue specific,
the brain by using peripheral tissue, such as placenta, there are also times that peripheral tissue can be
buccal cells, or blood. The assumption that chroma- useful. We feel that we can learn from information
tin marks that are found in peripheral tissues will gathered, even with its flaws, provided we under-
also be found in central tissues causes unease with stand these flaws and work to find evidence to sup-
some researchers (Boyce & Kobor, 2015). A consist- port our findings.
ent concern raised is that these tissue types include a
mixture of different cell types. In blood, for example, Genetic Contributions
it may be that methylation in leukocyte cells associ- Genetic factors contribute to individual differences
ated with immune responding is a confounding effect and transgenerational inheritance of DNA methyl-
of methylation in erythrocytes, which are associated ation. McRae and colleagues (2014) demonstrate

genetic heritability accounts for the majority of the epigenetic effects of natural disaster. For example,
similarities in DNA methylation. They also showed Project Ice Storm examined a severe ice storm in
that, of all individual differences found in DNA Quebec, the worst natural disaster in Canada’s his-
methylation, approximately 20% are caused by se- tory. Researchers followed a group of children
quence variation that is not located at the CpG whose mothers were pregnant during this storm and
sites (McRae et al., 2014). Twin studies reveal that found that exposure to stress—based on both objec-
DNA methylation is heritable near promoter re- tive and subjective appraisals—was related to DNA
gions (Kaminsky & Petronis, 2009). A growing methylation of genes involved in type 1 and type 2
body of literature also examines Genetic × Epigenetic diabetes in children 13 years later (Cao-Lei et al.,
interactions. For instance, DNA methylation of 2015) and alterations in immune system function
NR3c1 interacted with a common single nucleotide (Cao-Lei et al., 2014). These types of “natural ex-
polymorphism to predict attention in newborns. periments” allow for inference regarding causal effects
This illustrates an interaction between a genetic of environmental exposures on DNA methylation,
susceptibility and methylation, which was associ- particularly if DNA methylation is assessed prior to
ated with neurobehavioral outcomes (Bromer, the natural exposure.
Marsit, Armstrong, Padbury, & Lester, 2013). It is
possible, therefore, that the inconsistencies ob-
Conclusion
served in the epigenetic literature may be due to
Initial behavioral epigenetic studies, focused prima-
genetic variability.
rily on candidate epigenetic research, have “given
the gene a lifespan” (Lappe & Landecker, 2015,
Independent Replication p. 152). There is evidence that the epigenome
With the exception of a few recent meta-analyses changes with environmental inputs across the life
(Turecki & Meaney, 2016), the behavioral epig enetic course, which raises the possibility that epigenetic
literature suffers from a lack of replication studies marks may portend development of disease.
conducted in independent laboratories. Many epi- Discovering the role of epigenetic mechanisms in
genetic studies are susceptible to type I error. The risk for emotion dysregulation is an important goal,
field is plagued by low sample sizes and small effect given that this information could illuminate etiology
sizes, making replication unlikely. It is especially im- (e.g., as a mediator of early life stress on adverse out-
portant that we replicate findings if we seek to use comes) and identify who may be most susceptible to
epigenetic biomarkers as indicators of exposure to developing problems with emotion regulation (e.g.,
stress or treatment response. If the goal is to use this as a moderator of the association between early life
information to alleviate human suffering, replica- stress and emotion dysregulation). However, there is
tion is necessary before extensions to intervention a need to refine our assessments of how early expo-
work can be made. sures become biologically embedded via epigenetic
processes to increase risk for emotion dysregulation.
Causality Assumptions As the field stands, the overreliance on candidate
Most of the behavioral epigenetic work is based on epigenetic studies and the relative inaccessibility of
associations between DNA methylation phenotypes GWASs calls for a pathway-focused method of epi
of interest. To come closer to inferring causality, genetic analysis. The application of this method to
researchers could include DNA methylation in in- the etiology of emotion dysregulation could result
tervention research with random assignment of par- in novel therapeutic targets to prevent or alleviate
ticipants. Epigenetic data are currently being used suffering.
in intervention designs, notably in research with
African American males by Brody and colleagues
(2015). Greater levels of parent depressive symp- References
Allen, H. L., Estrada, K., Lettre, G., Berndt, S. I., Weedon,
toms at age 11 were related to accelerated epigenetic M. N., Rivadeneira, F., . . . Ferreira, T. (2010). Hundreds of
aging for children in a control, but not for children variants clustered in genomic loci and biological pathways
in a family-centered prevention program. These re- affect human height. Nature, 467, 832.
sults suggest that epigenetic processes are plastic and Auta, J., Smith, R. C., Dong, E., Tueting, P., Sershen, H., Boules,
S., . . . Guidotti, A. (2013). DNA-methylation gene network
amenable to treatment effects, though further re-
dysregulation in peripheral blood lymphocytes of
search is needed to target mechanistic questions re- schizophrenia patients. Schizophrenia Research, 150, 312–318.
lated to epigenetic processes. We can come closer to Baran, Y., Subramaniam, M., Biton, A., Tukiainen, T., Tsang,
inferring causality through research examining the E. K., Rivas, M. A., . . . Lappalainen, T. (2015). The landscape

of genomic imprinting across diverse adult human tissues. Canli, T., & Lesch, K. P. (2007). Long story short: The serotonin
Genome Research, 25, 927–936. transporter in emotion regulation and social cognition.
Barlow, D. P., & Bartolomei, M. S. (2014). Genomic imprinting Nature Neuroscience, 10, 1103–1109.
in mammals. Cold Spring Harbor Perspectives in Biology, 6, Cao-Lei, L., Dancause, K. N., Elgbeili, G., Massart, R., Szyf, M.,
a018382. Liu, A., . . . King, S. (2015). DNA methylation mediates the
Bau, C. H. D., Almeida, S., Costa, F. T., Garcia, C. E. D., Elias, impact of exposure to prenatal maternal stress on BMI and
E. P., Ponso, A. C., . . . Hutz, M. H. (2001). DRD4 and central adiposity in children at age 13 1/2 years: Project Ice
DAT1 as modifying genes in alcoholism: Interaction with Storm. Epigenetics, 10, 749–761.
novelty seeking on level of alcohol consumption. Molecular Cao-Lei, L., Massart, R., Suderman, M. J., Machnes, Z.,
Psychiatry, 6, 7–9. Elgbeili, G., Laplante, D. P., . . . King, S. (2014). DNA
Beauchaine, T. P., Crowell, S. E., & Hsiao, R. C. (2015). Post- methylation signatures triggered by prenatal maternal stress
dexamethasone cortisol, self-inflicted injury, and suicidal exposure to a natural disaster: Project Ice Storm. PLoS
ideation among depressed adolescent girls. Journal of ONE, 9, e107653.
Abnormal Child Psychology, 43, 619–632. Carey, N. (2013). The epigenetics revolution. New York, NY:
Beauchaine, T. P., Klein, D. N., Crowell, S. E., Derbidge, C., & Columbia University Press.
Gatzke-Kopp, L. (2009). Multifinality in the development of Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W.,
personality disorders: A Biology × Sex × Environment Harrington, H., . . . Poulton, R. (2003). Influence of life
interaction model of antisocial and borderline traits. stress on depression: Moderation by a polymorphism in the
Development and Psychopathology, 21, 735–770. 5-HTT gene. Science, 301, 386–389.
Beauchaine, T. P., Neuhaus, E., Zalewski, M., Crowell, S. E., & Chagnon, Y. C., Potvin, O., Hudon, C., & Preville, M. (2015).
Potapova, N. (2011). The effects of allostatic load on neural DNA methylation and single nucleotide variants in the
systems subserving motivation, mood regulation, and social brain-derived neurotrophic factor (BDNF) and oxytocin
affiliation. Development and Psychopathology, 23, 975–999. receptor (OXTR) genes are associated with anxiety/
Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as depression in older women. Frontiers in Genetics, 6, 230.
a transdiagnostic biomarker of psychopathology. International Champagne, F. A., Francis, D. D., Mar, A., & Meaney, M. J.
Journal of Psychophysiology, 98, 338–350. (2003). Variations in maternal care in the rat as a mediating
Beauchaine, T. P., Zisner, A. R., & Sauder, C. L. (2017). Trait influence for the effects of environment on development.
impulsivity and the externalizing spectrum. Annual Review of Physiology & Behavior, 79, 359–371.
Clinical Psychology, 13, 343–368. Charney, E. (2012). Behavior genetics and postgenomics.
Berridge, K. C., & Robinson, T. E. (1998). What is the role of Behavioral and Brain Sciences, 35, 331–410.
dopamine in reward: Hedonic impact, reward learning, or Chau, C. M., Ranger, M., Sulistyoningrum, D., Devlin, A. M.,
incentive salience? Brain Research Reviews, 28, 309–369. Oberlander, T. F., & Grunau, R. E. (2014). Neonatal pain
Bird, A. (2007). Perceptions of genetics. Nature, 447, 396–398. and COMT Val158Met genotype in relation to serotonin
Bird, E. D., Caro, A. J., & Pilling, J. B. (1974). A sex related transporter (SLC6A4) promoter methylation in very preterm
factor in the inheritance of Huntington’s chorea. Annals of children at school age. Frontiers in Behavioral Neuroscience,
Human Genetics, 37, 255–260. 8, 409.
Birney, E., Smith, G. D., & Greally, J. M. (2016). Epigenome- Coccaro, E. F., Kavoussi, R. J., Cooper, T. B., & Hauger, R. L.
wide association studies and the interpretation of disease- (1997). Central serotonin activity and aggression: Inverse
omics. PLoS Genetics, 12, e1006105. relationship with prolactin response to d-fenfluramine, but
Boehnke, M., Conneally, P. M., & Lange, K. (1983). Two models not CSF 5-HIAA concentration, in human subjects.
for a maternal factor in the inheritance of Huntington American Journal of Psychiatry, 154, 1430–1435.
disease. American Journal of Human Genetics, 35, 845–860. Conradt, E., Adkins, D., Crowell, S. E., Monk, K., & Kobor,
Booij, L., Szyf, M., Carballedo, A., Frey, E. M., Morris, D., M. S. (2018). An epigenetic pathway approach to
Dymov, S., . . . Frodl, T. (2015). DNA methylation of the investigating associations between prenatal exposure to
serotonin transporter gene in peripheral cells and stress- maternal mood disorder and newborn neurobehavior.
related changes in hippocampal volume: A study in depressed Development and Psychopathology, 30, 881–890.
patients and healthy controls. PLoS ONE, 10, e0119061. Conradt, E., Fei, M., LaGasse, L., Tronick, E., Guerin, D.,
Boyce, W. T., & Kobor, M. S. (2015). Development and the Gorman, D., . . . Lester, B. M. (2015). Prenatal predictors of
epigenome: The “synapse” of gene–environment interplay. infant self-regulation: The contributions of placental DNA
Developmental Science, 18, 1–23. methylation of NR3C1 and neuroendocrine activity. Frontiers
Brody, G. H., Yu, T., Miller, G. E., & Chen, E. (2015). in Behavioral Neuroscience, 9, 130.
Discrimination, racial identity, and cytokine levels among Coryell, W., & Schlesser, M. (2001). The dexamethasone
African-American adolescents. Journal of Adolescent Health, suppression test and suicide prediction. American Journal of
56, 496–501. Psychiatry, 158, 748–753.
Bromer, C., Marsit, C. J., Armstrong, D. A., Padbury, J. F., & Crowell, S. E., Beauchaine, T. P., & Linehan, M. M. (2009).
Lester, B. (2013). Genetic and epigenetic variation of the A biosocial developmental model of borderline personality:
glucocorticoid receptor (NR3C1) in placenta and infant Elaborating and extending Linehan’s theory. Psychological
neurobehavior. Developmental Psychobiology, 55, 673–683. Bulletin, 135, 495–510.
Buckholdt, K. E., Parra, G. R., & Jobe-Shields, L. (2014). Dadds, M. R., Schollar-Root, O., Lenroot, R., Moul, C., &
Intergenerational transmission of emotion dysregulation Hawes, D. J. (2016). Epigenetic regulation of the DRD4
through parental invalidation of emotions: Implications for gene and dimensions of attention-deficit/hyperactivity
adolescent internalizing and externalizing behaviors. Journal disorder in children. European Child and Adolescent Psychiatry,
of Child and Family Studies, 23, 324–332. 25, 1081–1089.

Deater-Deckard, K., Petrill, S. A., & Thompson, L. A. (2007). Glover, V. (2014). Maternal depression, anxiety and stress during
Anger/frustration, task persistence, and conduct problems in pregnancy and child outcome: What needs to be done. Best
childhood: A behavioral genetic analysis. Journal of Child Practice and Research Clinical Obstetrics and Gynaecology,
Psychology and Psychiatry, 48, 80–87. 28, 25–35.
Devlin, A. M., Brain, U., Austin, J., & Oberlander, T. F. (2010). Gotlib, I. H., Joorman, J., Minor, K. L., & Hallmayer, J. (2008).
Prenatal exposure to maternal depressed mood and the HPA-axis reactivity: A mechanism underlying the associations
MTHFR C677T variant affect SLC6A4 methylation in among 5-HTTLPR, stress, and depression. Biological Psychiatry,
infants at birth. PLoS ONE, 5, e12201. 63, 847–851.
Dick, D. M., Agrawal, A., Keller, M. C., Adkins, A., Aliev, F., Grace, A. A. (2016). Dysregulation of the dopamine system in
Monroe, S., . . . Sher, K. J. (2015). Candidate gene-environment the pathophysiology of schizophrenia and depression. Nature
interaction research: Reflections and recommendations. Reviews Neuroscience, 17, 524–532.
Perspectives in Psychological Science, 10, 37–59. Greally, J. M. (2018). A user’s guide to the ambiguous word
Dimaggio, G., Popolo, R., Montano, A., Velotti, P., Perrini, F., “epigenetics.” Nature Reviews Molecular Cell Biology, 19,
Buonocore, L., & Salvatore, G. (2017). Emotion dysregulation, 207–208.
symptoms, and interpersonal problems as independent Gurvits, I. G., Koenigsberg, H. W., & Siever, L. J. (2000).
predictors of a broad range of personality disorders in an Neurotransmitter dysfunction in patients with borderline
outpatient sample. Psychology and Psychotherapy: Theory, personality disorder. Psychiatric Clinics, 23, 27–40.
Research and Practice, 90, 586–599. Hariri, A. R., & Holmes, A. (2006). Genetics of emotional
Ding, K., Yang, J., Reynolds, G. P., Chen, B., Shao, J., regulation: The role of the serotonin transporter in neural
Liu, R., . . . Kang, C. (2017). DAT1 methylation is associated function. Trends in Cognitive Sciences, 10, 182–191.
with methylphenidate response on oppositional and Hariri, A. R., Mattay, V. S., Tessitore, A., Kolachana, B., Fera, F.,
hyperactive-impulsive symptoms in children and adolescents Goldman, D., . .
.
Weinberger, D. R. (2002). Serotonin
with ADHD. World Journal of Biological Psychiatry, 18, transporter genetic variation and the response of the human
291–299. amygdala. Science, 297, 400–403.
Flanagan, J. M. (2015). Epigenome-wide association studies Hood, S. D., Hince, D. A., Robinson, H., Cirillo, M.,
(EWAS): Past, present, and future. In M. Verma (Ed.), Christmas, D., & Kaye, J. M. (2006). Serotonin regulation
Cancer epigenetics: Risk assessments, diagnosis, treatments, and of the human stress response. Psychoneuroendocrinology, 31,
prognosis (pp. 51–63). New York, NY: Humana Press. 1087–1097.
Flint, J. (1992). Implications of genomic imprinting for Houseman, E., Accomando, W. P., Koestler, D. C.,
psychiatric genetics. Psychological Medicine, 22, 5–10. Christensen, B. C., Marsit, C. J., Nelson, H. H., . . . Kelsey,
Forbes, E. E., & Dahl, R. E. (2012). Research review: Altered K. T. (2012). DNA methylation arrays as surrogate
reward function in adolescent depression: What, when and measures of cell mixture distribution. BMC Bioinformatics,
how? Journal of Child Psychology and Psychiatry, 53, 3–15. 13, 86.
Forest, M., O’Donnell, K. J., Voisin, G., Gaudreau, H., Insel, T. (2014). The NIMH research domain criteria (RDoC)
MacIsaac, J. L., McEwen, L. M., . . . Greenwood, C. M. T. project: Precision medicine for psychiatry. American Journal
(2018). Agreement in DNA methylation levels from the of Psychiatry, 171, 395–397.
Illumina 450K array across batches, tissues, and time. Jacobs, B. L., & Azmitia, E. C. (1992). Structure and function
Epigenetics, 13, 19–32. of the brain serotonin system. Physiological Reviews, 72,
Fraga, M. F., Ballestar, E., Paz, M. F., Ropero, S., Setien, F. B., 165–229.
Heine-Suner, D., . . . Esteller, M. (2005). Epigenetic Jones, P. A. (2012). Functions of DNA methylation: Islands, start
differences arise during the lifetime of monozygotic twins. sites, gene bodies and beyond. Nature Reviews Genetics, 13,
Proceedings of the National Academy of Sciences of the United 484–492.
States of America, 102, 10604–10609. Joyce, P. R., McHugh, P. C., McKenzie, J. M., Sullivan, P. F.,
Friedel, R. O. (2004). Dopamine dysfunction in borderline Mulder, R. T., Luty, S. E., . . . Cloninger, C. R. (2006). A
personality disorder: A hypothesis. Neuropsychopharmacology, dopamine transporter polymorphism is a risk factor for
29, 1029–1039. borderline personality disorder in depressed patients.
Froehlich, T. E., Lanphear, B. P., Dietrich, K. N., Cory-Slechta, Psychological Medicine, 36, 807–813.
D. A., Wang, N., & Kahn, R. S. (2007). Interactive effects of Juster, R. P., Sindi, S., Marin, M. F., Perna, A., Hashemi, A.,
a DRD4 polymorphism, lead, and sex on executive functions Pruessner, J. C., & Lupien, S. J. (2011). A clinical allostatic
in children. Biological Psychiatry, 62, 243–249. load index is associated with burnout symptoms and
Ghasemi, A., Seifi, M., Baybordi, F., Danaei, N., & Rad, B. S. hypocortisolemic profiles in healthy workers. Psychoneuro
(2018). Association between serotonin 2A receptor genetic endocrinology, 36, 797–805.
variations, stressful life events and suicide. Gene, 658, 191–197. Kamali, M., Oquendo, M. A., & Mann, J. J. (2001).
Gilsbach, S., Neufang, S., Scherag, S., Vloet, T. D., Fink, G. R., Understanding the neurobiology of suicidal behavior.
Herpertz-Dahlmann, B., & Konrad, K. (2012). Effects of Depression and Anxiety, 14, 164–176.
the DRD4 genotype on neural networks associated with Kaminsky, Z., & Petronis, A. (2009). Methylation SNaPshot:
executive functions in children and adolescents. Developmental A method for the quantification of site-specific DNA
Cognitive Neuroscience, 2, 417–427. methylation levels. In J. Tost (Ed.) DNA methylation:
Gizer, I. R., Otto, J. M., & Ellingson, J. M. (2016). Molecular Methods and protocols (2nd ed., Vol. 507, pp. 241–255).
genetics of the externalizing spectrum. In T. P. Beauchaine & New York, NY: Humana Press.
S. P. Hinshaw (Eds.), The Oxford handbook of externalizing Keating, D. P. (2016). Transformative role of epigenetics in child
spectrum disorders (pp. 125–148). New York, NY: Oxford development research: Commentary on the special section.
University Press. Child Development, 87, 135–142.

Keller, J., Gomez, R., Williams, G., Lembke, A., Lazzeroni, L., Meaney, M. J. (2004). The nature of nurture: Maternal effects
Murphy, G. M., & Schatzberg, A. F. (2017). HPA axis in and chromatin remodeling. In J. T. Cacioppo, & G. G.
major depression: Cortisol, clinical symptomatology and Berntson (Eds.), Essays in social neuroscience (pp. 1–14).
genetic variation predict cognition. Molecular Psychiatry, 22, Cambridge: MIT Press.
527–536. Melas, P. A., Wei, Y., Wong, C. C., Sjoholm, L. K., Aberg, E.,
Kendler, K. S., Kuhn, J. W., Vittum, J., Prescott, C. A., & Mill, J., . . . Lavebratt, C. (2013). Genetic and epigenetic
Riley, B. (2005). The interaction of stressful life events and a associations of MAOA and NR3C1 with depression and
serotonin transporter polymorphism in the prediction of childhood adversities. International Journal of Neuropsycho
episodes of major depression. Archives of General Psychiatry, pharmacology, 16, 1513–1528.
62, 529–535. Mill, J., & Petronis, A. (2007). Molecular studies of major
Kluger, A. N., Siegfried, Z., & Ebstein, R. P. (2002). A meta- depressive disorder: The epigenetic perspective. Molecular
analysis of the association between DRD4 polymorphism Psychiatry, 12, 799–814.
and novelty seeking. Molecular Psychiatry, 7, 712–717. Mill, J., & Petronis, A. (2008). Pre- and peri-natal environmental
Koob, G. F., Arends, M. A., & Le Moal, M. (2014). Drugs, risks for attention-deficit hyperactivity disorder (ADHD):
addiction, and the brain. Oxford, UK: Elsevier. The potential role of epigenetic processes in mediating
Kopinathan, A., Scammells, P. J., Lane, J. R., & Capuano, B. susceptibility. Journal of Child Psychology and Psychiatry, 49,
(2016). Multivalent approaches and beyond: Novel tools for 1020–1030.
the investigation of dopamine D2 receptor pharmacology. Moore, D. S. (2015). The developing genome: An introduction to
Future Medicinal Chemistry, 8, 1349–1372. behavioral epigenetics. New York, NY: Oxford University Press.
Koss, K. J., & Gunnar, M. R. (2018). Annual Research Review: Myers, R. H., Madden, J. J., Teague, J. L., & Falek, A. (1982).
Early adversity, the hypothalamic–pituitary–adrenocortical Factors related to onset age of Huntington disease. American
axis, and child psychopathology. Journal of Child Psychology Journal of Human Genetics, 34, 481–488.
and Psychiatry, 59, 327–346. Na, K. S., Chang, H. S., Won, E., Han, K. M., Choi, S.,
Laakso, A., Wallius, E., Kajander, J., Bergman, J., Eskola, O., Tae, W. S., . . . Ham, B. J. (2014). Association between
Solin, O., . . . Hietala, J. (2003). Personality traits and striatal glucocorticoid receptor methylation and hippocampal
dopamine synthesis capacity in healthy subjects. American subfields in major depressive disorder. PLoS ONE, 9, e85425.
Journal of Psychiatry, 160, 904–910. Nantharat, M., Wanitchanon, T., Amesbutr, M., Tammachote, R.,
Lappe, M., & Landecker, H. (2015). How the genome got a life & Praphanphoj, V. (2015). Glucocorticoid receptor gene
span. New Genetics and Society, 34, 152–176. (NR3C1) promoter is hypermethylated in Thai females with
Lee, R. S., & Sawa, A. (2014). Environmental stressors and major depressive disorder. Genetics and Molecular Research,
epigenetic control of the hypothalamic-pituitary-adrenal 14, 19071–19079.
axis. Neuroendocrinology, 100, 278–287. Newcombe, R. G., Walker, D. A., & Harper, P. S. (1981). Factors
Lester, B. M., Conradt, E., & Marsit, C. J. (2016). Introduction influencing age at onset and duration of survival in Huntington’s
to the special section on epigenetics. Child Development, 87, chorea. Annals of Human Genetics, 45, 387–396.
29–37. Oakley, R. H., & Cidlowski, J. A. (2011). Cellular processing of
Lester, B. M., Marsit, C. J., Conradt, E., Bromer, C., & the glucocorticoid receptor gene and protein: New mechanisms
Padbury, J. F. (2012). Behavioral epigenetics and the for generating tissue-specific actions of glucocorticoids.
developmental origins of child mental health disorders. Journal of Biological Chemistry, 286, 3177–3184.
Journal of Developmental Origins of Health and Disease, 3, Oberlander, T. F., Weinberg, J., Papsdorf, M., Grunau, R., Misri,
395–408. S., & Devlin, A. M. (2008). Prenatal exposure to maternal
Linehan, M. M. (1987). Dialectical behavioral therapy for depression, neonatal methylation of human glucocorticoid
borderline personality disorder. Bulletin of the Menninger receptor gene (NR3C1) and infant cortisol stress responses.
Foundation Clinic, 51, 261–276. Epigenetics, 3, 97–106.
Liu, D., Diorio, J., Tannenbaum, B., Caldji, C., Francis, D., Olsson, C. A., Foley, D. L., Parkinson-Bates, M., Byrnes, G.,
Freedman, A., .
.
.
Meaney, M. J. (1997). Maternal care, McKenzie, M., Patton, G. C., & Saffery, R. (2010).
hippocampal glucocorticoid receptors, and hypothalamic- Prospects for epigenetic research within cohort studies of
pituitary-adrenal responses to stress. Science, 277, 1659–1662. psychological disorder: A pilot investigation of a peripheral
McEwen, B. S. (2004). Protection and damage from acute and cell marker of epigenetic risk for depression. Biological
chronic stress: Allostasis and allostatic overload and relevance Psychology, 83, 159–165.
to the pathophysiology of psychiatric disorders. Annals of the Palma-Gudiel, H., Cordova-Palomera, A., Leza, J. C., &
New York Academy of Sciences, 1032, 1–7. Fananas, L. (2015). Glucocorticoid receptor gene (NR3C1)
McEwen, B. S. (2017). Allostasis and the epigenetics of brain and methylation processes as mediators of early adversity in
body health over the life course: The brain on stress. JAMA stress-related disorders causality: A critical review. Neuroscience
Psychiatry, 74, 551–552. and Biobehavioral Reviews, 55, 520–535.
McGowan, P. O., Sasaki, A., D’Alessio, A. C., Dymov, S., Palma-Gudiel, H., & Fananas, L. (2017). An integrative review
Labonte, B., Szyf, M., . . . Meaney, M. J. (2009). Epigenetic of methylation at the serotonin transporter gene and its
regulation of the glucocorticoid receptor in human brain dialogue with environmental risk factors, psychopathology
associates with childhood abuse. Nature Neuroscience, 12, and 5-HTTLPR. Neuroscience and Biobehavioral Reviews, 72,
342–348. 190–209.
McRae, A. F., Powell, J. E., Henders, A. K., Bowdler, L., Hemani, Paquette, A., Lesseur-Perez, C., Armstrong, D., Koestler, D.,
G., Shah, S., . . . Montgomery, G. W. (2014). Contribution of Lester, B. M., & Marsit, C. J. (2013). Epigenetic modulation
genetic variation to transgenerational inheritance of DNA of the placental serotonin response pathway and its role in
methylation. Genome Biology, 15, R73. development. Reproductive Sciences, 20, 156A–157A.

Park, S. Y., & Kang, U. G. (2013). Hypothetical dopamine Schwarze, C. E., Hellhammer, D. H., Frieling, H., Mobascher,
dynamics in mania and psychosis—its pharmacokinetic A., & Lieb, K. (2017). Childhood sexual abuse predicts
implications. Progress in Neuro-Psychopharmacology and methylation of the glucocorticoid receptor gene (NR3C1) in
Biological Psychiatry, 43, 89–95. borderline personality disorder patients and controls.
Petronis, A. (2003). Epigenetics and bipolar disorder: New Psychoneuroendocrinology, 83, 44.
opportunities and challenges. American Journal of Medical Seckl, J. R., & Holmes, M. C. (2007). Mechanisms of disease:
Genetics Part C: Seminars in Medical Genetics, 123, 65–75. Glucocorticoids, their placental metabolism and fetal
Petronis, A. (2004). The origin of schizophrenia: Genetic thesis, “programming” of adult pathophysiology. Nature Reviews
epigenetic antithesis, and resolving synthesis. Biological Endocrinology, 3, 479.
Psychiatry, 55, 965–970. Smith, A. K., Conneely, K. N., Kilaru, V., Mercer, K. B., Weiss,
Pezawas, L., Meyer-Lindenberg, A., Drabant, E. M., Verchinski, T. E., Bradley, B., . . . Ressler, K. J. (2011). Differential
B. A., Munoz, K. E., Kolachana, B. S., . . . Weinberger, D. R. immune system DNA methylation and cytokine regulation
(2005). 5-HTTLPR polymorphism impacts human cingulate- in post-traumatic stress disorder. American Journal of
amygdala interactions: A genetic susceptibility mechanism Medical Genetics Part B: Neuropsychiatric Genetics, 156,
for depression. Nature Neuroscience, 8, 828–834. 700–708.
Philibert, R. A., Sandhu, H., Hollenbeck, N., Gunter, T., Adams, Smith, A. K., Kilaru, V., Kocak, M., Almli, L. M., Mercer, K. B.,
W., & Madan, A. (2008). The relationship of 5HTT Ressler, K. J., . . . Conneely, K. N. (2014). Methylation
(SLC6A4) methylation and genotype on mRNA expression quantitative trait loci (meQTLs) are consistently detected
and liability to major depression and alcohol dependence in across ancestry, developmental stage, and tissue type. BMC
subjects from the Iowa Adoption Studies. American Journal Genomics, 15, 145.
of Medical Genetics Part B: Neuropsychiatric Genetics, 147B, Smith, K. R., Hanson, H. A., Norton, M. C., Hollingshaus,
543–549. M. S., & Mineau, G. P. (2014). Survival of offspring
Plieger, T., Melchers, M., Vetterlein, A., Gortz, J., Kuhn, S., who experience early parental death: Early life conditions
Ruppel, M., & Reuter, M. (2017). The serotonin transporter and later-life mortality. Social Science and Medicine, 119,
polymorphism (5-HTTLPR) and coping strategies influence 180–190.
successful emotion regulation in an acute stress situation: Smith, S. M., & Vale, W. W. (2006). The role of the
Physiological evidence. International Journal of Psychophysiology, hypothalamic-pituitary-adrenal axis in neuroendocrine
114, 31–37. responses to stress. Dialogues in Clinical Neuroscience, 8,
Poulter, M. O., Du, I. C. G., Weaver, I. C., Palkovits, M., Faludi, 383–395.
G., Merali, Z., . . . Anisman, H. (2008). GABAA receptor Suomi, S. J. (2006). Risk, resilience, and gene × environment
promoter hypermethylation in suicide brain: Implications interactions in rhesus monkeys. Annals of the New York
for the involvement of epigenetic processes. Biological Academy of Sciences, 1094, 52–62.
Psychiatry, 64, 645–652. Suor, J. H., Sturge-Apple, M. L., Davies, P. T., Cicchetti, D., &
Provenzi, L., Giorda, R., Beri, S., & Montirosso, R. (2016). Manning, L. G. (2015). Tracing differential pathways of risk:
SLC6A4 methylation as an epigenetic marker of life adversity Associations among family adversity, cortisol, and cognitive
exposures in humans: A systematic review of literature. functioning in childhood. Child Development, 86, 1142–1158.
Neuroscience and Biobehavioral Reviews, 71, 7–20. Szyf, M., & Bick, J. (2013). DNA methylation: A mechanism for
Ptáček, R., Kuželová, H., & Stefano, G. B. (2011). Dopamine D4 embedding early life experiences in the genome. Child
receptor gene DRD4 and its association with psychiatric Development, 84, 49–57.
disorders. Medical Science Monitor, 17, RA215–RA220. Turecki, G., & Meaney, M. J. (2016). Effects of the social
Reul, J. M., Collins, A., Saliba, R. S., Mifsud, K. R., environment and stress on glucocorticoid receptor gene
Carter, S. D., Gutierrez-Mecinas, M., . . . Linthorst, A. C. methylation: A systematic review. Biological Psychiatry, 79,
(2015). Glucocorticoids, epigenetic control and stress 87–96.
resilience. Neurobiological Stress, 1, 44–59. van der Knaap, L. J., Riese, H., Hudziak, J. J., Verbiest, M. M.,
Rosas, S. L. B., Caballero, O. L., Dong, S. M., da Costa Verhulst, F. C., Oldehinkel, A. J., & van Oort, F. V. (2015).
Carvalho, M. da G., Sidransky, D., & Jen, J. (2001). Adverse life events and allele-specific methylation of the
Methylation status in the promoter region of the human serotonin transporter gene (SLC6A4) in adolescents: The
PGP9.5 gene in cancer and normal tissues. Cancer Letters, TRAILS study. Psychosomatic Medicine, 77, 246–255.
170, 73–79. van Ijzendoorn, M. H., Caspers, K., Bakermans-Kranenburg,
Roth, T. L., & Sweatt, J. D. (2011). Annual Research Review: M. J., Beach, S. R., & Philibert, R. (2010). Methylation
Epigenetic mechanisms and environmental shaping of the matters: Interaction between methylation density and
brain during sensitive periods of development. Journal of serotonin transporter genotype predicts unresolved loss or
Child Psychology and Psychiatry, 52, 398–408. trauma. Biological Psychiatry, 68, 405–407.
Russo, S. J., & Nestler, E. J. (2013). The brain reward circuitry in van Mil, N. H., Steegers-Theunissen, R. P. M., Bouwland-Both,
mood disorders. Nature Reviews Neuroscience, 14, 609–625. M. I., Verbiest, M. M. P. J., Rijlaarsdam, J., Hofman,
Sato, K. (2013). Placenta-derived hypo-serotonin situations in A., . . . Tiemeier, H. (2014). DNA methylation profiles at
the developing forebrain cause autism. Medical Hypotheses, birth and child ADHD symptoms. Journal of Psychiatric
80, 368–372. Research, 49, 51–59.
Schanen, N. C. (2006). Epigenetics of autism spectrum van Roekel, E., Verhagen, M., Engels, R. C. M. E., &
disorders. Human Molecular Genetics, 15, R138–R150. Kuppens, P. (2017). Variation in the serotonin transporter
Schultz, W. (2010). Dopamine signals for reward value and risk: polymorphism (5-HTTLPR) and inertia of negative and
Basic and recent data. Behavioral and Brain Functions, 6, 24. positive emotions in daily life. Emotion, 18, 229.

Walton, E., Hass, J., Liu, J., Roffman, J. L., Bernardoni, F., programming by maternal behavior. Nature Neuroscience, 7,
Roessner, V., . . . Ehrlich, S. (2016). Correspondence of 847–854.
DNA ethylation between blood and brain tissue and its Wise, R. A. (2004). Dopamine, learning and motivation. Nature
application to schizophrenia research. Schizophrenia Bulletin, Reviews Neuroscience, 5, 483–494.
42, 406–414. Yehuda, R., Cai, G., Golier, J. A., Sarapas, C., Galea, S.,
Wang, C., Tian, R., Zhao, Q., Xu, H., Meyer, C. A., Li, C., . . . Ising, M., . . . Buxbaum, J. D. (2009). Gene expression patterns
Liu, X. S. (2012). Computational inference of mRNA associated with posttraumatic stress disorder following
stability from histone modification and transcriptome profiles. exposure to the World Trade Center attacks. Biological
Nucleic Acids Research, 40, 6414–6423. Psychiatry, 66, 708–711.
Warde-Farley, D., Donaldson, S. L., Comes, O., Zuberi, K., Zannas, A. S., Wiechmann, T., Gassen, N. C., & Binder, E. B.
Badrawi, R., Chao, P., . . . Morris, Q. (2010). The GeneMANIA (2016). Gene-stress-epigenetic regulation of FKBP5: Clinical
prediction server: Biological network integration for gene and translational implications. Neuropsychopharmacology, 41,
prioritization and predicting gene function. Nucleic Acids 261–274.
Research, 38, W214–W220. Zisner, A., & Beauchaine, T. P. (2016). Neural substrates of trait
Watson, S., & Mackin, P. (2006). HPA axis function in mood impulsivity, anhedonia, and irritability: Mechanisms of
disorders. Psychiatry, 5, 166–170. heterotypic comorbidity between externalizing disorders and
Weaver, I. C., Cervoni, N., Champagne, F. A., D’Alessio, A. C., unipolar depression. Development and Psychopathology, 28,
Sharma, S., Seckl, J. R., . . . Meaney, M. J. (2004). Epigenetic 1179–1210.

CH A PTE R
Emotion Dysregulation and
17 Externalizing Spectrum Disorders
Tiffany M. Shader and Theodore P. Beauchaine
Abstract
As described in the literature for many years, a sizable number of children with hyperactive-impulsive
and combined subtypes/presentations of attention-deficit/hyperactivity disorder (ADHD)—especially
males—progress to more serious externalizing syndromes across development. Such outcomes
include oppositional defiant disorder, conduct problems, delinquency, substance use disorders, and in
some cases antisocial personality disorder, incarceration, and recidivism. This chapter summarizes a
developmental model that emphasizes different contributions of trait impulsivity, a highly heritable,
subcortically mediated vulnerability, versus emotion dysregulation, a highly socialized, cortically
mediated vulnerability, to externalizing progression. According to this perspective, trait impulsivity
confers vulnerability to all externalizing disorders, but this vulnerability is unlikely to progress beyond
ADHD in protective environments. In contrast, for children who are reared under conditions of
adversity—including poverty, family violence, deviant peer influences, and neighborhood violence/
criminality—neurodevelopment of prefrontal cortex structure and function is compromised, resulting
in failures to achieve age-expected gains in emotion regulation and other forms of executive control.
For these children, subcortical vulnerabilities to trait impulsivity are amplified by deficient cortical
modulation, which facilitates progression along the externalizing spectrum.
Keywords: ADHD, trait impulsivity, emotion dysregulation, externalizing disorders, neurodevelopment,

prefrontal cortex, emotion regulation, executive control, deficient cortical modulation
Introduction Manual of Mental Disorders, 5th edition (DSM-5;

Over the past several years, psychopathologists have American Psychiatric Association, 2013)—a docu-
increasingly embraced spectrum models of mental ment that throughout its history has strongly favored
illness, which group broad classes of etiologically a discrete disorder approach to classifying psychopa-
related disorders together. Although we focus here thology (see, e.g., Beauchaine & Klein, 2017).
on the externalizing spectrum, including attention- Although formalized spectrum accounts of psy-
deficit/hyperactivity disorder (ADHD), oppositional chopathology are a historically recent development,
defiant disorder (ODD), conduct disorder (CD), they are rooted in empirically based taxonomies
and antisocial personality disorder (ASPD; see, e.g., that appeared initially in the 1980s. At that time,
Beauchaine & Hinshaw, 2016), spectrum models of Achenbach and Edelbrock (1983) applied factor anal-
internalizing disorders, psychotic disorders, and ysis to symptoms expressed among large samples of
other forms of psychiatric impairment have also children and adolescents. These studies, and similar
gained traction in the last decade (e.g., Frazier et al., factor analyses of psychopathology symptoms ex-
2012; Lahey, Krueger, Rathouz, Waldman, & Zald, pressed by adults (e.g., Krueger, 1999), revealed a
2017). In fact, both schizophrenia and autism spec- consistent latent structure in which two higher order
tra are now included in the Diagnostic and Statistical factors—externalizing and internalizing—account
237
for much of the covariation among first-order adulthood for a preponderance of individuals
factors (behavioral syndromes). First-order exter- (Biederman, Petty, Evans, Small, & Faraone, 2010),
nalizing syndromes include constructs such as im- progression to more severe externalizing outcomes
pulsivity, aggression, delinquency, and substance is not foregone. Our ontogenic process perspective on
use, which map closely onto DSM-5 disruptive externalizing progression focuses on relative contri-
behavior and antisocial personality disorders. In butions of different but interconnected neural sys-
contrast, first-order internalizing syndromes include tems to (1) expression of hyperactivity-impulsivity, as
constructs such as anxiety, depression, and with- manifested very early in life by those with ADHD,
drawal, which map closely onto DSM-5 depressive versus (2) emotion dysregulation, as expressed in-
and anxiety disorders. This factor structure is ob- creasingly across development among those with
served in large population-based and twin studies; in ADHD who progress to delinquency and antisocial
child, adolescent, and adult samples; in male, behavior (Beauchaine & McNulty, 2013; Beauchaine
female, and mixed samples; and across self-, parent, et al., 2017; McDonough-Caplan & Beauchaine,
and teacher reports of symptoms (Achenbach & 2018). According to this perspective, subcortical
Edelbrock, 1983, 1991; Caspi et al., 2014; Lahey, vulnerabilities to impulsive behavior are expressed
Van Hulle, Singh, Waldman, & Rathouz, 2011; as ADHD during and even before the preschool
Lahey, Krueger, Rathouz, Waldman, & Zald, 2017; years. This impulsivity may be amplified or molli-
Lahey et al., 2014; Olino, Dougherty, Bufferd, fied by trajectories in cortical neuromaturation that
Carlson, & Klein, 2014; Tackett et al., 2013).1 unfold later in development. In protective environ-
The remarkable consistency of this factor structure ments, developmentally normative cortical neuro-
suggests there may be transdiagnostic etiological maturation results in effective emotion regulation,
influences on what were once seen as distinct
yielding lifelong persistent ADHD (i.e., “regulated”
disorders (see, e.g., McDonough-Caplan, Klein, & impulsivity). In contrast, in high-risk environments,
Beauchaine, 2018). Although elucidating transdiag- compromised cortical neuromaturation results in
nostic influences on internalizing disorder etiology emotion dysregulation and progression to more
is important, we do not consider internalizing dis- severe externalizing behavior across development
orders further in this chapter. Rather, a major goal (i.e., “unregulated” impulsivity). As outlined later, this
of our research is to specify transdiagnostic vulner- interpretation is consistent with several observations
abilities to externalizing spectrum disorders (see concerning vulnerability to delinquency among boys
Beauchaine & Hinshaw, 2016). Ten years ago, the with ADHD who are reared in high-risk environ-
notion of common liability to externalizing disor- ments (e.g., Lynam et al., 2000; Meier, Slutske,
ders enjoyed limited support. In the last decade, Arndt, & Cadoret, 2008) and with increasingly
however, considerable evidence for shared etiology well-characterized effects of environmental adver-
has emerged, including (1) highly overlapping heri- sity on cortical neuromaturation and self-regulation
tabilities, as indicated in behavioral genetics studies (e.g., Hanson et al., 2010; Luby et al., 2013). We
(e.g., Krueger et al., 2002); (2) common molecular begin by discussing trait impulsivity, which mani-
genetic vulnerabilities (e.g., Gizer, Otto, & Ellingson, fests very early in life as ADHD, as a predisposing
2016); (3) overlapping neural correlates in both sub- vulnerability to all externalizing disorders.
cortical brain regions implicated in impulsivity and
cortical brain regions implicated in poor self-control Trait Impulsivity as a Heritable,
and emotion dysregulation (e.g., Beauchaine, Subcortically Derived Vulnerability
Zisner, & Sauder, 2017); and (4) a well-characterized As already noted, trait impulsivity confers vulnera-
developmental trajectory from severe hyperactivity- bility to all externalizing disorders, beginning with
impulsivity (ADHD) very early in life to later ODD, development of ADHD during and even before the
CD, and eventual antisocial behavior, particularly preschool years (see, e.g., Beauchaine & McNulty,
among affected males (see Beauchaine & McNulty, 2013; Beauchaine et al., 2017). Consistent with
2013; Eme, 2015, 2017; Moffitt, 1993, 2006; Robins, the developmental theory of ADHD set forth by
1966).2 Sagvolden, Johansen, Aase, and Russell (2005), we
It is important to note, however, that many define trait impulsivity as a consistent preference for
hyperactive-impulsive children do not traverse
immediate rewards over larger, delayed rewards;
this developmental pathway to later ODD, CD, failures to plan ahead; and poor volitional control
and antisocial behavior. Even though ADHD is over one’s behaviors. Thus, trait impulsive individuals
highly heritable, with symptoms that persist into have difficulty delaying gratification and suppressing
238 Emotion Dysregul ation and Externalizing Disorders

prepotent responses in the service of long-term mood motivates individuals to engage in recurrent
goals (for more detailed discussion, see Beauchaine approach behaviors because such behaviors provide
et al., 2017; Neuhaus & Beauchaine, 2017). This temporary relief through phasic upregulation of DA
definition dovetails well with DSM-5 symptoms of neural firing in the ventral striatum (Zisner &
hyperactivity-impulsivity and closely related con- Beauchaine, 2016). However, as outlined by Sagvolden
structs (e.g., delay discounting, hyperbolic dis- et al. (2005), this phasic neural responding is brief
counting, low constraint), and reflects extreme ex- and of smaller magnitude for impulsive individuals
pression of a dimensional personality trait (see, than controls, so incessant external reinforcement
e.g., Plichta & Scheres, 2014). Notably, normal is sought, as manifested in hyperactive-impulsive
variation in impulsivity can be adaptive, as reflected behaviors.
in novelty seeking, extraversion, and exuberance— As this brief overview suggests, subcortically
core components of creativity and flexible think- generated affective responses help explain behavioral
ing (Degnan et al., 2011; Sagvolden et al., 2005). impulsivity—a transdiagnostic symptom of exter-
As foreseen by Sagvolden et al. (2005) in their nalizing spectrum disorders. Notably, however, nei-
foundational paper, a large and growing literature ther individual differences in striatal responding to
links trait impulsivity to striatal hyporesponding to incentives nor the mood states they imbue explain
incentives. Across childhood, adolescence, and why some affected individuals never progress from
adulthood, hyperactive-impulsive individuals exhibit ADHD to more intractable externalizing outcomes,
reduced neural reactivity compared with controls in whereas others exhibit increasingly delinquent and
the ventral (and sometimes dorsal) striatum while antisocial behavior as they mature. Understanding
anticipating reward cues (e.g., Cubillo, Halari, such progression requires that we also consider pat-
Smith, Taylor, & Rubia, 2012; Plichta & Scheres, terns of cortical neuromaturation that unfold across
2014). Importantly, this neural vulnerability is childhood, adolescence, and young adulthood.
observed in other externalizing disorders as well, A major function of the cortex is to inhibit im-
including CD and ASPD, and among individuals pulsive behaviors through top-down modulation of
with substance use disorders (SUDs)—even after subcortical neural responding, including striatal
extended periods of abstinence (e.g., Luijten, reactivity (e.g., Heatherton, 2011; Heatherton &
Schellekens, Kühn, Machielse, & Sescousse, 2017; Wagner, 2011). Developing effective top-down
Oberlin et al., 2012; Rubia et al., 2009). As reviewed modulation of subcortically generated impulses is a
elsewhere, blunted striatal responding is a complex major developmental task of adolescence, as mani-
endophenotype that is determined by multifactorial fested in emerging self- and emotion regulation skills
genetic influences, epigenetic factors, neurohormo- (Heller, Cohen, Dreyfuss, & Casey, 2016). As we
nal modulators, and environmental adversities (see describe next, cortical neuromaturation among those
Beauchaine & Constantino, 2017; Gatzke-Kopp, who progress along the externalizing spectrum is
2011; Gizer et al., 2016). Thus, low striatal function often compromised, resulting in poor emotion reg-
is a highly heritable and complex neural vulnerabil- ulation and executive control over behavior. Thus,
ity, but it is susceptible to further downregulation in among these individuals, a highly heritable sub-
adverse rearing environments (see Birn, Roeber, & cortical vulnerability to ADHD (blunted striatal
Pollak, 2017). responding) is met with inadequate top-down
According to reward-seeking models, blunted cortical regulation, increasing risk for more serious
striatal responding gives rise to impulsivity because externalizing behaviors (Beauchaine & McNulty,
it induces an aversive psychological state. The meso- 2013; Beauchaine et al., 2017).
limbic dopamine (DA) system, including the ventral
striatum, is a primary neural substrate of appetitive Emotion Dysregulation as a
motivation (for a review see Neuhaus & Beauchaine, Neuromaturational, Cortically
2017). Infusions of DA into the striatum and inter- Derived Vulnerability
connected mesolimbic structures produce pleasure The human prefrontal cortex (PFC) matures
(Berridge, 2003). Given this, it is unsurprising that throughout childhood, adolescence, and young
individual differences in central DA expression cor- adulthood (Brain Development Cooperative Group,
relate with trait positive affectivity (Ashby, Isen, & 2012; Casey, Getz, & Galvan, 2008). Among its
Turken, 1999), and low levels of striatal DA imbue core functions is volitional control over behavior
an irritable, anhedonic, discontented mood state and emotion (Castellanos-Ryan & Seguin, 2016;
(e.g., Laakso et al., 2003). This persistent aversive Macdonald, Goines, Novacek, & Walker, 2016).
Shader and Beauchaine 239

The orbitofrontal cortex and dorsolateral PFC play (Graziano & Garcia, 2016), and why emotion
especially important roles in inhibiting impulsivity dysregulation predicts both stability of ADHD

by exerting top-down control over striatal activity and development of aggressive behaviors across
and reactivity (see Beauchaine & Zisner, 2017; adolescence (Sasser, Kalvin, & Bierman, 2016).
Heatherton, 2011; Heatherton & Wagner, 2011). Finally, adolescent males with CD exhibit smaller
Such modulatory effects by the PFC on the striatum orbitofrontal cortex and anterior cingulate volumes
have been known for decades (e.g., Louilot, LeMoal, than controls (Huebner et al., 2008; Sauder,
& Simon, 1989). Beauchaine, Gatzke-Kopp, Shannon, & Aylward,
Even though subcortical brain regions including 2012), and smaller dorsolateral PFC volumes in
the striatum continue to develop throughout ado- early adolescence portend worsening externalizing
lescence (Galván, 2013), their neuromaturation symptoms—including binge drinking—in later
unfolds somewhat earlier than (yet overlaps with) adolescence (Brumback et al., 2016). In turn, heavy
neuromaturation of the PFC (Brain Development alcohol and other substance use can compromise
Cooperative Group, 2012; Gogtay et al., 2004). neurodevelopment of the PFC and its interconnec-
Compared with adults, children and adolescents tions further, magnifying self-regulation deficits
exhibit stronger striatal responses to rewards, yet (e.g., Bava, Jacobus, Thayer, & Tapert, 2013). Taken
their PFC responding is weaker and more dispersed together, this growing developmental literature
(Macdonald et al., 2016). These findings likely re- supports the assertion that ADHD and CD—and
flect neuromaturational differences in top-down to some extent SUDs—fall along a neurodevelop-
control over subcortical incentive processing. As we mental continuum in which severity of externalizing
have reviewed elsewhere and as alluded to previously, behavior is at least in part dependent on deficits in
typically developing children show increasingly PFC maturation and function, resulting in emotion
effective top-down inhibition of approach-related dysregulation and amplification of pre-existing
(and other) emotions as their self-regulation transi- subcortical vulnerability (see also Beauchaine &
tions from external sources—usually parents—to Gatzke-Kopp, 2012).
volitional control as they mature (Beauchaine, 2015). The previous sections suggest that despite their
For this reason, cortical mechanisms of emotion dysfunctional interdependence, bottom-up, subcortical
regulation take on increasing importance in impulse neural substrates of trait impulsivity are dissociable
control problems from childhood to adolescence from top-down, cortical neural substrates of self- and
(see Halperin & Schulz, 2006). For example, com- emotion regulation. In early childhood, individual
pared with controls, adolescent males with CD show differences in trait impulsivity (ADHD) derive in
reduced functional connectivity between striatal and large part from earlier maturing subcortical brain
frontal brain regions (Shannon, Sauder, Beauchaine, regions, with later maturing cortical brain regions
& Gatzke-Kopp, 2009). As outlined immediately to and functional connectivity between cortical and
follow, this reduced connectivity likely results from subcortical neural systems taking on increasing
delayed or even absent neuromaturation of prefron- importance in amplifying or mollifying trait impul-
tal structures. sivity across development. For those who progress to
Neurodevelopment of the PFC involves consid- increasingly intractable externalizing behaviors,
erable gray matter pruning and cortical surface cortical neuromaturation is compromised. In such
maturation across adolescence and young adult- cases, trait impulsivity is met with deficient top-
hood (e.g., Gogtay et al., 2004). These processes, down control over behavior and emotion, resulting
which are associated with improved efficiency in in “double jeopardy” for progression along the ex-
emotion regulation and executive function (e.g., ternalizing spectrum (see Beauchaine et al., 2017).
Vijayakumar et al., 2014), are disturbed among
children with ADHD and CD. Children with Environmental Influences on
ADHD show a roughly two-year lag in prefrontal Prefrontal Cortex Neuromaturation
neurodevelopment (Shaw et al., 2012), and boys and Emotion Regulation
with CD fail to exhibit PFC gray matter reductions As defined throughout this volume, emotion
from childhood to early adolescence (De Brito et al., regulation involves both volitional and automated
2009). This latter finding is illustrated in Figure 17.1. processes through which individuals shape their af-
Compromised PFC neurodevelopment may ex- fective experiences and expression in the service
plain why many children with ADHD exhibit of adaptive behavior (see, e.g., Beauchaine, 2015;
worsening emotion dysregulation as they mature Thompson, 1990). In contrast to trait impulsivity,

.75
.70
OFC gray matter concentration

r = .06
.65
.60
.55
r = –.57
.50
10.0 10.5 11.0 11.5 12.0 12.5 13.0 13.5
Age (years)
Figure 17.1 Associations between age and orbitofrontal cortex (OFC) gray matter density for typically developing boys (triangles)
versus boys with conduct disorder (circles). Age-expected gray matter reductions are not observed in the conduct disorder group.
Adapted with permission from De Brito et al. (2009).
which is highly heritable (e.g., Nikolas & Burt, 2010; working memory deficits (Hanson et al., 2012).
Thapar, Langley, Owen, & O’Donovan, 2007), most Thus, early-life adversity exerts widespread effects
measures of emotion regulation (ER) yield modest on neurodevelopment in cortical brain regions
heritability coefficients, suggesting significant so- that subserve emotion regulation. In fact, adults
cialization (e.g., Goldsmith, Pollak, & Davidson, who were reared in poverty during childhood show
2008). In fact, considerable research indicates reduced ventrolateral and dorsolateral PFC activ-
that ER, self-regulation, and executive functions on ity and fail to inhibit subcortical responses during
which they depend are shaped strongly across devel- effortful regulation of emotion (Kim et al., 2013).
opment by environmental influences, including Thus, effects of childhood poverty and stress extend
parent–child relationship dynamics, among others well into adulthood, with demonstrated effects on
(e.g., Beauchaine, Hinshaw, & Bridge, in press; ER capabilities. Although associated with altered
Beauchaine & Zalewski, 2016; Bell & Calkins, cortical neuromaturation and development of ex-
2000; Bernier, Carlson, & Whipple, 2010; Smith, ternalizing behavior (e.g., Santiago, Wadsworth,
Calkins, & Keane, 2006; Chapters 8 and 18, this & Stump, 2011), poverty of course is not the gen-
volume). Such findings are unsurprising given a erative mechanism through which either behavior
voluminous literature linking environmental en-
dysregulation or cortical brain development are
richment to PFC structure and function across effected (see Luby et al., 2013). Rather, correlated
development among both animals and humans (see adversities such as compromised parenting, neigh-
Baroncelli et al., 2010; Blair, 2016). borhood violence, deviant peer group affiliations,
In contrast to environmental enrichment, envi- and exposure to substances of abuse are likely
ronmental deprivation exerts profound negative mechanisms (Beauchaine, 2015). Perhaps unsur-
effects on PFC neurodevelopment and function, prisingly, these are the very influences associated with
with direct implications for emerging emotion progression from ADHD in early childhood to more
dysregulation and externalizing behavior (see
severe externalizing behaviors across development.
Beauchaine, 2015). Compared with controls,
children who are physically abused exhibit smaller Environmental Influences on
orbitofrontal cortex volumes than controls, which Externalizing Progression
predict both executive function deficits and social An impressively large literature specifies environ-
difficulties with peers (Hanson et al., 2010). mental risk factors that mediate progression of
Furthermore, poverty and associated stress sup- ADHD early in life to ODD, CD, ASPD, and
press cortical brain growth across childhood similar constructs, including aggression and de-
(Hanson et al., 2013). In turn, PFC structure me- linquency in later childhood, adolescence, and
diates links between early childhood stress and adulthood (Beauchaine & McNulty, 2013;

Beauchaine et al., 2017; Dishion & Hiatt Racer, et al., 2000; Meier et al., 2008). In contrast, impulsive
2013; McDonough-Caplan & Beauchaine, 2018). adolescents are no more likely than their nonimpul-
For example, coercive family relationship dynamics sive peers to offend in high SES neighborhoods
in which parent–child conflict, aggressive behaviors, where rates of violence and criminality are low.
physiological reactivity, and emotion dysregulation In addition, impulsivity predicts both early initi-
are negatively reinforced (see Beauchaine & ation of and increases in substance use in adolescence
Zalewski, 2016; Crowell et al., 2013) predict pro- (e.g., Iacono, Malone, & McGue, 2008). Adolescents
spective increases in children’s conduct problems— and young adults who fail to exhibit age-normative
including aggression—which then generalize to peer decreases in impulsive behavior across development
groups (e.g., Snyder, Edwards, McGraw, Kilgore, & show steeper escalation of cigarette, alcohol, and
Holton, 1994). Coercive family dynamics are par- marijuana use than their peers (Quinn & Harden,
ticularly potent mediators of longitudinal increases 2013). Furthermore, links between (1) ADHD and
in delinquency among children with ADHD. For other externalizing behaviors in childhood and (2)
example, Patterson, DeGarmo, and Knutson (2000) development of SUD symptoms are mediated by
demonstrated that prediction of antisocial and disrupted social relationships and affiliations with
delinquent behavior in ninth grade by hyperactivity- deviant peers (Marshal & Molina, 2006; Molina,
impulsivity in fourth grade was mediated fully by Pelham, Cheong, Marshal, & Gnagy, 2012). Finally,
coercive parental discipline. Notably, hyperactive- although mechanisms that mediate progression of
impulsive children who experienced more compe- childhood ADHD to later adult antisocial behavior
tent parenting did not progress to later delinquency. (e.g., Storebø & Simonsen, 2016) are not under-
More recent findings show that frequent parental stood fully, all of the mediating factors discussed
criticism mediates links between ADHD and emerg- here likely play some role, with particularly strong
ing ODD symptoms across adolescence (Musser, influences exerted by deviant peers (Dishion &
Karalunas, Dieckmann, Peris, & Nigg, 2016). Hiatt Racer, 2013).
Furthermore, nonsupportive parenting, including
discouragement and dismissal of emotions, predicts Conclusion
longitudinal increases in affective lability among Environmental risk factors contribute strongly to
children with ADHD (Breaux, McQuade, Harvey, & progression of externalizing behaviors among
Zakarian, 2018). In addition, parenting disruptions neurobiologically vulnerable children with ADHD.
associated with maternal depression mediate devel- According to our ontogenic process perspective,
opmental associations between ADHD in early depicted in Figure 17.2, subcortical vulnerabilities
childhood and conduct problems across intervals exert a particularly strong influence on trait impul-
spanning two to eight years (Chronis et al., 2007). sivity (ADHD) very early in life, with deficiencies in
Importantly, positive parenting protects against this cortical function taking on increasing importance
progression. Finally, children with ADHD who across development as externalizing behaviors prog-
incur abuse early in life are much more likely to show ress. Notably, cortical dysfunction, associated emotion
later externalizing behaviors than children with dysregulation, and progression along the externalizing
ADHD who do not endure abuse (Briscoe-Smith & spectrum are mediated by environmental influences
Hinshaw, 2006). that aggregate across development for children who are
In addition to family influences, deviant peer reared in conditions of adversity (see Beauchaine &
affiliations and neighborhood risk factors predict McNulty, 2013; Beauchaine & Zalewski, 2016).
longitudinal progression of externalizing behavior This formulation suggests that early intervention is
among vulnerable children. In fact, associating with crucial toward altering developmental trajectories
deviant peers predicts emergence of conduct prob- away from externalizing progression and emotion
lems from kindergarten through third to fourth dysregulation among children with ADHD (e.g.,
grade specifically among impulsive children (Snyder Beauchaine et al., 2013).
et al., 2008). Neighborhood effects on progression It is worth repeating that those with ADHD
of externalizing behavior among impulsive children who develop adequate top-down control over their
and adolescents are also well characterized. Impulsive behavior will nevertheless be affected by impulsive
adolescents in low socioeconomic-status (SES) tendencies throughout life, yet such individuals are
neighborhoods engage in higher rates of criminality, likely to be fully functioning members of society
including property crimes and violent offenses, (see Beauchaine, 2015; Beauchaine et al., 2017). In
than their peers in high SES neighborhoods (Lynam contrast, those who develop prefrontal dysfunction

emotion
vulnerability
trait (latent)
trait impulsivity dysregulation
subcortical, cortical, highly
highly heritable socialized
(observed)
behavioral
syndrome
ADHD oppositional conduct ASPD,

delinquency substance use, incarceration,
(HI/combined) defiant problems dependence recidivism
disorder
environmental
risk mediator
coercive deviant peer neighborhood availability, criminal

family group violence, opportunity, justice
processes affiliations criminality exposure involvement
preschool elementary school middle school adolescence adulthood
Developmental Period
Figure 17.2 A developmental model of progression along the externalizing spectrum for individuals with ADHD-HI/C (middle
panel, left). Early in life, ADHD behaviors derive largely from trait impulsivity, a highly heritable, subcortically mediated vulnerability
(top panel, left). For those who are reared in adverse contexts, myriad accumulating risk factors (bottom panel) mediate progression
along the externalizing spectrum in part by amplifying emotion dysregulation, a highly socialized cortical vulnerability (top panel,
right). According to this perspective, trait impulsivity confers vulnerability to all externalizing disorders across development (solid
arrows) but interacts increasingly with emotion dysregulation (thickening arrows) and related prefrontally mediated deficits in self-
control as externalizing behaviors escalate (see text; Beauchaine & McNulty, 2013; Beauchaine et al., 2017 for further details).
as a result of interactions between their neurobio- established. Indeed, children and adolescents who
logical vulnerabilities and environmental adversity are reared at or below 1.5 times the federal poverty
are far more likely to traverse a developmental level show widespread reductions in gray matter
pathway characterized by emerging oppositionality, volume compared with their peers, particularly in
conduct disturbance, delinquent behavior, problems frontal regions implicated in self-control (Hair,
with substance use, and in some cases criminality, Hanson, Wolfe, & Pollak, 2015). It is our hope
incarceration, and recidivism. This general devel- that specification of mechanisms will lead to more
opmental pathway has been described in the liter- widespread use of prevention and early interven-
ature for many years (Beauchaine & McNulty, tion programs that are known to improve emotion
2013; Moffitt, 1993; Robins, 1966), yet only re- regulation and reduce externalizing progression
cently has the field begun to elucidate complex (e.g., Beauchaine et al., 2013, in press; Webster-
mediating pathways from early-life ADHD to ad- Stratton, Reid, & Beauchaine, 2013). These pro-
olescent and adult externalizing behavior (e.g., grams therefore hold promise toward offsetting
Beauchaine et al., 2017; Eme, 2015, 2017; Moffitt, neurodevelopmental correlates of affect dysregula-
2006; Raine, 2018). In this chapter, we emphasize tion, failures of executive function, and progressive
that such developmental p rogression results from and therefore costly externalizing outcomes (see,
(1) interactions between subcortical vulnerabilities e.g., Beauchaine, Zisner, & Hayden, 2018).
to trait impulsivity and cortical neural vulnerabilities
to emotion dysregulation, (2) interactions between Acknowledgments
Work on this chapter was supported by grant DE025980 from
neurobiological vulnerabilities and environmental the National Institutes of Health, and by the National Institutes
adversities that shape emotion dysregulation, (3) of Health Science of Behavior Change (SoBC) Common Fund.
cumulative effects of c orrelated environmental risk
factors as they accrue across the lifespan, and Notes
therefore (4) complex developmental processes 1. Latent structural models also yield an even higher (third)-
order general liability factor onto which both externalizing
that cannot be understood fully at any single point
and internalizing factors load. This general liability factor is
in time. These processes eventuate in increasingly beyond the scope of this chapter. Interested readers are
poor top-down regulation of behavior and emo- referred elsewhere (e.g., Caspi et al., 2014; Lahey et al., 2011;
tion, which may be impossible to reverse once well Tackett et al., 2013).

2. Throughout this chapter, when discussing ADHD, we refer case for targeted prevention in preadolescence. Clinical
only to the hyperactive-impulsive (HI) and combined (C) Psychological Science.
presentations/subtypes. Evidence at behavioral, attentional, Beauchaine, T. P., & Klein, D. N. (2017). Classifying
neuropsychological, pharmacological, and neural levels of psychopathology: The DSM, empirically-based taxonomies,
analysis suggests that purely inattentive ADHD likely and the Research Domain Criteria. In T. P. Beauchaine &
emerges from a different pathophysiology than ADHD-HI S. P. Hinshaw (Eds.), Child and adolescent psychopathology
and ADHD-C. Most important for this chapter, no evidence (3rd ed., pp. 33–67). Hoboken, NJ: Wiley.
suggests that those with purely inattentive ADHD are Beauchaine, T. P., & McNulty, T. (2013). Comorbidities and
vulnerable to the externalizing trajectory we describe. Interested continuities as ontogenic processes: Towards a developmental
readers are referred elsewhere for further discussion (e.g., spectrum model of externalizing behavior. Developmental
Adams, Derefinko, Milich, & Fillmore, 2008; Beauchaine, Psychopathology, 25, 1505–1528.
Ben-David, & Sela, 2017; Fair et al., 2013). Beauchaine, T. P., & Zalewski, M. (2016). Physiological and
developmental mechanisms of emotional lability in coercive
References relationships. In T. J. Dishion & J. J. Snyder (Eds.), The
Achenbach, T. M., & Edelbrock, C. (1983). Manual for the child Oxford handbook of coercive relationship dynamics (pp. 39–52).
behavior checklist and revised child behavior profile. Burlington, New York, NY: Oxford University Press.
VT: University of Vermont Department of Psychiatry. Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion
Achenbach, T. M., & Edelbrock, C. S. (1991). Manual for the regulation, and the latent structure of psychopathology: An
child behavior checklist/4–18 and 1991 profile. Burlington, VT: integrative and convergent historical perspective.
University of Vermont Press. International Journal of Psychophysiology, 119, 108–118.
Adams, Z. W., Derefinko, K. J., Milich, R., & Fillmore, M. T. Beauchaine, T. P., Zisner, A. R., & Hayden, E. P. (2018).
(2008). Inhibitory functioning across ADHD subtypes: Neurobiological mechanisms of psychopathology and
Recent findings, clinical implications, and future directions. treatment action. In T. H. Ollendick, S. W. White, &
Developmental Disabilities Research Reviews, 14, 268–275. B. A. White (Eds.), The Oxford handbook of clinical child and
American Psychiatric Association. (2013). Diagnostic and statistical adolescent psychology (pp. 699–723). New York, NY: Oxford
manual of mental disorders (5th ed.). Arlington, VA: Author. University Press.
Ashby, F. G., Isen, A. M., & Turken, A. U. (1999). A Beauchaine, T. P., Zisner, A. R., & Sauder, C. L. (2017). Trait
neuropsychological theory of positive affect and its influence impulsivity and the externalizing spectrum. Annual Review of
on cognition. Psychological Review, 106, 529–550. Clinical Psychology, 13, 343–368.
Baroncelli, L., Braschi, C., Spolidoro, M., Begenisic, T., Sale, A., Bell, K. L., & Calkins, S. D. (2000). Relationships as inputs
& Maffei, L. (2010). Nurturing brain plasticity: Impact of and outputs of emotion regulation. Psychological Inquiry, 11,
environmental enrichment. Cell Death and Differentiation, 160–163.
17, 1092–1103. Bernier, A., Carlson, S. M., & Whipple, N. (2010). From external
Bava, S., Jacobus, J., Thayer, R. E., & Tapert, S. F. (2013). regulation to self-regulation: Early parenting precursors of
Longitudinal changes in white matter integrity among young children’s executive functioning. Child Development,
adolescent substance users. Alcohol Clinical and Experimental 81, 326–339.
Research, 37, E181–E189. Berridge, K. C. (2003). Pleasures of the brain. Brain and
Beauchaine, T. P. (2015). Future directions in emotion dysregulation Cognition, 52, 106–128.
and youth psychopathology. Journal of Clinical Child and Biederman, J., Petty, C. R., Evans, M., Small, J., & Faraone, S. V.
Adolescent Psychology, 44, 875–896. (2010). How persistent is ADHD? A controlled 10-year
Beauchaine, T. P., Ben-David, I., & Sela, A. (2017). Attention- follow-up study of boys with ADHD. Psychiatry Research,
deficit/hyperactivity disorder, delay discounting, and risky 177, 299–304.
financial behaviors: A preliminary analysis of self-report data. Birn, R. M., Roeber, B. J., & Pollak, S. D. (2017). Early
PLoS ONE, 12, e0176933. childhood stress exposure, reward pathways, and adult
Beauchaine, T. P., & Constantino, J. N. (2017). Redefining the decision making. Proceedings of the National Academy of
endophenotype concept to accommodate transdiagnostic Sciences, 114, 13549–13554.
vulnerabilities and etiological complexity. Biomarkers in Blair, C. (2016). Developmental science and executive function.
Medicine, 11, 769–780. Current Directions in Psychological Science, 25, 3–7.
Beauchaine, T. P., & Gatzke-Kopp, L. M. (2012). Instantiating the Brain Development Cooperative Group. (2012). Total and
multiple levels of analysis perspective in a program of study regional brain volumes in a population-based normative
on externalizing behavior. Development and Psychopathology, sample from 4 to 18 years: The NIH MRI Study of Normal
24, 1003–1018. Brain Development. Cerebral Cortex, 22, 1–12.
Beauchaine, T. P., Gatzke-Kopp, L. M., Neuhaus, E., Chipman, Breaux, R. P., McQuade, J. D., Harvey, E. A., & Zakarian, R. J.
J., Reid, M. J., & Webster-Stratton, C. (2013). Sympathetic- (2018). Longitudinal associations of parental emotion
and parasympathetic-linked cardiac function and prediction socialization and children’s emotion regulation: The
of externalizing behavior, emotion regulation, and prosocial moderating role of ADHD symptomatology. Journal of
behavior among preschoolers treated for ADHD. Journal of Abnormal Child Psychology, 46, 671–683.
Consulting and Clinical Psychology, 81, 481–493. Briscoe-Smith, A. M., & Hinshaw, S. P. (2006). Linkages
Beauchaine, T. P., & Hinshaw, S. P. (Eds.). (2016). The Oxford between child abuse and attention-deficit/hyperactivity
handbook of externalizing spectrum disorders. New York, NY: disorder in girls: Behavioral and social correlates. Child Abuse
Oxford University Press. and Neglect, 30, 1239–1255.
Beauchaine, T. P., Hinshaw, S. P., & Bridge, J. A. (in press). Brumback, T. Y., Worley, M., Nguyen-Louie, T. T., Squeglia,
Nonsuicidal self-injury and suicidal behaviors in girls: The L. M., Jacobus, J., & Tapert, S. F. (2016). Neural predictors

of alcohol use and psychopathology symptoms in adolescents. Gatzke-Kopp, L. M. (2011). The canary in the coalmine: The
Development and Psychopathology, 28, 1209–1216. sensitivity of mesolimbic dopamine to environmental
Casey, B. J., Getz, S., & Galvan, A. (2008). The adolescent brain. adversity during development. Neuroscience and Biobehavioral
Developmental Review, 28, 62–77. Reviews, 35, 794–803.
Caspi, A., Houts, R. M., Belsky, D. W., Goldman-Mellor, S. J., Gizer, I. R., Otto, J. M., & Ellingson, J. M. (2016). Molecular
Harrington, H., Israel, S., . . . Moffitt, T. E. (2014). The p genetics of the externalizing spectrum. In T. P. Beauchaine &
factor: One general psychopathology factor in the structure S. P. Hinshaw (Eds.), The Oxford handbook of externalizing
of psychiatric disorders? Clinical Psychological Science, 2, spectrum disorders (pp. 149–169). New York, NY: Oxford
119–137. University Press.
Castellanos-Ryan, N., & Séguin, J. R. (2016). Prefrontal and Gogtay, N., Giedd, J. N., Lusk, L., Hayashi, K. M., Greenstein,
anterior cingulate cortex mechanisms of impulsivity. In D., Vaituzis, A. C., . . . Thompson, P. M. (2004). Dynamic
T. P. Beauchaine & S. P. Hinshaw (Eds.), The Oxford mapping of human cortical development during childhood
handbook of externalizing spectrum disorders (pp. 201–219). through early adulthood. Proceedings of the National Academy
New York, NY: Oxford University Press. of Sciences, 101, 8174–8179.
Chronis, A. M., Lahey, B. B., Pelham, W. E., Williams, S. H., Goldsmith, H. H., Pollak, S. D., & Davidson, R. J. (2008).
Baumann, B. L., Kipp, H., .
.
.
Rathouz, P. J. (2007). Developmental neuroscience perspectives on emotion
Maternal depression and early positive parenting predict regulation. Child Development Perspectives, 2, 132–140.
future conduct problems in young children with attention- Graziano, P. A., & Garcia, A. (2016). Attention-deficit/
deficit/hyperactivity disorder. Developmental Psychology, 43, hyperactivity disorder and children’s emotion dysregulation:
70–82. A meta-analysis. Clinical Psychology Review, 46, 106–123.
Crowell, S. E., Baucom, B. R., Potapova, N. V., McCauley, E., Hair, N. L., Hanson, J. L., Wolfe, B. L., & Pollak, S. D. (2015).
Fittleson, M., Barth, H., . . . Beauchaine, T. P. (2013). Association of child poverty, brain development, and
Mechanisms of contextual risk for adolescent self-injury: academic achievement. JAMA Pediatrics, 169, 822–829.
Emotion invalidation and conflict escalation in mother-child Halperin, J. M., & Schulz, K. P. (2006). Revisiting the role of the
interactions. Journal of Clinical Child and Adolescent prefrontal cortex in the pathophysiology of attention-deficit/
Psychology, 42, 467–480. hyperactivity disorder. Psychological Bulletin, 132, 560–581.
Cubillo, A., Halari, R., Smith, A., Taylor, E., & Rubia, K. (2012). Hanson, J. L., Chung, M. K., Avants, B. B., Rudolph, K. D.,
A review of fronto-striatal and fronto-cortical brain Shirtcliff, E. A., Gee, J. C., . . . Pollak, S. D. (2012). Structural
abnormalities in children and adults with ADHD and new variations in prefrontal cortex mediate the relationship
evidence for dysfunction in adults with ADHD during between early childhood stress and spatial working memory.
motivation and attention. Cortex, 48, 194–214. Journal of Neuroscience, 32, 7917–7925.
De Brito, S. A., Mechelli, A., Wilke, M., Laurens, K. R., Jones, Hanson, J. L., Chung, M. K., Avants, B. B., Shirtcliff, E. A.,
A. P., Barker, G. J., . . . Viding, E. (2009). Size matters: Gee, J. C., Davidson, R. J., & Pollak, S. D. (2010). Early
Increased grey matter in boys with conduct problems and stress is associated with alterations in the orbitofrontal cortex:
callous-unemotional traits. Brain, 132, 843–852. A tensor-based morphometry investigation of brain structure
Degnan, K. A., Hane, A. A., Henderson, H. A., Moas, O. L., and behavioral risk. Journal of Neuroscience, 30, 7466–7472.
Reeb-Sutherland, B. C., & Fox, N. A. (2011). Longitudinal Hanson, J. L., Hair, N., Shen, D. G., Shi, F., Gilmore, J. H.,
stability of temperamental exuberance and social-emotional Wolfe, B. L., & Pollak, S. D. (2013). Family poverty affects the
outcomes in early childhood. Developmental Psychology, 47, rate of human infant brain growth. PLoS ONE, 8, e80954
765–780. Heatherton, T. F. (2011). Neuroscience of self and self-regulation.
Dishion, T. J., & Hiatt Racer, K. (2013). Development of adult Annual Review of Psychology, 62, 363–390.
antisocial behavior. In T. P. Beauchaine & S. P. Hinshaw Heatherton, T. F., & Wagner, D. D. (2011). Cognitive
(Eds.), Child and adolescent psychopathology (2nd ed., pp. neuroscience of self-regulation failure. Trends in Cognitive
453–488). Hoboken, NJ: Wiley. Sciences, 15, 132–139.
Eme, R. (2015). Beauchaine ontogenic process model of Heller, A. S., Cohen, A. O., Dreyfuss, M. F. W., & Casey, B. J.
externalizing psychopathology a biosocial theory of crime (2016). Changes in cortico-subcortical and subcortico-
and delinquency. Journal of Criminal Justice, 43, 443–449. subcortical connectivity impact cognitive control to
Eme, R. (2017). Longitudinal studies of antisocial outcome in emotional cues across development. Social Cognitive and
individuals with childhood attention deficit hyperactivity Affective Neuroscience, 11, 1910–1918.
disorder. Journal of Psychiatry and Psychiatric Disorders, 1, Huebner, T., Vloet, T. D., Marx, I., Konrad, K., Fink, G. R.,
180–189. Herpertz, S. C., & Herpertz-Dahlmann, B. (2008).
Fair, D. A., Nigg, J. T., Iyer, S., Bathula, D., Mills, K. L., Morphometric brain abnormalities in boys with conduct
Dosenbach, N. U. F., . . . Milham, M. P. (2013). Distinct neural disorder. Journal of the American Academy of Child and
signatures detected for ADHD subtypes after controlling for Adolescent Psychiatry, 47, 540–547.
micro-movements in resting state functional connectivity Iacono, W. G., Malone, S. M., & McGue, M. (2008). Behavioral
MRI data. Frontiers in Systems Neuroscience, 6, 80. disinhibition and the development of early-onset addiction:
Frazier, T. W., Youngstrom, E. A., Speer, L., Embacher, R., Law, Common and specific influences. Annual Review of Clinical
P., Constantino, J., . . . Eng, C. (2012). Validation of proposed Psychology, 4, 325–348.
DSM-5 criteria for autism spectrum disorder. Journal of the Kim, P., Evans, G. W., Angstadt, M., Ho, S. S., Sripada, C. S.,
American Academy of Child and Adolescent Psychiatry, 51, Swain, J. E., . . . Phan, K. L. (2013). Effects of childhood
28–40. poverty and chronic stress on emotion regulatory brain
Galván, A. (2013). The teenage brain: Sensitivity to rewards. function in adulthood. Proceedings of the National Academy of
Current Directions in Psychological Science, 22, 88–93. Sciences, 110, 18442–18447.

Krueger, R. F. (1999). The structure of common mental disorders. Moffitt, T. E. (1993). Adolescence-limited and life-course-persistent
Archives of General Psychiatry, 56, 921–926. antisocial behavior: A developmental taxonomy. Psychological
Krueger, R. F., Hicks, B. M., Patrick, C. J., Carlson, S. R., Review, 100, 674–701.
Iacono, W. G., & McGue, M. (2002). Etiologic connections Moffitt, T. E. (2006). Life-course-persistent versus adolescence-
among substance dependence, antisocial behavior, and limited antisocial behavior. In D. Cicchetti & D. J. Cohen
personality: Modeling the externalizing spectrum. Journal of (Eds.), Developmental psychopathology: Risk, disorder, and
Abnormal Psychology, 111, 411–424. adaptation (pp. 570–598). Hoboken, NJ: Wiley.
Laakso, A., Wallius, E., Kajander, J., Bergman, J., Eskola, O., Molina, B. S. G., Pelham, W. E., Cheong, J., Marshal, M. P., &
Solin, O., . . . Hietala, J. (2003). Personality traits and striatal Gnagy, E. M. (2012). Childhood attention-deficit/hyperactivity
dopamine synthesis capacity in healthy subjects. American disorder (ADHD) and growth in adolescent alcohol use:
Journal of Psychiatry, 160, 904–910. The roles of functional impairments, ADHD symptom
Lahey, B. B., Krueger, R. F., Rathouz, P. J., Waldman, I. D., & persistence, and parental knowledge. Journal of Abnormal
Zald, D. H. (2017). A hierarchical causal taxonomy of Psychology, 121, 922–935.
psychopathology across the lifespan. Psychological Bulletin, Musser, E. D., Karalunas, S. L., Dieckmann, N., Peris, T. S., &
143, 142–186. Nigg, J. T. (2016). Attention-deficit/hyperactivity disorder
Lahey, B. B., Rathouz, P. J., Keenan, K., Stepp, S. D., Loeber, R., developmental trajectories related to parental expressed
& Hipwell, A. E. (2014). Criterion validity of the general emotion. Journal of Abnormal Psychology, 125, 182–195.
factor of psychopathology in a prospective study of girls. Neuhaus, E., & Beauchaine, T. P. (2017). Impulsivity and
Journal of Child Psychology and Psychiatry, 56, 415–422. vulnerability to psychopathology. In T. P. Beauchaine &
Lahey, B. B., Van Hulle, C. A., Singh, A. L., Waldman, I. D., & S. P. Hinshaw (Eds.), Child and adolescent psychopathology
Rathouz, P. J. (2011). Higher-order genetic and environmental (3rd ed., pp. 178–212). Hoboken, NJ: Wiley.
structure of prevalent forms of child and adolescent Nikolas, M. A., & Burt, S. A. (2010). Genetic and environmental
psychopathology. Archives of General Psychiatry, 68, 181–189. influences on ADHD symptom dimensions of inattention
Louilot, A., LeMoal, M., & Simon, H. (1989). Opposite and hyperactivity: A meta-analysis. Journal of Abnormal
influences of dopaminergic pathways to the prefrontal cortex Psychology, 119, 1–17.
or the septum on the dopaminergic transmission in the Oberlin, B. G., Dzemidzic, M., Bragulat, V., Lehigh, C. A.,
nucleus accumbens: An in vivo voltammetric study. Talavage, T., O’Connor, S. J., & Kareken, D. A. (2012).
Neuroscience, 29, 45–56. Limbic responses to reward cues correlate with antisocial trait
Luby, J., Belden, A., Botteron, K., Marrus, N., Harms, M. P., density in heavy drinkers. NeuroImage, 60, 644–652.
Babb, C., . . . Barch, D. (2013). The effects of poverty Olino, T. M., Dougherty, L. R., Bufferd, S. J., Carlson, G. A.,
on childhood brain development. JAMA Pediatrics, 167, & Klein, D. N. (2014). Testing models of psychopathology
1135–1142. in preschool-aged children using a structured interview-
Luijten, M., Schellekens, A. F., Kühn, S., Machielse, M. W. J., & based assessment. Journal of Abnormal Child Psychology, 42,
Sescousse, G. (2017). Disruption of reward processing in 1201–1211.
addiction: An image-based meta-analysis of functional MRI Patterson, G. R., DeGarmo, D. S., & Knutson, N. M. (2000).
studies. JAMA Psychiatry, 74, 387–398. Hyperactive and antisocial behaviors: Comorbid or two
Lynam, D. R., Caspi, A., Moffitt, T. E., Wikstrom, P. H., Loeber, points in the same process? Development and Psychopathology,
R., & Novak, S. (2000). The interaction between impulsivity 12, 91–107.
and neighborhood context in offending: The effects of Plichta, M. M., & Scheres, A. (2014). Ventral-striatal responsiveness
impulsivity are stronger in poorer neighborhoods. Journal of during reward anticipation in ADHD and its relation to trait
Abnormal Psychology, 109, 563–574. impulsivity in the healthy population: A meta-analytic
Macdonald, A., Goines, K., Novacek, D., & Walker, E. (2016). review of the fMRI literature. Neuroscience and Biobehavioral
PFC mechanisms of comorbidity from a transdiagnostic and Reviews, 38, 125–134.
ontogenic perspective. Development and Psychopathology, 28, Quinn, P. D., & Harden, K. P. (2013). Differential changes in
1147–1175. impulsivity and sensation seeking and the escalation of
Marshal, M. P., & Molina, B. G. (2006). Antisocial behaviors substance use from adolescence to early adulthood.
moderate the deviant peer pathway to substance use in Development and Psychopathology, 25, 223–239.
children with ADHD. Journal of Clinical Child and Raine, A. (2018). Antisocial personality as a neurodevelopmental
Adolescent Psychology, 35, 216–226. disorder. Annual Review of Clinical Psychology, 14, 259–289.
McDonough-Caplan, H. M., & Beauchaine, T. P. (2018). Robins, L. N. (1966). Deviant children grown up. Baltimore,
Conduct disorder: A neurodevelopmental perspective. In MD: Williams & Wilkins.
M. M. Martel (Ed.), Disruptive, impulse-control, and conduct Rubia, K., Smith, A., Halari, R., Matukura, F., Mohammad, M.,
disorders: Assessment, pathways, and intervention (pp. 53–89). Taylor, E., & Brammer, M. J. (2009). Disorder-specific
Cambridge, MA: Elsevier. dissociation of orbitofrontal dysfunction in boys with pure
McDonough-Caplan, H., Klein, D. N., & Beauchaine, T. P. conduct disorder during reward and ventrolateral prefrontal
(2018). Comorbidity and continuity of depression and dysfunction in boys with pure attention-deficit/hyperactivity
conduct problems from elementary school to adolescence. disorder during sustained attention. American Journal of
Journal of Abnormal Psychology, 127, 326–337 . Psychiatry, 166, 83–94.
Meier, M. H., Slutske, W. S., Arndt, S., & Cadoret, R. J. (2008). Sagvolden, T., Johansen, E. B., Aase, H., & Russell, V. A. (2005).
Impulsive and callous traits are more strongly associated with A dynamic developmental theory of ADHD predominantly
delinquent behavior in higher risk neighborhoods among hyperactive/impulsive and combined subtypes. Behavioral
boys and girls. Journal of Abnormal Psychology, 117, 377–385. and Brain Sciences, 28, 397–419.

Santiago, C. D., Wadsworth, M. E., & Stump, J. (2011). Snyder, J., Schrepferman, L., McEachern, A., Barner, S.,
Socioeconomic status, neighborhood disadvantage, and Johnson, K., & Provines, J. (2008). Peer deviancy training
poverty-related stress: Prospective effects on psychological and peer coercion: Dual processes associated with early-onset
syndromes among diverse low-income families. Journal of conduct problems. Child Development, 79, 252–268.
Economic Psychology, 32, 218–230. Storebø, O. J., & Simonsen, E. (2016). The association between
Sasser, T. R., Kalvin, C. B., & Bierman, K. L. (2016). ADHD and antisocial personality disorder (ASPD): A review.
Developmental trajectories of clinically significant attention- Journal of Attention Disorders, 20, 815–824.
deficit/hyperactivity disorder (ADHD) symptoms from Tackett, J. L., Lahey, B. B., van Hulle, C., Waldman, I., Krueger,
grade 3 through 12 in a high-risk sample: Predictors and R. F., & Rathouz, P. J. (2013). Common genetic influences
outcomes. Journal of Abnormal Psychology, 125, 207–219. on negative emotionality and a general psychopathology
Sauder, C., Beauchaine, T. P., Gatzke-Kopp, L. M., Shannon, factor in childhood and adolescence. Journal of Abnormal
K. E., & Aylward, E. (2012). Neuroanatomical correlates of Psychology, 122, 1142–1153.
heterotypic comorbidity in externalizing male adolescents. Thapar, A., Langley, K., Owen, M. J., & O’Donovan, M. C.
Journal of Clinical Child and Adolescent Psychology, 41, (2007). Advances in genetic findings on attention deficit
346–352. hyperactivity disorder. Psychological Medicine, 37, 1681–1692.
Shannon, K. E., Sauder, C., Beauchaine, T. P., & Gatzke-Kopp, Thompson, R. A. (1990). Emotion and self-regulation. In
L. (2009). Disrupted effective connectivity between the R. A. Thompson (Ed.), Nebraska Symposium on Motivation:
medial frontal cortex and the caudate in adolescent boys with Vol. 36. Socioemotional development (pp. 383–483). Lincoln,
externalizing behavior disorders. Criminal Justice and Behavior, NE: University of Nebraska Press.
36, 1141–1157. Vijayakumar, N., Whittle, S., Yucel, M., Dennison, M.,
Shaw, P., Malek, M., Watson, B., Sharp, W., Evans, A., & Simmons, J., & Allen, N. B. (2014). Thinning of the lateral
Greenstein, D. (2012). Development of cortical surface area prefrontal cortex during adolescence predicts emotion
and gyrification in attention-deficit/hyperactivity disorder. regulation in females. Social Cognitive and Affective
Biological Psychiatry, 72, 191–197. Neuroscience, 9, 1845–1854.
Smith, C. L., Calkins, S. D., & Keane, S. P. (2006). The relation Webster-Stratton, C., Reid, M. J., & Beauchaine, T. P. (2013).
of maternal behavior and attachment security to toddlers’ One-year follow-up of combined parent and child
emotions and emotion regulation. Research in Human intervention for young children with ADHD. Journal of
Development, 3, 21–31. Clinical Child and Adolescent Psychology, 42, 251–261.
Snyder, J., Edwards, P., McGraw, K., Kilgore, K., & Holton, A. Zisner, A., & Beauchaine, T. P. (2016). Neural substrates of trait
(1994). Escalation and reinforcement in mother-child impulsivity, anhedonia, and irritability: Mechanisms of
conflict: Social processes associated with the development of heterotypic comorbidity between externalizing disorders and
physical aggression. Development and Psychopathology, 6, unipolar depression. Development and Psychopathology, 28,
305–321. 1179–1210.

CH A PTE R
18 Internalizing Spectrum Disorders
Camelia E. Hostinar and Dante Cicchetti
Abstract
Emotion dysregulation is a pattern of emotional experience or expression that interferes with

goal-directed behavior, and may set children and adolescents on developmental trajectories toward
psychopathology. Despite accumulating evidence linking emotion dysregulation to various forms of
internalizing psychopathology (e.g., depression, anxiety), several open questions remain. What are the
developmental pathways leading to emotion dysregulation and modifiable environmental conditions
that appear to foster it? What is the evidence that emotion dysregulation precedes or plays a causal
role in the development of internalizing spectrum disorders? What are the biological underpinnings of
emotion dysregulation, and how can we integrate this research with recent discoveries about internalizing
spectrum disorders from neuroscience, psychophysiology, genetics, and epigenetics? This review discusses
recent research pertinent to these three primary questions and concludes with suggestions for future
research and implications for interventions that promote resilience in youth.
Keywords: emotion, emotion dysregulation, child, adolescent, psychopathology, internalizing
Introduction disorders such as depression and anxiety (Aldao,

Our ability to manage difficult negative emotions is Nolen-Hoeksema, & Schweizer, 2010; Behar,
central for our mental and physical health, success- DiMarco, Hekler, Mohlman, & Staples, 2009;
ful social interactions, and accomplishing long-term Gotlib & Joormann, 2010; Mennin, Heimberg, Turk,
goals. In contrast, emotion dysregulation is a pattern & Fresco, 2002; Sheppes, Suri, & Gross, 2015).
of emotional experience or expression that interferes However, despite the heuristic value and accu-
with goal-directed behavior, and may set us on mulating empirical evidence supporting the utility
trajectories toward psychopathology (Beauchaine, of this construct for understanding the develop-
2015a; Beauchaine & Gatzke-Kopp, 2012). This ment and maintenance of psychopathology in gen-
failure to modulate emotional dynamics to achieve eral and internalizing spectrum disorders in particu-
beneficial outcomes can occur for any number of lar (Beauchaine, 2015a; Cole, Hall, & Hajal, 2010),
reasons. It can arise from the intensity of the emo- many open questions remain. For instance, what are
tions (which can make them more challenging to the developmental pathways leading to emotion
regulate), from mismatches between the emotional dysregulation and modifiable environmental condi-
experience and the situation, or from problems of tions that appear to foster it? What is the evidence
coordination between emotion and cognition or be- that emotion dysregulation precedes or plays a
tween emotion and action (Cicchetti, Ackerman, & causal role in the development of internalizing
Izard, 1995). Understanding the diverse causes and spectrum disorders, as opposed to simply being a
consequences of emotion dysregulation is critical correlate or consequence of psychopathology?
because it is a defining feature of many debilitating Furthermore, what are the biological underpinnings
forms of psychopathology, particularly internalizing of emotion dysregulation, and how can we integrate
249
this research with recent discoveries about internal- paradigms capturing independent manifestations
izing disorders from neuroscience, psychophysiol- of emotion and emotion regulation demonstrate
ogy, genetics, and epigenetics? This review aims to that these processes can be studied separately de-
discuss research focusing on these questions and has spite being closely related (Cole et al., 2004). For
three goals. First, we summarize leading theoretical example, in infants, facial expressions of emotion
perspectives on the developmental origins of and and behavioral indicators of emotion regulatory
potential pathways to emotion dysregulation. Second, strategies such as gaze aversion and self-soothing
we review current methods of assessing emotion can be captured independently from one another.
regulation and dysregulation in children and adoles- Second, studies identifying different neural corre-
cents and highlight some of the most recent findings lates for various emotion regulation strategies such
supporting its role as a specific and potentially causal as cognitive reappraisal and emotion suppression
risk factor that precedes the development of inter- elicited in the laboratory (e.g., Goldin, McRae,
nalizing spectrum disorders. Third, we describe recent Ramel, & Gross, 2008) suggest the utility of de-
research attempting to link emotion regulation/ scribing and classifying various forms of emotion
dysregulation with multilevel processes at neural, regulation to allow for closer mapping of complex
psychophysiological, genetic, and epigenetic levels thoughts and behaviors onto their corresponding
of analysis. Finally, we conclude by providing some neural circuitry.
future directions for research and implications for Another compelling rationale for studying
interventions and the promotion of resilience. We emotion regulation is to understand why and when
adopt a developmental psychopathology framework it goes awry, a phenomenon frequently observed in
(Cicchetti, 1984, 2016) throughout this review be- psychopathology. As mentioned earlier, emotion
cause we believe that understanding normal and ab- dysregulation can be defined as a pattern of emotional
normal trajectories of emotional development experience or expression that interferes with goal-
across childhood and adolescence can yield impor- directed behavior (Beauchaine, 2015a; Beauchaine
tant insights into adult endpoints like severe emo- & Gatzke-Kopp, 2012). Leading theories on the
tion dysregulation and clinical levels of symptoma- development of many types of psychopathology
tology. Furthermore, this developmental approach assign important etiological roles to emotion dys-
can inform decisions on when, where, and how to regulation (Aldao et al., 2010; Behar et al., 2009;
intervene before maladaptive emotional patterns Gotlib & Joormann, 2010; Mennin et al., 2002;
become fully consolidated. Before proceeding with Sheppes et al., 2015). These theories also specify
these central aims, we define the primary concepts different types of emotion regulatory failures as

of interest in this review. being involved in different disorders. For example,
the inability to disengage from negative affect is
Defining the Core Concepts more characteristic of depression (Gotlib &
Despite lingering theoretical disagreements on the Joormann, 2010), whereas overuse of avoidance and
ultimate nature of emotions, many scientists agree suppression of emotion are thought to promote
that emotions are processes that motivate and chronic worry and anxiety disorders (Mennin et al.,
organize behavior (Cicchetti et al., 1995) and that 2002). Although these theories have garnered sig-
they reflect an appraisal of a situation’s meaning nificant empirical support in the last two decades,
for individual well-being (Cole, Martin, & Dennis, an ongoing challenge in this area of research is that
2004). An important realization in research from psychopathology can be a result of problems with
the past two decades is that the qualities of our emotion generation, emotion regulation, or both.
emotional experiences (e.g., valence, intensity, du- Thus, it can be difficult to isolate specific effects of
ration) depend on our ability to modify emotional emotion regulation difficulties in the development
responses to accomplish individual goals, which of psychopathology (Cicchetti et al., 1995; Sheppes
has been termed emotion regulation (Thompson, et al., 2015). However, as we discuss later, there is
Lewis, & Calkins, 2008). The challenge of measuring emerging evidence to suggest a unique and additive
emotion and its regulation as separate processes role of emotion dysregulation in explaining variability
has raised a number of questions about the validity in mental health outcomes, over and above the role
of the construct of emotion regulation (Cole et al., of other constructs such as trait negative affectivity
2004). However, two streams of evidence have and exposure to stressful life events.
provided foundational evidence for the validity In this review, we focus specifically on internal-
and utility of the construct. First, experimental izing spectrum disorders, which are psychological
250 Emotion Dysregul ation and Internalizing Disorders

conditions with high levels of negative affectivity that greater risk of developing depression and anxiety
is self-directed or “intropunitive” and most often (Li, D’Arcy, & Meng, 2016; Nanni, Uher, &
covert (Tandon, Cardeli, & Luby, 2009). In the Danese, 2012; Nelson, Klumparendt, Doebler, &
Diagnostic and Statistical Manual of Mental Health Ehring, 2017). Furthermore, maltreatment predicts
Disorders, fifth edition (DSM-5) classification system, earlier onset, more severe course, and greater risk of
these include depressive disorders, anxiety disorders, recurring, persistent, and treatment-resistant mani-
obsessive-compulsive and related disorders, trauma festations of mood disorders (Nanni et al., 2012;
and stressor-related disorders, and dissociative disor- Nelson et al., 2017). Despite these robust associa-
ders (Regier, Kuhl, & Kupfer, 2013). In this review, tions, there is a dearth of studies examining the pro-
we focus primarily on depressive and anxiety disor- tective factors or other modifiable predictors of de-
ders, as most prior research on emotion dysregulation pression following maltreatment (Braithwaite,
with children and adolescents has centered on these O’Connor, Degli-Esposti, Luke, & Bowes, 2017).
subtypes of internalizing disorders. Internalizing Nevertheless, research from the past two decades
spectrum disorders are often characterized by ineffec- consistently reveals that maltreated children have
tive management of emotional arousal (particularly emotional difficulties with emotion perception, un-
sadness or fear) and are typically accompanied by derstanding, and regulation (Cicchetti & Ng, 2014;
alterations in physiology and neural function. These Luke & Banerjee, 2013; Pollak, 2015), and these al-
disorders are also more prevalent among those who terations likely explain a number of pathways to
have experienced major life stressors or emotionally mood and anxiety disorders. For instance, neglected
unsupportive environments during childhood or children struggle with discriminating emotional ex-
adolescence, as we discuss in the next section. pressions, whereas physically abused children show
Unlike temperamental predispositions for internal- attentional biases toward angry faces (Pollak,
izing symptoms, which show moderate levels of Cicchetti, Hornung, & Reed, 2000). Maltreated
heritability, emotion dysregulation is one of the children also show greater negative affect during
less heritable risk factors for psychopathology tasks that provoke anger or frustration (Shackman
(Beauchaine, 2015a). This suggests an important & Pollak, 2014). More specifically relevant to the
role for the social environment in shaping children’s development of depression, maltreated children
ability to develop consistent and effective strategies to show biased attention to sad faces after induction of
regulate their emotions, and the greater potential for a sad state, particularly if they have an affective style
plasticity if interventions occur early in development. that is high in rumination, an emotion regulation
strategy that is ineffective in dampening negative
Developmental Origins of affect and is a risk factor for depression (Romens &
Emotion Dysregulation Pollak, 2012). A recent meta-analysis of 51 empirical
The social milieu plays an important role in foster- studies showed that of all the emotional deficits
ing child and adolescent emotion dysregulation and studied in maltreated children, the greatest impair-
subsequent psychopathology. Childhood maltreat- ments are in the domain of emotion understanding,
ment, insecure or disorganized attachment, parental and these impairments are more prevalent in
psychopathology, negative family climate and prac- younger children compared to older children (Luke
tices, and peer rejection and victimization are all & Banerjee, 2013).
linked to greater odds of emotion dysregulation and One of the primary pathways through which
internalizing psychopathology. What remains to be maltreatment leads to emotion dysregulation ap-
understood are the pathways through which reject- pears to be through altered attentional processes,
ing or unpredictable family and peer groups lead to which can involve either poor attention modulation
these outcomes, though some evidence is beginning and attention deficits (Shields & Cicchetti, 1998) or
to illuminate these pathways. attentional biases toward threatening or sad stimuli
(for a recent review, see Pollak, 2015). These factors
Family Processes can lead children to dedicate more attentional re-
Maltreatment is a toxic social environment for chil- sources to negative stimuli, which generates more
dren that poses significant risk for development of negative affect that is then compounded by difficulties
both internalizing and externalizing psychopathology with disengaging or shifting attention away from
(Cicchetti & Ng, 2014; Cicchetti & Toth, 2005). negative stimuli. In addition to these biases, there is
Recent meta-analytic syntheses reveal that child- some evidence that another important pathway
hood maltreatment experiences are associated with may be that maltreated children develop atypical
Hostinar and Cicchet ti 251

patterns of processing positive stimuli and rewards. emotions. However, in situations of inconsistent,
For instance, one study with 8- to 14-year-olds emotionally unavailable, or frightened/frightening
revealed that maltreated youth were less likely to parenting, children develop insecure or disorgan-
modulate their behavioral responses based on re- ized attachment patterns and emotion regulation
wards, and those maltreated youth with depressive strategies that are not effective in downregulating
disorders were more likely to prefer low-risk/low- negative affect (Main & Solomon, 1986).
reward options than high-risk/high-reward options Children who develop an insecure-anxious
(Guyer et al., 2006). It is unclear whether this is due attachment pattern learn to amplify their own

to the relative infrequency of rewards in the envi- negative and fearful behaviors to elicit caregiving

ronment for maltreated children or due to stress- from inconsistent parents, whereas those with an
related neural alterations in reward circuitry that insecure-avoidant pattern learn to suppress and mask
shifts how rewards are processed. Overall, attention their negative affect to avoid eliciting rejection from
control deficits, attentional biases to threat, and their caregivers (Cassidy, 1994). Children with disor-
blunted responsivity to rewards form a triad of char- ganized attachment strategies develop i ncoherent and
acteristics that not only may independently increase contradictory strategies that leave them vulnerable in
the odds of developing depressive symptoms but the face of environmental challenges (Brumariu &
also may potentiate each other over time, though Kerns, 2010). Although all of these strategies are well
this possibility has yet to be tested empirically. adapted to specific caregiving circumstances children
Although extreme forms of harsh or neglectful find themselves in, they are not effective at managing
parenting can predispose children to emotion dys- negative affect in the long run and may predispose to
regulation and subsequent psychopathology, other psychopathology. Indeed, a review of this empirical
family characteristics and practices can have similar literature showed that overall, most studies suggest
effects, even in the absence of full-blown abuse or that early-life insecure attachment is related to a
neglect. There are three primary pathways through higher chance of subsequently developing depression
which families are thought to impact the develop- or anxiety, with associations being stronger when psy-
ment of children’s emotion regulation. First, chil- chopathology is assessed in preadolescence and ado-
dren first learn how to regulate their emotions lescence versus childhood (Brumariu & Kerns, 2010).
from their families via observation, which includes However, few studies have directly tested the hypoth-
processes such as observational learning, modeling, esis that emotion dysregulation mediates these asso-
and social referencing (Morris, Silk, Steinberg, ciations. One report from the Minnesota Longitudinal
Myers, & Robinson, 2007; Thompson & Meyer, Study of Parents and Children supported this hy-
2007). Second, there is evidence that specific par- pothesis and revealed that a history of attachment in-
enting practices and behaviors socialize children security assessed with the Strange Situation proce-
about emotions and their regulation (Calkins & dure during infancy was associated with parent- and
Hill, 2007). For instance, parents’ negative reactions teacher-reported anxiety in childhood, and this asso-
to children’s emotions, as well as parents’ own lim- ciation was mediated by preschool emotion regula-
itations in emotional expressivity, can set children tion skills as assessed by levels of distress, crying, and
on trajectories toward emotion dysregulation anger during a frustration task (Bosquet & Egeland,
(Calkins & Hill, 2007; Eisenberg, Cumberland, & 2006). Another study examining attachment repre-
Spinrad, 1998). Finally, the emotional climate of sentations in middle childhood and adolescence (ages
the family, which includes overall relationship 8 to 14 years old) found that attachment anxiety was
quality and attachment processes embedded in related to emotion dysregulation, whereas attachment
parent–child and marital relationships, also shape avoidance was associated with emotion suppression,
children’s emotion regulation abilities for better or and emotion dysregulation and suppression partially
for worse (Brumariu & Kerns, 2010; Morris et al., mediated associations with depressive symptoms in a
2007). Attachment research shows that sensitive, cross-sectional m ediation analysis (Brenning, Soenens,
responsive caregiving teaches children to use their Braet, & Bosmans, 2012).
parental figures as a safe haven and is an external Children’s biological predispositions also interact
regulator of distress and other negative emotions with features of the social environment to shape the
(Ainsworth, Bell, & Stayton, 1974). Over time, risk of developing internalizing spectrum disorders.
these processes become internalized and children For instance, children whose temperaments are high
begin to be able to regulate their own negative on behavioral inhibition or negative affectivity tend

to develop more symptoms of anxiety or depression Current Methods and Recent
when reared in negative, unsupportive environments Findings Explicating the Role
(Dougherty, Klein, Rose, & Laptook, 2011; N. A. of Emotion Dysregulation in
Fox, 1994; Yap, Allen, & Sheeber, 2007). Parental Youth Psychopathology
psychopathology is another risk factor for children’s Current Methods
internalizing symptoms, whether through genetic Emotional processes encompass behavioral, physio-
risk factors or through dysfunctional patterns of logical, phenomenological, cognitive, and sociocul-
parenting (e.g., parents with borderline personality tural aspects (Solomon, 2002) that are challenging
disorder tend to engage in more insensitive, hostile, to capture through any single measure or protocol.
or overprotective parenting, which in turn predicts Thus, it is not surprising that there are diverse ap-
children’s psychopathology; Eyden, Winsper, Wolke, proaches to assessing emotions and to inferring
Broome, & MacCallum, 2016). Moreover, these emotion regulatory processes. Four general strate-
parents may also possess biological vulnerabilities gies are widely used in research with children and
that serve as a diathesis for emotional lability in adolescents: self-report, other report (e.g., from
their offspring. teachers, parents, peers), observation, and neuro-
physiology (Zeman, Klimes-Dougan, Cassano, &
Peer Processes Adrian, 2007). These assessment tools need to be
In addition to the family environment, relationships tailored to the developmental stage of the participant.
with peers can also promote or hinder the develop- For instance, observation and neurophysiological
ment of emotion regulation abilities, as well as assessments (e.g., electroencephalogram [EEG],
subsequent psychopathology. Children between electrocardiogram [ECG], hormone production)
the ages of 8 and 13 years who are victims of rela- would be primary sources of information in infancy,
tional or overt victimization are at greater risk of whereas self-report becomes more central during
developing internalizing symptomatology, though childhood and adolescence, but would need to be
this association is moderated by genotype (e.g., the combined with other measures to enhance validity.
serotonin transporter gene variant; Banny, Cicchetti, In addition to capturing developmental stage, an-
Rogosch, Oshri, & Crick, 2013). Longitudinal other temporal dimension that would need to be
studies show a complex interplay between family considered is whether the measures reflect state or
and peer relationships, emotion dysregulation, and trait-level processes.
psychopathology. One such study revealed that Even within each of these four general approaches,
children ages 6 to 12 years who experienced mal- there is a wide variety of assessment methods. For
treatment by family members were more likely to instance, a recent review of emotion regulation studies
develop emotion dysregulation, which was linked from the past 35 years conducted with samples
to higher externalizing psychopathology and later ranging from infancy to adolescence revealed that
peer rejection (Kim & Cicchetti, 2010). In turn, these studies have used 28 self-report formats, 17
peer rejection was related to higher levels of psy- other-report formats, 47 observational paradigms,
chopathology, whereas higher levels of emotion and 8 physiological assessments to measure emotion
regulation served as a protective factor against es- regulation (Adrian, Zeman, & Veits, 2011). Given
calating levels of internalizing symptoms over time this diversity of approaches, there is a critical need
(Kim & Cicchetti, 2010). Another large longitudi- for increased standardization of methods and for
nal study of 1,065 adolescents between the ages of holistic models that could integrate information
11 and 14 years showed that peer victimization from these multimethod and multilevel approaches
predicted increases in emotion dysregulation over into a coherent representation of emotional processes
a 4-month period, which mediated increases in that will translate well to real-life and clinical settings.
internalizing symptoms over a 7-month period
In addition, the models developed should be infor-
(McLaughlin, Hatzenbuehler, & Hilt, 2009). Given mative in predicting behavior.
the frequency and salience of peer-related stressors Another limitation of existing methods is that so
in middle school and high school, these findings far most assessments of emotions and their regula-
have important implications for understanding tion/dysregulation have focused on the individual,
potentially modifiable risk factors for the develop- despite the fact that most emotion theories recog-
ment of emotion dysregulation and subsequent nize the person–environment interactions inher-
internalizing symptoms in these age groups. ently involved in any emotional responses (see also

Thompson & Waters, this volume). The social- is also linked to greater likelihood of anxiety
contextual embedding of individuals within their and depression (Nolen-Hoeksema, Wisco, &
environments is not usually considered when meas- Lyubomirsky, 2008).
uring emotions, and this is a limitation of current However, these overall associations between
research (Aldao, 2013). For instance, research thus emotion regulation strategies and internalizing
far has not dedicated sufficient attention to ques- psychopathology do not reveal whether emotion
tions such as the following: How typical are the ob- dysregulation precedes or plays a causal role in
served emotional reactions for the social, economic, (versus being a correlate or consequence of ) psy-
and cultural background of the participants? How chopathology. In adults, there is some correlational
do individual emotion regulation skills vary across evidence that emotion regulation explains risk of
social contexts, and how can we intervene to prevent internalizing psychopathology independent from
the generalization of emotion dysregulation from contributions of high-intensity negative affect and
one context (e.g., maltreating family) to another of childhood trauma (Bradley et al., 2011), suggesting
(e.g., school settings and interactions with peers)? that the association is not easily explained by other
Currently, there are no empirically validated taxon- potentially confounding factors. Causal inferences
omies for capturing the social contexts of emotion are challenging to extract from correlational data,
(Zeman et al., 2007); thus, this remains an impor- but prospective longitudinal studies can shed light
tant direction for future research. on the plausible direction of effects and potentially
rule out some reverse-causality pathways.
Recent Findings One such prospective longitudinal study with
Numerous correlational studies substantiate the hy- children (Kim-Spoon, Cicchetti, & Rogosch, 2013)
pothesis that emotion regulation strategies are asso- reported that early-life maltreatment was associated
ciated with internalizing symptoms. To illustrate with emotional negativity/lability at age 7, which
growing attention to these associations, a recent was associated with poor emotion regulation at age 8.
meta-analysis of 35 empirical studies conducted This, in turn, predicted internalizing psychopathol-
with youth and aggregating 68 effect sizes con- ogy at ages 8 and 9, controlling for prior levels of
firmed that the habitual use of adaptive emotion symptoms and emotion regulation (Kim-Spoon
regulation strategies (cognitive reappraisal, problem et al., 2013). This temporal ordering is consistent with
solving, and acceptance) appears protective against results from another longitudinal study showing
depressive and anxious symptoms in adolescence that maternal depression during the first few years
(Schafer, Naumann, Holmes, Tuschen-Caffier, & of life predicted children’s emotion dysregulation at
Samson, 2017). Cognitive reappraisal involves age 3 and worse socioemotional functioning at age
changing thoughts and beliefs about the meaning of 5 (Maughan, Cicchetti, Toth, & Rogosch, 2007). It
a situation and is a strategy that alters the emotional is also consistent with a mediational study with 4-
process early on before full-blown activation (Gross, to 6-year-old children revealing that maltreatment
2013). Problem solving is a regulatory strategy that history predicted emotion dysregulation, which
includes cognitive and behavioral responses that at- mediated associations between maltreatment and
tempt to eliminate the cause of negative emotions. anxious or depressed symptoms (Maughan &
In contrast, acceptance refers to allowing one’s emo- Cicchetti, 2002). Importantly, some studies show
tions to unfold without judgment or suppression that parenting moderates the association between
(Schafer et al., 2017). Maladaptive emotion regula- emotion dysregulation and subsequent psychopa-
tion strategies (avoidance, suppression, and rumina- thology. For instance, one study of 9- to 10-year-old
tion) are positively associated with internalizing girls showed that low levels of positive affect expres-
symptoms (Schafer et al., 2017). Avoidance consists sion and sadness regulation predict later depressive
of averting situations that may trigger negative symptoms only in girls whose parents are low in
emotions, whereas suppression refers to attempts to acceptance (Feng et al., 2009).
deny or prevent focusing on such emotions, and Prospective longitudinal studies with adolescents
these strategies have been linked to greater risk of also reveal that emotion dysregulation or poor emo-
psychopathology in youth (Schafer et al., 2017). Even tion identification skills can predict increases in
though avoidance and suppression are associated symptoms of anxiety, depression, aggression, and
with worse mental health, the opposite strategy of eating disorders, controlling for baseline symptoms
prolonged mental rehearsal of emotional experiences (Ciarrochi, Heaven, & Supavadeeprasit, 2008;
and their causes and consequences (i.e., rumination) Hatzenbuehler, McLaughlin, & Nolen-Hoeksema,

2008; McLaughlin, Hatzenbuehler, Mennin, & are thought to be complex psychobiological processes
Nolen-Hoeksema, 2011). For instance, one longitu- involving multiple neural, hormonal, and behavioral
dinal study following 667 high school students for systems that interact via mutual feedback loops
1 year found that low emotion identification skills (Thompson et al., 2008). Furthermore, emotion
in eighth grade predicted increases in fear and de- dysregulation is often conceptualized as the result of
creases in positive affect in the overall sample and interactions between “bottom-up” emotional pro-
increases in sad affect among boys from eighth grade cesses and “top-down” control or regulatory processes
to ninth grade (Ciarrochi et al., 2008). In a com- (Ochsner & Gross, 2005; Swartz & Monk, 2014);
munity sample of 1,071 middle school students thus, this construct could serve as a useful starting
(ages 11 to 14), sexual minority adolescents reported point for integrating findings on the interactions
higher levels of internalizing symptoms at the base- between processes occurring at these levels of
line and 7 months later (compared to nonminority analysis. In this section, we provide some examples
youth), with emotion regulation deficits mediating of how measures of emotion dysregulation have
changes in internalizing symptoms from baseline to started to be studied in conjunction with neural,
follow-up (Hatzenbuehler et al., 2008). In another psychophysiological, genetic, and epigenetic assess-
report, baseline psychopathology did not predict ments to begin formulating integrative psychobio-
changes in emotion dysregulation over time, but logical models for the etiology of internalizing
baseline emotion dysregulation predicted longitudi- symptoms.
nal increases in anxiety symptoms, aggressive behav-
ior, and eating pathology among 1,065 middle school Affective Neuroscience Findings
students ages 11 to 14 (McLaughlin et al., 2011). Research has begun probing neural correlates of
Overall, these prospective longitudinal studies emotion regulation and dysregulation (Ochsner &
suggest that emotion dysregulation most consistently Gross, 2005). Contemporary theories postulate
precedes the onset or exacerbation of future internal- that deficits in prefrontal control of subcortical
izing symptoms, but the reverse prediction is not regions play a critical role in failure to appropriately
true. Causal inference is difficult to draw from corre- contain or terminate emotions (Ahmed, Bittencourt-
lational findings, but the pattern of results thus far is Hewitt, & Sebastian, 2015; Beauchaine, 2015a;
more consistent with potential causal involvement of Davidson, Pizzagalli, Nitschke, & Putnam, 2002;
emotion dysregulation in the future development of Macdonald, Goines, Novacek, & Walker, 2016;
psychopathology, rather than being a consequence of Swartz & Monk, 2014). This is a particularly salient
or a simple correlate of psychopathology. issue in adolescence, when emotional reactivity in-
creases (Dahl & Gunnar, 2009) but prefrontally
What Are the Biological Underpinnings of mediated emotion regulation skills are slower to de-
Emotion Dysregulation? Recent Findings velop (Casey et al., 2010). This disparity is thought
and Open Questions to contribute to the rise in psychopathology during
Modern conceptualizations of mental health and ill- this life stage (Ahmed et al., 2015). Supporting the-
ness such as the Research Domain Criteria (RDoC) ories on the role of prefrontal–limbic interactions in
defined by the National Institute of Mental Health emotion regulation/dysregulation, a meta-analysis
(NIMH) are moving beyond descriptive, DSM-based of functional magnetic resonance imaging (fMRI)
categorical definitions of disorders toward under- studies of healthy adults engaged in emotion regula-
standing the continuum of emotional experiences tion found a relatively consistent set of neural regions
and pathophysiology (Insel et al., 2010). The goal of involved (Frank et al., 2014). Across 47 studies of
this new framework for psychiatric research is to emotion downregulation and 12 studies of emotion
map complex behaviors and symptoms onto their upregulation, cortical regions including the superior
corresponding neural circuits and underlying genetic frontal gyrus, cingulate, and premotor areas showed
profiles (Insel et al., 2010). This new generation of enhanced activity across all regulation conditions,
research faces the daunting task of integrating mul- whereas the amygdala was associated with emotional
tilevel, multimethod measures into coherent models intensity, revealing heightened activity during up-
of specific clusters of symptoms that are associated regulated states and lower activity in downregulated
with clinical impairment (Beauchaine & Cicchetti, states (Frank et al., 2014).
2016). We believe that emotion dysregulation could Results consistent with the role of the prefrontal
serve as a useful bridge between these multiple levels cortex in the cognitive control of negative affect are
of analysis, as emotion regulation and dysregulation also found in clinical samples of adults. A review of

neuroimaging studies comparing depressed and exhibiting signs of internalizing psychopathology
nondepressed adults reported an overall pattern of also show elevated activity in limbic regions in-
overactive amygdala, overactive anterior cingulate volved in emotion processing such as the amygdala
cortex, and underactive dorsolateral prefrontal cortex and hippocampus. For instance, one study of
(dlPFC) in major depressive disorder (Gotlib & depressed 4- to 6-year-old preschoolers revealed a
Hamilton, 2008). This is not surprising given the right-lateralized pattern of elevated amygdala,
role of the amygdala in processing affectively salient thalamus, inferior frontal gyrus, and angular gyrus
stimuli and the role of the dlPFC in cognitive control, activity during face processing in this group com-
which is frequently deficient in depressed patients. pared to the unaffected control group, and amyg-
A similar pattern emerges for anxiety. For instance, dala activity was correlated with parent-reported
one fMRI study (Ball, Ramsawh, Campbell-Sills, deficits in emotion regulation (Gaffrey, Barch, Singer,
Paulus, & Stein, 2013) found that adults with gen- Shenoy, & Luby, 2013). Consistent with this result,
eralized anxiety disorder (GAD) and panic disorder a study of 60 school-aged children showed that
showed lower activation in dlPFC and dorsomedial greater responses to sad faces in emotion reactivity
prefrontal cortex (dmPFC) regions during emotion neural regions (e.g., amygdala, hippocampus) pre-
reappraisal and emotion maintenance while viewing dicted lower emotion regulation skills and higher
negative images compared to healthy controls. These levels of depression (Pagliaccio, Luby, Luking, Belden,
findings suggest that insufficient top-down control & Barch, 2014). When samples at risk for emotion
of negative affect may be a risk factor for the devel- dysregulation and internalizing were examined, ad-
opment of depressive and anxious symptomatology olescents (ages 13 to 19) with a prior history of child
in adults. maltreatment exhibited greater activation in the
Neuroimaging studies of emotion regulation and salience network (including the amygdala, putamen,
dysregulation have begun emerging in children and and anterior insula) in response to negative versus
adolescents (for reviews, please see Ahmed et al., neutral stimuli when compared to an unexposed
2015; Swartz & Monk, 2014). Results thus far appear control group (McLaughlin, Peverill, Gold, Alves,
consistent with studies in adults. A recent review of & Sheridan, 2015). Furthermore, adults with a history
research on the role of amygdala–prefrontal connec- of childhood maltreatment exhibit positive connec-
tivity in emotion regulation concluded that functional tivity between the amygdala and the prefrontal cortex
and structural alterations in this circuit are related during an emotion-matching fMRI task, whereas
to the development of pediatric anxiety disorders nonmaltreated adults show negative amygdala–PFC
(Swartz & Monk, 2014), and similar evidence is connectivity, a pattern consistent with more effec-
accruing to support involvement of this circuit in tive emotion regulation (Jedd et al., 2015).
depressive symptoms. For instance, 8- to 12-year- Overall, these findings suggest that children and
old children who were instructed to regulate their adolescents who experience adversity and/or elevated
responses to negative affect after viewing sad photos levels of internalizing symptoms exhibit heightened
exhibit greater activation in prefrontal regions (ven- activity in limbic regions and/or altered cortico-
trolateral prefrontal cortex [vlPFC], dlPFC, and limbic functional and structural connectivity, which
dmPFC) compared to viewing the same photos pas- correlates with decreased emotion regulation abilities.
sively without reappraisal (Belden, Luby, Pagliaccio, This body of evidence supports theoretical models
& Barch, 2014). Furthermore, there is evidence of featuring cortico-limbic circuitry as a central under-
age-related improvements in recruitment of pre- lying neurobiological substrate for emotion regula-
frontal regions for reappraisal from childhood to ad- tion, and suggests it as a possible target for early iden-
olescence and into adulthood (McRae et al., 2012). tification of risk for psychopathology and a marker
Youth ages 7 to 15 years with a history of major de- for treatment efficacy in internalizing disorders.
pressive disorder show lower levels of activation in
the inferior frontal gyrus during a cognitive reap- Psychophysiological Findings
praisal task compared to their never-depressed Future neuroimaging studies should integrate these
counterparts (Belden, Pagliaccio, Murphy, Luby, & results with psychophysiological theories of emotion
Barch, 2015). This pattern of neural activity may dysregulation. Abnormalities in the activity of stress-
constitute a diathesis for developing depression or a mediating systems including the autonomic nerv-
scar of their prior depressive episodes. ous system (especially the parasympathetic branch)
In addition to evidence of weaker activation and the hypothalamic-pituitary-adrenocortical (HPA)
in frontal regions, youth exposed to adversity or axis not only can serve as useful peripheral indices

of emotional reactivity to stressors but also are involving the serotonin transporter (5-HTTLPR),
thought to indicate deficient prefrontal control of monoamine oxidase A, and CRHR1 genes with
emotion (Appelhans & Luecken, 2006; Beauchaine, environmental adversity, rendering some youth

2015a; Thayer & Lane, 2009). For instance, respi- more vulnerable to internalizing psychopathology
ratory sinus arrhythmia (RSA), an index of para- than others (for recent reviews, see Cicchetti, 2013;
sympathetic influence on cardiac activity, is con- Jaffee, 2017).
sistently associated with better emotion regulation Recent studies are also beginning to reveal
and executive function skills (Appelhans & Luecken, evidence of G×G×E interactions. For example, one
2006), and it is thought to reflect medial PFC in- large study of 1,096 maltreated and nonmaltreated
fluences on the peripheral nervous system (Beauchaine, African American children found evidence of
2015b). Conversely, low RSA has been linked to a G×G×E interactions between 5-HTTLPR and the
wide range of mental health conditions, including norepinephrine transporter gene, 5-HTTLPR and
depression and anxiety, but also attention problems, the BDNF gene, and maltreatment as predictors of
conduct disorder, and self-injury (for reviews, see depressive symptomatology (Cicchetti & Rogosch,
Beauchaine, 2015a; Shader et al., 2018). Importantly, 2014). In addition, there was a G×G×E interaction
recent research suggests that adolescents’ RSA in between the BDNF gene, CRHR1 haplotype, and
response to emotion-eliciting stimuli (e.g., film clips) maltreatment in predicting psychopathology
interacts with maternal emotion socialization prac- (Cicchetti & Rogosch, 2014).
tices to predict internalizing symptoms (Hastings, Adding another layer of complexity to G×E
Klimes-Dougan, Kendziora, Brand, & Zahn-Waxler, interactions, research has also found evidence of
2014). This interaction is such that less supportive G×E×E interactions. For example, one longitudinal
and more punitive maternal socialization and greater study identified interactions between genetics
RSA suppression jointly predict greater levels of (CRHR1 and 5-HTTLPR genes) and both early-life
fear and sadness in youth (Hastings et al., 2014). (before age 5) and recent chronic stress proximal to
In another study, low levels of RSA among children age 20 in predicting depressive symptoms (Starr,
conferred significant risk for depression in con- Hammen, Conway, Raposa, & Brennan, 2014). The
texts of maternal depression, whereas high RSA overall pattern of results suggests that early-life ad-
offered protection (Shannon, Beauchaine, Brenner, versity sensitizes individuals to the effects of later
Neuhaus, & Gatzke-Kopp, 2007). Although these chronic stress on depressive symptoms, but genetic
initial findings are promising, more research is risk moderated this association such that some indi-
needed to establish connections between periph- viduals were more vulnerable to this sensitizing
eral physiology, neural activity, subjective reports effect than others (Starr et al., 2014).
of emotions or emotion regulation strategies, and Another novel line of G × E research implicates
psychopathology. inflammatory processes in the pathophysiology of at
least some depression subtypes (Raison & Miller,
Genetics 2011). In children, one recent study found that vari-
Similarly, research on genetic markers or modera- ation in inflammatory genetic variants (specifically
tors of risk for internalizing disorders has burgeoned the interleukin-1β gene, IL-1β) interacts with con-
in the past decade, adding another level of analysis textual stressors to predict symptoms of major de-
to psychobiological models in developmental psy- pressive disorder in 3- to 5-year-old preschoolers,
chopathology (Cicchetti & Natsuaki, 2014). Advances some of whom were exposed to child maltreatment
in molecular genetics support the hypothesis that (Ridout et al., 2014). IL-1β is a proinflammatory
individual differences in emotional behavior and cytokine whose production can increase after
the ability to regulate one’s emotions are affected by psychosocial stressors, and animal models demon-
genetic variation, even though the proportion of strate its role in perturbing stress neurobiology, with
variance explained by genes alone tends to be small implications for depressive-like behaviors (Dantzer,
and more often than not Gene × Environment (G×E) O’Connor, Freund, Johnson, & Kelley, 2008).
interactions qualify associations found (Hariri & There is increasing recognition that neuroimmune
Holmes, 2006). For instance, we discussed that interactions play a role in the development of stress-
child maltreatment is associated with greater risk for related psychopathology (Hostinar, Nusslock, &
emotion dysregulation and internalizing symptoms, Miller, 2018). However, more research is needed to
but these associations are moderated by genotype. examine these processes developmentally and to
There is increasing evidence of G×E interactions elucidate the specific neural pathways through

which inflammation confers these risks in human and psychopathology in some studies (Palma-Gudiel,
studies. Cordova-Palomera, Leza, & Fananas, 2015).
In sum, genetic variation appears to interact with In youth, higher levels of methylation of NR3C1
environmental characteristics to predict psychopa- in varying biological specimens (saliva, whole blood)
thology, but more research is needed to reveal the are associated with psychosocial adversity in pre-
intermediary pathways underlying these associa- schoolers (Tyrka et al., 2015), older children
tions in humans: from genes, to proteins, to neural (Cicchetti & Handley, 2017), and adolescents
function and processing of environmental input, (Romens, McDonald, Svaren, & Pollak, 2015; van
and finally to emotion and behavior. der Knaap et al., 2014). However, more research is
needed to then link NR3C1 methylation to emotion
Epigenetics regulation/dysregulation and to psychopathology in
In addition to G×E interactions, there is growing youth. There is some emerging evidence that these
recognition that the epigenetic regulation of genes associations may be important to investigate. For
is another pathway through which the environ- example, one study comparing maltreated and non-
ment can confer risk for emotion dysregulation maltreated children found that hypermethylation of
and psychopathology. Epigenetic changes (e.g., NR3C1 was associated with prior experiences of
DNA methylation, posttranslational histone mod- maltreatment and also to greater emotional lability/
ifications, noncoding RNA molecules) are mecha- negativity and greater depressive symptoms among
nisms that silence or activate gene expression based 9-year-old children (Cicchetti & Handley, 2017).
on environmental input, including social, nutri- The findings we summarized here are significant
tional, and toxicological input (Champagne, 2016). because they begin to build the conceptual and em-
There is growing evidence, based on animal models, pirical bridges necessary to create multilevel, mech-
that prenatal and even preconception social adver- anistic models of how mood and anxiety symptoms
sity experienced by the mother or father can alter develop. Most human research on genetics and epi-
gene expression in the offspring (Champagne, genetics in psychopathology thus far has focused on
2016; Doherty & Roth, 2016). This can occur both “bottom-up” influences on emotion regulation/dys-
directly, by affecting the germline, and indirectly, regulation (i.e., influences on biological processes
by negatively affecting parental behavior toward involved in stress and emotional reactivity). As a
offspring such that parents exposed to stressors result, we understand little about genetic (or G×E)
provide lower quality caregiving (Champagne, and epigenetic influences on cognitive control pro-
2016; Meaney & Szyf, 2005). The early-life social cesses that would attempt to modulate or terminate
environment of offspring then continues to mold emotional reactions to adverse stimuli and experi-
the epigenetic landscape, often in sex-specific ways ences. We also understand little about how genetic
(Massart et al., 2016). and epigenetic influences on emotional processes
Emerging evidence in humans links epigenetic may constrain the repertoire and effectiveness of
alterations to child and adolescent psychopathology. emotion regulation strategies that youth can acquire
For instance, studies using salivary DNA specimens and deploy. Furthermore, more research is needed
and conducting genome-wide methylation analyses to connect findings at neural, physiological, genetic,
reveal that children who experience maltreatment epigenetic, and sociocultural levels of analysis to un-
show differential methylation of numerous genes derstand which risk factors for emotion dysregula-
involved in mental health, but also in physical health tion are independent from each other versus part of
(e.g., immune functioning, cancer) compared to a network of interconnected alterations in behavior,
nonmaltreated children (Cicchetti, Hetzel, Rogosch, the brain, stress physiology, and genes.
Handley, & Toth, 2016; Yang et al., 2013). Most
other epigenetic studies in youth (and adults) have Conclusions, Future Directions, and
focused on the epigenetic profiles of genes involved Implications for Interventions
in the regulation of the HPA axis, especially the In this brief review, we focused on the developmental
glucocorticoid receptor gene, NR3C1 (Tyrka, Ridout, origins of emotion dysregulation, findings on the
& Parade, 2016). A meta-analysis of 23 studies con- temporal ordering and potential causal involvement
ducted with samples of various ages found evidence of emotion dysregulation in internalizing psychopa-
that prenatal and early-life social adversity are both thology, and some putative biological underpinnings
associated with hypermethylation of NR3C1, which of emotion dysregulation. We concisely summarize
was correlated with greater cortisol stress responses our conclusions here.

From a developmental perspective, a well- emotions as simple responses of the individual to
established body of evidence now suggests that stimuli in the environment. Future research could
early-life experiences within the family and peer benefit from contextualizing individual emotion
contexts are critical for the development of emotion regulation/dysregulation more, by devoting greater
processing and emotion regulation systems. Adding attention to the social learning history of the indi-
to this evidence, novel findings from epigenetics vidual and to any current interpersonal relationships,
also suggest that the effects of social adversity on the their affective tone, and their encouragement or dis-
neurobiology of emotion and stress may begin pre- couragement of specific emotion regulatory strategies.
natally or even preconception and can be transmit- Finally, as illustrated in this review, interest in the
ted intergenerationally. This suggests that emotion neurobiological, physiological, genetic, and epigenetic
dysregulation and psychopathology may have some processes involved in the development of internal-
of their origins much earlier than previously izing disorders has grown exponentially in the past
thought, though later social environments continue decade. However, what remains unspecified is how
to shape developmental trajectories. We also know exactly emotional stimuli lead to responses (i.e.,
that environmental enrichment at various develop- what the intermediary links are between them and
mental stages (from prenatal to adult) can lead to how the organism determines the sequence of neu-
epigenetic changes that promote positive long-term rocognitive and peripheral physiological changes
behavioral adaptation (Doherty & Roth, 2016). The that are appropriate to deploy for each situation;
implication is that efforts to promote resilience A. S. Fox, Lapate, Davidson, & Shackman, in press).
against psychopathology could begin much earlier We also understand little about the long-term de-
in development, with the potential to have positive velopmental processes through which momentary
ramifications for mental and physical health across instances of emotion dysregulation accumulate and
the lifespan. However, an important gap in the lit- interact with environmental contingencies to create
erature is to better characterize early stages in the more persistent states, moods, and ultimately disor-
development of emotion dysregulation (e.g., prena- ders associated with clinical impairment that will
tal influences and infancy), as most research on require treatment or intervention.
emotion dysregulation and psychopathology thus What future waves of research also need to reveal
far has been conducted with children, adolescents, are the many missing links between indices of
and adults. neural, physiological, genetic, and epigenetic activ-
As summarized previously, accumulating evidence ity and internalizing symptoms. The constructs of
also suggests that emotion dysregulation often pre- emotion, emotion regulation, and emotion dysreg-
cedes and may contribute causally to the develop- ulation may prove fruitful as starting points in this
ment of internalizing symptoms. However, what search for psychobiological mediators and possible
remains unclear is the extent to which emotion dys- targets for intervention, as these constructs are prov-
regulation as an antecedent factor is independent ing themselves to be a useful and intuitive interface
from social-contextual stressors, or simply a proxy between the biological and psychological levels of
measure of their occurrence. Currently, emotion analysis, as highlighted in various studies we discussed
regulation and dysregulation have been largely stud- here. Additionally, integrative conceptual and com-
ied as individual-level processes, with insufficient putational models that synthesize the wealth of in-
attention being dedicated to the role of the current formation gleaned from such multilevel analyses
social context in shaping what is adaptive or mala- need to be developed to improve theoretical models
daptive (Aldao, 2013). Greater attention to individ- of internalizing spectrum disorders, as well as the
ual sociodemographic characteristics (age, sex, race/ prediction and treatment of mental illness.
ethnicity), the ecological validity of the emotion As far as implications for preventative interven-
stimuli used, and interpersonal interactions has the tions are concerned, it is evident that reducing the
potential to reveal novel and important dimensions of incidence of child maltreatment and peer victimi-
emotion and emotion dysregulation. For instance, zation, as well as training parents to model healthier
emerging findings on the contagious nature of affect emotion regulation strategies for their own benefit
and on the dynamic physiological synchrony of the and for that of their children, would likely result
sympathetic and parasympathetic nervous system in in reductions in the prevalence of internalizing
dyads (e.g., mothers and infants; Waters, West, symptoms. Furthermore, multilevel models in de-
Karnilowicz, & Mendes, 2017) suggest that we might velopmental psychopathology suggest that resilience
be missing significant information if we consider can be sparked at any level (neural, physiological,

behavioral, etc.), but environmental supports need Beauchaine, T. P., & Gatzke-Kopp, L. M. (2012). Instantiating
to be in place to create and maintain positive syner- the multiple levels of analysis perspective in a program of
study on externalizing behavior. Development and
gies within children and adolescents that will result Psychopathology, 24, 1003–1018.
in optimal mental and physical health outcomes Behar, E., DiMarco, I. D., Hekler, E. B., Mohlman, J., &
across the lifespan. Staples, A. M. (2009). Current theoretical models of
generalized anxiety disorder (GAD): Conceptual review
Acknowledgments and treatment implications. Journal of Anxiety Disorders,
The authors’ effort on this manuscript was supported by funding 23, 1011–1023.
from the National Science Foundation (NSF; SMA1327768) to Belden, A. C., Luby, J. L., Pagliaccio, D., & Barch, D. M. (2014).
Camelia E. Hostinar and from the Jacobs Foundation to Dante Neural activation associated with the cognitive emotion
Cicchetti. regulation of sadness in healthy children. Developmental
Cognitive Neuroscience, 9, 136–147.
Belden, A. C., Pagliaccio, D., Murphy, E. R., Luby, J. L., &
References Barch, D. M. (2015). Neural activation during cognitive
Adrian, M., Zeman, J., & Veits, G. (2011). Methodological emotion regulation in previously depressed compared to
implications of the affect revolution: A 35-year review of healthy children: Evidence of specific alterations. Journal of
emotion regulation assessment in children. Journal of the American Academy of Child and Adolescent Psychiatry, 54,
Experimental Child Psychology, 110(2), 171–197. doi:10.1016/j. 771–781.
jecp.2011.03.009 Bosquet, M., & Egeland, B. (2006). The development and
Ahmed, S. P., Bittencourt-Hewitt, A., & Sebastian, C. L. (2015). maintenance of anxiety symptoms from infancy through
Neurocognitive bases of emotion regulation development in adolescence in a longitudinal sample. Development and
adolescence. Developmental Cognitive Neuroscience, 15, 11–25. Psychopathology, 18, 517–550.
doi:10.1016/j.den.2015.07.006 Bradley, B., DeFife, J. A., Guarnaccia, C., Phifer, J., Fani, N.,
Ainsworth, M. D. S., Bell, S. M., & Stayton, D. J. (1974). Ressler, K. J., & Westen, D. (2011). Emotion dysregulation
Infant-mother attachment and social development: and negative affect: Association with psychiatric symptoms.
“Socialisation” as a product of reciprocal responsiveness to Journal of Clinical Psychiatry, 72, 685–691.
signals. In M. P. Richards (Ed.), The integration of the child Braithwaite, E. C., O’Connor, R. M., Degli-Esposti, M., Luke,
into a social world (pp. 99–135). London, UK: Cambridge N., & Bowes, L. (2017). Modifiable predictors of depression
University Press. following childhood maltreatment: A systematic review and
Aldao, A. (2013). The future of emotion regulation research: meta-analysis. Translational Psychiatry, 7, e1162.
Capturing context. Perspectives on Psychological Science, 8(2), Brenning, K. M., Soenens, B., Braet, C., & Bosmans, G. (2012).
155–172. doi:10.1177/1745691612459518 Attachment and depressive symptoms in middle childhood
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion- and early adolescence: Testing the validity of the emotion
regulation strategies across psychopathology: A meta-analytic regulation model of attachment. Personal Relationships, 19,
review. Clinical Psychology Review, 30(2), 217–237. 445–464.
doi:10.1016/j.cpr.2009.11.004 Brumariu, L. E., & Kerns, K. A. (2010). Parent-child attachment
Appelhans, B. M., & Luecken, L. J. (2006). Heart rate variability and internalizing symptoms in childhood and adolescence:
as an index of regulated emotional responding. Review of A review of empirical findings and future directions.
General Psychology, 10(3), 229–240. doi:10.1037/1089- Development and Psychopathology, 22, 177–203.
2680.10.3.229 Calkins, S., & Hill, A. (2007). Caregiver influences on
Ball, T. M., Ramsawh, H. J., Campbell-Sills, L., Paulus, M. P., & emerging emotion regulation: Biological and environmental
Stein, M. B. (2013). Prefrontal dysfunction during emotion transactions in early development. In J. J. Gross (Ed.),
regulation in generalized anxiety and panic disorders. Handbook of emotion regulation (pp. 229–248). New York,
Psychological Medicine, 43(7), 1475–1486. doi:10.1017/ NY: Guilford Press.
S0033291712002383 Casey, B. J., Jones, R. M., Levita, L., Libby, V., Pattwell, S. S.,
Banny, A. M., Cicchetti, D., Rogosch, F. A., Oshri, A., & Ruberry, E. J., . . . Somerville, L. H. (2010). The storm and
Crick, N. R. (2013). Vulnerability to depression: A moderated stress of adolescence: Insights from human imaging and
mediation model of the roles of child maltreatment, mouse genetics. Developmental Psychobiology, 52, 225–235.
peer victimization, and serotonin transporter linked Cassidy, J. (1994). Emotion regulation: Influences of attachment
polymorphic region genetic variation among children from relationships. Monographs of the Society for Research in Child
low socioeconomic status backgrounds. Development and Development, 59, 228–249.
Psychopathology, 25, 599–614. Champagne, F. A. (2016). Epigenetic legacy of parental
Beauchaine, T. P. (2015a). Future directions in emotion experiences: Dynamic and interactive pathways to inheritance.
dysregulation and youth psychopathology. Journal of Clinical Development and Psychopathology, 28, 1219–1228.
Child and Adolescent Psychology, 44, 875–896. Ciarrochi, J., Heaven, P. C. L., & Supavadeeprasit, S. (2008).
Beauchaine, T. P. (2015b). Respiratory sinus arrhythmia: A The link between emotion identification skills and socio-
transdiagnostic biomarker of emotion dysregulation and emotional functioning in early adolescence: A 1-year
psychopathology. Current Opinion in Psychology, 3, 43–47. longitudinal study. Journal of Adolescence, 31, 565–582.
Beauchaine, T. P., & Cicchetti, D. (2016). A new generation of Cicchetti, D. (1984). The emergence of developmental
comorbidity research in the era of neuroscience and the psychopathology. Child Development, 55, 1–7.
Research Domain Criteria. Development and Psychopathology, Cicchetti, D. (2013). Annual Research Review: Resilient
28, 891–894. functioning in maltreated children—past, present, and

future perspectives. Journal of Child Psychology and Psychiatry, Eisenberg, N., Cumberland, A., & Spinrad, T. L. (1998). Parental
54, 402–422. socialization of emotion. Psychological Inquiry, 9, 241–273.
Cicchetti, D. (2016). Socioemotional, personality, and biological Eyden, J., Winsper, C., Wolke, D., Broome, M. R., &
development: Illustrations from a multilevel developmental MacCallum, F. (2016). A systematic review of the parenting
psychopathology perspective on child maltreatment. Annual and outcomes experienced by offspring of mothers with
Review of Psychology, 67, 187–211. borderline personality pathology: Potential mechanisms and
Cicchetti, D., Ackerman, B. P., & Izard, C. E. (1995). Emotions clinical implications. Clinical Psychology Review, 47, 85–105.
and emotion regulation in developmental psychopathology. Feng, X., Keenan, K., Hipwell, A. E., Henneberger, A. K.,
Development and Psychopathology, 7, 1–10. Rischall, M. S., Butch, J., .
.
.
Babinski, D. E. (2009).
Cicchetti, D., & Handley, E. D. (2017). Methylation of the Longitudinal associations between emotion regulation and
glucocorticoid receptor gene (NR3C1) in maltreated and depression in preadolescent girls: Moderation by the caregiving
nonmaltreated children: Associations with behavioral environment. Developmental Psychology, 45, 798–808.
undercontrol, emotional lability/negativity, and externalizing Fox, A. S., Lapate, R. C., Davidson, R. J., & Shackman, A. J. (in
and internalizing symptoms. Development and Psychopathology, press). Epilogue—The nature of emotion: A research agenda
29, 1795–1806. for the 21st century. In A. S. Fox, R. C. Lapate,
Cicchetti, D., Hetzel, S., Rogosch, F. A., Handley, E. D., & A. J. Shackman, & R. J. Davidson (Eds.), The nature of
Toth, S. L. (2016). An investigation of child maltreatment emotion: Fundamental questions (2nd ed.). New York, NY:
and epigenetic mechanisms of mental and physical health Oxford University Press.
risk. Development and Psychopathology, 28, 1305–1317. Fox, N. A. (Ed.). (1994). The development of emotion regulation:
Cicchetti, D., & Natsuaki, M. N. (2014). Multilevel developmental Biological and behavioral considerations. Chicago, Ill: Society
perspectives toward understanding internalizing psycho for Research in Child Development.
pathology: Current research and future directions. Frank, D. W., Dewitt, M., Hudgens-Haney, M., Schaeffer, D. J.,
Development and Psychopathology, 26, 1189–1190. Ball, B. H., Schwarz, N. F., .
.
.
Sabatinelli, D. (2014).
Cicchetti, D., & Ng, R. (2014). Emotional development in Emotion regulation: Quantitative meta-analysis of functional
maltreated children. Children and Emotion: New Insights into activation and deactivation. Neuroscience and Biobehavioral
Developmental Affective Science, 26, 29–41. Reviews, 45, 202–211.
Cicchetti, D., & Rogosch, F. A. (2014). Genetic moderation of Gaffrey, M. S., Barch, D. M., Singer, J., Shenoy, R., & Luby, J. L.
child maltreatment effects on depression and internalizing (2013). Disrupted amygdala reactivity in depressed 4- to
symptoms by serotonin transporter linked polymorphic region 6-year-old children. Journal of the American Academy of Child
(5-HTTLPR), brain-derived neurotrophic factor (BDNF), and Adolescent Psychiatry, 52, 737–746.
norepinephrine transporter (NET), and corticotropin Goldin, P. R., McRae, K., Ramel, W., & Gross, J. J. (2008). The
releasing hormone receptor 1 (CRHR1) genes in African neural bases of emotion regulation: Reappraisal and suppression
American children. Development and Psychopathology, 26, of negative emotion. Biological Psychiatry, 63, 577–586.
1219–1239. Gotlib, I. H., & Hamilton, J. P. (2008). Neuroimaging and
Cicchetti, D., & Toth, S. L. (2005). Child maltreatment. Annual depression: Current status and unresolved issues. Current
Review of Clinical Psychology, 1, 409–438. Directions in Psychological Science, 17, 159–163.
Cole, P. M., Hall, S. E., & Hajal, N. J. (2010). Emotion Gotlib, I. H., & Joormann, J. (2010). Cognition and depression:
dysregulation as a vulnerability to psychopathology. In Current status and future directions. Annual Review of
T. Beauchaine & S. Hinshaw (Eds.), Child and adolescent Clinical Psychology, 6, 285–312.
psychopathology (3rd ed., pp. 346–386). Hoboken, NJ: Wiley. Gross, J. J. (2013). Emotion regulation: Taking stock and moving
Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion forward. Emotion, 13(3), 359–365.
regulation as a scientific construct: Methodological challenges Guyer, A. E., Kaufman, J., Hodgdon, H. B., Masten, C. L.,
and directions for child development research. Child Jazbec, S., Pine, D. S., & Ernst, M. (2006). Behavioral
Development, 75, 317–333. alterations in reward system function: The role of childhood
Dahl, R. E., & Gunnar, M. R. (2009). Heightened stress maltreatment and psychopathology. Journal of the American
responsiveness and emotional reactivity during pubertal Academy of Child and Adolescent Psychiatry, 45, 1059–1067.
maturation: Implications for psychopathology. Development Hariri, A. R., & Holmes, A. (2006). Genetics of emotional
and Psychopathology, 21, 1–6. regulation: The role of the serotonin transporter in neural
Dantzer, R., O’Connor, J. C., Freund, G. G., Johnson, R. W., & function. Trends in Cognitive Sciences, 10, 182–191.
Kelley, K. W. (2008). From inflammation to sickness and Hastings, P. D., Klimes-Dougan, B., Kendziora, K. T., Brand, A.,
depression: When the immune system subjugates the brain. & Zahn-Waxler, C. (2014). Regulating sadness and fear from
Nature Reviews Neuroscience, 9, 46–56. outside and within: Mothers’ emotion socialization and
Davidson, R. J., Pizzagalli, D., Nitschke, J. B., & Putnam, K. adolescents’ parasympathetic regulation predict the
(2002). Depression: Perspectives from affective neuroscience. development of internalizing difficulties. Development and
Annual Review of Psychology, 53, 545–574. Psychopathology, 26, 1369–1384.
Doherty, T. S., & Roth, T. L. (2016). Insight from animal models Hatzenbuehler, M. L., McLaughlin, K. A., & Nolen-Hoeksema,
of environmentally driven epigenetic changes in the S. (2008). Emotion regulation and internalizing symptoms
developing and adult brain. Development and Psychopathology, in a longitudinal study of sexual minority and heterosexual
28, 1229–1243. adolescents. Journal of Child Psychology and Psychiatry, 49,
Dougherty, L. R., Klein, D. N., Rose, S., & Laptook, R. S. 1270–1278.
(2011). Hypothalamic-pituitary-adrenal axis reactivity in the Hostinar, C. E., Nusslock, R., & Miller, G. E. (2018). Future
preschool-age offspring of depressed parents: Moderation by directions in the study of early-life stress and physical and
early parenting. Psychological Science, 22, 650–658. emotional health: Implications of the neuroimmune network

hypothesis. Journal of Clinical Child and Adolescent Psychology, McLaughlin, K. A., Peverill, M., Gold, A. L., Alves, S., &
47(1), 142–156. Sheridan, M. A. (2015). Child maltreatment and neural
Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D. S., systems underlying emotion regulation. Journal of the American
Quinn, K., . . . Wang, P. (2010). Research Domain Criteria Academy of Child and Adolescent Psychiatry, 54, 753–762.
(RDoC): Toward a new classification framework for research McRae, K., Gross, J. J., Weber, J., Robertson, E. R., Sokol-
on mental disorders. American Journal of Psychiatry, 167, Hessner, P., Ray, R. D., . . . Ochsner, K. N. (2012). The
748–751. development of emotion regulation: An fMRI study of
Jaffee, S. R. (2017). Child maltreatment and risk for cognitive reappraisal in children, adolescents and young
psychopathology in childhood and adulthood. Annual adults. Social Cognitive and Affective Neuroscience, 7, 11–22.
Review of Clinical Psychology, 13, 525–551. Meaney, M. J., & Szyf, M. (2005). Environmental programming
Jedd, K., Hunt, R. H., Cicchetti, D., Hunt, E., Cowell, R. A., of stress responses through DNA methylation: Life at the
Rogosch, F. A., . . . Thomas, K. M. (2015). Long-term interface between a dynamic environment and a fixed
consequences of childhood maltreatment: Altered amygdala genome. Dialogues in Clinical Neuroscience, 7, 103–123.
functional connectivity. Development and Psychopathology, Mennin, D. S., Heimberg, R. G., Turk, C. L., & Fresco, D. M.
27(4), 1577–1589. (2002). Applying an emotion regulation framework to
Kim, J., & Cicchetti, D. (2010). Longitudinal pathways linking integrative approaches to generalized anxiety disorder.
child maltreatment, emotion regulation, peer relations, and Clinical Psychology-Science and Practice, 9, 85–90.
psychopathology. Journal of Child Psychology and Psychiatry, Morris, A. S., Silk, J. S., Steinberg, L., Myers, S. S., & Robinson,
51, 706–716. L. R. (2007). The role of the family context in the development
Kim-Spoon, J., Cicchetti, D., & Rogosch, F. A. (2013). of emotion regulation. Social Development, 16, 361–388.
A longitudinal study of emotion regulation, emotion Nanni, V., Uher, R., & Danese, A. (2012). Childhood
lability-negativity, and internalizing symptomatology in maltreatment predicts unfavorable course of illness and
maltreated and nonmaltreated children. Child Development, treatment outcome in depression: A meta-analysis. American
84, 512–527. Journal of Psychiatry, 169, 141–151.
Li, M., D’Arcy, C., & Meng, X. (2016). Maltreatment in Nelson, J., Klumparendt, A., Doebler, P., & Ehring, T. (2017).
childhood substantially increases the risk of adult depression Childhood maltreatment and characteristics of adult
and anxiety in prospective cohort studies: Systematic review, depression: Meta-analysis. British Journal of Psychiatry, 210,
meta-analysis, and proportional attributable fractions. 96–104.
Psychological Medicine, 46, 717–730. Nolen-Hoeksema, S., Wisco, B. E., & Lyubomirsky, S. (2008).
Luke, N., & Banerjee, R. (2013). Differentiated associations Rethinking rumination. Perspectives on Psychological Science,
between childhood maltreatment experiences and social 3, 400–424.
understanding: A meta-analysis and systematic review. Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of
Developmental Review, 33, 1–28. emotion. Trends in Cognitive Sciences, 9, 242–249.
Macdonald, A. N., Goines, K. B., Novacek, D. M., & Walker, Pagliaccio, D., Luby, J. L., Luking, K. R., Belden, A. C., &
E. F. (2016). Prefrontal mechanisms of comorbidity from a Barch, D. M. (2014). Brain-behavior relationships in the
transdiagnostic and ontogenic perspective. Development and experience and regulation of negative emotion in healthy
Psychopathology, 28, 1147–1175. children: Implications for risk for childhood depression.
Main, M., & Solomon, J. (1986). Discovery of a new, insecure- Development and Psychopathology, 26, 1289–1303.
disorganized/disoriented attachment pattern. In Palma-Gudiel, H., Cordova-Palomera, A., Leza, J. C., &
T. B. Brazelton & M. Yogman (Eds.), Affective development in Fananas, L. (2015). Glucocorticoid receptor gene (NR3C1)
infancy (pp. 95–124). Norwood, NJ: Ablex. methylation processes as mediators of early adversity in
Massart, R., Nemoda, Z., Suderman, M. J., Sutti, S., Ruggiero, stress-related disorders causality: A critical review.
A. M., Dettmer, A. M., . . . Szyf, M. (2016). Early life adversity Neuroscience and Biobehavioral Reviews, 55, 520–535.
alters normal sex-dependent developmental dynamics of Pollak, S. D. (2015). Multilevel developmental approaches
DNA methylation. Development and Psychopathology, 28, to understanding the effects of child maltreatment:
1259–1272. Recent advances and future challenges. Development and
Maughan, A., & Cicchetti, D. (2002). Impact of child Psychopathology, 27, 1387–1397.
maltreatment and interadult violence on children’s emotion Pollak, S. D., Cicchetti, D., Hornung, K., & Reed, A. (2000).
regulation abilities and socioemotional adjustment. Child Recognizing emotion in faces: Developmental effects of child
Development, 73, 1525–1542. abuse and neglect. Developmental Psychology, 36, 679–688.
Maughan, A., Cicchetti, D., Toth, S. L., & Rogosch, F. A. Raison, C. L., & Miller, A. H. (2011). Is depression an inflam
(2007). Early-occurring maternal depression and maternal matory disorder? Current Psychiatry Reports, 13, 467–475.
negativity in predicting young children’s emotion regulation Regier, D. A., Kuhl, E. A., & Kupfer, D. J. (2013). The DSM-5:
and socioemotional difficulties. Journal of Abnormal Child Classification and criteria changes. World Psychiatry, 12,
Psychology, 35, 685–703. 92–98.
McLaughlin, K. A., Hatzenbuehler, M. L., & Hilt, L. M. (2009). Ridout, K. K., Parade, S. H., Seifer, R., Price, L. H., Gelernter,
Emotion dysregulation as a mechanism linking peer J., Feliz, P., & Tyrka, A. R. (2014). Interleukin 1B
victimization to internalizing symptoms in adolescents. gene (IL1B) variation and internalizing symptoms in
Journal of Consulting and Clinical Psychology, 77, 894–904. maltreated preschoolers. Development and Psychopathology,
McLaughlin, K. A., Hatzenbuehler, M. L., Mennin, D. S., & 26, 1277–1287.
Nolen-Hoeksema, S. (2011). Emotion dysregulation and Romens, S. E., McDonald, J., Svaren, J., & Pollak, S. D. (2015).
adolescent psychopathology: A prospective study. Behaviour Associations between early life stress and gene methylation in
Research and Therapy, 49, 544–554. children. Child Development, 86, 303–309.

Romens, S. E., & Pollak, S. D. (2012). Emotion regulation predicts Thayer, J. F., & Lane, R. D. (2009). Claude Bernard and the
attention bias in maltreated children at-risk for depression. heart-brain connection: Further elaboration of a model of
Journal of Child Psychology and Psychiatry, 53, 120–127. neurovisceral integration. Neuroscience and Biobehavioral
Schafer, J. O., Naumann, E., Holmes, E. A., Tuschen-Caffier, B., Reviews, 33, 81–88.
& Samson, A. C. (2017). Emotion regulation strategies in Thompson, R. A., Lewis, M. D., & Calkins, S. D. (2008).
depressive and anxiety symptoms in youth: A meta-analytic Reassessing emotion regulation. Child Development Perspectives,
review. Journal of Youth and Adolescence, 46, 261–276. 2, 124–131.
Shackman, J. E., & Pollak, S. D. (2014). Impact of physical Thompson, R. A., & Meyer, S. (2007). Socialization of emotion
maltreatment on the regulation of negative affect and regulation in the family. In J. J. Gross (Ed.), Handbook of
aggression. Development and Psychopathology, 26, 1021–1033. emotion regulation (pp. 249–268). New York, NY: Guilford
Shader, T. M., Gatzke-Kopp, L. M., Crowell, S. E., Reid, M. J., Press.
Thayer, J. F., Vasey, M. W., . . . Beauchaine, T. P. (2018). Tyrka, A. R., Parade, S. H., Eslinger, N. M., Marsit, C. J.,
Quantifying respiratory sinus arrhythmia: Effects of Lesseur, C., Armstrong, D. A., .
.
.
Seifer, R. (2015).
misspecifying breathing frequencies across development. Methylation of exons 1D, 1F, and 1H of the glucocorticoid
Development and Psychopathology, 30(1), 351–366. receptor gene promoter and exposure to adversity in
Shannon, K. E., Beauchaine, T. P., Brenner, S. L., Neuhaus, E., preschool-aged children. Development and Psychopathology,
& Gatzke-Kopp, L. (2007). Familial and temperamental 27, 577–585.
predictors of resilience in children at risk for conduct Tyrka, A. R., Ridout, K. K., & Parade, S. H. (2016). Childhood
disorder and depression. Development and Psychopathology, adversity and epigenetic regulation of glucocorticoid
19, 701–727. signaling genes: Associations in children and adults.
Sheppes, G., Suri, G., & Gross, J. J. (2015). Emotion regulation Development and Psychopathology, 28, 1319–1331.
and psychopathology. Annual Review of Clinical Psychology, van der Knaap, L. J., Riese, H., Hudziak, J. J., Verbiest,
11, 379–405. M. M. P. J., Verhulst, F., Oldehinkel, A. J., & van Oort,
Shields, A., & Cicchetti, D. (1998). Reactive aggression among F. V. A. (2014). Glucocorticoid receptor gene (NR3C1)
maltreated children: The contributions of attention and methylation following stressful events between birth and
emotion dysregulation. Journal of Clinical Child Psychology, adolescence. The TRAILS study. Translational Psychiatry, 4,
27, 381–395. e381.
Solomon, R. C. (2002). Back to basics: On the very idea of Waters, S. F., West, T. V., Karnilowicz, H. R., & Mendes, W. B.
“basic emotions.” Journal for the Theory of Social Behaviour, (2017). Affect contagion between mothers and infants:
32, 115–144. Examining valence and touch. Journal of Experimental
Starr, L. R., Hammen, C., Conway, C. C., Raposa, E., & Psychology-General, 146, 1043–1051.
Brennan, P. A. (2014). Sensitizing effect of early adversity on Yang, B. Z., Zhang, H., Ge, W., Weder, N., Douglas-Palumberi,
depressive reactions to later proximal stress: Moderation by H., Perepletchikova, F., . . . Kaufman, J. (2013). Child abuse
polymorphisms in serotonin transporter and corticotropin and epigenetic mechanisms of disease risk. American Journal
releasing hormone receptor genes in a 20-year longitudinal of Preventive Medicine, 44, 101–107.
study. Development and Psychopathology, 26, 1241–1254. Yap, M. B. H., Allen, N. B., & Sheeber, L. (2007). Using an
Swartz, J. R., & Monk, C. S. (2014). The role of corticolimbic emotion regulation framework to understand the role of
circuitry in the development of anxiety disorders in children temperament and family processes in risk for adolescent
and adolescents. Current Topics in Behavioral Neuroscience, depressive disorders. Clinical Child and Family Psychology
16, 133–148. Review, 10, 180–196.
Tandon, M., Cardeli, E., & Luby, J. (2009). Internalizing Zeman, J., Klimes-Dougan, B., Cassano, M., & Adrian, M.
disorders in early childhood: A review of depressive and (2007). Measurement issues in emotion research with
anxiety disorders. Child and Adolescent Psychiatric Clinics of children and adolescents. Clinical Psychology-Science and
North America, 18, 593–610. Practice, 14, 377–401.

CH A PTE R
19 Childhood Trauma
Patricia K. Kerig
Abstract
This chapter describes theoretical models and empirical research devoted to understanding the a ftermath
of childhood trauma exposure and discusses the value of considering posttraumatic stress from an
emotion dysregulation perspective. After describing definitional controversies in the field related to both
trauma and posttraumatic stress, this chapter summarizes research on the effects of chronic, prolonged,
and repeated traumatic experiences in childhood, such as maltreatment, with particular attention to its
potential to compromise development of adaptive emotion regulation capacities. The role of emotion
dysregulation in leading theoretical models of posttraumatic stress is presented, as well as empirical
research testing the hypothesis that emotion dysregulation represents an underlying developmental
mechanism through which childhood trauma affects functioning over the lifespan. Future directions
include a need for clarification in conceptualization and measurement, further developmental processes
to be considered, and opportunities for translational work to inform intervention efforts.
Keywords: emotion dysregulation, trauma, posttraumatic stress, PTSD, maltreatment, allostasis,

LHPA axis, gene-environment interaction, overmodulation, undermodulation
Introduction psychiatric morbidity over the lifespan, including

The aftermath of exposure to childhood trauma— for posttraumatic stress disorder . . . This facilitation
what has been termed “overwhelming experience” of risk may be partly the result of cascading
(van der Kolk, McFarlane, & Weisaeth, 2006)—can neurobiological changes over the course of
be construed as consisting of, at its essence, a problem development that influence neurocognitive and
of dysregulation. The experience of extreme stress in emotion regulation abilities and ultimately interfere
the early years of life disrupts emerging neurobio- with adaptive stress responses.
logical and psychological processes in ways that in- To this end, this chapter describes current
terfere with the capacity to regulate physiological, nderstanding in the study of childhood trauma
u
emotional, cognitive, and interpersonal functions and emotion dysregulation, controversies in the
(Cicchetti, 2016; Cicchetti & Toth, 2016). Prolonged, field, and future directions for theory and research
chronic, and cumulative traumatic stress exposures on the topic.
negatively affect central regulatory systems of the
brain, body, and psyche, particularly those related
Defining Trauma: Definitional and
to the limbic hypothalamic-pituitary adrenal (LHPA)
Conceptual Controversies
axis, in ways that have significant repercussions for
Before discussing the role of trauma in the devel-
emotion and self-regulation. As summarized by
opmental psychopathology of emotion dysregulation,
Cross, Fani, Powers, and Bradley (2017, p. 111):
it is important to acknowledge the existence of
A clear dose-response relationship exists between long-standing definitional and conceptual dis-
exposure to stress or trauma in early life and risk for agreements (for reviews, see Friedman, Resick, &
265
Keane, 2014; Kerig, 2017). Since its inaugural in- a child’s perspective, certain events that do not
clusion in the third edition of the Diagnostic and meet Criterion A, including separation from a
Statistical Manual (DSM-III; American Psychiatric caregiver even under conditions when the child is
Association, 1980), the term “trauma” has become physically safe, a caregiver’s emotional unavailabil-
widely used in the research literature but as applied ity, or failure of a caregiver to protect the child
to a range of diverse types of experiences and out- from dangers, can be experienced as traumatic
comes. Moreover, these definitions have shifted (Bowlby, 1973/1998; Kerig, 2017; Pynoos et al.,
with each revision of the DSM, and appear to be 2009). In Bowlby’s (1973/1998) words, for a child,
shifting further in draft criteria for the forthcom- no stressor “is likely to be more frightening than
ing edition of the International Classification of the possibility that an attachment figure will be
Diseases (ICD) manual (Keeley et al., 2016), in absent or, in more general terms, unavailable when
ways that continue to incite controversy. wanted” (p. 234). Overall, appraisals are key, in
that it is whether individuals find events to be
What Is a “Traumatic” Experience? distressing—and, tellingly for emotion dysregulation
In the DSM-5 (American Psychiatric Association, researchers, whether individuals perceive those
2013), there was an intentional narrowing of the events as disorganizing and overwhelming their
definition of trauma in an attempt to avoid “crite- ability to cope—that determines whether experi-
rion creep” (Kilpatrick, Resnick, & Acierno, 2009). ences will result in psychopathology (Bovin &
Nonetheless, a growing body of evidence indicates Marx, 2011; Kerig & Bennett, 2013). In fact, re-
that, especially among children and adolescents, a search involving youth has found that peritrau-
wider range of experiences precipitate posttraumatic matic distress and disorganization—indicators of
stress reactions than those encompassed within dysregulated emotions—are more powerful predic-
DSM criteria, which are specific to life threat or tors of posttraumatic stress than are the objective
sexual violence. Additional experiences that are characteristics of the event itself, including whether
associated with posttraumatic stress symptoms in it meets the criteria specified in DSM Criterion A
youth include some specifically precluded by the (Bennett, Modrowski, Kerig, & Chaplo, 2015; Bui
DSM-5 definition, such as exposure to upsetting et al., 2010; Giannopoulou et al., 2006; Stallard,
events solely through the media (Gil-Rivas, Silver, Velleman, & Baldwin, 1998; Trickey, Siddaway,
Holman, McIntosh, & Poulin, 2007; Lengua, Meiser-Stedman, Serpell, & Field, 2012; Verlinden
Long, Smith, & Meltzoff, 2005) and anticipated, et al., 2013).
nonviolent deaths of loved ones (Kaplow, Howell, At the same time, a growing body of research is
& Layne, 2014). In addition, studies have identified being devoted to the study of the many interrelated
a wide range of childhood adversities that do not cumulative early-life adversities, including poverty,
meet DSM-5 criteria for trauma but which are as- family dysfunction, and chronic life stress, that
sociated with posttraumatic stress symptoms, in- contribute to allostatic load (McEwen, 2017) and
cluding separations from caregivers, incarceration increase the risk of posttraumatic stress disorder
or deportation of family members, bullying victim- (PTSD), as well as other stress-related mental and
ization, teenage pregnancy, romantic breakups, ju- physical health problems (e.g., Anda et al., 2006;
venile incarceration, and racial discrimination (Chou, Myers et al., 2015; Wang, Shelton, & Dwivedi,
Asnaani, & Hofmann, 2012; Copeland, Keeler, 2017; Willard, Long, & Phipps, 2016). As Shalev
Angold, & Costello, 2010; Costello, Erkanli, Fairbank, (2007) has pointed out, although the DSM and
& Angold, 2002; Flores, Tschann, Dimas, Pasch, & ICD criteria were originally intended to be specific
de Groat, 2010; Holman, Garfin, & Silver, 2014; to catastrophic events, such as wars and disasters,
Idsoe, Dyregrov, & Idsoe, 2012; Lansing, Plante, & “events that do not involve extreme stress can be
Beck, 2017; Nielsen, Tangen, Idsoe, Matthiesen, & perceived by some survivors as threatening and by
Magerøy, 2015; Rojas-Flores, Clements, Hwang others as challenging. . . . Indeed, no one has success-
Koo, & London, 2017; Taylor & Weems, 2009). fully distinguished traumatic from stressful events”
Consistent with cognitive and developmental (p. 92). To date, little empirical research is available
psychology, scholarship in the field of traumatic stress to illuminate whether the phenomenology and un-
appears to support views that what is traumatic is in derlying processes involved are equivalent for life
the eyes of the beholder and, moreover, that what is threat–related events that meet DSM-5’s Criterion
traumatic for young people depends on the child’s- A versus other more chronic and pervasive trau-
eye point of view (Kerig, 2017). For example, from matic stressors, and so this is an issue upon which
266 Emotion Dysregul ation and Childhood Trauma

the jury is still out and which thus represents a Maercker et al., 2013) further simplify the diagnosis
potential growth point for the field. by focusing on the three “core elements” that are
characteristic of PTSD and differentiate it most
What Is a Traumatized Response? clearly from other disorders: re-experiencing of the
A second way in which the term “trauma” is used is event as if recurring in the present, avoidance, and
to refer not to a potentially traumatic experience but perceptions of current threat. In contrast to the
to its aftermath. A major shift in the prevailing un- DSM-5, the ICD-11 also includes a separate diagno-
derstanding of posttraumatic stress is indicated by sis of complex PTSD (C-PTSD), a concept origi-
the DSM-5’s removal of the PTSD diagnosis from nally proposed by Herman (1994) to account for
the anxiety disorders spectrum and its placement in the distinct set of posttraumatic reactions that arise
a separate category of “trauma and stress-related dis- in the context of chronic, repeated, prolonged inter-
orders”; no longer is posttraumatic stress seen as rep- personal traumas such as childhood maltreatment.
resenting a fear-based reaction akin to an extreme As defined by the ICD-11, C-PTSD symptoms
state of anxiety. Instead, the more recent conceptual- include all three of the core PTSD symptoms in
ization of PTSD is informed by research confirming addition to pervasive problems with affect regula-
that a range of distressing emotions quite distinct tion, persistent negative beliefs about the self, and
from fear—including shame, disgust, and anger— difficulty sustaining close relationships. To date, some
characterize those affected by trauma (Resick & research has emerged indicating that the C-PTSD
Miller, 2009). Specific symptoms of a traumatized diagnosis can be distinguished reliably from related
response as defined by the DSM-5 criteria for disorders in adults, such as borderline personality
PTSD include unbidden intrusions of trauma-related (Cloitre, Garvert, Brewin, Bryant, & Maercker,
thoughts, images, and sensations on daily function- 2013), and that, in children, those with long-term
ing; effortful attempts to avoid internal and external maltreatment histories show specific deficits in affect
trauma reminders; negative changes in prevailing and self-regulation that are consistent with the
cognitions or mood; and increases in arousal. In ad- C-PTSD diagnosis and distinguishable from more
dition, the DSM-5 specifies a dissociative subtype in typical PTSD symptoms shown by children who
which the other symptoms of PTSD are accompa- have experienced single-incident traumas such as
nied by perceptions of derealization (e.g., the sensa- accidents or disasters (Sachser, Keller, & Goldbeck,
tion of disconnection from one’s body) or deperson- 2017).
alization (e.g., experiencing the environment as However, trauma research also illustrates the
unreal). Although a separate set of criteria are speci- developmental psychopathology concept of multifi-
fied for the diagnosis of PTSD in children under the nality (Cicchetti & Rogosch, 1996), in that not all
age of 6, the differences are mostly quantitative, in individuals exposed to traumatic stressors will de-
that they require fewer symptoms to be evidenced in velop a fully fledged disorder and, among those who
young children, with the only significant qualitative do develop psychopathology, PTSD is not the only
difference being the removal of symptoms that are disorder that emerges following traumatic events. In
developmentally inappropriate for preschoolers (e.g., fact, through disrupting important neurobiological
distorted cognitions, engagement in risk-taking ac- and neuropsychological regulatory processes, trauma
tivities). Many of the DSM-5 PTSD symptoms can exposure can be viewed as a “gateway” (Kenardy, De
be construed as representing problems of emotion Young, & Charlton, 2012) to the development of a
dysregulation, in relation to both underregulation wide array of psychopathologies. Through its effects
(e.g., distress in response to reminders in the intru- on the developing brain, including hyperactivity of
sions cluster; irritability, angry outbursts, hypervigi- corticotropin-releasing factor and other neurotrans-
lance, exaggerated startle response, and problems mitter systems, early trauma exposure increases
with sleep and concentration in the arousal cluster) reactivity to stressors and acts as a diathesis, leaving
and overregulation (e.g., efforts to avoid distressing the individual vulnerable to a range of disorders, in-
feelings associated with reminders in the avoidance cluding depression and anxiety (Heim & Nemeroff,
cluster; detachment and inability to experience posi- 2001). In this regard, Bremner (2016) has proposed
tive emotions in the alterations in cognition and the concept of “trauma-spectrum disorders” to en-
mood cluster; derealization and depersonalization in compass the range of psychological problems associ-
the dissociative subtype). ated with a history of childhood trauma, including
Regarding the forthcoming ICD-11, the draft not only PTSD but also borderline personality,
criteria released to date (Keeley et al., 2016; dissociative identity disorders, substance abuse,
Kerig 267
epression, and psychosomatic problems following
d Importantly for the present chapter, many of the
child abuse. key neurobiological functions, structures, and neu-
ropsychological connections that are affected by
Biopsychosocial Processes Underlying childhood trauma are implicated directly in emotion
Childhood Trauma and Emotion regulation. Among studies focusing on childhood
Dysregulation maltreatment, these include executive functions in-
The consequences of traumatic stress have been volving inhibitory control and cognitive flexibility,
conceptualized by many scholars as fundamentally as well as the capacities to identify, interpret, and
composing a disorder of dysregulation (Dvir, Ford, modulate emotions, and to tolerate and downregu-
Hill, & Frazier, 2014; Ford, 2005; Frewen & Lanius, late distress (Cross et al., 2017; McLaughlin, Peverill,
2006; Gray, 1988; Horowitz, 2011). As van der Kolk Gold, Alves, & Sheridan, 2015; Pollak, 2008;
(2006) states: “The lack or loss of self-regulation is Shields, Cicchetti, & Ryan, 1994; Shipman, Zeman,
possibly the most far-reaching effect of psychologi- Penza, & Champion, 2000), in which a shift from
cal trauma in both children and adults” (p. 187). prefrontal cortex–governed to amygdala-dominated
Moreover, dysregulation is seen across multiple de- processing is implicated (Ganzel, Kim, Gilmore,
veloping systems in interaction with one another, Tottenham, & Temple, 2013; McLaughlin et al.,
including cognitive, emotional, self, interpersonal, 2015). The diminutions in executive functions re-
and, underlying and integrating all of these, the bio- sulting from unrelenting trauma exposure have direct
logical (Bremner, 2016). implications for emotion dysregulation in that they
Although a comprehensive discussion of the disrupt necessary underlying capacities for managing
neurobiology of the stress response system is beyond emotions.
the scope of the current chapter, a number of recent
Executive function contributes to emotion regulation
well-articulated primers and reviews of the relevant
by controlling the contents of working memory to
research are available (Bremner, 2016; Cross et al.,
prevent excessive attention to negative thoughts or
2017; Ford, 2009; Koss & Gunnar, 2018; Lupien,
stimuli . . ., shifting to new coping strategies when old
McEwen, Gunnar, & Heim, 2009; McCoy, 2013;
ones are no longer effective . . ., and inhibiting
Rasmussen & Shalev, 2014); in addition, a review of
automatic emotional, behavioral, or cognitive
the biological processes underlying resilience in
responses that do not fit the situation or one’s
the face of traumatic stress can be found in Russo,
goals . . ., such as during cognitive reappraisal.
Murrough, Han, Charney, and Nestler (2012). Briefly,
(Cross et al., 2017, p. 115)
repeated exposure to threat, particularly early in
development, activates the LHPA axis and alters Research on biological sequelae of traumatic stress
regulation of glucocorticoids, including cortisol, exposure encompasses multiple systems, including
which can have toxic effects on the developing brain neuropsychological, neurotransmitter, neuroendo-
(Lupien et al., 2009), particularly through inter- crine, physiological, pro- and anti-inflammatory, and
fering with gene expression, protein synthesis, and immune response systems (McEwen, 2017). Recent
communication between the prefrontal cortex and research also yields a complex set of findings in which
hippocampus (Cross et al., 2017). As summarized dysfunctions across these systems are highly variable
by Rasmussen and Shalev (2014), exposure to across individuals and thus no one biological process
chronic stressors such as maltreatment sensitizes can be pinpointed as a source of vulnerability or pro-
neuronal structures in the amygdala to subsequent tection against PTSD. “Instead, these individually
stimulation by other stressors, compromises prefron- variable and often redundant systems appear to in-
tal cortex functioning through dendritic atrophy, teract in complex ways to facilitate or reduce PTSD
and leads to hyperreactivity in the sympathetic risk and recovery, as well as to influence vulnerability
nervous system and a dysregulated response to envi- to a variety of PTSD comorbid . . . conditions”
ronmental challenges. Brain imaging studies of chil- (Rasmussen & Shalev, 2014, p. 276); consequently,
dren exposed to maltreatment and family violence researchers in the field are called upon to take a
show heightened amygdala activation (McCrory dynamic systemic approach that can account for
et al., 2013; McCrory et al., 2011) and reductions in complex interactions and “deep translational rela-
white mater connectivity, particularly within the tionships between individually v ariable component
ventromedial prefrontal cortex, which, in turn, are neurobiological processes in PTSD” (p. 276).
associated with cortisol attenuation and maladapta- Epigenetic mechanisms also may come into play,
tion (Puetz et al., 2017). with studies of infants, children, adolescents, and

adults showing that childhood trauma is associated of neuronal circuits, resulting in higher risk for
with gene-expression changes that are mediated by trauma-associated psychiatric disorders” (Cross et al.,
DNA methylation, a process that typically inhibits 2017, p. 113). Other genetic markers also have
gene transcription and appears to be related to a been found that are associated with differential vul-
range of internalizing and externalizing problems nerability to psychopathology in the aftermath of
(Barker, Walton, & Cecil, 2018; Vinkers et al., trauma exposure. For example, twin studies show
2015). Tellingly, in some studies, these alterations in that levels of DNA methylation are highly heritable
DNA methylation are observed to be specific to and that individual differences, which can be de-
participants with a history of childhood maltreat- tected at birth, are associated with increased sensi-
ment as opposed to those whose trauma exposure tivity to environmental stressors and resulting mal-
occurred in adulthood (Klengel et al., 2013; Mehta adaptation in their aftermath (Barker et al., 2018).
et al., 2013). A fine-tuned examination by Cecil and Low vagal tone, an index of reduced capacity to
colleagues (2016) with a sample of high-risk youth regulate emotions in the face of stress, also repre-
found that maltreatment in the form of physical sents a biological vulnerability (Beauchaine, 2001;
abuse was most strongly related to DNA methyla- Beauchaine, Gatzke-Kopp, & Mead, 2007; Porges,
tion, although all types of abuse were associated 2007), albeit one that develops partially in response
with “a ‘common’ epigenetic signature enriched for to context, including parental emotion socializa-
biological processes related to regulation of nervous tion strategies (Katz, Maliken, & Stettler, 2012).
system development” (Barker et al., 2018, p. 310). Children with poor regulatory capacities, as
Limitations of much of this research include that it indexed by respiratory sinus arrhythmia or by a
has been cross-sectional, and thus unable to estab- lack of coordination between parasympathetic and
lish temporal precedence, and that most studies sympathetic responding, are differentially likely to
have examined outcomes related to general psycho- develop maladaptation in response to traumas
pathology rather than posttraumatic stress–related such as family and community violence (El-Sheikh
disorders specifically. However, prospective longitu- et al., 2009; McLaughlin, Rith-Najarian, Dirks, &
dinal studies of adults have identified alteration in Sheridan, 2013).
DNA methylation as a source of increased risk for In the psychosocial realm, risk factors that in-
the development of PTSD in the aftermath of trau- crease the likelihood that youth will develop PTSD
mas such as combat exposure (Rutten et al., 2018), symptoms in the aftermath of trauma exposure in-
and so this is a promising avenue for future research. clude a prior history of such exposures, preexisting
psychopathology, low social support, White ethnic-
Individual Differences in Vulnerability ity, and female gender (McLaughlin, Koenen, et al.,
and Resilience 2013; Milan, Zona, Acker, & Turcios-Cotto, 2013).
Research on Gene × Environment interactions and Further, in a meta-analysis spanning 64 studies in-
individual differences in sensitivity to context sug- cluding over 32,000 children and adolescents,
gests that polymorphisms in certain genes may Trickey and colleagues (2012) found that, above
confer vulnerability to PTSD, as well as other disor- and beyond preexisting vulnerabilities, PTSD in
ders in the aftermath of childhood trauma, which the aftermath of trauma exposure was predicted by
have relevance specifically for the development of ongoing posttrauma difficulties, including family
emotion regulation capacities. One of these genes, dysfunction and low support, as well as maladap-
FKBP5, is involved in regulating glucocorticoid tive coping strategies, particularly those involving
sensitivity, which, when reduced, leads to LHPA withdrawal, suppression, and anger. These findings
axis hyperresponsivity in the absence of threat. As suggest the importance of considering transactional
summarized by Cross et al. (2017), several studies associations among trauma exposure, emotion dys-
show that FKBP5 polymorphisms interact with regulation, and maladaptation and point to the po-
childhood maltreatment specifically to predict PTSD, tential value of targeting adaptive emotion regula-
as well as psychosis, depression, and executive function in interventions for trauma-exposed youth.
tion deficits, in adulthood. “Epigenetic changes in
the form of differential transcriptional activation of Parenting Contributions
FKBP5 by glucocorticoid receptor activation in the Parents’ own distress and emotion dysregulation in
presence of childhood abuse may enhance FKPB5 the aftermath of trauma exposure also have been
responsiveness, leading to both long-term changes implicated as factors increasing risk for negative
in the body’s stress response system and alterations child outcomes (Landolt, Ystrom, Sennhauser,
Kerig 269
Gnehm, & Vollrath, 2012; Nugent, Ostrowski, Theoretical Models of Emotion
Christopher, & Delahanty, 2007; Ostrowski et al., Dysregulation in Posttraumatic Stress
2011). In turn, parenting support in the aftermath Although, as noted, PTSD is not the only maladap-
of trauma exposure plays an important protective tive outcome associated with exposure to childhood
role, one that has been examined directly in relation trauma, and not all trauma-exposed young people
to its beneficial effects on children’s capacity to develop psychopathology, theoretical models of
manage emotions (Katz et al., 2012; Shipman & PTSD are useful because they highlight emotion
Zeman, 2001). Significantly, from infancy onward, dysregulation as an essential feature of the disorder.
emotion regulation capacities develop in the con- Although the DSM and ICD list disparate symp-
text of attachment relationships (Calkins & Hill, toms associated with the disorder, a variety of theo-
2007; Cassidy, 1994; Sroufe, 1996), and parents’ retical models have been offered in an attempt to
modeling, provision, and socialization of emotion lend central coherence to these lists by placing them
regulation strategies have a profound effect on those in a dysregulation framework.
of their children (Eisenberg et al., 2003; Grolnick
& Farkas, 2002). Particularly in the case of child Phasic Dysregulation Model
maltreatment, however, when a caregiver also is the One of the seeming internal contradictions to the
source of trauma, children are likely to be exposed PTSD diagnosis is its requirement that individuals
to poor models of emotion regulation and to experi- demonstrate simultaneously symptoms that are dia-
ence insecure and disorganized attachments that metrically opposed such as intrusions and avoid-
promote development of maladaptive self-soothing ance, or numbing and arousal. Horowitz’s (2011)
strategies and increase the likelihood of posttrau- seminal work has proposed that these symptoms are
matic stress reactions (Kobak, Cassidy, & Zir, best understood as representing distinct phases in
2004). For example, in an observational study com- the posttraumatic response cycle, which is organized
paring a sample of physically maltreating and non- around efforts to engage, and resultant failures, in
maltreating mothers, Shipman and colleagues (2000) emotion regulation. Given the aversiveness of the
found that maltreating mothers engaged in more traumatic event and the emotions surrounding it,
invalidation of their school-age children’s emotions attempts at affect suppression, such as avoidance,
and exhibited less supportive emotion coaching; in numbing, and denial, may be an adaptation strategy
addition, mothers’ emotion socialization styles ac- that is effective in the short term. However, efforts
counted for associations between maltreatment and at suppressing strong emotions are ultimately drain-
children’s adaptive emotion regulation skills. ing and difficult to maintain over a longer term; as
Even when the parent is not the source of the the individual’s suppressive coping strategies
trauma, parents may themselves be affected by trau- become exhausted, posttraumatic symptoms such as
matic experiences, whether historically due to their intrusions and arousal begin to break through, once
own childhood traumas, contemporaneously when again prompting attempts at emotion suppression.
they and the child are victims of the same event, or
indirectly when parents are distressed by the fact Overmodulation Versus Undermodulation
that harm has come to their child. Effects of trauma Although the term “emotion dysregulation” often is
on parenting should also be viewed in the context of used to refer to an impaired ability to downregulate
the larger family in which they radiate and cascade affect, scholars studying emotion dysregulation
dynamically among all members of the system have long pointed out that dysregulated emotion
(Kerig & Alexander, 2013). Parents’ own PTSD processing can take two forms: underregulation and
symptoms, distress, and poor affect regulation can overregulation (Cole, Michel, & Teti, 1994). Just as
compromise their parenting and contribute to chil- the inability to moderate emotions contributes to
dren’s dysregulation and maladaptation to traumatic maladaptation, so lack of access and expression of
events (Lambert, Holzer, & Hasbun, 2014; Marsac, emotions appropriate to an experience “interferes
Kassam-Adams, Delahanty, Widaman, & Barakat, with such adaptive functions as affective communi-
2014; Nugent et al., 2007). Research also supports cation in close relationships and successful problem
an intergenerational transmission of vulnerability to resolution” (Cole et al., 1994, p. 85). In this regard,
PTSD, the mechanisms of which appear to be in new thinking in the field of PTSD has focused on
the realms of both shared biology and socialization the role that specific symptoms play in the distress
processes (Leen-Feldner et al., 2013; Yehuda, regulation process, differentiating between those
Halligan, & Grossman, 2001). that represent attempts to overmodulate emotions

by restricting or suppressing them (i.e., avoidance, Trauma-Linked Callousness
numbing, and dissociation) versus those that repre- Another concept potentially related to the over-
sent heightened emotional reactivity and undermodulation of emotion in the aftermath of trauma
modulation (i.e., intrusions and arousal; Frewen & is that of acquired callousness (Kerig & Becker,
Lanius, 2006; Hopper, Frewen, van der Kolk, & 2010), the proposition that some youth utilize emo-
Lanius, 2007; Lanius, Brand, Vermetten, Frewen, tion suppression in an attempt to dampen down
& Spiegel, 2012; Lanius et al., 2010). Research has distress arising from childhood trauma, which then
reliably identified two subtypes of individuals with becomes generalized into a callous-unemotional
PTSD who display symptom profiles dominated by (CU) interpersonal style. For example, in a cross-
one or the other type of dysregulation. In a series of sectional study of detained youth, Kerig, Bennett,
studies utilizing psychophysiological and neuroim- Thompson, and Becker (2012) found that posttrau-
aging methods, Frewen and Lanius (2006) have matic emotional numbing statistically mediated the
found that, when exposed to trauma-relevant cues, association between trauma exposure and interper-
adults evidencing undermodulation display increased sonal callousness, consistent with the hypothesis
heart rate and reduced activation in the medial pre- that such traits could arise as a function of emo-
frontal cortex and anterior cingulate cortex (ACC), tional constriction in the aftermath of trauma.
consistent with a loss of regulatory control over Research on youth with high CU traits recognizes
emotional arousal. In addition, in comparison to the presence of a subtype defined by the presence of
controls who evidenced activation of the left hemi- high levels of anxiety (e.g., Docherty, Boxer,
sphere in combination with the right ACC during Huesmann, O’Brien, & Bushman, 2016; Kimonis,
trauma recall, suggestive of a verbally mediated re- Frick, Cauffman, Goldweber, & Skeem, 2012).
sponse, those with the undermodulation profile of Across studies, youth in the secondary group are dif-
PTSD showed coactivation with the right ACC and ferentiated by their histories of trauma exposure, as
other structures of the right hemisphere, evidencing well as their demonstration of higher levels of emo-
a more nonverbal and negatively valenced pattern of tional distress and reactivity to others’ emotions in
emotional reactivity. In contrast, functional mag- comparison to youth in the primary CU group. In
netic resonance imaging (fMRI) scans of trauma- these ways, the responses of those in the secondary
tized individuals showing the overmodulation pat- group appear similar to maltreated youth who also
tern of PTSD revealed increased activation in the display heightened reactivity to others’ emotions
inferior frontal gyrus, medial prefrontal cortex, and (Leist & Dadds, 2009; Masten et al., 2008; Pollak,
ACC, all indicative of the inhibition of emotional 2008), leading them to be dubbed as “callous and
arousal. In another study of adults diagnosed with emotional” (Gill & Stickle, 2016, p. 295).
PTSD, Nicholson and colleagues (2017) conducted In fact, although most research has distinguished
resting-state stochastic dynamic causal modeling between these two high-CU groups on the basis of
comparisons of those with and without the dissoci- self-reported anxiety, theory regarding the origins of
ative subtype. They found that dissociation was this secondary type suggests that the developmental
characterized by a distinctly different pattern of top- trajectory is precipitated by trauma rather than trait
down modulation from the medial prefrontal cortex anxiety (Karpman, 1941; Porter, 1996). Indeed, a
to decreased activation in the amygdala and periaq- significant body of research confirms that the sec-
ueductal gray area, resulting in emotional detach- ondary group also is differentiated by high levels of
ment and hypoarousal. posttraumatic stress symptoms (Kahn et al., 2013;
Attempts to confirm the over-/undermodulation Krischer & Sevecke, 2008; Tatar, Cauffman, Kimonis,
model in samples of youth are still in their infancy & Skeem, 2012; Vaughn, Edens, Howard, & Smith,
but are emergent. For example, in recent work 2009) and can be reliably distinguished from the
drawing upon a sample of traumatized youth re- primary group on that basis (Bennett & Kerig,
cruited from a detention center, our lab found that 2014). A study of emotion processing comparing
the over-/undermodulation subtypes could be reliably the two groups found that, in a sample of detained
distinguished. Further, tests of indirect effects were adolescents, those in the acquired (high-CU, high-
consistent with the hypothesis that interpersonal PTSD) category were more accurate in recognizing
trauma exposure was related to nonsuicidal self- complex emotions and reported higher levels of
injury through its association with elevated post- emotional numbing in comparison to youth in the
traumatic overmodulation of emotions (Modrowski, primary (high-CU, low-PTSD) group (Bennett &
Chaplo, Mozley, & Kerig, under review). Kerig, 2014). In addition, youth identified as
Kerig 271
“acquired CU” endorsed elevated levels of emotion psychological patterns among individuals whose
dysregulation, including nonacceptance of emo- PTSD symptoms are reflective of each of these dif-
tions and lack of emotional clarity. These data are ferent forms of defensive reaction (Gray, 2003;
suggestive of the possibility that some traumatized Koutsikou et al., 2014; Lanius et al., 2014).
youth may wear a “mask” of callousness, beneath
which their functioning is better described as unreg- Developmental Trauma Disorder Proposal
ulated than unemotional (Kerig, Bennett et al., One of the most fully developed conceptualizations
2012), or as exhibiting emotional distress rather of trauma as essentially composing a disorder of
than emotion deficit (Skeem, Johansson, Andershed, dysregulation was a proposal presented to the
Kerr, & Louden, 2007). DSM-5 planning committee by a group of leading
developmental psychopathologists who articulated
Defensive Regulation Model the case for a new diagnosis termed Developmental
Gray’s (1988, 2003) model of the stress response Trauma Disorder, or DTD (van der Kolk, Pynoos
system also emphasizes the role of affective and be- et al., 2009). Citing the conceptual foundations laid
havioral dysregulation in PTSD, a disorder that is down by Terr (1991) and Herman (1994), as well as
conceptualized as arising from an overreliance on a decades of subsequent research, the authors pointed
limited set of regulatory strategies that are no longer to a constellation of symptoms displayed consist
adaptive to the situation. Further, Gray proposes ently by children who had undergone complex trau-
that the prototypical stress-related “flight, fight, matic experiences involving disruptions in caregiving
freeze” (and, more recently added, “faint”; Schauer during their early years, in addition to other
& Elbert, 2010) not only represent different types of Criterion A trauma exposures, such as interpersonal
reactions but also can be understood meaningfully violence. Taken singly, these symptoms could be
as hierarchically sequenced, escalating responses for seen as consistent with a wide variety of diagnoses
regulating emotions and behavior in response to spanning both the internalizing and externalizing
threat. The “freeze” response, as seen in posttrau- spectra, and indeed, children with this complex
matic symptoms such as hypervigilance, behavioral trauma history commonly receive a toxic stew of
inhibition, and emotional constriction, may repre- multiple severe psychiatric diagnoses and accompa-
sent an adaptive initial response that allows us to nying major psychotropic medications. However,
limit our exposure to harm and buy time to appraise the authors argued, these symptoms could be law-
our options. If the threat continues, the next stage fully arranged under the umbrella of dysregulation
of escalation in the stress response system is to and viewed as resulting meaningfully from early
engage in “flight,” seen in symptoms such as avoid- developmental processes disrupted by trauma. The
ance. If flight is not possible, the next defensive re- resulting clarity and parsimony, in which a diverse
sponse is to turn and “fight,” represented by PTSD set of symptoms could be understood as arising
symptoms such as arousal, reactivity, and irritability. from a single pathogenic process, would allow for
Should all previous stress response reactions prove a better identification of the associated change
ineffective, and physical evasion is not possible, processes to be targeted by effective treatments
the next stage in the process is “freeze,” defined by (D’Andrea, Ford, Stolbach, Spinazzola, & van der
attempts to leave the scene psychologically, as Kolk, 2012; van der Kolk, 2005).
evidenced by tonic immobility and dissociation. The DTD proposal identified three domains of
A final stage proposed is that of “faint,” in which, dysregulation, involving key developmental pro-
when all else fails, the system shuts down entirely cesses that are disrupted by childhood trauma in the
and consciousness is abandoned to protect the or- absence of a buffering relationship with a reliable
ganism from experiencing unbearable pain directly attachment figure. First, affective and physiological
(Schauer & Elbert, 2010). dysregulation emerges as an inability to modulate,
As Schauer and Elbert (2010) suggest, these pat- recover from, or tolerate strong emotional states;
terns can be understood as emerging from changes disturbances in regulation of bodily functions or
in the biological circuitry involved, moving from physical sensations; and impaired awareness of
sympathetic activation in the early stages of the or capacity to describe emotions or bodily states.
stress response system to parasympathetic activation Second, attentional and behavioral dysregulation
in the latter stages. Consistent with this model, re- may take the form of either preoccupation with or
search also is beginning to emerge showing differ- diminished capacity to recognize threat, as well as
ent neuropsychological, psychophysiological, and maladaptive attempts at self-soothing, self-harm,

and difficulty initiating or sustaining goal-directed dissociation), and problem-focused versus avoidant
behavior. Third, self and relational dysregulation is coping responses. Results showed a nonlinear shift
seen in avoidance of or anxiety about attachment in posttraumatic symptom levels over time as a
figures; negative self-concept; pervasive distrust, de- function of decreasing peritraumatic dissociation in
fiance, or lack of reciprocity in close relationships; combination with low perceived self-efficacy. Further,
inappropriate attempts to achieve emotional inti- low self-efficacy interacted with avoidant coping
macy with others; and impaired capacity to regulate responses in leading to increased posttraumatic

empathic responses, whether in the form of dimin- distress. As the authors conclude, these findings
ished empathy, intolerance of others’ distress, or point to the centrality of “the self-regulation process
empathic overresponsiveness. whereby coping behaviors and self-evaluative ap-
The fact that the DTD proposal was rejected and praisals interact to influence a dynamic upward shift
the diagnosis not included in the DSM-5 has in [posttraumatic] symptoms” (Benight et al., 2017,
thwarted research on the topic, although some p. 339).
emerging validation studies of the draft criteria have
shown promise in studies of children and adoles- Dysregulation as a Mechanism
cents (Stolbach et al., 2013; Wamser-Nanney & Linking Childhood Trauma
Vandenberg, 2013). Further, as noted, the ICD-11 Exposure to Psychopathology
draft criteria released to date include a separate diag- A large body of research has confirmed that there
nosis for complex PTSD, which, although not spe- are associations among childhood maltreatment,
cific to childhood-onset trauma and different in emotion dysregulation, and maladaptation in sam-
some other respects from the DTD concept, may ples of both young persons and adults (Heleniak,
revitalize empirical investigations in this area. King, McLaughlin, & Monahan, 2017; Maughan
& Cicchetti, 2002; Shipman et al., 2000). As sum-
Self-Regulation Shift Theory marized by Doyle and Cicchetti (2017), across a
More recently, Benight, Shoji, and Delahanty host of studies, maltreated children exhibit delays
(2017) have proposed a novel conceptualization of and deficits in many facets of emotion regulation,
posttraumatic reactions from a dynamic systems including the capacities to identify, interpret, and
perspective, termed self-regulation shift theory mange feelings. Further, emotion dysregulation in
(SRST), in which the role of dysregulation is central. the aftermath of childhood maltreatment accounts
SRST proposes that, as “dynamic living systems” for functional impairments in occupational, social,
(p. 334), all humans engage in self-regulation in and family realms in adulthood (Cloitre, Miranda,
order to achieve a state of equilibrium conducive to Stoveall-McClough, & Han, 2005). Among stud-
meeting our biopsychosocial goals. Reactions to ies focusing on the outcome of PTSD specifically,
stressors, in turn, arise as a function of a perceived cross-sectional research also has found indirect
state of disequilibrium in combination with per- effects consistent with the hypothesis that trauma
ceived self-efficacy about one’s ability to cope or to exposure contributes to PTSD through the pur-
return to normal state. Under conditions of trau- ported mechanism of emotion dysregulation (see
matic stress, a critical threshold may be reached Seligowski, Lee, Bardeen, & Orcutt, 2015 for a
such that the discrepancy between one’s expected meta-analysis and Messman-Moore & Bhuptani,
and current self-efficacy is beyond one’s perceived 2017 for a recent narrative review).
future ability to cope, and a nonlinear shift to a new Research focused on the adolescent period also
impaired steady state emerges that is characterized by has investigated emotion dysregulation in the
psychological distress, disorganized coping responses, aftermath of trauma as a factor contributing to in-
and posttraumatic stress symptoms. In an initial test creased risk-taking, which is a developmentally
of the theory, the investigators used cusp catastro- salient precipitator of a range of adolescent prob-
phe modeling, which demonstrates a shift (cusp) lems, including substance abuse, delinquency,
from one stable state to another as a function of interpersonal violence, and health-risk behaviors
controlling and bifurcating factors that contribute such as dangerous driving, disordered eating, unsafe
to that shift. To this end, the investigators studied sexual activities, and self-harm (Kerig, 2014, 2017;
changes in posttraumatic stress symptoms over time Pat-Horenczyk et al., 2007). For example, in a series
in a sample of adult motor vehicle accident survivors of studies including youth involved in the juvenile
as a function of perceived self-efficacy (the bifurca- justice system, our lab has found that emotion dys-
tion catalyst), a controlling variable (peritraumatic regulation, as measured by youth self-reports on
Kerig 273
the Difficulties in Emotion Regulation Scale 2009). An advance offered by this research design
(DERS; Gratz & Roemer, 2004), accounts for the was the creation of an emotion dysregulation latent
association between trauma exposure and post- construct containing measures assessing lack of
traumatic stress symptoms (Bennett, Chaplo, emotional awareness and understanding, dysregu-
Modrowski, & Kerig, 2016), nonsuicidal self-injury lated emotion expression, and rumination.
(Chaplo, Kerig, Bennett, & Modrowski, 2015), Research outside the realm of childhood also
and recurrent involvement in law-violating behav- suggests that emotion dysregulation can act as a
ior (Chaplo, Kerig, Modrowski, & Bennett, 2017). vulnerability for the development of PTSD in the
More compellingly, longitudinal studies confirm aftermath of trauma exposure in emerging adult-
the hypothesis that emotion dysregulation acts as a hood. For example, Bardeen, Kumpula, and Orcutt
mediator of the association between trauma expo- (2013) gathered self-report DERS data from a sample
sure and PTSD, as well as other negative outcomes. of college students prior to a campus shooting.
In a study comparing maltreated and nonmal- Preexisting emotion regulation difficulties predicted
treated school-age children followed over the course the emergence of posttraumatic stress symptoms in
of a year, Kim and Cicchetti (2010) found that ne- the immediate aftermath of the shooting and 8
glect, physical abuse, sexual abuse, experiencing months later; moreover, posttraumatic symptoms
multiple forms of abuse, and early onset of abuse reciprocally predicted increased emotion dysregula-
were related to higher emotion dysregulation as tion over time.
rated by summer camp counselors on the Emotion
Regulation Checklist (Shields & Cicchetti, 1998). Facets of Emotion Dysregulation
Further, over time, emotion dysregulation pre- Related to PTSD
dicted peer rejection and externalizing problems, as A variety of measures with varying underlying
measured by peer nominations and teacher reports, conceptualizations of emotion regulation have been
respectively, which, in turn, exacerbated one an- used to study the association between emotion reg-
other’s negative effects. In a subsequent study fol- ulation, dysregulation, and PTSD. For example,
lowing a similar sample over a 3-year period, this Seligowski and colleagues’ (2015) meta-analysis of
research team found that early-onset maltreatment 57 studies of adults identified 12 measures encom-
was associated with emotional lability and negativity passing eight different aspects of emotion regulation:
at age 7, which predicted emotion dysregulation at general emotion dysregulation, acceptance, experi-
age 8; emotion dysregulation was in turn associated ential avoidance, expressive suppression, reappraisal,
with internalizing problems at age 9 (Kim-Spoon, rumination, thought suppression, and worry. Results
Cicchetti, & Rogosch, 2013). In a study focusing across studies showed the largest effect sizes for an
on a community sample of youth followed over association between PTSD and general emotion
5 years, Heleniak, Jenness, Vander Stoep, McCauley, regulation, rumination, thought suppression, and
and McLaughlin (2016) found that self-reported experiential avoidance.
emotional reactivity and deficient emotion regulation Many studies focusing on adults and adolescents
capacities as measured on the Emotion Reactivity with maltreatment histories have operationalized
Scale (Nock, Wedig, Holmberg, & Hooley, 2008) emotion dysregulation through self-reports on the
mediated associations between childhood maltreat- DERS (Gratz & Roemer, 2004), which assesses six
ment and both internalizing and externalizing dimensions: lack of emotional awareness, lack of
problems. emotional clarity, difficulty controlling behavior
Expanding this research to more general life when upset, difficulty maintaining goal-directed
stressors, in a series of studies following a large behavior, nonacceptance of emotions, and limited
community sample of early adolescents over time, access to emotion regulation strategies. Some re-
McLaughlin and colleagues demonstrated that search suggests that, among these facets of emotion
self-reported emotion dysregulation mediated the dysregulation, difficulty maintaining goal-directed
association between stressful life events and youth behavior, difficulty controlling behavior, lack of
aggression (Herts, McLaughlin, & Hatzenbuehler, emotional clarity, and limited access to effective
2012) and internalizing symptoms (McLaughlin & emotion regulation strategies are those most strongly
Hatzenbuehler, 2009). Further, this team found associated with PTSD among adults with histories
that emotion regulation difficulties accounted for of child abuse–related trauma (e.g., Weiss, Tull,
the association between peer victimization and in- Lavender, & Gratz, 2013). In contrast, in a study of
ternalizing (McLaughlin, Hatzenbuehler, & Hilt, detained adolescents with histories of exposure to

multiple forms of interpersonal and noninterpersonal Methodological and Conceptual Dilemmas
traumas, Bennett, Chaplo, Modrowski, and Kerig One major challenge for the field, as is implicit in
(2016) found that the DERS scales of difficulty con- the foregoing review of the methods used in this re-
trolling behavior and lack of emotion regulation search, is a need for clarification of the boundaries
strategies were those most robustly associated with and delineation of the dimensions that compose the
PTSD symptoms overall. However, looking at the construct of emotion dysregulation, which has been
individual symptom clusters associated with PTSD, conceptualized and operationalized in various ways
the investigators found that the DERS scales of lack and with disparate measures. A potential rich avenue
of emotional clarity and goal-directed behavior were for future research will be to wed refinements in the
most strongly associated with PTSD symptoms in- conceptualization and measurement of emotion
dicative of emotion underregulation (i.e., intrusions dysregulation to those simultaneously ongoing in
and arousal), whereas the DERS scale of nonaccep- recent reconceptualizations of the posttraumatic re-
tance of emotions was differentially associated with sponse from a dysregulation perspective (Frewen &
PTSD symptoms related to emotion overregulation Lanius, 2006; Lanius et al., 2010). Another needed
(i.e., avoidance and numbing). These findings sug- methodological advance will be the incorporation
gest the importance of considering both under- and of dynamic systems and multilevel perspectives
overmodulation of emotions as dysregulatory pro- that, as in the field of developmental psychopathol-
cesses underlying associations between trauma ex- ogy more widely, incorporate biopsychosocial
posure and PTSD. contributors to the study of maladaptation and re-
silience in the aftermath of trauma (Bremner, 2016;
Summary and Integration Cicchetti, 2016). Psychophysiological methods in
Major conceptual models and the existing body of particular offer an alternative to the overreliance in
empirical research on childhood trauma confirm the field on self-reports assessing important constructs
the value of considering posttraumatic stress from such as emotion dysregulation, overmodulation,
an emotion dysregulation perspective. Childhood and undermodulation, particularly given evidence
chronic, prolonged, and repeated trauma exposure that traumatized youth exhibit deficits in their ca-
in particular has negative effects on brain develop- pacities to accurately access, label, and report their
ment that compromise emotion regulation capacities. emotions (Kerig, 2018). Even more challenging,
Although emotion dysregulation in the aftermath of fundamental disagreements about the nature and
childhood trauma exposure may be considered a definition of traumatic stress have proven difficult
transdiagnostic risk factor for a wide range of to resolve. However, the somewhat separate litera-
psychopathologies (Heleniak et al., 2016), it also ture that has been amassing on allostatic load and
appears to play a particularly salient role in post- adverse childhood experiences more broadly offers
traumatic stress reactions. Emotion dysregulation opportunities to expand our perspective on trauma
acts as a preexisting vulnerability for children who as a construct in ways that allow for a more develop-
lack effective strategies for managing the emotional mentally sensitive and person-centered view.
distress precipitated by traumatic experiences,
whether as a function of their biological makeup or Needed Developmental Considerations
failures in the “average expectable environment” Within a developmental psychopathology frame-
(Cicchetti & Valentino, 2006) provided by a secure work, there are at least three important challenges
attachment relationship, in which the capacities for for future work devoted to the consequences of
emotion regulation are first modeled, experienced, childhood trauma, as specifically defined, and ad-
and internalized. In turn, emotion dysregulation verse childhood experiences, as more broadly con-
emerges as a lasting pathogenic aftereffect for youth ceived. One relatively neglected factor in research to
whose emerging emotion management capacities date concerns the need to carefully attend to the
are disrupted by biologically, psychologically, and developmental epoch(s) during which trauma oc-
socially “overwhelming” experiences. curred and how that might affect the developing
person differentially (Cowell, Cicchetti, Rogosch,
Future Directions & Toth, 2015), depending on the stage of emerging
A number of unresolved issues and controversies brain structures and processes such as myelination
challenge the study of emotion dysregulation and and pruning (Bremner, 2016). Of note, trauma ap-
childhood trauma, but these also offer growth points pears to alter LHPA axis functioning differently
for future research. among infants, children, adolescents, and adults
Kerig 275
(Lupien et al., 2009), with potentially significant childhood trauma within similar developmental
consequences for emotion dysregulation across the epochs; moreover, many studies of trauma-exposed
lifespan. There also may be sensitive periods for samples find high rates of retraumatization and
brain structures that make them more individually revictimization that make it challenging to deter-
vulnerable to the effects of traumatic stress at par- mine with any specificity which experiences have
ticular points in development; in addition, these potentiated particular posttraumatic reactions
differences in maturation rates may contribute to (Kerig, 2017).
disruptions in coordination and communication
among regions that ordinarily operate as a cohesive Translational Research Opportunities
network in responding to environmental challenges, The enhancement of adaptive emotion regulation
including the hippocampus, prefrontal cortex, and capacities is encompassed within the leading
amygdala (Cross et al., 2017), with clear implica- evidence-based interventions for child and adolescent
tions for emotion regulation capacity. PTSD (Cohen, Mannarino, & Deblinger, 2017).
Another relatively neglected developmental The scaffolding of healthy regulation capacities is
factor concerns the length of time that has elapsed particularly central to interventions developed for
since the traumatic event(s) and at what point in (Ford, 2015; Ford & Russo, 2006; Ford, Steinberg,
the trajectory of the stress adaptation process that Hawke, Levine, & Zhang, 2012) and adapted to
measurements are taken. For example, in the im- (Cohen, Mannarino, Kliethermes, & Murray, 2012)
mediate aftermath of a traumatic event, cortisol youth with complex PTSD/DTD. However, addi-
levels are generally elevated, whereas with repeated tional research deconstructing these treatment ef-
and prolonged childhood trauma exposure, cortisol fects would be valuable to better inform the field
becomes depleted over the course of the transition about the role of emotion regulation in recovery
from childhood to adolescence (Trickett, Noll, from trauma. For example, in a prospective study of
Susman, Shenk, & Putnam, 2010); therefore, adult combat veterans, Boden and colleagues (2013)
measures taken at different time points may present found that self-reported attempts to manage emo-
contradictory pictures regarding the associations tions through suppression, as measured by the
among traumatic stress, neurochemistry, and Emotion Regulation Questionnaire (Gross & John,
psychological symptoms and behavior. Studies of 2003), were associated with higher levels of PTSD
psychophysiology and neurobiological processes initially and that reductions in emotion suppression
involved in childhood trauma generally have been over time accounted for the beneficial effects of
conducted either in the immediate aftermath of cognitive-behavioral therapy on PTSD symptoms.
exposure to discrete stressors (Kirsch, Wilhelm, & Studies showing similar mechanisms of effect for
Goldbeck, 2011) or in an indeterminately variable child treatment components targeting emotion dys-
period afterward in the case of childhood exposure regulation would be of value. In addition, future
to chronic traumas, such as maltreatment (Cross translational research should be guided by new work
et al., 2017); thus, type of trauma exposure and evidencing typologies of posttraumatic response,
timing of posttraumatic response are inextricably which suggest that different interventions may be
entangled. needed to address different underlying processes
A third developmental consideration arises represented by such distinctions as overmodulation
from the developmental psychopathology concept versus overmodulation of emotions. The development
of stage-salient issues, which suggests that trauma’s of a more nuanced understanding of the posttrau-
effects also will differ as a function of the child’s matic response holds promise for the development
emergent capacities and the prevailing develop- of more targeted and effective treatments.
mental tasks that the child is attempting to master
(Becker-Blease & Kerig, 2016; Kerig, Ludlow, &
References
Wenar, 2012). Although consideration of these de- American Psychiatric Association. (1980). Diagnostic and statistical
velopmental factors promises to shed important manual of mental disorders, 3rd edition (DSM-III).
light on the emergence, expression, and phenome- Washington, DC: Author.
nology of posttraumatic processes, they will be American Psychiatric Association. (2013). Diagnostic and
statistical manual of mental disorders, 5th edition (DSM-5).
challenging to research in a systematic way. Other
Washington, DC: Author.
than in the case of discrete natural disasters, it is Anda, R. F., Felitti, V. F., Walker, J., Whitfield, C. L., Bremner,
challenging to recruit into studies children or J. D., Perry, B. D. . . . Giles, W. H. (2006). The enduring
adults who have experienced similar forms of effects of abuse and related adverse experiences in childhood.

European Archives of Psychiatry and Clinical Neuroscience, Cassidy, J. (1994). Emotion regulation: Influences of attachment
256, 174–186. relationships. Monographs of the Society for Research in Child
Bardeen, J. R., Kumpula, M. J., & Orcutt, H. K. (2013). Development, 59, 228–249.
Emotion regulation difficulties as a prospective predictor of Cecil, C. A. M., Smith, R. G., Walton, E., Mill, J., McCrory,
posttraumatic stress symptoms following a mass shooting. E. J., & Viding, E. (2016). Epigenetic signatures of childhood
Journal of Anxiety Disorders, 27, 188–196. abuse and neglect: Implications for psychiatric vulnerability.
Barker, E. D., Walton, E., & Cecil, C. A. M. (2018). Annual Journal of Psychiatric Research, 83, 184–194.
Research Review: DNA methylation as a mediator in the Chaplo, S. D., Kerig, P. K., Bennett, D. C., & Modrowski, C. A.
association between risk exposure and child and adolescent (2015). The roles of emotion dysregulation and dissociation
psychopathology. Journal of Child Psychology and Psychiatry, in the association between sexual abuse and self-injury
59, 303–322. among juvenile justice-involved youth. Journal of Trauma
Beauchaine, T. P. (2001). Vagal tone, development, and Gray’s and Dissociation, 16, 272–285.
motivational theory: Toward an integrated model of Chaplo, S. D., Kerig, P. K., Modrowski, C. A., & Bennett, D. C.
autonomic nervous system functioning in psychopathology. (2017). Gender differences in the sequelae of childhood
Development and Psychopathology, 13, 183–214. sexual abuse: An examination of borderline features,
Beauchaine, T. P., Gatzke-Kopp, L., & Mead, H. K. (2007). dissociation, emotion dysregulation, and delinquent
Polyvagal theory and developmental psychopathology: behaviors among detained adolescents. Journal of Child and
Emotion dysregulation and conduct problems from Adolescent Trauma, 10, 29–39.
preschool to adolescence. Biological Psychology, 74, 174–184. Chou, T., Asnaani, A., & Hofmann, S. G. (2012). Perception of
Becker-Blease, K., & Kerig, P. K. (2016). Child maltreatment: racial discrimination and psychopathology across three
A developmental traumatology perspective. Washington, DC: U.S. ethnic minority groups. Cultural Diversity and Ethnic
American Psychological Association Press. Minority Psychology, 18, 74–81.
Benight, C. C., Shoji, K., & Delahanty, D. L. (2017). Self- Cicchetti, D. (2016). Socioemotional, personality, and biological
regulation shift theory: A dynamic systems approach to development: Illustrations from a multilevel developmental
traumatic stress. Journal of Traumatic Stress, 30, 333–342. psychopathology perspective on child maltreatment. Annual
Bennett, D. C., Chaplo, S. D., Modrowski, C., & Kerig, P. K. Review of Psychology, 67, 187–211.
(2016). Facets of emotion dysregulation as mediators of the Cicchetti, D., & Rogosch, F. A. (1996). Editorial: Equifinality
association between trauma exposure and posttraumatic stress and multifinality in developmental psychopathology.
symptoms in justice-involved adolescents. Traumatology, 22, Development and Psychopathology, 8, 597–600.
174–183. Cicchetti, D., & Toth, S. L. (2016). Child maltreatment and
Bennett, D. C., & Kerig, P. K. (2014). Investigating the construct developmental psychopathology: A multilevel perspective. In
of trauma-related acquired callousness among delinquent D. Cicchetti (Ed.), Developmental psychopathology, Vol. II:
youth: Differences in emotion processing. Journal of Maladaptation and psychopathology (pp. 457–512). New York,
Traumatic Stress, 27, 415–422. NY: John Wiley & Sons.
Bennett, D. C., Modrowski, C. A., Kerig, P. K., & Chaplo, S. D. Cicchetti, D., & Valentino, K. (2006). An ecological-
(2015). Investigating the dissociative subtype of posttraumatic transactional perspective on child maltreatment: Failure of
stress disorder in a sample of traumatized detained youth. the average expectable environment and its influence on
Psychological Trauma: Theory, Research, Practice, and Policy, 7, child development. In D. Cicchetti & D. J. Cohen (Eds.),
465–472. Developmental psychopathology. Vol. III: Risk, disorder and
Boden, M. T., Westermann, S., McRae, K., Kuo, J., Alvarez, J., adaptation (Vol. 2, pp. 129–201). New York, NY: Wiley.
Kulkarni, M. R., . . . Bonn-Miller, M. O. (2013). Emotion Cloitre, M., Garvert, D. W., Brewin, C. R., Bryant, R. A., &
regulation and posttraumatic stress disorder: A prospective Maercker, A. (2013). Evidence for proposed ICD-11 PTSD
investigation. Journal of Social and Clinical Psychology, 32, and complex PTSD: A latent profile analysis. European
296–314. Journal of Psychotraumatology, 4.
Bovin, M. J., & Marx, B. P. (2011). The importance of the Cloitre, M., Miranda, R., Stoveall-McClough, K. C., &
peritraumatic experience in defining traumatic stress. Han, H. (2005). Beyond PTSD: Emotion regulation and
Psychological Bulletin, 137, 47–57. interpersonal problems as predictors of functional
Bowlby, J. (1973/1998). Attachment and loss, Vol. II: Separation. impairment in survivors of childhood abuse. Behavior Therapy,
London, UK: Pimlico. 36, 119–124.
Bremner, J. D. (2016). Traumatic stress from a multilevel Cohen, J. A., Mannarino, A. J., & Deblinger, E. (2017). Treating
developmental psychopathology perspective. In D. Cicchetti trauma and traumatic grief in children and adolescents (2nd
(Ed.), Developmental psychopathology (3rd ed., Vol. 3). ed.). New York, NY: Guilford.
New York, NY: Wiley. Cohen, J. A., Mannarino, A. P., Kliethermes, M., & Murray,
Bui, E., Brunet, A., Allenou, C., Camassel, C., Raynaud, J. P., L. A. (2012). Trauma-focused CBT for youth with complex
Claudet, I., . . . Birmes, P. (2010). Peritraumatic reactions and trauma. Child Abuse and Neglect, 36, 528–541.
posttraumatic stress symptoms in school-aged children Cole, P. M., Michel, M. K., & Teti, L. O. (1994). The
victims of road traffic accident. General Hospital Psychiatry, development of emotion regulation and dysregulation: A
32, 330–333. clinical perspective. Monographs of the Society for Research in
Calkins, S. D., & Hill, A. (2007). Caregiver influences on Child Development, 59, 73–102.
emerging emotion regulation. In J. J. Gross (Ed.), Handbook Copeland, W. E., Keeler, G., Angold, A., & Costello, E. J.
of emotion regulation (pp. 229–248). New York, NY: (2010). Posttraumatic stress without trauma in children.
Guilford. American Journal of Psychiatry, 167, 1059–1065.
Kerig 277
Costello, E. J., Erkanli, A., Fairbank, J. A., & Angold, A. (2002). Frewen, P. A., & Lanius, R. A. (2006). Toward a psychobiology
The prevalence of potentially traumatic events in childhood of posttraumatic self-regulation. Annals of the New York
and adolescence. Journal of Traumatic Stress, 15, 99–112. Academy of Sciences, 1071, 110–124.
Cowell, R. A., Cicchetti, D., Rogosch, F. A., & Toth, S. L. Friedman, M. J., Resick, P. A., & Keane, T. M. (2014). PTSD
(2015). Childhood maltreatment and its effect on from DSM-III to DSM-5: Progress and challenges. In
neurocognitive functioning: Timing and chronicity matter. M. J. Friedman, T. M. Keane, & P. A. Resick (Eds.),
Development and Psychopathology, 27, 521–533. Handbook of PTSD (pp. 3–20). New York, NY: Guilford.
Cross, D., Fani, N., Powers, A., & Bradley, B. (2017). Ganzel, B. L., Kim, P., Gilmore, H., Tottenham, N., & Temple,
Neurobiological development in the context of childhood E. (2013). Stress and the healthy adolescent brain: Evidence
trauma. Clinical Psychology: Science and Practice, 24, 111–124. for the neural embedding of life events. Development and
D’Andrea, W., Ford, J., Stolbach, B., Spinazzola, J., & van der Psychopathology, 25, 879–889.
Kolk, B. A. (2012). Understanding interpersonal trauma in Giannopoulou, I., Strouthos, M., Smith, P., Dikaiakou, A.,
children: Why we need a developmentally appropriate Galanopoulou, V., & Yule, W. (2006). Post-traumatic stress
trauma diagnosis. American Journal of Orthopsychiatry, 82, reactions of children and adolescents exposed to the Athens
187–200. 1999 earthquake. European Psychiatry, 21, 160–166.
Docherty, M., Boxer, P., Huesmann, L. R., O’Brien, M., & Gil-Rivas, V., Silver, R. C., Holman, E. A., McIntosh, D. N., &
Bushman, B. J. (2016). Exploring primary and secondary Poulin, M. (2007). Parental response and adolescent
variants of psychopathy in adolescents in detention and in adjustment to the September 11, 2001 terrorist attacks.
the community. Journal of Clinical Child and Adolescent Journal of Traumatic Stress, 20, 1063–1068.
Psychology, 45, 564–578. Gill, A. D., & Stickle, T. R. (2016). Affective differences between
Doyle, C., & Cicchetti, D. (2017). From the cradle to the grave: psychopathy variants and genders in adjudicated youth.
The effect of adverse caregiving environments on attachment Journal of Abnormal Child Psychology, 44, 295–307.
and relationships throughout the lifespan. Clinical Psychology: Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment
Science and Practice, 24, 203–217. of emotion regulation and dysregulation: Development,
Dvir, Y., Ford, J. D., Hill, M., & Frazier, J. A. (2014). Childhood factor structure, and initial validation of the difficulties in
maltreatment, emotional dysregulation, and psychiatric emotion regulation scale. Journal of Psychopathology and
comorbidities. Harvard Review of Psychiatry, 22, 149–161. Behavioral Assessment, 26, 41–54.
Eisenberg, N., Valiente, C., Morris, A. S., Fabes, R. A., Gray, J. A. (1988). The psychology of fear and stress (2nd ed.).
Cumberland, A., Reiser, M., .
.
. Losoya, S. (2003). New York, NY: Cambridge University Press.
Longitudinal relations among parental emotional expressivity, Gray, J. A. (2003). The neuropsychology of anxiety: An enquiry into
children’s regulation, and quality of socioemotional the functions of the septo-hippocampal system. New York, NY:
functioning. Developmental Psychology, 39, 3–19. Oxford University Press.
El-Sheikh, M., Kouros, C. D., Erath, S., Cummings, E. M., Grolnick, W. S., & Farkas, M. (2002). Parenting and the
Keller, P., Staton, L., .
.
.
Moore, G. A. (2009). Marital development of children’s self-regulation. In M. H. Bornstein
conflict and children’s externalizing behavior: Interactions (Ed.), Handbook of parenting, Vol. 5: Practical issues in
between parasympathetic and sympathetic nervous system parenting (pp. 89–110). Mahwah, NJ: Erlbaum.
activity. Monographs of the Society for Research in Child Gross, J. J., & John, O. P. (2003). Individual differences in two
Development, 74, vii–79. emotion regulation processes: Implications for affect,
Flores, E., Tschann, J. M., Dimas, J. M., Pasch, L. A., & de relationships, and well-being. Journal of Personality and Social
Groat, C. L. (2010). Perceived racial/ethnic discrimination, Psychology, 85, 348–362.
posttraumatic stress symptoms, and health risk behaviors Heim, C., & Nemeroff, C. B. (2001). The role of childhood
among Mexican American adolescents. Journal of Counseling trauma in the neurobiology of mood and anxiety disorders:
Psychology, 57, 264–273. Preclinical and clinical studies. Biological Psychiatry, 49,
Ford, J. (2015). An affective cognitive neuroscience-based 1023–1039.
approach to PTSD psychotherapy: The TARGET Model. Heleniak, C., Jenness, J. L., Vander Stoep, A., McCauley, E., &
Journal of Cognitive Psychotherapy, 29, 68–91. McLaughlin, K. A. (2016). Childhood maltreatment exposure
Ford, J. D. (2005). Treatment implications of altered affect and disruptions in emotion regulation: A transdiagnostic
regulation and information processing following child pathway to adolescent internalizing and externalizing psycho
maltreatment. Psychiatric Annals, 35, 410–419. pathology. Cognitive Therapy and Research, 40, 394–415.
Ford, J. D. (2009). Neurobiological and developmental research: Heleniak, C., King, K. M., McLaughlin, K. A., & Monahan,
Clinical implications. In M. A. Courtois & J. D. Ford (Eds.), K. C. (2017). Disruptions in emotion regulation as a
Treating complex traumatic stress disorders: An evidence-based mechanism linking community violence exposure to
guide (pp. 31–58). New York, NY: Routledge. adolescent internalizing problems. Journal of Research on
Ford, J. D., & Russo, E. (2006). Trauma-focused, present- Adolescence, 28, 229–244.
centered, emotional self-regulation approach to integrated Herman, J. L. (1994). Sequelae of prolonged and repeated
treatment for posttraumatic stress and addiction: Trauma trauma: Evidence for a complex posttraumatic syndrome
Adaptive Recovery Group Education and Therapy (DESNOS). In J. R. T. Davidson & E. G. Foa (Eds.),
(TARGET). American Journal of Psychotherapy, 60, 335–355. Posttraumatic stress disorder (pp. 213–228). Washington, DC:
Ford, J. D., Steinberg, K. L., Hawke, J., Levine, J., & Zhang, W. American Psychiatric Press.
(2012). Randomized trial comparison of emotion regulation Herts, K. L., McLaughlin, K. A., & Hatzenbuehler, M. L.
and relational psychotherapies for PTSD with girls involved (2012). Emotion dysregulation as a mechanism linking stress
in delinquency. Journal of Clinical Child and Adolescent exposure to adolescent aggressive behavior. Journal of
Psychology, 41, 27–37. Abnormal Child Psychology, 40, 1111–1122.

Holman, E. A., Garfin, D. R., & Silver, R. C. (2014). Media’s posttraumatic stress symptoms among traumatized
role in broadcasting acute stress following the Boston delinquent youth. Psychological Trauma, 5, 431–438.
Marathon bombings. Proceedings of the National Academy of Kerig, P. K., Bennett, D. C., Thompson, M., & Becker, S. P.
Sciences, 111, 93–98. (2012). “Nothing really matters”: Emotional numbing as a
Hopper, J. W., Frewen, P. A., van der Kolk, B. A., & Lanius, link between trauma exposure and callousness in delinquent
R. A. (2007). Neural correlates of reexperiencing, avoidance, youth. Journal of Traumatic Stress, 25, 272–279.
and dissociation in PTSD: Symptom dimensions and Kerig, P. K., Ludlow, A., & Wenar, C. (2012). Developmental
emotion dysregulation in responses to script-driven trauma psychopathology: From infancy through adolescence (6th ed.).
imagery. Journal of Traumatic Stress, 20, 713–725. Maidenhead, UK: McGraw-Hill.
Horowitz, M. J. (2011). Stress response syndromes. Northvale, NJ: Kilpatrick, D. G., Resnick, H. S., & Acierno, R. (2009). Should
Aronson. PTSD Criterion A be retained? Journal of Traumatic Stress,
Idsoe, T., Dyregrov, A., & Idsoe, E. C. (2012). Bullying and 22, 374–383.
PTSD symptoms. Journal of Abnormal Child Psychology, 40, Kim, J., & Cicchetti, D. (2010). Longitudinal pathways linking
901–911. child maltreatment, emotion regulation, peer relations, and
Kahn, R. E., Frick, P. J., Youngstrom, E. A., Youngstrom, J. K., psychopathology. Journal of Child Psychology and Psychiatry,
Feeny, N. C., & Findling, R. L. (2013). Distinguishing 51, 706–716.
primary and secondary variants of callous-unemotional traits Kim-Spoon, J., Cicchetti, D., & Rogosch, F. A. (2013).
among adolescents in a clinic-referred sample. Psychological A longitudinal study of emotion regulation, emotion
Assessment, 25, 966–978. lability-negativity, and internalizing symptomatology in
Kaplow, J. B., Howell, K. H., & Layne, C. M. (2014). Do maltreated and nonmaltreated children. Child Development,
circumstances of the death matter? Identifying 84, 512–527.
socioenvironmental risks for grief-related psychopathology Kimonis, E. R., Frick, P. J., Cauffman, E., Goldweber, A., &
in bereaved youth. Journal of Traumatic Stress, 27, 42–49. Skeem, J. (2012). Primary and secondary variants of juvenile
Karpman, B. (1941). On the need of separating psychopathy into psychopathy differ in emotional processing. Development and
two distinct clinical types: The symptomatic and the Psychopathology, 24, 1091–1103.
idiopathic. Journal of Criminal Psychopathology, 3, 112–137. Kirsch, V., Wilhelm, F. H., & Goldbeck, L. (2011).
Katz, L. F., Maliken, A. C., & Stettler, N. M. (2012). Parental Psychophysiological characteristics of PTSD in children
meta-emotion philosophy: A review of research and and adolescents: A review. Journal of Traumatic Stress, 24,
theoretical framework. Child Development Perspectives, 6, 146–154.
417–422. Klengel, T., Mehta, D., Anacker, C., Rex-Haffner, M., Pruessner,
Keeley, J. W., Reed, G. M., Roberts, M. C., Evans, S. C., J. C., Pariante, C. M., . . . Binder, E. B. (2013). Allele-specific
Robles, R., Matsumoto, C., . .
.
Maercker, A. (2016). FKBP5 DNA demethylation mediates gene-childhood
Disorders specifically associated with stress: A case- trauma interactions. Nature: Neuroscience, 16, 33–41.
controlled field study for ICD-11 Mental and Behavioural Kobak, R., Cassidy, J., & Zir, Y. (2004). Attachment-related
Disorders. International Journal of Clinical and Health trauma and posttraumatic stress disorder. In W. S. Rholes &
Psychology, 16, 109–127. J. A. Simpson (Eds.), Adult attachment: Theory, research, and
Kenardy, J., De Young, A., & Charlton, E. (2012, November). clinical implications (pp. 388–407). New York, NY: Guilford.
PTSD as a “gateway” disorder in young children. Paper Koss, K. J., & Gunnar, M. R. (2018). Annual research review:
presented at the Annual Meeting of the International Society Early adversity, the hypothalamic–pituitary–adrenocortical
for Traumatic Stress Studies, Los Angeles, CA. axis, and child psychopathology. Journal of Child Psychology
Kerig, P. K. (2014). Maltreatment and trauma in adolescence: and Psychiatry, 59, 327–346.
A time of heightened risk and potential resilience. StressPoints, Koutsikou, S., Crook, J. J., Earl, E. V., Leith, J. L., Watson, T. C.,
28, 1–21. Lumb, B. M., & Apps, R. (2014). Neural substrates underlying
Kerig, P. K. (2017). Posttraumatic stress disorder in childhood and fear-evoked freezing: The periaqueductal grey–cerebellar link.
adolescence: A developmental psychopathology perspective. Journal of Physiology, 592, 2197–2213.
New York, NY: Momentum Press. Krischer, M. K., & Sevecke, K. (2008). Early traumatization
Kerig, P. K. (2018). Polyvictimization and girls’ involvement in and psychopathy in female and male juvenile offenders.
the juvenile justice system: Investigating gender-differentiated International Journal of Law and Psychiatry, 31, 253–262.
patterns of risk, recidivism, and resilience. Journal of Lambert, J. E., Holzer, J., & Hasbun, A. (2014). Association
Interpersonal Violence, 33, 789–809. between parents’ PTSD severity and children’s psychological
Kerig, P. K., & Alexander, J. F. (2013). Family matters: Integrating distress: A meta-analysis. Journal of Traumatic Stress, 27,
trauma treatment into Functional Family Therapy with 9–17.
delinquent youth. In P. K. Kerig (Ed.), Psychological trauma Landolt, M. A., Ystrom, E., Sennhauser, F. H., Gnehm, H. E., &
and juvenile delinquency (pp. 122–140). London, UK: Vollrath, M. E. (2012). The mutual prospective influence of
Routledge. child and parental post-traumatic stress symptoms in
Kerig, P. K., & Becker, S. P. (2010). From internalizing to pediatric patients. Journal of Child Psychology and Psychiatry,
externalizing: Theoretical models of the processes linking 53, 767–774.
PTSD to juvenile delinquency. In S. J. Egan (Ed.), Lanius, R. A., Brand, B., Vermetten, E., Frewen, P. A., & Spiegel,
Posttraumatic stress disorder (PTSD): Causes, symptoms and D. (2012). The dissociative subtype of posttraumatic stress
treatment (pp. 1–46). Hauppauge, NY: Nova Science disorder: Rationale, clinical and neurobiological evidence,
Publishers. and implications. Depression and Anxiety, 29, 701–708.
Kerig, P. K., & Bennett, D. C. (2013). Beyond fear, helplessness, Lanius, R. A., Vermetten, E., Loewenstein, R. J., Brand, B.,
and horror: Peritraumatic reactions associated with Schmahl, C., Bremner, J., & Spiegel, D. (2010). Emotion
Kerig 279
modulation in PTSD: Clinical and neurobiological evidence McLaughlin, K. A., & Hatzenbuehler, M. L. (2009). Mechanisms
for a dissociative subtype. American Journal of Psychiatry, 167, linking stressful life events and mental health problems in a
640–647. prospective, community-based sample of adolescents. Journal
Lanius, R. A., Wolf, E. J., Miller, M. W., Frewen, P. A., of Adolescent Health, 44, 153–160.
Vermetten, E., Brand, B., & Spiegel, D. (2014). The McLaughlin, K. A., Hatzenbuehler, M. L., & Hilt, L. M. (2009).
dissociative subtype of PTSD. In M. J. Friedman, Emotion dysregulation as a mechanism linking peer
T. M. Keane, & P. A. Resick (Eds.), Handbook of PTSD (2nd victimization to internalizing symptoms in adolescents.
ed., pp. 234–250). New York, NY: Guilford. Journal of Consulting and Clinical Psychology, 77, 894–904.
Lansing, A. E., Plante, W. Y., & Beck, A. N. (2017). Assessing McLaughlin, K. A., Koenen, K. C., Hill, E. D., Petukhova, M.,
stress-related treatment needs among girls at risk for poor Sampson, N. A., Zaslavsky, A. M., & Kessler, R. C. (2013).
functional outcomes: The impact of cumulative adversity, Trauma exposure and posttraumatic stress disorder in a
criterion traumas, and non-criterion events. Journal of national sample of adolescents. Journal of the American
Anxiety Disorders, 48, 36–44. Academy of Child and Adolescent Psychiatry, 52, 815–830.
Leen-Feldner, E. W., Feldner, M. T., Knapp, A., Bunaciu, L., McLaughlin, K. A., Peverill, M., Gold, A. L., Alves, S., &
Blumenthal, H., & Amstadter, A. B. (2013). Offspring Sheridan, M. A. (2015). Child maltreatment and neural systems
psychological and biological correlates of parental underlying emotion regulation. Journal of the American
posttraumatic stress: Review of the literature and research Academy of Child and Adolescent Psychiatry, 54, 753–762.
agenda. Clinical Psychology Review, 33, 1106–1133. McLaughlin, K. A., Rith-Najarian, L., Dirks, M. A., & Sheridan,
Leist, T., & Dadds, M. R. (2009). Adolescents’ ability to read M. A. (2013). Low vagal tone magnifies the association
different emotional faces relates to their history of between psychosocial stress exposure and internalizing
maltreatment and type of psychopathology. Clinical Child psychopathology in adolescents. Journal of Clinical Child and
Psychology and Psychiatry, 14, 237–250. Adolescent Psychology, 44, 314–328.
Lengua, L. J., Long, A. C., Smith, K. I., & Meltzoff, A. N. (2005). Mehta, D., Klengel, T., Conneely, K. N., Smith, A. K., Altmann,
Pre-attack symptomatology and temperament as predictors of A., Pace, T. W., . . . Binder, E. B. (2013). Childhood
children’s responses to the September 11 terrorist attacks. maltreatment is associated with distinct genomic and
Journal of Child Psychology and Psychiatry, 46, 631–645. epigenetic profiles in posttraumatic stress disorder. Proceedings
Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. of the National Academy of Sciences, 110, 8302–8307.
(2009). Effects of stress throughout the lifespan on the brain, Messman-Moore, T. L., & Bhuptani, P. H. (2017). A review of
behaviour and cognition. Nature Reviews Neuroscience, 10, the long-term impact of child maltreatment on posttraumatic
434–445. stress disorder and its comorbidities: An emotion
Maercker, A., Brewin, C. R., Bryant, R. A., Cloitre, M., Reed, dysregulation perspective. Clinical Psychology: Science and
G. M., van Ommeren, M., . . . Saxena, S. (2013). Proposals Practice, 24, 154–169.
for mental disorders specifically associated with stress in the Milan, S., Zona, K., Acker, J., & Turcios-Cotto, V. (2013).
International Classification of Diseases-11. The Lancet, 381, Prospective risk factors for adolescent PTSD: Sources of
1683–1685. differential exposure and differential vulnerability. Journal of
Marsac, M. L., Kassam-Adams, N., Delahanty, D. L., Abnormal Child Psychology, 41, 339–353.
Widaman, K. F., & Barakat, L. P. (2014). Posttraumatic stress Modrowski, C. A., Chaplo, S. D., Mozley, M. M., & Kerig, P. K.
following acute medical trauma in children: A proposed (under review). The associations among trauma exposure,
model of bio-psycho-social processes during the peri- posttraumatic overmodulation and undermodulation, and non-
trauma period. Clinical Child and Family Psychology Review, suicidal self-injury in traumatized justice-involved adolescents.
17, 399–411. Manuscript submitted for publication.
Masten, C., Guyer, A., Hodgdon, H., McClure, E., Charney, D., Myers, H. F., Wyatt, G. E., Ullman, J. B., Loeb, T. B., Chin, D.,
Ernst, M., . . . Monk, C. (2008). Recognition of facial emotions Prause, N., . . . Liu, H. (2015). Cumulative burden of lifetime
among maltreated children with high rates of post-traumatic adversities: Trauma and mental health in low-SES African
stress disorder. Child Abuse and Neglect, 32, 139–153. Americans and Latino/as. Psychological Trauma, 7, 243–251.
Maughan, A., & Cicchetti, D. (2002). Impact of child Nicholson, A. A., Friston, K. J., Zeidman, P., Harricharan, S.,
maltreatment and interadult violence on children’s emotion McKinnon, M. C., Densmore, M., . . . Lanius, R. A. (2017).
regulation abilities and socioemotional adjustment. Child Dynamic causal modeling in PTSD and its dissociative
Development, 73, 1525–1542. subtype: Bottom-up versus top-down processing within fear
McCoy, D. C. (2013). Early violence exposure and self-regulatory and emotion regulation circuitry. Human Brain Mapping,
development: A bioecological systems perspective. Human 38, 5551–5561.
Development, 56, 254–273. Nielsen, M. B., Tangen, T., Idsoe, T., Matthiesen, S. B., &
McCrory, E. J., De Brito, S. A., Kelly, P. A., Bird, G., Sebastian, Magerøy, N. (2015). Post-traumatic stress disorder as a
C. L., Mechelli, A., . . . Viding, E. (2013). Amygdala activation consequence of bullying at work and at school. A literature
in maltreated children during pre-attentive emotional review and meta-analysis. Aggression and Violent Behavior, 21,
processing. British Journal of Psychiatry, 202, 269–276. 17–24.
McCrory, E. J., De Brito, S. A., Sebastian, C. L., Mechelli, A., Nock, M. K., Wedig, M. M., Holmberg, E. B., & Hooley, J. M.
Bird, G., Kelly, P. A., & Viding, E. (2011). Heightened neural (2008). The emotion reactivity scale: Development, evaluation,
reactivity to threat in child victims of family violence. and relation to self-injurious thoughts and behaviors. Behavior
Current Biology, 21, 947–948. Therapy, 39, 107–116.
McEwen, B. S. (2017). Allostasis and the epigenetics of brain and Nugent, N. R., Ostrowski, S., Christopher, N. C., & Delahanty,
body health over the life course: The brain on stress. JAMA D. L. (2007). Parental posttraumatic stress symptoms as a
Psychiatry, 74, 551–552. moderator of child’s acute biological response and subsequent

posttraumatic stress symptoms in pediatric injury patients. Shalev, A. Y. (2007). Stress versus traumatic stress: From acute
Journal of Pediatric Psychology, 32, 309–318. homeostatic reactions to chronic psychopathology. In B. van
Ostrowski, S. A., Ciesla, J. A., Lee, T. J., Irish, L., Christopher, der Kolk (Ed.), Traumatic stress: The effects of overwhelming
N. C., & Delahanty, D. L. (2011). The impact of caregiver experience on mind, body, and society (pp. 77–101). New York,
distress on the longitudinal development of child acute post- NY: Guilford.
traumatic stress disorder symptoms in pediatric injury Shields, A., & Cicchetti, D. (1998). Reactive aggression among
victims. Journal of Pediatric Psychology, 36, 806–815. maltreated children: The contributions of attention and
Pat-Horenczyk, R., Peled, O., Miron, T., Brom, D., Villa, Y., & emotion dysregulation. Journal of Clinical Child Psychology,
Chemtob, C. (2007). Risk-taking behaviors among Israeli 27, 381–395.
adolescents exposed to recurrent terrorism: Provoking danger Shields, A. M., Cicchetti, D., & Ryan, R. M. (1994). The
under continuous threat? American Journal of Psychiatry, 164, development of emotional and behavioral self-regulation and
66–72. social competence among maltreated school-age children.
Pollak, S. D. (2008). Mechanisms linking early experience and Development and Psychopathology, 6, 57–76.
the emergence of emotions: Illustrations from the study of Shipman, K., Zeman, J., Penza, S., & Champion, K. (2000).
maltreated children. Current Directions in Psychological Science, Emotion management skills in sexually maltreated and
17, 370–375. nonmaltreated girls: A developmental psychopathology
Porges, S. W. (2007). The polyvagal perspective. Biological perspective. Development and Psychopathology, 12, 47–62.
Psychology, 74, 116–143. Shipman, K. L., & Zeman, J. (2001). Socialization of children’s
Porter, S. (1996). Without conscience or without active emotion regulation in mother-child dyads: A developmental
conscience? The etiology of psychopathy revisited. Aggression psychopathology perspective. Development and Psychopathology,
and Violent Behavior, 1, 179–180. 13, 317–336.
Puetz, V. B., Parker, D., Kohn, N., Dahmen, B., Verma, R., & Skeem, J., Johansson, P., Andershed, H., Kerr, M., & Louden,
Konrad, K. (2017). Altered brain network integrity after J. E. (2007). Two subtypes of psychopathic violent offenders
childhood maltreatment: A structural connectomic DTI- that parallel primary and secondary variants. Journal of
study. Human Brain Mapping, 38, 855–868. Abnormal Psychology, 116, 395–409.
Pynoos, R. S., Steinberg, A. M., Layne, C. M., Briggs, E. C., Sroufe, L. A. (1996). Emotional development: The organization of
Ostrowski, S. A., & Fairbank, J. A. (2009). DSM-V PTSD emotional life in the early years. New York, NY: Cambridge
diagnostic criteria for children and adolescents: A University Press.
developmental perspective and recommendations. Journal of Stallard, P., Velleman, R., & Baldwin, S. (1998). Prospective study
Traumatic Stress, 22, 391–398. of post-traumatic stress disorder in children involved in road
Rasmussen, A. M., & Shalev, A. Y. (2014). Integrating the traffic accidents. British Medical Journal, 317, 1619–1623.
neuroendocrinology, neurochemistry, and neuroimmunology Stolbach, B. C., Minshew, R., Rompala, V., Dominguez, R. Z.,
of PTSD to date and the changes ahead. In M. J. Friedman, Gazibara, T., & Finke, R. (2013). Complex trauma exposure
T. M. Keane, & P. A. Resick (Eds.), Handbook of PTSD. and symptoms in urban traumatized children: A preliminary
New York, NY: Guilford. test of the proposed criteria for Developmental Trauma
Resick, P. A., & Miller, M. W. (2009). Posttraumatic stress Disorder. Journal of Traumatic Stress, 26, 483–491.
disorder: Anxiety or traumatic stress disorder? Journal of Tatar, J. R., Cauffman, E., Kimonis, E. R., & Skeem, J. L.
Traumatic Stress, 22, 384–390. (2012). Victimization history and posttraumatic stress: An
Rojas-Flores, L., Clements, M. L., Hwang Koo, J., & London, J. analysis of psychopathy variants in male juvenile offenders.
(2017). Trauma and psychological distress in Latino citizen Journal of Child and Adolescent Trauma, 5, 102–113.
children following parental detention and deportation. Taylor, L. K., & Weems, C. F. (2009). What do youth report as
Psychological Trauma: Theory, Research, Practice, and Policy, 9, a traumatic event? Toward a developmentally informed
352–361. classification of traumatic stressors. Psychological Trauma, 1,
Russo, S. J., Murrough, J. W., Han, M.-H., Charney, D. S., & 91–106.
Nestler, E. J. (2012). Neurobiology of resilience. Nature: Terr, L. C. (1991). Childhood traumas: An outline and overview.
Neuroscience, 15, 1475–1484. American Journal of Psychiatry, 148, 10–20.
Rutten, B. P., Vermetten, E., Vinkers, C. H., Ursini, G., Trickett, P. K., Noll, J. G., Susman, E. J., Shenk, C. E., &
Daskalakis, N. P., Pishva, E., .
.
.
Jaffe, A. E. (2018). Putnam, F. W. (2010). Attenuation of cortisol across
Longitudinal analyses of the DNA methylome in deployed development for victims of sexual abuse. Development and
military servicemen identify susceptibility loci for post- Psychopathology, 22, 165–175.
traumatic stress disorder. Molecular Psychiatry, 23, 1145–1156. Trickey, D., Siddaway, A. P., Meiser-Stedman, R., Serpell, L., &
Sachser, C., Keller, F., & Goldbeck, L. (2017). Complex PTSD as Field, A. P. (2012). A meta-analysis of risk factors for post-
proposed for ICD-11: Validation of a new disorder in children traumatic stress disorder in children and adolescents. Clinical
and adolescents and their response to Trauma-Focused Psychology Review, 32, 122–138.
Cognitive Behavioral Therapy. Journal of Child Psychology van der Kolk, B. A. (2005). Developmental trauma disorder:
and Psychiatry, 58, 160–168. Toward a rational diagnosis for children with complex
Schauer, M., & Elbert, T. (2010). Dissociation following traumatic trauma histories. Psychiatric Annals, 35, 401–408.
stress. Zeitschrift für Psychologie/Journal of Psychology, 218, van der Kolk, B. A. (2006). The complexity of adaptation to
109–127. trauma: Self-regulation, stimulus discrimination, and
Seligowski, A. V., Lee, D. J., Bardeen, J. R., & Orcutt, H. K. characterological development. In B. van der Kolk,
(2015). Emotion regulation and posttraumatic stress A. C. McFarlane & L. Weisaeth (Eds.), Traumatic stress: The
symptoms: A meta-analysis. Cognitive Behaviour Therapy, 44, effects of overwhelming experience on mind, body, and society
87–102. (pp. 182–213). New York, NY: Guilford.
Kerig 281
van der Kolk, B. A., McFarlane, A. C., & Weisaeth, L. (2006). Wamser-Nanney, R., & Vandenberg, B. R. (2013). Empirical
Traumatic stress: The effects of overwhelming experience on support for the definition of a complex trauma event in children
mind, body, and society. New York, NY: Guilford. and adolescents. Journal of Traumatic Stress, 26, 671–678.
van der Kolk, B. A., Pynoos, R. S., Cicchetti, D., Cloitre, M., Wang, Q., Shelton, R. C., & Dwivedi, Y. (2017). Interaction
D’Andrea, W., Ford, J. D., . . . Teicher, M. (2009). Proposal to between early-life stress and FKBP5 gene variants in major
include a developmental trauma disorder diagnosis for children depressive disorder and post-traumatic stress disorder:
and adolescents in DSM-V. Los Angeles, CA: National Child A systematic review and meta-analysis. Journal of Affective
Traumatic Stress Network Developmental Trauma Disorder Disorders, 225, 422–428.
Taskforce. Weiss, N. H., Tull, M. T., Lavender, J., & Gratz, K. L. (2013).
Vaughn, M. G., Edens, J. F., Howard, M. O., & Smith, S. T. Role of emotion dysregulation in the relationship between
(2009). An investigation of primary and secondary childhood abuse and probable PTSD in a sample of substance
psychopathy in a statewide sample of incarcerated youth. abusers. Child Abuse and Neglect, 37, 944–954.
Youth Violence and Juvenile Justice, 7, 172–188. Willard, V. W., Long, A., & Phipps, S. (2016). Life stress versus
Verlinden, E., Schippers, M., Van Meijel, E. P., Beer, R., traumatic stress: The impact of life events on psychological
Opmeer, B. C., Olff, M., . . . Lindauer, R. J. (2013). What functioning in children with and without serious illness.
makes a life event traumatic for a child? The predictive Psychological Trauma: Theory, Research, Practice, and Policy, 8,
values of DSM-Criteria A1 and A2. European Journal of 63–71.
Psychotraumatology, 4. Yehuda, R., Halligan, S. L., & Grossman, R. (2001). Childhood
Vinkers, C. H., Kalafateli, A. L., Rutten, B. P., Kas, M. J., Kaminsky, trauma and risk for PTSD: Relationship to intergenerational
Z., Turner, J. D., & Boks, M. P. (2015). Traumatic stress and effects of trauma, parental PTSD, and cortisol excretion.
human DNA methylation. Epigenomics, 7, 593–608. Development and Psychopathology, 13, 733–753.

CH A PTE R
Emotion Dysregulation in
20 Autism Spectrum Disorder
Emily Neuhaus
Abstract
Autism spectrum disorder (ASD) is defined by deficits in social communication and interaction, and
restricted and repetitive behaviors and interests. Although current diagnostic conceptualizations of
ASD do not include emotional difficulties as core deficits, the disorder is associated with emotion
dysregulation across the lifespan, with considerable implications for long-term psychological, social,
and educational outcomes. The overarching goal of this chapter is to integrate existing knowledge of
emotion dysregulation in ASD and identify areas for further investigation. The chapter reviews the
prevalence and expressions of emotion dysregulation in ASD, discusses emerging theoretical models
that frame emotion dysregulation as an inherent (rather than associated) feature of ASD, presents
neurobiological findings and mechanisms related to emotion dysregulation in ASD, and identifies
continuing controversies and resulting research priorities.
Keywords: autism, dysregulation, anxiety, depression, externalizing, comorbidity
Introduction infants with typical development (Garon et al.,

By definition, autism spectrum disorder (ASD) is a 2009; Konstantareas & Stewart, 2006). In addi-
social-communication disorder, with hallmark deficits tion, early childhood among those with ASD is
in social reciprocity, verbal and nonverbal commu- often marked by broad dysregulation, including
nication, and social relationships, which are self-injurious behavior, physical aggression, and
accompanied by restricted and repetitive behaviors emotional reactivity (Lecavalier, 2006). By middle
and interests (American Psychiatric Association, childhood, children with ASD display higher than
2013). Conspicuously absent from current diagnos- normal levels of internalizing and externalizing
tic criteria are explicit references to emotional symptoms (Capps, Kasari, Yirmiya, & Sigman,
experiences and difficulties among children and 1993; Neuhaus, Bernier, & Beauchaine, 2014;
adults with ASD. Although alterations in emotional Simonoff et al., 2008; Samson, Wells, Phillips,
experience and processing can be inferred from Hardan, & Gross, 2015) and heightened emotional
symptoms such as atypical use and understanding lability (Ashburner, Ziviani, & Rodger, 2010). By
of facial expressions, difficulties with empathy and adulthood, nearly 80% of those with ASD meet
perspective taking, and limited emotional reci- diagnostic criteria for a psychiatric disorder, of

procity, these deficits are typically construed as which anxiety and depression are most common
social-cognitive in nature. (Lever & Geurts, 2016). Rates of suicidal ideation
Nevertheless, disruptions to emotional well-being and behavior are correspondingly elevated relative
among individuals with ASD are evident from very to both the general population and complex clinical
early in life. Parents of infants later diagnosed with samples (Cassidy & Rodgers, 2017; Horowitz et al.,
ASD report high levels of negative reactivity, low 2017; Segers & Rawana, 2014), affecting up to two
positive affect, and poorer soothability relative to thirds of adults with ASD (Cassidy et al., 2014).
283
Lack of attention to emotion dysregulation in that interfere with adaptive function (see Beauchaine,
ASD is all the more striking given that behavioral 2015a; Thompson, 1990). Inherent within this view
difficulties such as aggression, irritability, and self- is recognition that expectations for normative
injury are frequent presenting concerns in clinical emotional experiences and displays differ across

settings, and are often the bases from which both development. As expectations of adaptive function
diagnostic referrals for ASD and need for treatment change, both the degree and frequency of dysregula-
arise (Arnold et al., 2003; Lecavalier, 2006). High tion vary greatly over the course of childhood,
levels of behavior and emotion dysregulation some- adolescence, and adulthood among typically de-
times complicate the diagnostic process for children veloping individuals. For instance, developmental
with ASD (Yee & Millichap, 2015), and constitute a expectations for normative “dysregulation” among
leading source of stress for caregivers of children toddlers differ dramatically from those for older
with ASD (Davis & Carter, 2008). As a consequence, children and adults (e.g., Osterman & Björkqvist,
emotion dysregulation is a frequent target of behav- 2010). As a result, terminology and experimental
ioral and pharmacological intervention efforts in both methods related to emotion dysregulation differ
outpatient and inpatient settings, with dramatically across development as well. During infancy and
increased use of psychiatric services relative to indi- childhood, we often interpret behavioral and emo-
viduals without ASD (Croen, Najjar, Ray, Lotspeich, tional reactivity within the context of temperament
& Bernal, 2006). Together, these findings reveal a (e.g., surgency, reactivity, emotional control,
developmental trajectory marked by pervasive yet soothability), and we use these temperamental con-
poorly documented emotion regulation difficulties structs as markers to index (dys)regulation (e.g.,
across the lifespan for many individuals with ASD. Garon et al., 2009; Putnam, Gartstein, & Rothbart,
In this chapter, I call attention to the role of 2006). By school age, measures of broad dimen-
emotion dysregulation in expression of ASD. I begin sions of internalizing and externalizing difficulties
by considering the prevalence and expressions of are informative, with further differentiation into
emotion dysregulation in both core and associated diagnostic categories such as depression or anxiety
features of ASD. Next, I present theoretical models emerging thereafter.
that integrate these findings, review current under- We also recognize that dysregulation can be
standings of emotion dysregulation in ASD across expressed across a range of both time frames and
neurobiological levels of analysis, and highlight levels of analysis, from momentary fluctuations in
current controversies in the literature. I close with a response to particular stimuli (e.g., event-related
discussion of unanswered questions and suggest pri- changes in skin conductance) to relatively
orities for future studies of emotion dysregulation long-standing patterns of behavior that are stable
in ASD. Given the objectives of this volume, my and resistant to change (e.g., personality traits).
focus is explicitly on emotion dysregulation, so I touch Consistent with this variety in expression across
only briefly on emotion regulation. Although disrup- time and levels of analysis, we consider a range of
tions are likely present in both (White et al., 2014), methodological approaches, from molecular genetic
emotion dysregulation is a transdiagnostic trait, and to subjective experience. This inclusive view of
often precedes and necessitates efforts at emotion emotion dysregulation allows for a more compre-
regulation. Emotion dysregulation may therefore be hensive understanding of emotional experience and
more fundamental to our understanding of these expression among individuals with ASD.
concepts in ASD.
Theoretical Perspectives
Terms and Concepts Historically, mental health concerns among indi-
Despite its broad relevance, emotion dysregulation is viduals with developmental disabilities have been
not universally defined, nor is it clearly and consist poorly recognized due to diagnostic overshadowing,
ently differentiated from the emotional variation in which emotional or psychiatric difficulties are
expected in daily life. Here, I conceptualize dysregu- attributed to the identified disability, and conse-
lation as emotional experiences that differ in inten- quently are overlooked as phenomena warranting
sity, valence, duration, or patterns of reactivity when clinical attention (Kerns et al., 2015; Levitan &
compared to same-age peers without ASD. This is Reiss, 1983). These early misconceptions likely im-
by and large consistent with the definition of emo- peded access to necessary mental health evaluations
tion dysregulation used throughout this volume— and care. Fortunately, views have evolved over time,
patterns of emotional experience and/or expression with growing awareness of emotional difficulties
284 Emotion Dysregul ation in Autism Spectrum Disorder

among individuals with ASD. In recent years, 2006), with significant risk for depression and sui-
conceptualizations of emotion dysregulation in
cidal ideation and behavior throughout adulthood
ASD have largely followed two themes. In the first, (Cassidy et al., 2014).
emotion dysregulation is viewed as the result of Externalized expressions of emotion dysregulation
co-occurring psychiatric disorders that are diagnos- emerge concurrently with internalizing symptoms.
tically distinct from ASD. In contrast, in more Longitudinal data reveal high comorbidity rates
recent accounts, emotion dysregulation is viewed as among preschool children with ASD, with a sub-
integral to ASD, with shared cognitive and neurobi- stantial number following a trajectory of high,
ological substrates across emotion dysregulation and stable levels of both internalizing and externalizing
ASD symptoms. These perspectives are discussed in difficulties over the course of early childhood
turn. (Vaillancourt et al., 2017). Externalizing concerns
frequently include tantrums, irritability, and aggres-
Dysregulation as Comorbidity sive behavior (Mazefsky & White, 2014). These
Emotion dysregulation in ASD is often evidenced problems often persist beyond developmental ex-
by heightened rates of numerous comorbid psychi- pectations. However, patterns of symptom change
atric diagnoses. Prevalence estimates for anxiety, for over time vary markedly across individuals. Although
example, vary across studies (see White et al., 2009), adolescence brings a decrease in externalizing
but data suggest that over half of children with ASD behavior for some with ASD, others experience in-
meet diagnostic criteria for an anxiety disorder (de creases during this transition (Gray et al., 2012).
Bruin, Ferdinand, Meester, de Nijs, & Verheij, Even in adulthood, externalizing difficulties remain
2007), and that up to 84% display significant anxi- high for many with ASD, with significant implica-
ety in the absence of a formal anxiety-related diag- tions for their long-term independence and quality
nosis (Muris, Steerneman, Merckelbach, Holdrinet, of life (Ballaban-Gil, Rapin, Tuchman, & Shinnar,
& Meesters, 1998). Most frequently, anxiety symp- 1996).
toms fall within diagnostic categories of simple pho-
bias, generalized anxiety disorder, separation anxi- Dysregulation as Integral to Autism
ety, and social phobia (White et al., 2009). Anxiety Spectrum Disorder
symptoms remain high into and throughout adult- Much of the research discussed thus far frames dys-
hood (Lever & Geurts, 2016), although prevalence regulation of emotion-related processes as distinct
rates of disorders within the larger umbrella of anxi- from ASD, implicitly conceptualizing such dysregu-
ety may shift with age (Lever & Geurts, 2016) and lation as a sort of psychiatric overlay that occurs
may vary according to individual differences in in- against a neurodevelopmental background of autism.
tellectual ability (White et al., 2009). Yet boundaries between ASD and so-called comor-
Mood-related concerns are also elevated among bid symptoms are often, if not usually, ambiguous.
individuals with ASD, occurring frequently in con- Consider social avoidance and diminished social
junction with anxiety disorders (Lever & Geurts, approach, which characterize many individuals with
2016). As early as infancy, children later diagnosed social anxiety. When should this behavioral style in-
with ASD appear to experience less positive affect dicate the presence of clinically meaningful social
(e.g., positive anticipation, observed smiling) and anxiety, and when might it reflect the core social
more negative affect than their peers without ASD deficits of ASD? Similarly, consider ritualized
(Filliter et al., 2015; Garon et al., 2009). A similar behaviors or inflexible cognitions associated with
pattern (heightened fear and sadness, reduced joy) obsessive-compulsive disorders, and compare them
continues into childhood (Capps et al., 1993; with the “insistence on sameness, inflexible adher-
Samson et al., 2015). By school age, children with ence to routines, or ritualized verbal or nonverbal
ASD exhibit greater degrees of anger and shame behavior” (American Psychiatric Association, 2013,
(Capps et al., 1993) and more depressive symptoms p. 50) described in the current diagnostic formulation
than their peers without ASD, according to both of ASD. Given such overlap between core features
parent and self-report, as well as categorical and of ASD and a number of psychiatric disorders, dis-
dimensional assessments (Neuhaus, Bernier, &
tinguishing cleanly between them becomes difficult.
Beauchaine, 2014; Rieffe, De Bruine, De Rooij, & Rather than attempt to parse emotion dysregu-
Stockmann, 2014; Simonoff et al., 2008). Rates lation and ASD as entirely separate entities, an
of mood-related symptoms increase as individuals alternate and rather recent view contends that at
move into adolescence (Brereton, Tonge, & Einfeld, least some so-called comorbid emotion-related
Neuhaus 285
symptoms are better understood as inherent com- of one’s internal emotional states may interact with
ponents of ASD. Several models that assert such atypical thresholds for sensory input, leading to in-
have been articulated, perhaps most comprehensively creased anxiety when internal and external sensory
by Mazefsky and colleagues (e.g., Mazefsky et al., cues are misinterpreted. In support of this model,
2013; Mazefsky & White, 2014), who developed a imaging studies indicate that neural activation in
model of emotion dysregulation as intrinsic to ASD. sensory and limbic regions in response to auditory
In this framework, a number of ASD-related behav- stimuli correlates with parent-reported anxiety
iors may stem from or represent underlying emotion (Green et al., 2013, 2015). Moreover, the relation
dysregulation. For instance, self-injurious behaviors between ASD and anxiety is mediated largely by a
such as head-banging may be nonverbal indicators of latent factor composed of alexithymia, acceptance
emotional lability (Magnuson & Constantino, 2011). of emotional experience, and uncertainty tolerance
Similarly, repetitive motor movements (e.g., body (Maisel et al., 2016).
rocking, hand-flapping) and sensory-seeking behavior Finally, White et al. (2014) propose a model
(e.g., tactile exploration)—both diagnostic criteria grounded in a developmental psychopathology
for ASD—may be manifestations of dysregulation, framework, whereby emotion dysregulation in ASD
efforts to engage in self-soothing, or both (Mazefsky results from a number of different etiological mech-
et al., 2013). anisms, and is then shaped in its expression (e.g.,
Based on these observations, the Mazefsky et al. anxiety vs. aggression) by a range of psychological
(2013) model describes emotion-related symptoms and social-cognitive moderators. In this view, emo-
among individuals with ASD as unique interactions tion dysregulation is conceptualized as a transdiag-
between emotion dysregulation (conceptualized as a nostic trait common to many forms of psychopa-
transdiagnostic feature of psychopathology) and thology, but both its development and its expression
ASD-specific traits, yielding patterns of lability and are shaped by ASD-specific factors such that it is
dysregulation that are phenomenologically distinct intrinsically related to ASD itself. For example,
from individuals without ASD. According to this ASD may be characterized by heightened physiolog-
model, ASD is characterized by altered physiologi- ical arousal (discussed in more detail in the following
cal functioning and reactivity, as well as atypical section), leading to dysregulation that could take
connectivity among neural regions implicated in any number of forms. When coupled with ASD-
emotion regulation, leading to heightened baseline specific deficits in processing of facial and vocal
levels of negative affect. Layered upon this foun- information, perspective taking, and cognitive

dation are ASD-specific cognitive factors such as flexibility, such dysregulation may take the form of
rigidity, perseveration, deficits in social cognition, intense anxiety and avoidance in social settings,
and idiosyncratic triggers for emotional reactions. since peers’ behaviors and comments can appear
Together, these factors produce dysregulation that is unpredictable and sometimes threatening (White
manifested in unique ways, generating many of the et al., 2014). Emotion dysregulation can be further
behaviors frequently observed in ASD (e.g., sensory exacerbated by the ruminative, perseverative cognitive
seeking, repetitive motor movements). This model style often observed in ASD, resulting in frequent
suggests that individuals with ASD exhibit greater and enduring internalizing symptoms (Burrows,
intraindividual variability in their emotional re- Timpano, & Uddin, 2017).
sponses from day to day, yielding a complex and
seemingly unpredictable constellation of emotional Current Methods and Findings
and behavioral symptoms (Mazefsky et al., 2013). All of the models described specify mechanisms of
Other models link behavior and emotion dys- emotion dysregulation across behavioral and neuro-
regulation to core features of ASD, particularly with biological levels of analysis. Consistent with this, a
respect to internalizing symptoms. In one such variety of research methods currently inform our
model, the combination of atypical sensory process- understanding of emotion dysregulation in ASD
ing, alexithymia (inability to identify and describe and reveal a range of possible mechanisms for the
one’s own emotions), and intolerance of uncertainty emotion dysregulation so often observed in the dis-
forms a pathway to emotion dysregulation (South order. Empirical research has only begun to examine
& Rodgers, 2017). Each of these traits is prominent comprehensive models in a coordinated manner,
among diagnostic criteria for ASD, and together may and most studies focus on single biological systems
operate synergistically to produce anxiety symptoms. rather than integrating mechanisms across biologi-
For example, reduced awareness and understanding cal systems. Given this, we organize findings by

broad method in this section, moving upstream from to social and reward-based tasks differ among those
peripheral biomarkers to central nervous system with ASD, who exhibit links between electrodermal
mechanisms, and finally to genetic substrates. reactivity and both internalizing and externalizing
symptoms (Baker et al., 2017; Faja, Murias,
Psychophysiology Beauchaine, & Dawson, 2013; Mathersul, McDonald,
Some of the earliest research on emotional experi- & Rushby, 2013; Kylliainen & Hietanen, 2006;
ences of individuals with ASD assessed markers of Kylliainen et al., 2012; Neuhaus, Bernier, &
autonomic nervous system (ANS) activity and pro- Beauchaine, 2015).
vided compelling evidence for altered function in Additional insight into emotional reactivity is
both the parasympathetic and sympathetic branches. provided through investigations of the reflexive
Parasympathetic activity is often indexed by high- startle response. Although not a direct measure of
frequency heart rate variability (i.e., respiratory sinus neural activity, startle modulation provides a non-
arrhythmia [RSA]), which quantifies respiration- invasive index of amygdala functioning under
related variability in heart rate (see, e.g., Beauchaine, appropriate stimulus conditions, thus reflecting

2001). Higher resting RSA is associated with adaptive amygdala-mediated processes. Although some fea-
behavior in response to environmental challenges, tures of the startle response appear to be intact in
including social interactions (Porges, 2001; Porges, ASD (Bernier, Dawson, Panagiotides, & Webb,
Doussard-Roosevelt, & Maiti, 1994). In typically 2005; McAlonan et al., 2002; Ornitz, Lane,
developing samples, higher resting RSA is associated Sugiyama, & de Traversay, 1993), there may be
with better socio-emotional functioning, whereas subtle alterations in affective modulation of the
lower levels are associated with emotion dysregulation startle response. In contrast to the typical pattern
across multiple forms of psychopathology, including of startle potentiation following negative stimuli
depression, anxiety, panic, and nonsuicidal self- and attenuation following positive stimuli, both
injury (see Beauchaine, 2001, 2015b; Eisenberg positive and negative stimuli increase startle among
et al., 1995; Fabes et al., 1993; Heilman et al., 2007; individuals with autism (Salmond, de Haan, Friston,
Henderson et al., 2004; Patriquin et al., 2014). Gadian, & Vargha-Khadem, 2003; Wilbarger,
Individuals with ASD display reduced resting RSA McIntosh, & Winkielman, 2009). This might suggest
relative to peers and altered RSA reactivity during heightened sensitivity to threat, particularly in
social-emotional tasks and interactions (Bal et al., light of positive correlations between startle response
2010; Neuhaus, Bernier, & Beauchaine, 2016; and measures of anxiety, difficulties with uncer-
Van Hecke et al., 2009). Furthermore, altered tainty, and repetitive behavior (Chamberlain et al.,
parasympathetic function correlates with both in- 2013).
ternalizing and externalizing symptoms in children Autism is also characterized by altered function
with ASD (Guy, Souders, Bradstreet, DeLussey, & within the limbic hypothalamic-pituitary-adrenal
Herrington, 2014; Neuhaus et al., 2014). (L-HPA) axis, a major component of the body’s
In contrast to the parasympathetic branch of the stress response system, reactivity of which can be
ANS, which subserves restorative functions, the indexed by salivary cortisol (see Tarullo & Gunnar,
sympathetic branch facilitates approach behaviors 2006). Among typically developing samples, corti-
and active responses to threat by increasing heart sol levels follow a diurnal pattern, peaking in the
rate, mobilizing physiological resources for activity, early morning and decreasing gradually over the
including “fight or flight” responding. Studies of course of the day (Glaser, 2000). In addition, corti-
sympathetic markers among individuals with ASD sol is released in response to both acute and chronic
are not fully consistent, but many suggest a state of stressors, with long-term effects on physical and
hyperarousal in ASD. Relative to their peers, boys mental health including depression, anxiety, and
with ASD display elevated heart rate and a tendency externalizing symptoms (Adam et al., 2017; Mead,
toward increased sympathetic cardiac influence Beauchaine, & Shannon, 2010). Thus, both daily
during naturalistic social interactions (Neuhaus, fluctuations and acute responses to stimuli provide
Bernier, & Beauchaine, 2016). Electrodermal activ- insight into function of the HPA axis.
ity, a sympathetic marker often construed as reflect- A number of studies suggest atypical functioning
ing anxious arousal, appears to be comparable across of the HPA axis in ASD, with correlations between
samples with and without ASD at rest (van Engeland, cortisol and emotion dysregulation. Although chil-
1984; Zahn, Rumsey, & Van Kammen, 1987), but dren with ASD generally display higher cortisol in
patterns of electrodermal reactivity and habituation the morning, consistent with non-ASD samples,
Neuhaus 287
they demonstrate greater variability in daily rhythms familial risk for ASD differ from low-risk infants
(Corbett, Mendoza, Abdullah, Wegelin, & Levine, in their patterns of EEG asymmetry at 6 months
2006). Stressors such as blood draws and magnetic of age, with markedly different trajectories of
resonance imaging exams elicit greater increases in asymmetry over the course of the following
cortisol among those with ASD relative to peers 12 months (Gabard-Durnam, Tierney, Vogel-Farley,
without ASD, with higher cortisol peaks that last Tager-Flusberg, & Nelson, 2015). This body of
longer and return to baseline more slowly (Corbett findings suggests that ASD may be characterized
et al., 2006; Spratt et al., 2012). Among those with by altered patterns of left versus right cortical ac-
ASD, atypical cortisol rhythms are associated with tivity, with possible implications for social and
depression, anxiety, irritability, and repetitive be- emotional functioning. Encouragingly, early evidence
haviors (Bitsika, Sharpley, Sweeney, & McFarlane, suggests that patterns of EEG asymmetry among
2014; Hollocks, Howlin, Papadopoulos, Khondoker, children with ASD may be malleable (at least in
& Simonoff, 2014; Lydon et al., 2015; Mikita et al., some regions), and may more closely approximate
2015; Sharpley, Bitsika, Andronicos, & Agnew, that of typically developing children following ap-
2016). Thus, HPA dysfunction is a clear and con propriate intervention (Van Hecke et al., 2015).
sistent correlate of emotion dysregulation in ASD.
Neuroimaging
Electrophysiology A rich literature documents alterations in amygdala
A long history of research in electroencephalography structure and function among those with ASD.
(EEG) links resting-state neural activity with Although tied initially to social (dys)function in
various forms of psychopathology and individual ASD (see Neuhaus, Beauchaine, & Bernier, 2010
differences in emotion dysregulation. Frontal EEG for a review), the amygdala’s role in emotion-related
asymmetry, often computed as ratios of alpha power processes such as evaluating emotional and motiva-
across hemispheres of the brain, tends to be stable tional significance of stimuli, detecting threats, and
over time and is linked to affective style, approach/ identifying emotions is indisputable (Adolphs, 2003;
withdrawal behavior, and motivational tendencies Grelotti et al., 2002). Accordingly, its contributions
(Davidson, 1998; Coan & Allen, 2003). Relatively to emotion dysregulation in ASD are increasingly
greater activity over left frontal regions is associated evident.
with a greater tendency toward approach (and as- From very early in life, the amygdala follows an
sociated positive emotions; Sutton et al., 2005) and atypical developmental trajectory among children
greater trait positive affect (Tomarken, Davidson, & with ASD. Early on, these children display increased
Henriques, 1990), whereas relatively less left frontal amygdala volumes relative to peers without ASD
activity is associated with withdrawal and depressed (Munson et al., 2006; Sparks et al., 2002), which
mood. Associations with anxiety are more nuanced, correspond to symptoms of anxiety and depression
and it appears that greater left asymmetry is associ- (Juranek et al., 2006). During adolescence, amyg-
ated with anxiety in the form of apprehension and dala volumes are similar across individuals with and
worry, whereas right asymmetry correlates with without ASD, but anxiety symptoms correlate with
anxiety in the form of panic-related symptoms and decreased right amygdala volumes (Herrington
heightened physiological arousal (Heller, Nitschke, et al., 2017). By adulthood, overall amygdala volumes
Etienne, & Miller, 1997; Nusslock et al., 2015). are reduced more broadly in ASD (Pierce et al.,
Based on these relations, variations in frontal EEG 2001). Together, these findings indicate a pattern of
asymmetry index individuals’ propensity to anxiety early overgrowth and subsequent deceleration relative
and dysregulated mood (Davidson, 1998; Nusslock to typical development, with effects on internalizing
et al., 2015). behaviors across development (Schumann & Amaral,
Disruptions to typical patterns of EEG asym- 2006).
metry are observed in autism. Among school-age Amygdala function differs in ASD as well.
children with ASD, left frontal asymmetry is asso- Activation in the amygdala is diminished relative to
ciated with better social functioning but also with peers without ASD across a variety of tasks, includ-
greater anxiety and social stress (Sutton et al., 2005). ing emotion discrimination (Critchley et al., 2000)
Left frontal asymmetry is also associated with and viewing of fearful faces (Ashwin, Baron-Cohen,
higher levels of self-reported anger and obsessive- Wheelwright, O’Riordan, & Bullmore, 2007).
compulsive thoughts and behaviors (Burnette Habituation of amygdala activation to neutral and
et al., 2011). Longitudinally, infants at elevated emotional faces is also slower (Kleinhans et al.,

2009; Swartz, Wiggins, Carrasco, Lord, & Monk, between regions of the DMN in ASD (Cherkassky
2013). However, anxiety may moderate amygdala et al., 2006; Jann et al., 2015), and longitudinal
function, as individuals with ASD who also exhibit findings reveal that functional connectivity within
anxiety show increased activation during social- the DMN predicts the level and change in ASD
cognitive tasks (Herrington, Miller, Pandey, & symptoms over time (Plitt, Barnes, Wallace,
Schultz, 2016; Kleinhans et al., 2010). Kenworthy, & Martin, 2015). Few studies have ex-
More broadly, amygdala interactions with other amined explicit links between emotion dysregulation
regions and structures in the brain have implica- and DMN function in ASD. However, patterns of
tions for emotion dysregulation in ASD. Structural DMN attenuation during tasks of social perception
connections between the amygdala and other sub- are related to both anxiety and externalizing behav-
cortical structures such as the striatum correlate ior in children and adolescents with ASD (Yang et al.,
with parent-reported need for sameness among 2017).
adolescents and young adults with ASD (Eisenberg,
Wallace, Kenworthy, Gotts, & Martin, 2015). Genetics
Altered functional connectivity between the amyg- Several candidate genes contribute to emotion dys-
dala and thalamus, which is critical in filtering and regulation in both typically developing and ASD
relaying of incoming sensory information (Sherman, samples. Among these are genes that affect seroto
2005), may offer one pathway through which ASD’s nin (5-HT) function, a neurotransmitter that sub-
atypical sensory experiences and associated dysregu- serves mood, arousal, social affiliation, and early
lation arise (Green, Hernandez, Bookheimer, & neural developmental functions, across both limbic
Dapretto, 2017; Shen et al., 2016). Decreased func- and cortical regions (Anderson, 2002; Lam et al.,
tional connectivity between the amygdala and the 2006; Whitaker-Azmitia, 2001). Early research sug-
prefrontal cortex (PFC) may be particularly influen- gested that a functional polymorphism in 5-HTT,
tial, given the PFC’s role in modulating subcortical the serotonin transporter gene, might affect risk of
brain regions and regulating emotional responses to ASD (Huang & Santangelo, 2008). More recent
subcortical input (Beauchaine, 2015a; South & findings suggest that serotonin transporter vulnera-
Rodgers, 2017; White et al., 2014). Consistent with bility is not specific to ASD, although allelic variation
this notion, connectivity between the amygdala and in the promotor region (5-HTTLPR) might influ-
prefrontal cortex is reduced relative to controls and ence symptom profile and expression (Yang, Menga,
also predicts amygdala habituation to emotional Li, & Huang, 2017). Low-expressing 5-HTTLPR
faces (Swartz et al., 2013). Finally, within the amyg- genotypes are associated with increased amygdala
dala itself, connectivity may vary across subregions; responding to emotional faces among individuals
whereas social difficulties in ASD correspond to de- with ASD, in contrast to decreased responses dem-
creased connectivity between the basolateral nuclei onstrated by both peers with ASD who have higher
of the amygdala and associated structures, symp- expressing genotypes and by those without ASD
toms of depression are associated with increased (Wiggins, Swartz, Martin, Lord, & Monk, 2014).
connectivity (Kleinhans et al., 2016). The same allelic variant among children with ASD
Also relevant to discussions of connectivity is also corresponds to stronger connectivity between the
functioning of the default-mode network (DMN; amygdala and subgenual anterior cingulate cortex
Raichle et al., 2001), a set of regions that collectively (Velasquez et al., 2017), a region implicated in in-
activate while the brain is at rest, yet deactivate at hibiting amygdala responses (McDonald, 1998).
the onset of a goal-directed behavior (Broyd et al., Finally, high-expressing 5-HTTLPR genotypes are
2009). Composed in part of the medial prefrontal associated with heightened tactile sensitivity in
cortex, precuneus/posterior cingulate cortex, and ASD (Schauder, Muller, Veenstra-VanderWeele, &
medial, lateral, and inferior parietal cortex, DMN Cascio, 2015).
activation is associated with self-referential and in- Gene variants that affect dopamine (DA) neuro-
trospective processes, including emotional reflection transmission are less characterized in ASD, but DA’s
(Broyd et al., 2009). Given this, alterations in DMN roles in impulsive behavior and depression are
function may underlie at least some of the difficul- well established. Both externalizing disorders and
ties with emotional awareness and expression that depression are associated with altered midbrain DA
are central to ASD (Kennedy & Courchesne, 2008). function, as well as allelic variants that confer
Indeed, research thus far documents atypical DMN individual differences in activity and reactivity of
attenuation and decreased functional connectivity the dorsal and ventral striatum (see Beauchaine &
Neuhaus 289
Constantino, 2017; Beauchaine, Neuhaus, Zalewski, traits such as harm avoidance and reward dependence
Crowell, & Potapova, 2011; Zisner & Beauchaine, (Picardi et al., 2015). In addition, principal compo-
2016). Of particular interest with regard to emotion nents analysis reveals that core features of ASD and
in ASD are DA transporter (e.g., DAT1) and recep- emotional/behavioral concerns load onto two inde-
tor (e.g., DRD2, DRD4) genes. As in the general pendent factors—one composed of emotional and
population, various polymorphisms in DAT1 appear repetitive features and one composed of social-
to modulate symptoms of anxiety, depression, and communication difficulties (Georgiades et al.,
hyperactivity among those with ASD (Gadow, 2011). These findings all raise questions regarding
Pinsonneault, Perlman, & Sadee, 2014; Gadow, the degree to which emotional difficulties should be
Roohi, DeVincent, & Hatchwell, 2008). Also as in differentiated from ASD. Nevertheless, consensus
the general population, DA receptor variants are on whether emotion dysregulation constitutes a
associated with parent reports of externalizing
core symptom of ASD awaits additional research on
symptoms such as oppositionality, and internalizing genetic underpinnings, neural mechanisms, covari-
symptoms related to separation anxiety (Gadow, ation with intervention, and developmental time
DeVincent, Olvet, Pisarevskaya, & Hatchwell, course of ASD and associated behavior and emotion
2010; Gadow et al., 2014). Finally, variants in two dysregulation.
genes involved in degrading serotonin and dopamine Even more foundational to understanding
(the monoamine oxidase [MAO-A] and catechol-O- emotion dysregulation is the issue of how best to
methyltransferase [COMT] genes) may confer vul- assess it among individuals with ASD. In this chapter,
nerability to generalized anxiety (Roohi, DeVincent, I review findings from a variety of methods, encom-
Hatchwell, & Gadow, 2009) and social anxiety passing observational, parent-report, self-report,
(Gadow, Roohi, DeVincent, Kirsch, & Hatchwell, neurobiological, and genetic approaches. Yet limita-
2009), respectively, among children with ASD. tions exist with each of these methods, and these
limitations are likely exacerbated by intrinsic features
Unresolved Controversies of ASD. For example, self-reports of emotional
As outlined previously, a primary issue in under- experiences can be limited due to diminished

standing ASD and other psychiatric syndromes emotional insight and self-awareness, unique inter-
concerns disentangling whether emotion dysregula- pretations of physiological cues related to arousal
tion is part and parcel of the disorder or is a largely and emotion, use of idiosyncratic language to un-
independent trait that interacts with core features of derstand and express internal emotional experiences,
disorders to increase functional impairment. The and difficulties with abstract and/or figurative lan-
latter perspective is consistent with recent models of guage (Ben Shalom et al., 2006; Mazefsky et al.
psychopathology that view emotion dysregulation 2013). Parent and teacher ratings of behaviors and
as a superordinate vulnerability that potentiates emotions can be similarly problematic, and discrep-
expression of most any individual difference (e.g., ancies observed between self- and other-report
negative affectivity, social anxiety, impulsivity; see measures are not easily resolved (e.g., Mazefsky et al.,
Beauchaine & Constantino, 2017; Beauchaine & 2013; White, Schry, & Maddox, 2012). Observational
Zisner, 2017). Clinical features such as intense reac- and neurobiological methods circumvent some of
tions to changes in routines or agenda, ritualized or these concerns but require that participants com-
seemingly compulsive behaviors, diminished eye prehend and comply with task instructions, as well
contact, and social avoidance, among others, can as tolerate stressful protocols (e.g., magnetic reso-
stem from core ASD deficits and/or anxiety and nance imaging scans, blood draws) despite commu-
mood disorders. Thus, diagnostic boundaries are nication and sensory challenges.
not clear. Although current estimates indicate that Further complicating this issue is the question of
the majority of individuals with ASD receive a co- whether emotion-related constructs as they are cur-
morbid psychiatric diagnosis, recent research suggests rently conceptualized have equal validity, structure,
that when psychiatric assessment tools are adapted and neurobiological correlates for individuals with
to account for ASD features, rates of “comorbid” and without ASD. For example, factor analysis of a
diagnoses drop dramatically, from nearly 80% to popular questionnaire to assess anxiety disorders,
approximately 50% (Mazefsky et al., 2012). Twin the Multidimensional Anxiety Scale for Children
studies suggest shared genetic and environmental (MASC; March, Parker, Sullivan, Stallings, &
etiologies between ASD and emotional difficulties Conners, 1997), indicates different factor structure
(Tick et al., 2016), and between ASD and personality for children with ASD relative to their nonaffected

peers, and different correlations between anxiety fort, and abrupt transitions or changes to routines;
and cortisol patterns depending on the reporter and (2) shape the experience and expression of that dys-
children’s age (Bitsika, Sharpley, Andronicos, & regulation, resulting in significant anxiety, mood
Agnew, 2015; Bitsika et al., 2016). Whether these concerns, and disruptive and repetitive behaviors;
findings reflect differential experiences of anxiety and (3) limit the availability and effectiveness of
among children with and without ASD, method- strategies typically used to regulate emotions, due to
ological factors, or measurement error is uncertain. limited emotional insight, fewer expressive verbal
Development of ASD-informed assessments (e.g., and nonverbal communication strategies, and
Bearss et al., 2015; Mazefsky et al., 2012, 2016) that poorer social skills with which to recruit emotional
differentiate between symptoms of ASD and potential support from others (Mazefsky, Borue, Day, &
comorbid disorders and that account for features Minshew, 2014; Mazefsky & White, 2014; South &
of ASD in the expression and quality of emotion- Rodgers, 2017; White et al., 2014). Thus, although
related processes represents a valuable step toward underlying emotion dysregulation is a transdiagnos-
resolving these questions. tic vulnerability shared by many, if not all, psychiat-
A key quality of ASD is heterogeneity in profiles ric diagnoses (e.g., Beauchaine & Zisner, 2017),
of strengths and weaknesses among affected indi- behavioral and neurobiological facets unique to
viduals. Although recognition of this heterogeneity ASD influence most aspects of that dysregulation.
is increasing with regard to core symptoms, our Autism spectrum disorder is a disorder of social
understanding of factors moderating emotional
communication. Perhaps because of that, across
experience and dysregulation in ASD lags. Some re- many of the neurobiological mechanisms discussed
search suggests that intellectual ability may influence here in the context of emotion (dys)regulation, we
vulnerability to comorbid diagnoses such as depres- see tremendous overlap with mechanisms responsi-
sion and anxiety, such that increased cognitive ble for social and communication processes. For
ability promotes awareness of one’s social difficul- example, neural regions such as the amygdala and
ties, thereby increasing vulnerability to internalizing prefrontal cortex, and neurotransmitters such as ser
symptoms (Sterling, Dawson, Estes, & Greenson otonin and dopamine, form the bases of social cog-
2008). As in other populations, sex and gender may nition and behavior (see Neuhaus, Beauchaine, &
moderate the presence and expression of dysregula- Bernier, 2010 for review). Comprehensive models
tion. For example, consistent with the general pop- detailing links between social and emotional pro-
ulation, girls with ASD are more likely than boys to cesses specific to autism are incomplete, but studies
experience anxiety and depression, whereas boys are among typically developing samples indicate recip-
more likely to exhibit aggressive and repetitive be- rocal relations between these domains. Porges’s
haviors (Werling & Geschwind, 2013). Similarly, polyvagal theory (Porges, 2001) offers one frame-
sex may moderate combined trajectories of internal- work for understanding that relationship, describ-
izing and externalizing disorders over the course of ing social and emotional functioning as emerging
early childhood differentially among children with from a complex interplay of neurobiological func-
and without ASD (Vaillancourt et al., 2017). Finally, tions and processes (see also Beauchaine, 2001).
accumulating evidence indicates complex, multifac- Indeed, research across biomarkers suggests shared
torial etiologies for ASD (e.g., Stessman et al., 2017; mechanisms for social and emotional outcomes. For
Weiner et al., 2017). As a result, no single gene vari- example, autonomic research with children with
ant or mutation is necessary or sufficient for devel- ASD reveals independent contributions of social
opment of the disorder. Thus, individual differences and emotional difficulties to RSA (Neuhaus et al.,
in genetic burden may moderate vulnerability to 2014). Similarly, EEG research highlights links be-
and expression of emotion dysregulation over time. tween an event-related potential long associated
with social perception and cognition (response to
Theoretical Synthesis faces during early childhood) and levels of anxiety
Taken together, models and data reviewed thus far several years later (Neuhaus et al., 2016).
suggest that ASD-specific features such as social dif-
ficulties, sensory aversions, and diminished cogni- Future Directions
tive and behavioral flexibility (1) contribute to Findings discussed herein also highlight several av-
unique and idiosyncratic triggers for behavior and enues through which we might better understand
emotion dysregulation, including aversive sensory the phenomenology and mechanisms of emotion
experiences, social misunderstandings and discom- dysregulation in ASD. Perhaps most apparent is the
Neuhaus 291
need for better assessment of the construct, including and psychological outcomes (Gotham et al., 2015).
methods and instruments that have been developed Indeed, the transition from adolescence to adulthood,
or adapted specifically to improve validity and relia- and the corresponding transition out of pediatric
bility among individuals with ASD (e.g., Mazefsky health care and public education settings, is a critical
et al., 2016). Through these more specialized and turning point for individuals with ASD and their
comprehensive evaluations, we can better parse families (Taylor & Seltzer, 2010). Lack of attention
boundaries between ASD and comorbid condi- to adulthood and later life for individuals with ASD
tions. Because emotion-related processes can occur is particularly disappointing with regard to emotion-
across various timeframes, assessments must span related processes, as their influences are wide-ranging.
timeframes from momentary events (e.g., sudden Whereas internalizing symptoms can decrease over
responses to discrete stimuli) to longer experiences the course of late adolescence, they tend to plateau
lasting weeks or months (e.g., gradual onset of for some adults with ASD, moderated by factors
mood or anxiety symptoms). Given limitations in- such as cognitive ability and family income (Taylor
herent in measurement, multimodal assessments, in & Seltzer, 2010). Among adults with ASD, contin-
which complementary information is gathered from ued psychiatric symptoms in adulthood are associ-
multiple reporters and methods, will likely offer the ated with poorer physical health, increased familial
richest and most comprehensive information. Central stress, and decreased relationship quality for indi-
to this approach will be inclusion of subjective, viduals and their parents (Hartley, Barker, Baker,
self-report information gathered directly from indi- Seltzer, & Greenberg, 2012; Kring, Greenberg, &
viduals with ASD. Despite potential difficulties with Seltzer, 2008). Thus, understanding risk and protec-
emotional insight, first-hand reports offer access to tive factors, mediators, and consequences of emo-
internal psychological and physical processes that tion dysregulation across the lifespan offers promise
are not otherwise accessible, and recognize the unique for improved quality of life across most, if not all,
experiences of each individual. domains of functioning.
On a foundation of solid assessment, a second Ultimately, my goal in writing this chapter was
priority will be to explore vulnerabilities to and risk to highlight the importance of integrating knowl-
factors for development of emotion dysregulation edge regarding emotion dysregulation into concep-
among individuals with ASD. Decades of research tualizations of ASD, by reviewing emerging theo-
within the context of typical development identify retical models of dysregulation and its relation to
familial, environmental, and psychosocial risk factors core features of ASD, considering research findings
through which individuals’ emotional difficulties spanning multiple levels of analysis, highlighting a
are shaped, including coercive escalation within number of unanswered questions, and suggesting
families (Patterson, 1982), trauma and maltreat- areas for continued investigation. Put most simply,
ment (Mead, Beauchaine, & Shannon, 2010), prob- emotion-related symptoms and challenges represent
lematic peer interactions (Snyder et al., 2005), pa- substantial determinants of current functioning and
rental psychopathology (Kaufman et al., 2017), and long-term outcomes for individuals with autism,
many more. Although one might predict that despite falling outside of historically recognized di-
patterns of risk and resilience would hold constant agnostic boundaries for ASD, influencing social,
among individuals with ASD, this cannot be assumed psychological, and educational outcomes. By ex-
without empirical evidence. It may be that the unique ploring these avenues in a comprehensive and
social, cognitive, and behavioral features of ASD integrated fashion, those who study ASD have the
alter relationships between putative risk factors and potential not only to gain a greater scientific under-
emotion-related outcomes, either amplifying or standing of the disorder but also to have positive,
blunting their effects relative to peers without ASD. meaningful, and enduring effects on the lives of
Finally, further understanding of how emotion affected individuals and their families across the
dysregulation influences long-term ASD trajectories lifespan.
across the lifespan will be essential. Originally iden-
tified among young children (Kanner, 1943) and References
often construed as a childhood disorder, ASD is a Adam, E. K., Quinn, M. E., Tavernier, R., McQuillan, M. T.,
Dahlke, K. A., & Gilbert, K. E. (2017). Diurnal cortisol
lifelong neurodevelopmental condition, with broad
slopes and mental and physical health outcomes: A systematic
effects across all stages of life. Adults with ASD are review and meta-analysis. Psychoneuroendocrinology, 83, 2541.
traditionally underrepresented in nearly all areas of Adolphs, R. (2003). Cognitive neuroscience of human social
research, to the detriment of social, occupational, behavior. Nature Reviews Neuroscience, 4, 165–178.

American Psychiatric Association. (2013). Diagnostic and statistical Normal physiological emotions but differences in expression
manual of mental disorders (5th ed.). Arlington, VA: Author. of conscious feelings in children with high-functioning
Anderson, G. M. (2002). Genetics of childhood disorders: XLV. autism. Journal of Autism and Developmental Disorders, 36,
Autism, part 4: Serotonin in autism. Journal of the American 395–400.
Academy of Child and Adolescent Psychiatry, 41, 1513–1516. Bernier, R., Dawson, G., Panagiotides, H., & Webb, S. (2005).
Arnold, L. E., Vitiello, B., McDougle, C., Scahill, L., Shah, B., Individuals with autism spectrum disorder show normal
Gonzalez, N. M., . .
.
Tierney, E. (2003). Parent-defined responses to a fear potential startle paradigm. Journal of
target symptoms respond to risperidone in RUPP autism Autism and Developmental Disorders, 35, 575–583.
study: Customer approach to clinical trials. Journal of the Bitsika, V., Sharpley, C. F., Andronicos, N. M., & Agnew, L. L.
American Academy of Child and Adolescent Psychiatry, 42, (2015). Hypothalamic-pituitary-adrenal axis daily
1443–1450. fluctuation, anxiety, and age interact to predict cortisol
Ashburner, J., Ziviani, J., & Rodger, S. (2010). Surviving in the concentrations in boys with an autism spectrum disorder.
mainstream: Capacity of children with autism spectrum Physiology and Behavior, 138, 200–207.
disorders to perform academically and regulate their Bitsika, V., Sharpley, C. F., Andronicos, N. M., & Agnew, L. L.
emotions and behavior at school. Research in Autism Spectrum (2016). Prevalence, structure and correlates of anxiety-
Disorders, 4, 18–27. depression in boys with an autism spectrum disorder.
Ashwin, C., Baron-Cohen, S., Wheelwright, S., O’Riordan, M., Research in Developmental Disabilities, 49–50, 302–311.
& Bullmore, E. T. (2007). Differential activation of the Bitsika, V., Sharpley, C. F., Sweeney, J. A., & McFarlane, J. R.
amygdala and the ‘social brain’ during fearful face-processing (2014). HPA and SAM axis responses as correlates of self- vs
in Asperger syndrome. Neuropsychologia, 45, 2–14. parental ratings of anxiety in boys with an autistic disorder.
Baker, J. K., Fenning, R. M., Erath, S. A., Baucom, B. R., Physiology and Behavior, 127, 1–7.
Moffitt, J., & Howland, M. A. (2017). Sympathetic under- Brereton, A. V., Tonge, B. J., & Einfeld, S. L. (2006).
arousal and externalizing behavior problems in children with Psychopathology in children and adolescents with autism
autism spectrum disorder. Journal of Abnormal Psychology. compared to young people with intellectual disability.
Advance online publication. Journal of Autism and Developmental Disorders, 36, 863–870.
Bal, E., Harden, E., Lamb, D., Van Hecke, A. V., Denver, J. W., Broyd, S. J., Demanuele, C., Debener, S., Helps, S. K., James,
& Porges, S. W. (2010). Emotion recognition in children C. J., & Sonuga-Barke, E. J. S. (2009). Default-mode brain
with autism spectrum disorders: Relations to eye gaze and dysfunction in mental disorders: A systematic review.
autonomic state. Journal of Autism and Developmental Neuroscience and Biobehavioral Reviews, 33, 279–296.
Disorders, 40, 358–370. Burnette, C. P., Henderson, H. A., Inge, A. P., Zahka, N. E.,
Ballaban-Gil, K., Rapin, I., Tuchman, R., & Shinnar, S. (1996). Schwartz, C. B., & Mundy, P. C. (2011). Anterior EEG
Longitudinal examination of the behavioral, language, and symmetry and the modifier model of autism. Journal of
social changes in a population of adolescents and young adults Autism and Developmental Disorders, 41, 1113–1124.
with autistic disorder. Pediatric Neurology, 15, 217–223. Burrows, C. A., Timpano, K. R., & Uddin, L. Q. (2017).
Bearss, K., Taylor, C. A., Aman, M. G., Whittemore, R., Putative brain networks underlying repetitive negative
Lecavalier, L., Miller, J., . . . Scahill, L. (2015). Using qualitative thinking and comorbid internalizing problems in autism.
methods to guide scale development for anxiety in youth Clinical Psychological Science, 5, 522–536.
with autism spectrum disorder. Autism, 20, 663–672. Capps, L., Kasari, C., Yirmiya, N., & Sigman, M. (1993).
Beauchaine, T. (2001). Vagal tone, development, and Gray's Parental perception of emotional expressiveness in children
motivational theory: Toward an integrated model of with autism. Journal of Consulting and Clinical Psychology, 61,
autonomic nervous system functioning in psychopathology. 475–484.
Development and Psychopathology, 13, 183–214. Cassidy, S., Bradley, P., Robinson, J., Allison, C., McHugh, M.,
Beauchaine, T. P. (2015a). Future directions in emotion & Baron-Cohen, S. (2014). Suicidal ideation and suicide
dysregulation and youth psychopathology. Journal of Clinical plans or attempts in adults with Asperger’s syndrome
Child and Adolescent Psychology, 44, 875–896. attending a specialist diagnostic clinic: A clinical cohort
Beauchaine, T. P. (2015b). Respiratory sinus arrhythmia: A study. Lancet Psychiatry, 1, 142–147.
transdiagnostic biomarker of emotion dysregulation and Cassidy, S., & Rodgers, J. (2017). Understanding and prevention
psychopathology. Current Opinion in Psychology, 3, 43–47. of suicide in autism. Lancet Psychiatry, 4, e11.
Beauchaine, T. P., & Constantino, J. N. (2017). Redefining the Chamberlain, P. D., Rodgers, J., Crowley, M. J., White, S. E.,
endophenotype concept to accommodate transdiagnostic Freeston, M. H., & South, M. (2013). A potentiated startle
vulnerabilities and etiological complexity. Biomarkers in study of uncertainty and contextual anxiety in adolescents
Medicine. Advance online publication. diagnosed with autism spectrum disorder. Molecular Autism,
Beauchaine, T. P., Neuhaus, E., Zalewski, M., Crowell, S. E., 4, 31.
& Potapova, N. (2011). Effects of allostatic load on neural Cherkassky, V. L., Kana, R. K., Keller, T. A., & Just, M. A.
systems subserving motivation, mood regulation, and (2006). Functional connectivity in a baseline resting-state
social affiliation. Development and Psychopathology, 23, network in autism. NeuroReport, 17, 1687–1690.
975–999. Coan, J. A., & Allen, J. J. B. (2003). Frontal EEG asymmetry
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion and the behavioral activation and inhibition systems.
regulation, and the latent structure of psychopathology: Psychophysiology, 40, 106–114.
An integrative and convergent historical perspective. Corbett, B. A., Mendoza, S., Abdullah, M., Wegelin, J. A., &
International Journal of Psychophysiology, 119, 108–118. Levine, S. (2006). Cortisol circadian rhythms and response
Ben Shalom, D., Mostofsky, S. H., Hazlett, R. L., Goldberg, to stress in children with autism. Psychoneuroendocrinology,
M. C., Landa, R. J., Faran, Y., . . . Hoehn-Saric, R. (2006). 31, 59–68.
Neuhaus 293
Critchley, H. D., Daly, E. M., Bullmore, E. T., Williams, ADHD and tics in children with autism spectrum disorder.
S. C. R., Van Amelsvoort, T., Robertson, D. M., . . . Murphy, Journal of Autism and Developmental Disorders, 39,
D. G. (2000). The functional neuroanatomy of social 1542–1551.
behaviour: Changes in cerebral blood flow when people Garon, N., Bryson, S. E., Zwaigenbaum, L., Smith, I. M., Brian,
with autistic disorder process facial expressions. Brain, 123, J., Roberts, W., & Szatmari, P. (2009). Temperament and its
2203–2212. relationship to autistic symptoms in a high-risk infant sib
Croen, L. A., Najjar, D. V., Ray, G. T., Lotspeich, L., & Bernal, cohort. Journal of Abnormal Child Psychology, 37, 59–78.
P. (2006). A comparison of health care utilization and costs Georgiades, S., Szatmari, P., Duku, E., Zwaigenbaum, L.,
of children with and without autism spectrum disorders in a Bryson, S., Roberts, W., . . . Thompson, A. (2011). Phenotypic
large group-model health plan. Pediatrics, 118, e1203–e1211. overlap between core diagnostic features and emotional/
Davidson, R. J. (1998). Anterior electrophysiological asymmetries, behavioral problems in preschool children with autism
emotion, and depression: Conceptual and methodological spectrum disorder. Journal of Autism and Developmental
conundrums. Psychophysiology, 35, 607–614. Disorders, 41, 1321–1329.
Davis, N. O., & Carter, A. S. (2008). Parenting stress in mothers Glaser, D. (2000). Child abuse and neglect and the brain—A
and fathers of toddlers with autism spectrum disorders: review. Journal of Child Psychology and Psychiatry, 41, 97–116.
Associations with child characteristics. Journal of Autism and Gotham, K., Marvin, A. R., Taylor, J. L., Warren, Z., Anderson,
Developmental Disabilities, 38, 1278–1291. C. M., Law, P. A., . . . Lipkin, P. H. (2015). Characterizing the
de Bruin, E. I., Ferdinand, R. F., Meester, S., de Nijs, P. F., & daily life, needs, and priorities of adults with ASD from
Verheij, F. (2007). High rates of psychiatric co-morbidity in Interactive Autism Network data. Autism, 19, 794–804.
PDD-NOS. Journal of Autism and Developmental Disorders, Gray, K., Keating, C., Taffe, J., Brereton, A., Einfeld, S., &
37, 877–886. Tonge, B. (2012). Trajectory of behavior and emotional
Eisenberg, N., Fabes, R. A., Murphy, B., Maszk, P., Smith, M., & problems in autism. American Journal on Intellectual and
Karbon, M. (1995). The role of emotionality and regulation Developmental Disabilities, 117, 121–133.
in children's social functioning: A longitudinal study. Child Green, S. A., Hernandez, L., Bookheimer, S. Y., & Dapretto, M.
Development, 66, 1360–1384. (2017). Reduced modulation of thalamocortical connectivity
Eisenberg, I. W., Wallace, G. L., Kenworthy, L., Gotts, S. J., & during exposure to sensory stimuli in ASD. Autism Research,
Martin, A. (2015). Insistence on sameness relates to increased 10, 801–809.
covariance of gray matter structure in autism spectrum Green, S. A., Hernandez, L., Tottenham, N., Krasileva, K.,
disorder. Molecular Autism, 6, 54. Bookheimer, S. Y., & Dapretto, M. (2015). Neurobiology of
Fabes, R. A., Eisenberg, N., & Eisenbud, L. (1993). Behavioral sensory overresponsivity in youth with autism spectrum
and physiological correlates of children’s reactions to others disorders. JAMA Psychiatry, 72, 778–786.
in distress. Developmental Psychology, 29, 655–663. Green, S. A., Rudie, J. D., Colich, N. L., Wood, J. J., Shirinyan,
Faja, S., Murias, M., Beauchaine, T. P., & Dawson, G. (2013). D., Hernandez, L., . . . Bookheimer, S. Y. (2013). Over-
Reward-based decision making and electrodermal responding reactive brain responses to sensory stimuli in youth with
by young children with autism spectrum disorders during a autism spectrum disorders. Journal of the American Academy
gambling talk. Autism Research, 6, 494–505. of Child and Adolescent Psychiatry, 52, 1158–1173.
Filliter, J. H., Longard, J., Lawrence, M. A., Zwaigenbaum, L., Grelotti, D. J., Gauthier, I., & Schultz, R. T. (2002). Social
Brian, J., Garon, N., . . . Bryson, S. E. (2015). Positive affect interest and the development of cortical face specialization:
in infant siblings of children diagnosed with autism What autism teaches us about face processing. Developmental
spectrum disorder. Journal of Abnormal Child Psychology, Psychobiology, 40, 213–225.
43, 567–575. Guy, L., Souders, M., Bradstreet, L., Delussey, C., & Herrington,
Gabard-Durnam, L., Tierney, A. L., Vogel-Farley, V., Tager- J. D. (2014). Brief report: Emotion regulation and respiratory
Flusberg, H., & Nelson, C. A. (2015). Alpha asymmetry in sinus arrhythmia in autism spectrum disorder. Journal of
infants at risk for autism spectrum disorders. Journal of Autism and Developmental Disorders, 44, 2614–2620.
Autism and Developmental Disorders, 45, 473–480. Hartley, S. L., Barker, E. T., Baker, J. K., Seltzer, M. M., &
Gadow, K. D., DeVincent, C. J., Olvet, D. M., Pisarevskaya, V., Greenberg, J. S. (2012). Marital satisfaction and life
& Hatchwell, E. (2010). Association of DRD4 polymorphism circumstances of grown children with autism across 7 years.
with severity of oppositional defiant disorder, separation Journal of Family Psychology, 26, 688–697.
anxiety disorder and repetitive behaviors in children with Heilman, K. J., Bal, E., Bazhenova, O. V., & Porges, S. W.
autism spectrum disorder. European Journal of Neuroscience, (2007). Respiratory sinus arrhythmia and tympanic membrane
32, 1058–1065. compliance predict spontaneous eye gaze behaviors in young
Gadow, K. D., Pinsonneault, J., Perlman, G., & Sadee, W. children: A pilot study. Developmental Psychobiology, 49,
(2014). Association of dopamine gene variants, emotion 531–542.
dysregulation and ADHD in autism spectrum disorder. Heller, W., Nitschke, J. B., Etienne, M. A., & Miller, G. A.
Research in Developmental Disabilities, 35, 1658–1665. (1997). Patterns of regional brain activity differentiate types
Gadow, K. D., Roohi, J., DeVincent, C. J., & Hatchwell, E. of anxiety. Journal of Abnormal Psychology, 106, 376–385.
(2008). Association of ADHD, tics, and anxiety with Henderson, H. A., Marshall, P. J., Fox, N. A., & Rubin, K. H.
dopamine transporter (DAT1) genotype in autism spectrum (2004). Psychophysiological and behavioral evidence for
disorder. Journal of Child Psychology and Psychiatry, 49, varying forms and functions of nonsocial behavior in
1331–1338. preschoolers. Child Development, 75, 251–263.
Gadow, K. D., Roohi, J., DeVincent, C. J., Kirsch, S., & Herrington, J. D., Maddox, B. B., Kerns, C. M., Rump, K.,
Hatchwell, E. (2009). Association of COMT (Val158Met) Worley, J. A., Bush, J. C., . . . Miller, J. S. (2017). Amygdala
and BDNF (Val66Met) gene polymorphisms with anxiety, volume differences in autism spectrum disorder are related to

anxiety. Journal of Autism and Developmental Disorders, 47, Konstantareas, M. M., & Stewart, K. (2006). Affect regulation
3682–3691. and temperament in children with autism spectrum disorder.
Herrington, J. D., Miller, J. S., Pandey, J., & Schultz, R. T. Journal of Autism and Developmental Disorders, 36, 143–154.
(2016). Anxiety and social deficits have distinct relationships Kring, S. R., Greenberg, J. S., & Seltzer, M. M. (2008).
with amygdala function in autism spectrum disorder. Social Adolescents and adults with autism with and without co-
Cognitive and Affective Neuroscience, 11, 907–914. morbid psychiatric disorders: Differences in maternal well-
Hollocks, M. J., Howlin, P., Papadopoulos, A. S., Khondoker, being. Journal of Mental Health Research in Intellectual
M., & Simonoff, E. (2014). Differences in HPA-axis and Disabilities, 1, 53–74.
heart rate responsiveness to psychosocial stress in children Kylliainen, A., & Hietanen, J. K. (2006). Skin conductance
with autism spectrum disorders with and without co-morbid responses to another person’s gaze in children with autism.
anxiety. Psychoneuroendocrinology, 46, 32–45. Journal of Autism and Developmental Disorders, 36, 517–525.
Horowitz, L. M., Thurm, A., Farmer, C., Mazefsky, C., Kylliainen, A., Wallace, S., Coutanche, M. N., Leppanen, J. M.,
Lanzillo, E., Bridge, J. A., . . . Siegel, M. (2017). Talking Cusack, J., Bailey, A. J., & Hietanen, J. K. (2012). Affective-
about death or suicide: Prevalence and clinical correlates in motivational brain responses to direct gaze in children with
youth with autism spectrum disorder in the psychiatric autism spectrum disorder. Journal of Child Psychology and
inpatient setting. Journal of Autism and Developmental Psychiatry, 53, 790–797.
Disorders. Advance online publication. Lam, K. S. L., Aman, M. G., & Arnold, L. E. (2006).
Huang, C. H., & Santangelo, S. L. (2008). Autism and serotonin Neurochemical correlates of autistic disorder: A review of
transporter gene polymorphisms: A systematic review and the literature. Research in Developmental Disabilities, 27,
meta-analysis. American Journal of Medical Genetics Part 254–289.
B-Neuropsychiatric Genetics, 147B, 903–913. Lecavalier, L. (2006). Behavioral and emotional problems in
Jann, K., Hernandez, L. M., Beck-Pancer, D., McCarron, R., young people with pervasive developmental disorders:
Smith, R. X., Dapretto, M., & Wang, D. J. J. (2015). Altered Relative prevalence, effects of subject characteristics, and
resting perfusion and functional connectivity of default empirical classification. Journal of Autism and Developmental
mode network in youth with autism spectrum disorder. Disorders, 36, 1101–1114.
Brain and Behavior, 5, e00358. Lever, A. G., & Geurts, H. M. (2016). Psychiatric co-occurring
Juranek, J., Filipek, P. A., Berenji, G. R., Modahl, C., Osann, K., symptoms and disorders in young, middle-aged, and older
& Spence, M. A. (2006). Association between amygdala adults with autism spectrum disorder. Journal of Autism and
volume and anxiety level: Magnetic resonance imaging Developmental Disorders, 46, 1916–1930.
(MRI) study in autistic children. Journal of Child Neurology, Levitan, G. W., & Reiss, S. (1983). Generality of diagnostic
21, 1051–1058. overshadowing across disciplines. Applied Research in Mental
Kanner, L. (1943). Autistic disturbances of affective contact. Retardation, 4, 59–64.
Nervous Child, 2, 217–250. Lydon, S., Healy, O., Roche, M., Henry, R., Mulhern, T., &
Kaufman, E. A., Puzia, M. E., Mead, H. K., Crowell, S. E., Hughes, B. M. (2015). Salivary cortisol levels and challenging
McEachern, A., & Beauchaine, T. P. (2017). Children’s behavior in children with autism spectrum disorder. Research
emotion regulation difficulties mediate the association in Autism Spectrum Disorders, 10, 78–92.
between maternal borderline and antisocial symptoms and Magnuson, K. M., & Constantino, J. N. (2011).
youth behavior problems over one year. Journal of Personality Characterization of depression in children with autism
Disorders, 31, 170–192. spectrum disorders. Journal of Developmental and Behavioral
Kennedy, D. P., & Courchesne, E. (2008). Functional Pediatrics, 32, 332–340.
abnormalities of the default network during self- and other- Maisel, M. E., Stephenson, K. G., South, M., Rodgers, J.,
reflection in autism. Social Cognitive and Affective Neuroscience, Freeston, M. H., & Gaigg, S. B. (2016). Modeling the
3, 177–190. cognitive mechanisms linking autism symptoms and
Kerns, C. M., Kendall, P. C., Zickgraf, H., Franklin, M. E., anxiety in adults. Journal of Abnormal Psychology, 125,
Miller, J., & Herrington, J. (2015). Not to be overshadowed 692–703.
or overlooked: Functional impairments associated with March, J. S., Parker, J. D., Sullivan, K., Stallings, P., & Conners,
comorbid anxiety disorders in youth with ASD. Behavior C. K. (1997). The Multidimensional Anxiety Scale for
Therapy, 46, 29–39. Children (MASC): Factor structure, reliability, and validity.
Kleinhans, N. M., Johnson, L. C., Richards, T., Mahurin, R., Journal of the American Academy of Child and Adolescent
Greenson, J., Dawson, G., & Aylward, E. (2009). Reduced Psychiatry, 36, 554–565.
neural habituation in the amygdala and social impairments Mathersul, D., McDonald, S., & Rushby, J. A. (2013).
in autism spectrum disorders. American Journal of Psychiatry, Psychophysiological correlates of social judgement in high-
166, 467–475. functioning adults with autism spectrum disorder. International
Kleinhans, N. M., Reiter, M. A., Neuhaus, E., Pauley, G., Journal of Psychophysiology, 87, 88–94.
Martin, N., Dager, S., & Estes, A. (2016). Subregional Mazefsky, C. A., Borue, X., Day, T. N., & Minshew, N. J. (2014).
differences in intrinsic amygdala hyper and hypo Emotion regulation patterns in adolescents with high-
connectivity in autism spectrum disorder. Autism Research, functioning autism spectrum disorder: Comparison to typically
9, 760–772. developing adolescents and association with psychiatric
Kleinhans, N. M., Richards, T., Weaver, K., Johnson, L. C., symptoms. Autism Research, 7, 344–354.
Greenson, J., Dawson, G., & Aylward, E. (2010). Association Mazefsky, C. A., Day, T. N., Siegel, M., White, S. W., Yu, L., &
between amygdala response to emotional faces and social Pilkonis, P. A. (2016). Development of the Emotion
anxiety in autism spectrum disorders. Neuropsychologia, 48, Dysregulation Inventory: A PROMISing method for
3665–3670. creating sensitive and unbiased questionnaires for autism
Neuhaus 295
spectrum disorders. Journal of Autism and Developmental Osterman, K., & Björkqvist, K. (2010). A cross-sectional study
Disorders. Advance online publication. of onset, cessation, frequency, and duration of children’s
Mazefsky, C. A., Herrington, J., Siegel, M., Scarpa, A., Maddox, temper tantrums in a nonclinical sample. Psychological
B. B., Scahill, L., & White, S. W. (2013). The role of emotion Reports, 106, 448–454.
regulation in autism spectrum disorder. Journal of the American Patriquin, M. A., Lorenzi, J., Scarpa, A., & Bell, M. A. (2014).
Academy of Child and Adolescent Psychiatry, 52, 679–688. Developmental trajectories of respiratory sinus arrhythmia:
Mazefsky, C. A., Oswald, D. P., Day, T. N., Eack, S. M., Associations with social responsiveness. Developmental
Minshew, N. J., & Lainhart, J. E. (2012). ASD, a psychiatric Psychobiology, 56, 317–326.
disorder, or both? Psychiatric diagnoses in adolescents with Patterson, G. R. (1982). Coercive family process. Eugene, OR:
high-functioning ASD. Journal of Clinical Child and Castalia.
Adolescent Psychology, 41, 516–523. Picardi, A., Fagnani, C., Medda, E., Toccaceli, V., Brambilla, P.,
Mazefsky, C. A., & White, S. W. (2014). Emotion regulation: & Stazi, M. A. (2015). Genetic and environmental influences
Concepts and practice in autism spectrum disorder. Child and underlying the relationship between autistic traits and
Adolescent Psychiatric Clinics of North America, 23, 15–24. temperament and character dimensions in adulthood.
McAlonan, G. M., Daly, E., Kumari, V., Critchley, H. D., van Comprehensive Psychiatry, 58, 178–188.
Amelsvoort, T., Suckling, J., . . . Murphy, D. G. M. (2002). Pierce, K., Muller, R.-A., Ambrose, J., Allen, G., & Courchesne,
Brain anatomy and sensorimotor gating in Asperger’s E. (2001). Face processing occurs outside the fusiform ‘face
syndrome. Brain, 127, 1594–1606. area’ in autism: Evidence from functional MRI. Brain, 124,
McDonald, A. J. (1998). Cortical pathways to the mammalian 2059–2073.
amygdala. Progress in Neurobiology, 55, 257–332. Plitt, M., Barnes, K. A., Wallace, G. L., Kenworthy, L., &
Mead, H. K., Beauchaine, T. P., & Shannon, K. E. (2010). Martin, A. (2015). Resting-state functional connectivity
Neurobiological adaptations to violence across development. predicts longitudinal change in autistic traits and adaptive
Development and Psychopathology, 22, 1–22. functioning in autism. Proceedings of the National Academy of
Mikita, N., Hollocks, M. J., Papadopoulos, A. S., Aslani, A., Sciences, 112, E6699–E6706.
Harrison, S., Leibenluft, E., . . . Stringaris, A. (2015). Porges, S. W. (2001). The polyvagal theory: Phylogenetic
Irritability in boys with autism spectrum disorders: An substrates of a social nervous system. International Journal of
investigation of physiological reactivity. Journal of Child Psychophysiology, 42, 123–146.
Psychology and Psychiatry, 56, 1118–1126. Porges, S. W., Doussard-Roosevelt, J. A., & Maiti, A. K. (1994).
Munson, J., Dawson, G., Abbott, R., Faja, S., Webb, S. J., Vagal tone and the physiological regulation of emotion.
Friedman, S. D., . . . Dager, S. R. (2006). Amygdalar volume Monographs of the Society for Research in Child Development,
and behavioral development in autism. Archives of General 59, 167–186.
Psychiatry, 63, 686–693. Putnam, S. P., Gartstein, M. A., & Rothbart, M. K. (2006).
Muris, P., Steerneman, P., Merckelbach, H., Holdrinet, I., & Measurement of fine-grained aspects of toddler temperament:
Meesters, C. (1998). Comorbid anxiety symptoms in children The Early Childhood Behavior Questionnaire. Infant
with pervasive developmental disorders. Journal of Anxiety Behavior and Development, 29, 386–401.
Disorders, 12, 387–393. Raichle, M. E., MacLeod, A. M., Snyder, A. Z., Powers, W. J.,
Neuhaus, E., Beauchaine, T. P., & Bernier, R. (2010). Gusnard, D. A., & Shulman, G. L. (2001). A default mode
Neurobiological correlates of social functioning in autism. of function. Proceedings of the National Academy of Sciences,
Clinical Psychology Review, 30, 733–748. 98, 676–682.
Neuhaus, E., Bernier, R. A., & Beauchaine, T. P. (2014). Social Rieffe, C., De Bruine, M., De Rooij, M., & Stockmann, L.
skills, internalizing and externalizing symptoms, and (2014). Approach and avoidant emotion regulation prevent
respiratory sinus arrhythmia in autism. Journal of Autism and depressive symptoms in children with an autism spectrum
Developmental Disorders, 44, 730–737. disorder. International Journal of Developmental Neuroscience,
Neuhaus, E., Bernier, R. A., & Beauchaine, T. P. (2015). 39, 37–43.
Electrodermal response to reward and non-reward among Roohi, J., DeVincent, C. J., Hatchwell, E., & Gadow, K. D.
children with autism. Autism Research, 8, 357–370. (2009). Association of a monoamine oxidase-A gene promoter
Neuhaus, E., Bernier, R. A., & Beauchaine, T. P. (2016). Children polymorphism with ADHD and anxiety in boys with autism
with autism show altered autonomic adaptation to novel and spectrum disorder. Journal of Autism and Developmental
familiar social partners. Autism Research, 9, 579–591. Disorders, 39, 67–74.
Neuhaus, E., Jones, E. J. H., Barnes, K., Sterling, L., Estes, A., Salmond, C. H., de Haan, M., Friston, K. J., Gadian, D. G., &
Munson, J., Dawson, G., & Webb, S. J. (2016). The Vargha-Khadem, F. (2003). Investigating individual
relationship between early neural responses to emotional differences in brain abnormalities in autism. Philosophical
faces at age 3 and later autism and anxiety symptoms in Transactions of the Royal Society of London, Series B: Biological
adolescents with autism. Journal of Autism and Developmental Sciences, 358, 405–413.
Disorders, 46, 2450–2463. Samson, A. C., Wells, W. M., Phillips, J. M., Hardan, A. Y., &
Nusslock, R., Walden, K., & Harmon-Jones, E. (2015). Gross, J. J. (2015). Emotion regulation in autism spectrum
Asymmetrical frontal cortical activity associated with disorder: Evidence from parent interviews and children’s
differential risk for mood and anxiety disorder symptoms. An daily diaries. Journal of Child Psychology and Psychiatry, 56,
RDoC perspective. International Journal of Psychophysiology, 903–913.
98, 249–261. Schauder, K. B., Muller, C. L., Veenstra-VanderWeele, J., &
Ornitz, E. M., Lane, S. J., Sugiyama, T., & de Traversay, J. Cascio, C. J. (2015). Genetic variation in serotonin transporter
(1993). Startle modulation studies in autism. Journal of modulates tactile hyperresponsiveness in ASD. Research in
Autism and Developmental Disorders, 23, 619–637. Autism Spectrum Disorders, 10, 93–100.

Schumann, C. M., & Amaral, D. G. (2006). Stereological Thompson, R. A. (1990). Emotion and self-regulation. In
analysis of amygdala neuron number in autism. Journal of R. A. Thompson (Ed.), Nebraska symposium on motivation:
Neuroscience, 26, 7674–7679. Vol. 36. Socioemotional development (pp. 383–483). Lincoln,
Segers, M., & Rawana, J. (2014). What do we know about NE: University of Nebraska Press.
suicidality in autism spectrum disorder? A systematic review. Tick, B., Colvert, E., McEwen, F., Stewart, C., Woodhouse, E.,
Autism Research, 7, 507–521. Gillan, N., . . . Rijsdijk, F. (2016). Autism spectrum disorders
Sharpley, C. F., Bitsika, V., Andronicos, N. M., & Agnew, L. L. and other mental health problems: Exploring etiological
(2016). Further evidence of HPA-axis dysregulation and its overlaps and phenotypic causal associations. Journal of the
correlation with depression in autism spectrum disorder: American Academy of Child and Adolescent Psychiatry, 55,
Data from girls. Physiology and Behavior, 167, 110–117. 106–113.
Shen, M. D., Li, D. D., Keown, C. L., Lee, A., Johnson, R. T., Tomarken, A. J., Davidson, R. J., & Henriques, J. B. (1990).
Angkustsiri, K., . . . Nordahl, C. W. (2016). Functional Resting frontal brain asymmetry predicts affective responses
connectivity of the amygdala is disrupted in preschool-aged to films. Journal of Personality and Social Psychology, 59I,
children with autism spectrum disorder. Journal of the American 791–801.
Academy of Child and Adolescent Psychiatry, 55, 817–824. Vaillancourt, T., Haltigan, J.D., Smith, I., Zwaigenbaum, L.,
Sherman, S. M. (2005). Thalamic relays and cortical functioning. Szatmari, P., Fombonne, E. .
.
.
Bryson, S. (2017). Joint
Progress in Brain Research, 149, 107–126. trajectories of internalizing and externalizing problems in
Simonoff, E., Pickles, A., Charman, T., Chandler, S., Loucas, T., preschool children with autism spectrum disorder.
& Baird, G. (2008). Psychiatric disorders in children with Development and Psychopathology, 29, 203–214.
autism spectrum disorders: Prevalence, comorbidity, and van Engeland, H. (1984). The electrodermal orienting response
associated factors in a population-derived sample. Journal of to auditive stimuli in autistic children, normal children,
the American Academy of Child and Adolescent Psychiatry, 47, mentally retarded children, and child psychiatric patients.
921–929. Journal of Autism and Developmental Disorders, 14, 261–279.
Snyder, J., Schrepferman, L., Oeser, J., Patterson, G., Stoolmiller, Van Hecke, A. V., Lebow, J., Bal, E., Lamb, D., Harden, E.,
M., Johnson, K., & Snyder, A. (2005). Deviancy training Kramer, A., . . . Porges, S. W. (2009). Electroencephalogram
and association with deviant peers in young children: and heart rate regulation to familiar and unfamiliar people in
Occurrence and contribution to early-onset conduct children with autism spectrum disorders Child Development,
problems. Development and Psychopathology, 17, 397–413. 80, 1118–1133.
South, M., & Rodgers, J. (2017). Sensory, emotional and Van Hecke, A. V., Stevens, S., Carson, A. M., Karst, J. S., Dolan,
cognitive contributions to anxiety in autism spectrum B., Schohl, K., .
.
.
Brockman, S. (2015). Measuring the
disorders. Frontiers in Human Neuroscience, 11, 20. plasticity of social approach: A randomized controlled trial of
Sparks, B. F., Friedman, S. D., Shaw, D. W., Aylward, E. H., the effects of the PEERS intervention on EEG asymmetry in
Echelard, D., Artru, A. A., . . . Dager, S. R. (2002). Brain adolescents with autism spectrum disorders. Journal of
structural abnormalities in young children with autism Autism and Developmental Disorders, 45, 316–335.
spectrum disorder. Neurology, 59, 184–192. Velasquez, F., Wiggins, J. L., Mattson, W. I., Martin, D. M.,
Spratt, E. G., Nicholas, J. S., Brady, K. T., Carpenter, L. A., Lord, C., & Monk, C. S. (2017). The influence of 5-HTTLPR
Hatcher, C. R., . . . Charles, J. M. (2012). Enhanced cortisol transporter genotype on amygdala-subgenual anterior
response to stress in children in autism. Journal of Autism and cingulate cortex connectivity in autism spectrum disorder.
Developmental Disorders, 42, 75–81. Developmental Cognitive Neuroscience, 24, 12–20.
Sterling, L., Dawson, G., Estes, A., & Greenson, J. (2008). Weiner, D. J., Wigdor, E. M., Ripke, S., Walters, R. K.,
Characteristics associated with presence of depressive Kosmicki, J. A., Grove, J., . . . Robinson, E. B. (2017).
symptoms in adults with autism spectrum disorder. Journal Polygenic transmission disequilibrium confirms that
of Autism and Developmental Disorders, 38, 1011–1018. common and rare variation act additively to create risk for
Stessman, H. A. F., Xiong, B., Coe, B. P., Wang, T., Hoekzema, autism spectrum disorders. Nature Genetics, 49, 978–985.
K., Fenckova, M., . . . Eichler, E. E. (2017). Targeted Werling, D. M., & Geschwind, D. H. (2013). Sex differences in
sequencing identifies 91 neurodevelopmental disorder risk autism spectrum disorder. Current Opinion in Neurology, 26,
genes with autism and developmental disability biases. 146–153.
Nature Genetics, 49, 515–526. Whitaker-Azmitia, P. M. (2001). Serotonin and brain
Sutton, S. K., Burnette, C. P., Mundy, P. C., Meyer, J., Vaughan, A., development: Role in human developmental diseases. Brain
Sanders, C., & Yale, M. (2005). Resting cortical brain activity Research Bulletin, 56, 479–485.
and social behavior in higher functioning children with White, S. W., Mazefsky, C. A., Dichter, G. S., Chiu, P. H.,
autism. Journal of Child Psychology and Psychiatry, 46, 211–222. Richey, J. A., & Ollendick, T. H. (2014). Social-cognitive,
Swartz, J. R., Wiggins, J. L., Carrasco, M., Lord, C., & Monk, physiological, and neural mechanisms underlying emotion
C. S. (2013). Amygdala habituation and prefrontal functional regulation impairments: Understanding anxiety in autism
connectivity in youth with autism spectrum disorders. Journal spectrum disorder. International Journal of Developmental
of the American Academy of Child and Adolescent Psychiatry, Neuroscience, 39, 22–36.
52, 84–93. White, S. W., Oswald, D., Ollendick, T., & Scahill, L. (2009).
Tarullo, A. R., & Gunnar, M. R. (2006). Child maltreatment Anxiety in children and adolescents with autism spectrum
and the developing HPA axis. Hormones and Behavior, 50, disorder. Clinical Psychology Review, 29, 216–229.
632–639. White, S. W., Schry, A. R., & Maddox, B. B. (2012). Brief report:
Taylor, J. L., & Seltzer, M. M. (2010). Changes in the autism The assessment of anxiety of high-functioning adolescents
behavioral phenotype during the transition to adulthood. with autism spectrum disorder. Journal of Autism and
Journal of Autism and Developmental Disorders, 40, 1431–1446. Developmental Disorders, 42, 1138–1145.
Neuhaus 297
Wiggins, J. L., Swartz, J. R., Martin, D. M., Lord, C., & Yee, M. M., & Millichap, J. G. (2015). Relationship between age
Monk, C. S. (2014). Serotonin transporter genotype at diagnosis of ADHD and ASD. Pediatric Neurology Briefs,
impacts amygdala habituation in youth with autism spectrum 29, 78.
disorders. Social Cognitive and Affective Neuroscience, 9, Zahn, T. P., Rumsey, J. M., & Van Kammen, D. P. (1987).
832–838. Autonomic nervous system activity in autistic, schizophrenic,
Wilbarger, J. L., McIntosh, D. N., & Winkielman, P. (2009). and normal men: Effects of stimulus significance. Journal of
Startle modulation in autism: Positive affective stimuli Abnormal Psychology, 96, 135–144.
enhance startle response. Neuropsychologia, 47, 1323–1331. Zisner, A., & Beauchaine, T. P. (2016). Neural substrates of trait
Yang, P., Menga, Y., Li, T., & Huang, Y. (2017). Associations of impulsivity, anhedonia, and irritability: Mechanisms of
endocrine stress-related gene polymorphisms with risk of heterotypic comorbidity between externalizing disorders and
autism spectrum disorders: Evidence from an integrated unipolar depression. Development and Psychopathology, 28,
meta-analysis. Autism Research, 10, 1722–1736. 1179–1210.

CH A PTE R
21 Psychosis Spectrum Disorders
Gemma T. Wallace and Anna R. Docherty
Abstract
Psychosis spectrum disorders (PSDs) are complex, highly heritable psychiatric conditions with high
economic and societal costs. PSDs have historically been conceptualized as neurocognitive disorders in
which psychotic episodes and impairments in social and emotional functioning are attributed to deficits
in neurocognition. Although cognitive pathways play an important role in the etiology and presentation
of PSDs, recent research suggests that interrelations between cognition and emotion are highly
relevant. Moreover, aberrant emotion regulation likely plays a significant role in the presentation of
PSDs. Emotion dysregulation (ED) may underlie and exacerbate both negative and positive symptoms
in PSDs, such as blunted affect, avolition, disorganized speech and behavior, poor social cognition, and
delusions and hallucinations. Advances in measurement of emotion dysregulation—including self-reports,
behavioral paradigms, neuroimaging paradigms, and neurophysiological assessment—have informed
etiological models of emotion dysregulation in PSDs. This chapter reviews research on emotion
regulation and dysregulation in PSDs. Notably, more severe presentations of emotion symptoms and
greater emotion regulation impairments are associated with worse outcomes in PSDs. It may therefore
be the case that focusing on ED as an early risk factor and intervention target could improve outcomes
and prevention approaches for psychotic disorders.
Keywords: psychosis spectrum disorders, emotion dysregulation, emotion regulation strategies,

negative symptoms, positive symptoms
Psychosis Spectrum Disorders: schizoaffective disorder, up to 4.6% for schizotypal

Prevalence and Features personality disorder, up to 0.7% for schizophrenia,
Psychosis spectrum disorders (PSDs) are among the and a prevalence similar to that observed in schizo-
most complex, varied, and debilitating of psychiatric phrenia for schizophreniform disorder; American
disorders, involving a range of cognitive and Psychiatric Association 2013). PSDs are among the
affective impairments. PSDs have heterogeneous top 25 global causes of disability (Lopez Mathers,
and nonspecific signs and symptoms. Schizophrenia Ezzati, Jamison, & Murray, 2006; Vos et al., 2013)
is more common in males than in females and impose massive social, economic, and emotional
(Aleman, Kahn, & Selten, 2003), with a prevalence burdens on diagnosed patients and their relatives,
ratio of about 1.4:1 in males relative to females caregivers, and the public (Chong et al., 2016). No
(Regier et al., 1993; Jablensky & Kalaydjieva, 2003). single symptom is considered “core” to schizophrenia,
According to the Diagnostic and Statistical Manual though some symptoms may be more closely related
of Mental Disorders, fifth edition (DSM-5; American to underlying pathophysiology than others. In ad-
Psychiatric Association, 2013), PSDs have a com- dition, schizophrenia and other PSDs show multi-
bined incidence of about 6.5% of the general factorial genetic inheritance, with hundreds or even
population (0.2% for delusional disorder, 0.3% for thousands of genes, copy number variants, and
299
even de novo mutations contributing to vulnera- Emotion and Emotion Regulation
bility (Purcell et al., 2009; Ripke et al., 2014). Abnormalities in PSDs
In turn, these vulnerabilities interact strongly with Multiple forms of affective disturbance are observed
environmental risk factors (e.g., Gottesman & in PSDs (van Rijn et al., 2011, Kring & Elis, 2013).
Gould, 2003). Thus, there is significant incentive Abnormalities in emotion, including blunted affect,
for integrative research that targets etiology, pre- heightened negative emotionality, diminished
vention, and treatment strategies for PSDs. positive emotionality (anhedonia), and increased
Three symptom dimensions characterize schizo- emotional reactivity (lability), are well documented,
phrenia and related disorders, including positive, beginning with the earliest descriptions of schizo-
disorganized, and negative symptoms. These occur phrenia and related disorders (e.g., Bleuler, 1950).
at varying levels of severity across affected individuals Notably, affective difference often precedes the
and conditions (e.g., subthreshold schizotypy to onset and diagnosis of PSDs (Kim et al., 2013;
acute psychosis). In sections to follow, we review Meyer et al., 2014; Kimhy et al., 2016), and patients
emotion dysregulation in contexts of these symptom who experience more severe negative symptoms
dimensions. Core positive symptoms of psychosis have poorer prognoses (Mueser Penn, Blanchard,
include delusions and hallucinations, whereas disor- & Bellack, 1997; Milev, Beng-Choon, Arndt, &
ganized symptoms include disordered behaviors, Andreasen, 2005; Gur et al., 2006; Henry et al.,
disorganized thinking and speech, and generalized 2007; Foussias & Remington, 2010). However, re-
cognitive impairments. Negative symptoms include search on the nature of affective disturbance lags
flattened affect, social withdrawal, decreased motiva- behind studies of cognition (Aleman & Kahn, 2005;
tion (avolition), and decreased attention to emotion van der Velde, Opmeer, et al., 2015). Prior to the
(American Psychiatric Association, 2013). Negative DSM-5, schizophrenia was classified as a “nonaf-
symptoms are associated with poorer concurrent fective” psychosis by the American Psychiatric
and long-term functioning, and are particularly Association (1952, 1968, 1980, 1994). These previous
heritable (Piskulic et al., 2012; Kim et al., 2013; classification schemes may have discouraged re-
Meyer et al., 2014; Schlosser et al., 2015). A large search on affect in PSDs by implying that patients’
part of this review will focus on these important, emotional impairments were a reaction to symptoms
emotion-related symptoms. or experiences of schizophrenia, rather than causal
Although diagnostic criteria include affective or core to the disorder. However, advances in
deficits (American Psychiatric Association 2013), affective science (see, e.g., Kring & Moran, 2008;
PSDs have historically been conceptualized as neu- Kring & Caponigro, 2010) have led to a growing
rocognitive disorders, in which psychotic episodes literature on affective experiences and presentations
and impairments in social, cognitive, and emotional of PSD patients.
functioning are attributed to neurocognitive se- It is now recognized that both emotion regulation
quelae. Large effect sizes are observed in differences and emotion dysregulation may be central to
between people with schizophrenia and healthy PSD severity and treatment outlook (Livingstone,
controls on measures of executive function, working Harper, & Gillanders, 2009; Cohen & Minor, 2010).
memory, and attention (for reviews see Heinrichs & Emotion regulation, as used here, is defined as pro-
Zakzanis, 1998; Green, Kern, Braff, & Mintz, 2000; cesses through which individuals monitor, evaluate,
Pantelis & Maruff, 2002). These cognitive impair- and alter their emotional reactions and experiences
ments are also observed to a lesser extent in in the service of adaptive behavior (e.g., Gross, 2002;
first-degree relatives (for reviews see Sitskoom, Thompson, 1990). Although emotion regulation
Aleman, Ebisch, Appels, & Kahn, 2004; Snitz, has been examined as a component of and vulner-
Macdonald, & Carter, 2006). Cognitive pathways ability to many psychiatric disorders (see Aldao,
are implicated in disorganized thinking and behavior, Nolen-Hoeksema, & Schweizer, 2010), emotion
emotional disturbances, and psychotic symptoms regulation paradigms have only recently found a
(e.g., Brewer et al., 2006; Berenbaum, Kerns, Vernon, foothold in PSD research (Livingstone et al., 2009;
& Gomez, 2008a, 2008b, 2008c; Campellone, Elis, Kimhy et al., 2012; Kimhy et al., 2016). In contrast to
Mote, Sanchez, & Kring, 2016). However, addi- the goal-oriented nature of emotion regulation, emo-
tional consideration and awareness of the intersection dysregulation is conceptualized as emotional pro-
tion of cognition and emotion has furthered current cesses that interfere with healthy emotion regulation
understanding of these disorders. and goal-directed behavior (see Beauchaine, 2015).
300 Emotion Dysregul ation and Schizophrenia Disorders

Compared with other psychological disorders and prevention of these disorders. In the following
(e.g., borderline personality disorder; Glenn & sections, we (1) provide an overview of emotion
Klonsky, 2009), in PSD research, the term emotion regulation research on PSDs, (2) describe symptom
dysregulation is used far less frequently. Nonetheless, facets that appear more related to emotion dys-
emotion dysregulation constructs have been central regulation, (3) discuss current methodological frame-
to research on affect in PSDs. To date, such studies works for studying emotion dysregulation in PSDs,
have focused primarily on five areas of emotion: (1) and (4) offer recommendations for future transla-
disjointed emotional experience and presentation, tional research in the area of emotion dysregulation.
(2) dysregulated negative and positive emotionality,
(3) emotional reactivity, (4) emotional awareness, Emotion Regulation Deficits in PSDs
and (5) reliance on different emotion regulation Initial evidence suggests that PSD patients use
strategies from those of healthy controls. The first different emotion regulation strategies than con-
four of these topics represent facets of emotion trols (e.g., Henry et al., 2007; Henry et al., 2009;
dysregulation, whereas research on strategies falls Livingstone et al., 2009; van der Meer, van’t Wout,
under the umbrella of emotion regulation. & Aleman, 2009; Horan, Hajcak, Wynn, & Green,
Emotion regulation and dysregulation differences 2013; Strauss et al., 2013). PSD patients appear to
in schizophrenia may be linked to the severity and rely more on dysfunctional emotion regulation
development of negative, positive, and disorganized strategies and less on healthy strategies. In particular,
(cognitive) symptoms (Berenbaum et al., 2006; individuals with PSDs seem to rely less on
Strauss et al., 2013). Affective symptoms tend to antecedent-focused strategies, which involve modi-
precede the onset of psychotic symptoms in schizo- fying emotional responses before they fully activate,
phrenia, suggesting a possible association of affect than on response-focused strategies, which alter
dysfunction in psychosis (Livingstone et al., 2009). emotional responses after they emerge (Gross, 1998).
Although psychotic symptoms are often attributed Antecedent-focused strategies are often considered
to cognitive dysfunctions (e.g., Waters et al., 2012), more adaptive than response-focused techniques,
emotion dimensions may influence individual because they adjust successive emotional responses
differences in psychotic symptom severity and
and experiences (Gross & John, 2003).
distress (Garety, Kuipers, Fowler, Freeman, &
To date, most studies of PSD emotion regulation
Bebbington, 2001). For many people managing strategies have focused on expressive suppression
schizophrenia, psychotic symptoms are terrifying, and cognitive reappraisal. Suppression is a response-
and an acute psychotic episode is a highly emotional focused strategy that involves decreasing behavioral,
experience. In addition, recent foci on avolition and outward expressions of emotion. Although suppres-
reward processing in PSDs, both of which are sion reduces external emotionality, it often increases
relevant to social and work role function, suggest subjective intensity of negative emotions and re-
fundamental differences in incentive processing, duces positive emotionality (Gross & Levenson,
with implications for valuating emotion stimuli and 1997). In contrast, reappraisal is an antecedent-
engaging different emotion regulation strategies focused “cognitive change” strategy in which
(Barch, 2005; for reviews see Gard, Kring, Gard, emotionally charged stimuli are retrospectively re-
Horan, & Green, 2007; Frost & Strauss, 2016). framed in unemotional terms, thereby making a
Specific interrelations between cognitive, motiva- stimulus less emotionally disturbing (Gross, 1998).
tional, and affective disturbances in PSD emotion In general, cognitive change strategies decrease the
(dys)regulation impairments remain unclear, but intensity and duration of negative emotions and in-
these symptoms likely involve both shared and crease positive emotionality; they are therefore
distinct neural processes (see Gross, 2002; Taylor & considered more effective than suppression (Gross
Liberzon, 2007, Foussias & Remington, 2010; & John, 2003; Goldin, McRae, Ramel, & Gross,
Strauss et al., 2013). 2008). In two case-control studies examining assess-
To date, many complementary and contradictory ment of emotional stimuli, healthy controls used
studies highlight potential emotion regulation and reappraisal more than suppression, but PSD sub-
dysregulation differences in PSDs, and emotion jects relied heavily on suppression (van der Meer
dysregulation represents an exciting point of growth et al., 2009; Kimhy et al., 2012). Those who are
for the field. Examination of both regulation and highly vulnerable to developing psychosis—as as-
dysregulation could inform research on treatment sessed by family history of PSD and prodromal
Wall ace and Dochert y 301

symptoms (Nelson, Yuen, & Yung, 2011)—show with negative emotionality, reduced positive affect,
greater use of suppression (Kimhy et al., 2016; and less social interaction (Moran, Culbreth, &
although see Livingstone et al., 2009, for a differ- Barch, 2017). Failures in cognitive change strategies
ent result). that successfully down-regulate negative emotions
Notably, however, these results may depend on may therefore contribute to and/or exacerbate
sample and/or study characteristics. Although multiple symptom dimensions of PSDs. In addi-
some neurophysiological (Strauss et al., 2013) and tion, inability to amplify emotion expressions may
self-report (Livingstone et al., 2009; van der Meer contribute to flattened affect (Henry et al., 2007;
et al., 2009; Kimhy et al., 2012) studies find lower Henry et al., 2009). Importantly, these emotion
use of cognitive change strategies among those regulation strategies are not unique to PSDs and
with PSDs compared with controls, others are similar to observations across numerous psy-
using identical measures (e.g., Emotion Regulation chiatric conditions (Campbell-Sills, Barlow, Brown,
Questionnaire) find no differences (Henry, Rendell, & Hofmann, 2006; Livingstone et al., 2009; Aldao
Green, McDonald, & O’Donnell, 2008; Badcock, et al., 2010).
Paulik, & Maybery, 2011; Perry, Henry, & Grisham, The degree to which less adaptive emotion regu-
2011; Strauss et al., 2013). Findings using self-reports lation strategies reflect innate biological differences
may yield more variable effects, and it may be versus social or environmental factors across
that PSD subjects do not perceive themselves as development remains unclear. Neuroimaging and
using less effective emotion regulation strategies. neurophysiological studies have provided potential
Discrepancy in self-report outcomes may also be insights into neural bases of emotion regulation
confounded with alexithymia (decreased awareness deficits in PSDs, including impaired neurophysio-
of emotion) in individuals with PSDs, as the ability logical ability to down-regulate emotional responses
to readily understand one’s emotional responses is (Horan et al., 2013; Strauss et al., 2013), altered
a prerequisite for using emotion regulation skills volumes of limbic structures (Aleman & Kahn,
effectively (Thompson, 1994). Further investiga- 2005; Giuliani, Drabant, Bhatnagar, & Gross, 2011;
tion of factors underlying inconsistent findings Giuliani, Drabant, & Gross, 2011), and decreased
is needed. prefrontal cortex (PFC) activation (van der Velde,
To date, few studies have examined other Opmeer, et al., 2015). For example, amygdala and
emotion regulation strategies in PSDs. One line of insula activation appears to increase during suppres-
investigation suggests that individuals with PSDs sion but decrease during reappraisal (Goldin et al.,
may use maladaptive attentional deployment 2008). Cognitive change strategies may down-
relative to controls. For example, PSD subjects
regulate negative emotions by decreasing limbic
demonstrate increased rumination (Badcock et al., system activity and increasing PFC activity (Goldin
2011), a response-focused, repetitive focus on nega- et al., 2008, van der Velde, Opmeer, et al., 2015);
tive emotionality that is associated with emotional PSD patients may struggle to engage the PFC and/
distress (Nolen-Hoeksema, 2000). Additionally, or inhibit limbic system processes when attempt-
PSD patients show reduced ability to amplify ing to use cognitive change strategies. Therefore,
emotional responses to positive stimuli (Henry it is possible that PSD subjects may be constrained
et al., 2007, Henry et al., 2009), and use less in their ability to use healthier emotion regulation
mindfulness-based emotion acceptance strategies strategies and to down-regulate negative emotional
than controls (Perry et al., 2011). Both of these char- responses. Whether any constraints may cause
acteristics are risk factors for psychopathology (see or result from different PSD symptoms remains
Aldao et al., 2010). unclear.
Despite inconsistencies in the literature, emotion
regulation deficits may influence multiple facets of Emotion Dysregulation and PSD
PSDs. Overreliance on suppression is associated Symptom Dimensions
with negative affect (perceiving neutral stimuli PSD symptom dimensions appear moderately
negatively), increased emotion reactivity, and flat- interrelated. Next, we discuss relations of symptoms
tened external affect (see Aldao et al., 2010), to emotion as they reflect current trends in emotion
which are common to PSDs. In a recent study using research. We do not examine all PSD symptoms in
ecological momentary assessment, PSD patients this chapter; interested readers are referred to other
who used cognitive reappraisal reported higher pos- sources for reviews on avolition/abnormal reward-
itive emotionality, whereas suppression was associated seeking behaviors (Barch, Pagliaccio, & Luking, 2015;

Reddy, Horan, & Green, 2015; Frost & Strauss, Herbener, Rosen, Khine, & Sweeney, 2007; Strauss,
2016), reduced social cognition (Couture, Penn, & 2013; Wash-Messinger et al., 2014) and are less re-
Roberts, 2006; Green, Horan, & Lee, 2015), and trievable for retrospective savoring and relating to
facial emotion perception deficits (Kohler, Walker, future anticipation. Psychological impairments may
Martin, Healey, & Moberg, 2010). also contribute to this anhedonia, as PSD patients
demonstrate reduced abilities to believe in and
Emotion Dysregulation and estimate pleasurable experiences (Strauss, 2013).

Affective Symptoms Anhedonic and emotional responses may also vary
PSDs are characterized by several affective deficits, with symptom severity (Bodapati & Herbener, 2014),
many of which are associated with emotion dysreg- emotion and social stimulus content (Llerena, Strauss,
ulation. One of the most prominent features of & Cohen, 2012), and sex (Kring & Moran, 2008).
PSDs is the “emotion paradox”—an apparent dis- Although positive emotionality appears dimin-
junction between external emotion expression and ished outside the present moment, PSD patients
subjective emotional experience. Individuals with report heightened negative emotionality in all situa-
PSDs often present with blunted or flattened affect tions. Individuals with schizophrenia report higher
and show diminished facial and vocal emotion ex- negative emotion responses to neutral and negatively
pressions to both positive and negative stimuli valenced stimuli in the present (Kring & Moran,
(Berenbaum & Oltmanns, 1992; Kring & Moran, 2008; Cohen & Minor, 2010). Heightened negativ-
2008). This is often one of the earliest PSD symptoms ity may be associated with poor physiological and
to develop, is typically chronic, and is associated emotion regulation (Strauss et al., 2013). Regulation
with poorer outcomes and reduced social efficacy impairments may exacerbate negative emotional
(Aghevli, Blanchard, & Horan, 2003; Gur et al., states via impaired negative emotion down-regulation
2006). The emotion paradox may result in part or enhanced negative emotion arousal. Chronically
from impairments in certain emotion regulation heightened emotional negativity may hinder effec-
strategies. Reduced ability to amplify and up-regulate tive emotion regulation strategies, and there may be
emotional responses may lead to decreases in typical differences in processes used to regulate positive
expression (Kring & Werner, 2004; Henry et al., versus negative emotions (Gross & Levenson, 1997).
2007; Henry et al., 2008). Additionally, overreliance In addition, increased negative emotionality and
on suppression strategies may diminish external reduced positive emotionality across tenses may
emotions (Ellgring & Smith, 1998). be related to motivational deficits (Frost &
Given reduced emotional expression, it was once Strauss, 2016).
presumed that individuals with PSDs would In addition to elevated negativity, some indi-
have diminished subjective experience of emotion. viduals with schizophrenia exhibit intensified
However, emotion experience in individuals with emotional reactivity and instability in physiological
PSDs may instead vary across current, retrospective, and behavioral assessments. Some individuals with
and prospective “tenses.” In emotion induction and PSDs exhibit emotional overarousal and tend to
self-report studies, those with flattened affect assign more negative emotional importance to neu-
demonstrate no differences in their subjective tral and negative stimuli than controls (Haralanova,
emotional responses to stimuli compared to controls Haralanov, Beraldi, Moller, & Hennig-Fast, 2012),
and patients without flattened affect (see Cohen & and exhibit more pronounced sympathetic nervous
Minor, 2010; Strauss, 2013). However, although system responses to emotional stimuli (Strauss
PSD patients’ in-the-moment emotion experiences et al., 2013). Amplified emotional reactivity may be
are intact, their retrospective and prospective re- related to reduced abilities to down-regulate emo-
ports of pleasure are diminished relative to controls. tion responses. However, these observations are
Thus, hedonic emotion experience appears normal in somewhat obfuscated by concurrent flattened affect
the present, but patients report anhedonia for previ- and by studies reporting general reduced limbic
ous and anticipated pleasurable experiences, suggest- system activation in PSD (Aleman & Kahn, 2005).
ing a reduced ability to experience pleasure outside Because reduced amygdala activation could weaken
of the present moment (Gard et al., 2007; Kring & emotional response pathways, enhanced emotion
Moran, 2008; Strauss & Gold, 2012; Strauss, 2013). reactivity may reflect a different mechanism of emo-
This abnormality may reflect emotional memory tion dysregulation, and may be related to symptoms
impairment, whereby positive experiences are not of paranoia (van der Gaag, 2006; Haralanova,
accurately encoded (Robinson & Clore, 2002; Haralanov, & Shkodrova, 2007).

Impaired emotion perception and processing— adults (Docherty et al., 2017). This could indicate—
typically studied as decreased emotional awareness at least in part—genetic risk for emotion dysregula-
and recognition—is another hallmark of PSDs tion. However, more research is necessary to address
(Aleman & Kahn, 2005). Diminished emotional this question. Neuroimaging studies implicate
awareness (alexithymia) includes reduced emotion lowered amygdala activation and reduced PFC
clarity and attention to emotion, and can be interconnectivity in PSDs, whereby (in lay terms)
measured as both “internal” and “external.” Internal the “emotion” brain may not effectively activate,
alexithymia is the ability to identify, understand, communicate with, and be modulated by higher
and pay attention to one’s own emotions, whereas cognitive processes (for general discussion see
external alexithymia relates to awareness of others’ Beauchaine, 2015). (For reviews of neural contribu-
emotions. Awareness of emotions, both in oneself tors to emotion impairments in PSDs specifically,
and others, is considered essential for effective social see Phillips, Drevets, Rauch, & Lane, 2003a, 2003b;
adaptation and may be a prerequisite for healthy Aleman & Kahn, 2005; van Rijn, Aleman, Swaab,
emotion regulation (van Rijn et al., 2011; O’Driscoll, & Kahn, 2005.) From an environmental standpoint,
Laing, & Mason, 2014). External alexithymia may stressful life events that perpetuate an imbalance in
be core to impaired social cognition and compe- dopaminergic systems may lead to increased stress
tence in PSDs (Green et al., 2000), including poor sensitization, anxiety, and autonomic arousal (Myin-
facial expression recognition (Abram et al., 2014; Germeys, Krabbendam, Delespaul, & Van Os,
Addington & Addington, 1998; Addington, Penn, 2003; Read, van Os, Morrison, & Ross, 2005).
Woods, Addington, & Perkins, 2008; Strauss, Jetha, Thus, traumatic experiences can cause long-term
Ross, Duke, & Allen, 2010; Turetsky et al., 2007), emotion dysregulation issues that may compound
deficient vocal emotion cue identification (Edwards, other PSD symptoms (Yuii, Suzuki, & Kurachi,
Jackson, & Pattison, 2002), misinterpreting others’ 2007; Benedetti et al., 2011). Comorbid conditions,
intentions in persecutory delusions (D’Antonio, psychiatric medications, social stigma, family
Kahn, McKelvey, Berenbaum, & Serper, 2015), and dynamics, and interpersonal difficulties may also
impaired theory of mind (Green, Olivier, Crawley, influence ways in which emotion impairments
Penn, & Silverstein, 2005). Internal alexithymia present and develop in PSDs. In physiological assays,
measures are correlated negatively with measures of PSD patients sometimes show heightened autonomic
emotional intelligence (Parker, Taylor, & Bagby, arousal (Horan et al., 2013; Strauss et al., 2013),
2001). Although sometimes attributed to lower IQ, suggesting inability to down-regulate emotional
lower emotion awareness scores in PSD patients are responses. Notably, dysregulated autonomic nervous
not fully explained by intelligence. Thus, low system (ANS) processes are relevant to numerous
emotion awareness may be distinct from primary forms of psychopathology (see, e.g., Wielgus,
deficits in intellectual function (van der Meer et al., Aldrich, Mezulis, & Crowell, 2016).
2009; van Rijn et al., 2011). Low emotion awareness
often presents in the early prodrome, so alexithymia Emotion Dysregulation and
scores may prove useful as vulnerability markers Cognitive Symptoms
(van Rijn et al., 2011, van der Velde, Swart, et al., General cognitive deficits are feature of PSDs, and
2015). Of note, one study reported higher alexithymia cognitive decline in the prodromal period of
as measured by behavioral paradigm in PSDs, but schizophrenia is common. Until the 1990s, cogni-
self-report measures indicated emotional awareness tive and emotional impairments were studied
to be equivalent among PSD patients and controls somewhat separately in PSDs, yet we know these
(Henry, Bailey, von Hippel, Rendell, & Lane, 2010). domains are linked (Ortony, Clore, & Collins,
Thus, PSD patients’ perception of their emotional 1990). For example, the circumplex model of
function may contrast with task-based studies. affect suggests that all emotional states and experi-
Affective symptoms in PSDs almost certainly ences across arousal (high/low) and valence (posi-
involve overlapping biological and environmental tive/negative) develop from cognitive interpretations
etiologic factors, some of which are transdiagnostic. of neural stimuli (Barrett & Russell, 1999; Posner
Broadly, polygenic risk for psychosis, major depressive et al., 2005). Similar conceptual frameworks,
disorder, and neuroticism overlap, and genome- which parse emotion facets and relate them to
wide polygenic risk for psychosis is associated with cognition, have greatly informed research on both
self-reported neuroticism, anxiety, smoking behaviors, schizotypy and schizophrenia (e.g., Kring, Barrett,
and depressive symptoms in healthy emerging & Gard, 2003).

Several specific emotion and cognition impair- paranormal beliefs). These symptoms, across PSDs,
ments in PSDs influence one another directly, and can include paranoia, odd perceptions and beliefs,
problems with social cognition, executive function, and suspiciousness.
and memory encoding may accentuate and contrib- In general, enhanced negative affect is associated
ute to emotion dysregulation problems. Although with stronger and more persistent psychotic
affective impairment is not associated consistently symptoms, and positive and negative emotions
with decreased performance on neurocognitive seem to largely control the content of psychotic ex-
tasks (Berenbaum et al., 2008b), emotion dysregu- periences (Freeman & Garety, 2003). Hallucination
lation appears closely related to poor social cogni- and delusion severity increases with poorer emo-
tion and functional outcomes (Penn, Sanna, & tional awareness in schizophrenia, including lower
Roberts, 2008; Tso, Grove, & Taylor, 2010). Deficits emotional clarity and greater attention to emotion
in social cognition and difficulties processing (Serper & Berenbaum, 2008; D’Antonio et al.,
complex social stimuli may intensify emotion re- 2015). Self-report measures of schizotypy symptoms,
sponses (Bigelow et al., 2006; Couture et al., 2006). including paranoid beliefs and suspiciousness,
Executive function is also impaired in most schiz- demonstrate positive associations with lower emo-
ophrenia patients, likely interfering with related tion clarity scores (Berenbaum et al., 2006). In
functions critical to evaluation and reappraisal of other words, PSD patients who focus more attention
negative emotions (John & Gross, 2007; Gyurak on their emotions and are less able to identify and
et al., 2009). Thus, enhanced negative emotionality understand their emotions are more likely to report
observed in schizophrenia and PSDs may result frequent and intense psychotic symptoms.
largely from executive function deficits. Moreover, Greater attention to emotion also predicts the
memory encoding impairments could account in extent to which emotionally valenced stimuli in-
part for both retrospective and anticipatory anhedo- fluence judgment (Gasper & Clore, 2000; Clore &
nia observed in some PSDs, offering an explanation Huntsinger, 2007). This suggests that patients who
for disjointed emotion experience across tense attend more to emotion may perceive stimuli as
(see Emotion Dysregulation and Affective Symptoms; more emotionally significant or threatening and
Strauss, 2013; Walsh-Messinger et al., 2014). Other have less tolerance to distress caused by stimuli.
complex cognitive sequelae may exist: individuals’ Physiologically, lower ANS regulation ability, a
noticeable cognitive and/or psychotic symptoms characteristic of emotionally dysregulated tempera-
may generate social stress or self-stigma, which ment, is associated with auditory hallucination (AH)
could in turn aggravate pre-existing emotion regula- severity ratings (Kimhy et al., 2016). Schizophrenia
tion issues (Birchwood et al., 2007). This section patients who have experienced AHs show higher
includes only a handful of associations of emotion limbic system activation in response to verbal
with cognitive symptoms in PSDs, but there are emotional stimuli than PSD patients who have
many (Posner, Russell, & Peterson, 2005; Anticevic never reported AHs, implying a connection of
& Corlett, 2012; Anticevic, Schleifer, & Youngsun, limbic system activity to psychotic symptoms
2015). Future studies that examine these relations (Escarti et al., 2010).
have the potential to propel PSD nosology forward Research on emotion regulation strategies in
and inform assessment and intervention. schizophrenia suggests an association between
heavier reliance on suppression and AHs (Badcock
Emotion Dysregulation and et al., 2011), possibly resulting from suppression-
Psychotic Symptoms induced increased ANS arousal. However, suppres-
Emotion dysregulation in PSDs may be related to sion does not appear to be associated with subse-
the magnitude and emergence of psychotic symp- quent paranoia (Westermann, Kesting, & Lincoln,
toms. Hallucinations involve aberrant perception of 2012) or delusions (Henry et al., 2008, Westermann
stimuli, whereas delusions are defined as strongly & Lincoln, 2011; Westermann, Rief, & Lincoln,
held beliefs that persist despite evidence of their 2014). Failures in cognitive reappraisal may increase
falsehood. These symptoms are present at sub- state paranoia (Westermann et al., 2012; Westermann
threshold levels in schizotypy and schizotypal per- et al., 2014). Depressive (ruminating) and anxious
sonality disorder: for example, individuals in these (worrying) thought processes about negative ex-
groups may experience subtle perceptual aberrations periences might provide the content of many
(e.g., shadows, fleeting visual experiences) or psychotic symptoms (Fowler et al., 2006; Startup,
magical thinking (e.g., subtle paranoid ideation, Freeman, & Garety, 2007). Excessive rumination

and worrying are associated with both risk for Criteria, 2016). Continued use of RDoC could help
(Jones & Fernyhough, 2009) and distress from clarify inconsistencies in the literature on PSD
AHs (Badcock et al., 2011) and delusions (Hartley, emotion impairments (Nusslock & Alloy, 2017). In
Haddock, Vasconcelos, Emsley, & Barrowclough, their current form, DSM-5 diagnostic criteria for
2014). distinguishing between PSDs are based largely in
Psychotic symptoms are also associated with different presentations and thresholds of cognitive
stress experiences and responses. Adverse life events and psychotic symptoms, whereas emotion abnor-
(ALEs) and stressors have known associations with malities tend to vary widely among patients across
psychotic symptom onset risk and severity (Garety PSD diagnoses. These symptoms are described
et al., 2001; Bentall et al., 2014; Valmaggia et al., loosely in the DSM, and emotion dysregulation is
2015; Hardy et al., 2016). ALEs also show links with not included in current symptom lists.
emotion dysregulation, and emotion dysregulation The new HiTOP initiative (Kotov et al., 2017)
may mediate stressful life event and trauma contri- has promise for addressing limitations in current
butions to psychotic symptoms (Laloyaux, Dessart, diagnostic criteria and research methods. HiTOP is
Van der Linden, Lemaire, & Laroi, 2016). Although a consortium of researchers and clinicians devoted
few studies have examined associations between to a data-driven reorganization of psychological
specific psychotic symptoms and emotion dysregu- symptom dimensions. HiTOP incorporates con-
lation, treatment approaches that target emotion tinuous measures of emotion, cognition, and per-
dysregulation and trauma processing may aid sonality. A more empirically derived system of
psychotic symptom management for PSD patients. diagnosis may further our knowledge of emotion
dysregulation in psychopathology and the accuracy
Research Methodologies and Frameworks and validity of psychiatric research.
To date, most studies on emotion (dys)regulation in In addition to introduction of new research
PSDs have employed case-control models in which frameworks, PSD emotion research will benefit
a small number of clinical participants are com- from varied research approaches. Experience sam-
pared with nonclinical controls in nonparametric pling techniques, via smartphone or electronic
statistical group comparisons. These statistical auditory recording device, may clarify inconsis-
models are often simple, given sample size limita- tencies in the literature by minimizing erroneous
tions and the need to maximize power. Although laboratory and retrospective self-report findings
case-control studies contribute groundbreaking in PSDs, since emotional reactions and responses
insights to the nature of schizophrenia signs and can vary across socio-environmental contexts
symptoms, they can neglect symptom dimensions (Myin-Germeys et al., 2009).
across the schizophrenia spectrum (e.g., Insel et al., In addition, ANS measures have recently
2010). The National Institute of Mental Health’s been used to evaluate emotion dysregulation in
recent Research Domain Criteria (RDoC) initiative psychiatric disorders and intervention develop-
(https://www.nimh.nih.gov/research-priorities/ ments (e.g., Skowron, Cipriano-Essel, Gatzke-
rdoc/index.shtml) and the Hierarchical Taxonomy Kopp, Teti, & Ammerman, 2014). Autonomic
of Psychopathology (HiTOP) initiative (Kotov measurements have only been used in a handful of
et al., 2017) encourage viewing psychological symp- sufficiently powered papers examining emotion
toms and traits dimensionally. Thus, consistent with regulation in PSDs but may benefit this research
the theme of this volume, emotion dysregulation is area, particularly if used to corroborate psycho-
not considered as unique to specific disorders (see metric, behavioral, self-report, genetic, and neu-
Beauchaine & Thayer, 2015). There is much overlap roimaging data. In genetic research, large-scale
of symptom dimensions across different psychiatric genome-wide association study cohorts and poly-
conditions. The RDoC framework includes five genic risk methods have improved assessment of
primary symptom domains and specifies research genetic liability to different symptom dimensions
constructs for each. Specific RDoC measures, such in PSDs (Kendler, 2015). There is preliminary
as those for positive and negative valence systems, evidence for enriched polygenic risk for emotion
are useful in standardizing research approaches regulation in overall genetic risk for these disor-
and data interpretations for complex affective and ders (van Os et al., 2017). Further polygenic
cognitive symptom dimensions (National analyses of emotion regulation and dysregulation
Advisory Mental Health Council Workgroup on constructs may improve our understanding of risk
Tasks and Measures for Research Domain for these symptoms.

Conclusions and Directions for Future events but struggled to describe them in detail.
Translational Research It remains unclear whether targeting skills rele-
Emotion dysregulation research is relatively new to vant to recall of positive emotional events can
the PSD literature. It represents a promising area of improve with practice and elicit clinically mean-
growth for research both specific to schizophrenia ingful change. Affective impairments that appear
and to psychopathology in general. Research to date early in the prodrome, including factors that
suggests that PSD patients use less adaptive emotion contribute to diminished emotion regulation abil-
regulation strategies than controls, and that emo- ities, may be effective vulnerability markers
tion dysregulation issues may influence PSD (van Rijn et al., 2011, van der Velde, Opmeer,
symptom dimensions, including affective impair- et al., 2015; van der Velde, Swart, et al., 2015). If
ments, cognitive deficits, and psychotic symptoms. assessed in early screenings, these risk indices have
Emotion regulation patterns in PSDs appear similar the potential to improve early diagnostic criteria,
to those observed in other mental health disorders, thereby improving outcomes with earlier, more
corroborating emotion regulation deficits and targeted interventions.
dysregulation as dimensional abnormalities across
psychopathologies. However, the specific nature of References
emotion dysregulation has been much better studied Abram, S. V., Karpouzian, T. M., Reilly, J. L., Derntl, B., Habel, U.,
in other disorders, and several unanswered questions & Smith, M. J. (2014). Accurate perception of negative
remain about relations between emotion dysregula- emotions predicts functional capacity in schizophrenia.
Psychiatry Research, 216, 6–11.
tion and the course and outcomes of PSDs. The
Addington, J., & Addington, D. (1998). Facial affect recognition
PSD literature also consists of numerous small and information processing in schizophrenia and bipolar
studies in which researchers have viewed these dis- disorder. Schizophrenia Research, 32(3), 171–181.
orders primarily through either cognitive or affective Addington, J., Penn, D., Woods, S. W., Addington, D., &
lenses, based on laboratory expertise. Integrative de- Perkins, D. O. (2008). Facial affect recognition in individuals
at clinical high risk for psychosis. British Journal of Psychiatry,
signs that investigate both cognition and affect will
192, 67–68.
explicate shared and distinct mechanisms for these Aghevli, M. A., Blanchard, J. J., & Horan, W. P. (2003). The
impairments (Anticevic & Corlett, 2012). expression and experience of emotion in schizophrenia: A
Focusing on emotion regulation and dysregulation study of social interactions. Psychiatry Research, 119, 261–270.
may have important implications for prevention Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
Emotion-regulation strategies across psychopathology:
and intervention science in PSDs. In addition to
A meta-analytic review. Clinical Psychology Review, 30,
traditional PSD treatment regimens, implementing 217–237.
therapies that target emotion regulation skills could Aleman, A., & Kahn, R. S. (2005). Strange feelings: Do
help PSD patients better manage their symptoms amygdala abnormalities dysregulate the emotional brain in
(van der Meer et al., 2009). Cognitive behavioral schizophrenia? Progress in Neurobiology, 77, 283–298.
Aleman, A., Kahn, R. S., & Selten, J. P. (2003). Sex differences
therapy (CBT) and dialectical behavior therapy
in the risk of schizophrenia: Evidence from meta-analysis.
(DBT) teach cognitive change skills to reduce Archives of General Psychiatry, 60, 565–571.
emotional avoidance and improve adaptive emotion American Psychiatric Association. (1952). Diagnostic and
regulation tactics. This may not only reduce patients’ statistical manual of mental disorders. Washington, DC:
emotion dysregulation but also reduce other symp- Author.
toms exacerbated by maladaptive emotion regulation
statistical manual of mental disorders (2nd ed.). Washington,
patterns. For example, CBT for psychosis adapts DC: Author.
traditional CBT principles to PSDs and shows American Psychiatric Association. (1980). Diagnostic and
promise for promoting mindfulness, increased statistical manual of mental disorders (3rd ed.). Washington,
emphasis on positive emotions, cognitive-change DC: Author.
strategies, and emotion acceptance (see Khoury &
statistical manual of mental disorders (4th ed.). Washington,
Lecomte, 2012). Given abnormal temporal dynamics DC: Author.
in positive emotionality, interventions that target American Psychiatric Association. (2013). Diagnostic and
recollection of emotional events may enhance statistical manual of mental disorders (5th ed.). Arlington,
emotion regulation and social function. For exam- VA: Author.
Anticevic, A., & Corlett, P. R. (2012). Cognition-emotion
ple, Gruber and King (2008) developed a narrative
dysinteraction in schizophrenia. Frontiers in Psychology,
assessment of emotional awareness that rates an in- 3, 392.
dividual’s ability to describe and recount emotional Anticevic, A., Schleifer, C., & Youngsun, T. C. (2015). Emotional
life events. PSD patients could recall emotional life and cognitive dysregulation in schizophrenia and depression:

Understanding common and distinct behavioral and neural Bodapati, A. S., & Herbener, E. S. (2014). The impact of social
mechanisms. Dialogues in Clinical Neuroscience, 17, 421–434. content and negative symptoms on affective ratings in
Badcock, J. C., Paulik, G., & Maybery, M. T. (2011). The role of schizophrenia. Psychiatry Research, 218, 25–30.
emotion regulation in auditory hallucinations. Psychiatry Brewer, W. J., Wood, S. J., Phillips, L. J., Francey, S. M.,
Research, 185, 303–308. Pantelis, C., Yung, A. R., . . . McGorry, P. D. (2006).
Barch, D. M. (2005). The relationships among cognition, Generalized and specific cognitive performance in
motivation, and emotion in schizophrenia: How much and clinical high-risk cohorts: A review highlighting potential
how little we know. Schizophrenia Bulletin, 31, 875–881. vulnerability markers for psychosis. Schizophrenia Bulletin,
Barch, D. M., Pagliaccio, D., & Luking, K. (2015). Mechanisms 32, 538–555.
underlying motivational deficits in psychopathology: Campbell-Sills, L., Barlow, D. H., Brown, T. A., & Hofmann,
Similarities and differences in depression and schizophrenia. S. G. (2006). Acceptability and suppression of negative
In E. H. Simpson & P. D. Balsam (Eds.), Behavioral emotion in anxiety and mood disorders. Emotion, 6, 587–595.
neuroscience of motivation (Vol. 27, pp. 411–449). Cham, Campellone, T. R., Elis, O., Mote, J., Sanchez, A. H., & Kring,
Switzerland: Springer International Publishing. A. M. (2016). Negative symptoms in psychometrically
Barrett, L. F., & Russell, J. A. (1999). The structure of current defined schizotypy: The role of depressive symptoms.
affect: Controversies and emerging consensus. Current Psychiatry Research, 240, 181–186.
Directions in Psychological Science, 8, 10–14. Chong, H. Y., Teoh, S. L., Wu, D. B., Kotirum, S., Chiou, C. F.,
Beauchaine, T. P. (2015). Future directions in emotion & Chaiyakunapruk, N. (2016). Global economic burden of
dysregulation and youth psychopathology. Journal of Clinical schizophrenia: A systematic review. Neuropsychiatric Disease
Child and Adolescent Psychology, 44, 875–896. and Treatment, 12, 357–373.
Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as Clore, G. L., & Huntsinger, J. R. (2007). How emotions inform
a transdiagnostic biomarker of psychopathology. International judgment and regulate thought. Trends in Cognitive Sciences,
Journal of Psychophysiology, 98, 338–350. 11, 393–399.
Benedetti, F., Radaelli, D., Poletti, S., Falini, A., Cavallaro, R., Cohen, A. S., & Minor, K. S. (2010). Emotional experience in
Dallaspezia, S., . . . Smeraldi, E. (2011). Emotional reactivity patients with schizophrenia revisited: Meta-analysis of
in chronic schizophrenia: Structural and functional brain laboratory studies. Schizophrenia Bulletin, 36, 143–150.
correlates and the influence of adverse childhood experiences. Couture, S. M., Penn, D. L., & Roberts, D. L. (2006). The
Psychological Medicine, 41, 509–519. functional significance of social cognition in schizophrenia:
Bentall, R. P., de Sousa, P., Varese, F., Wickham, S., Sitko, K., A review. Schizophrenia Bulletin, 32, S44–S63.
Haarmans, M., & Read, J. (2014). From adversity to D’Antonio, E., Kahn, J., McKelvey, J., Berenbaum, H., &
psychosis: Pathways and mechanisms from specific adversities Serper, M. R. (2015). Emotional awareness and delusions in
to specific symptoms. Social Psychiatry and Psychiatric schizophrenia and schizoaffective disorder. Comprehensive
Epidemiology, 49, 1011–1022. Psychiatry, 57, 106–111.
Berenbaum, H., Boden, M. T., Baker, J. P., Dizen, M., Thompson, Docherty, A. R., Moscati, A., Dick, D., Savage, J., Salvatore, J.,
R. J., & Abramowitz, A. (2006). Emotional correlates of the Cooke, M., . . . Kendler, K. S. (2017). Polygenic prediction of
different dimensions of schizotypal personality disorder. the phenome, across ancestry, in emerging adulthood.
Journal of Abnormal Psychology, 115, 359–368. Psychological Medicine, 48, 1814–1823.
Berenbaum, H., Kerns, J. G., Vernon, L. L., & Gomez, J. J. Edwards, J., Jackson, H. J., & Pattison, P. E. (2002). Emotion
(2008a). Cognitive correlates of schizophrenia signs and recognition via facial expression and affective prosody in
symptoms: I. Verbal communication disturbances. Psychiatry schizophrenia: A methodological review. Clinical Psychology
Research, 159, 147–156. Review, 22, 789–832.
Berenbaum, H., Kerns, J. G., Vernon, L. L., & Gomez, J. J. Ellgring, H., & Smith, M. (1998). Affect regulation during
(2008b). Cognitive correlates of schizophrenia signs and psychosis. In J. D. Flack & J. D. Laird (Eds.), Emotions in
symptoms: II. Emotional disturbances. Psychiatry Research, psychopathology: Theory and research (pp. 323–325). New
159, 157–162. York, NY: Oxford University Press.
Berenbaum, H., Kerns, J. G., Vernon, L. L., & Gomez, J. J. Escarti, M. J., de la Iglesia-Vaya, M., Marti-Bonmati, L., Robles,
(2008c). Cognitive correlates of schizophrenia signs and M., Carbonell, J., Lull, J. J., . . . Sanjuan, J. (2010). Increased
symptoms: III. Hallucinations and delusions. Psychiatry amygdala and parahippocampal gyrus activation in
Research, 159, 163–166. schizophrenic patients with auditory hallucinations: An
Berenbaum, H., & Oltmanns, T. F. (1992). Emotional experience fMRI study using independent component analysis.
and expression in schizophrenia and depression. Journal of Schizophrenia Research, 117, 31–41.
Abnormal Psychology, 101, 37–44. Foussias, G., & Remington, G. (2010). Negative symptoms in
Bigelow, N. O., Paradiso, S., Adolphs, R., Moser, D. J., Arndt, schizophrenia: Avolition and Occam’s razor. Schizophrenia
S., Heberlein, A., . . . Andreasen, N. C. (2006). Perception of Bulletin, 36, 359–369.
socially relevant stimuli in schizophrenia. Schizophrenia Fowler, D., Freeman, D., Steel, C., Hardy, A., Smith, B.,
Research, 83, 257–267. Hackman, C., . . . Bebbington, P. (2006). The catastrophic
Birchwood, M., Trower, P., Brunet, K., Gilbert, P., Iqbal, Z., & interaction hypothesis. In W. Larken & A. P. Morrison
Jackson, C. (2007). Social anxiety and the shame of (Eds.), Trauma and psychosis: New directions for theory and
psychosis: A study in first episode psychosis. Behaviour therapy. New York, NY: Taylor & Francis.
Research and Therapy, 45, 1025–1037. Freeman, D., & Garety, P. A. (2003). Connecting neurosis and
Bleuler, E. (1950). Dementia praecox or the group of schizophrenias psychosis: The direct influence of emotion on delusions
(J. Zinkin, trans.). Madison, CT: International Universities and hallucinations. Behaviour Research and Therapy, 41,
Press (Originally published, 1911). 923–947.

Frost, K. H., & Strauss, G. P. (2016). A review of anticipatory spontaneously and when instructed to suppress? Cognitive,
pleasure in schizophrenia. Current Behavioral Neuroscience Affective, and Behavioral Neuroscience, 9, 144–152.
Reports, 3, 232–247. Haralanova, E., Haralanov, S., Beraldi, A., Moller, H. J., &
Gard, D. E., Kring, A. M., Gard, M. G., Horan, W. P., & Hennig-Fast, K. (2012). Subjective emotional over-arousal to
Green, M. F. (2007). Anhedonia in schizophrenia: neutral social scenes in paranoid schizophrenia. European
Distinctions between anticipatory and consummatory Archives of Psychiatry and Clinical Neuroscience, 262, 59–68.
pleasure. Schizophrenia Research, 93, 253–260. Haralanova, E., Haralanov, S., & Shkodrova, D. (2007).
Garety, P. A., Kuipers, E., Fowler, D., Freeman, D., & Emotional dysregulation and psychotic-symptom formation
Bebbington, P. E. (2001). A cognitive model of the positive in paranoid schizophrenia. Bulgarian Neurological and
symptoms of psychosis. Psychological Medicine, 31, 189–195. Psychiatric Practice, 4, 13–16.
Gasper, K., & Clore, G. L. (2000). Do you have to pay attention Hardy, A., Emsley, R., Freeman, D., Bebbington, P., Garety,
to your feelings to be influenced by them? Personality and P. A., Kuipers, E. E., . . . Fowler, D. (2016). Psychological
Social Psychology Bulletin, 26, 698–711. mechanisms mediating effects between trauma and psychotic
Giuliani, N. R., Drabant, E. M., Bhatnagar, R., & Gross, J. J. symptoms: The role of affect regulation, intrusive trauma
(2011). Emotion regulation and brain plasticity: Expressive memory, beliefs, and depression. Schizophrenia Bulletin, 42,
suppression use predicts anterior insula volume. Neuroimage, S34–S43.
58, 10–15. Hartley, S., Haddock, G., Vasconcelos, E. S. D., Emsley, R., &
Giuliani, N. R., Drabant, E. M., & Gross, J. J. (2011). Anterior Barrowclough, C. (2014). An experience sampling study of
cingulate cortex volume and emotion regulation: Is bigger worry and rumination in psychosis. Psychological Medicine,
better? Biological Psychology, 86, 379–382. 44, 1605–1614.
Glenn, C. R., & Klonsky, D. (2009). Emotion dysregulation as Heinrichs, R. W., & Zakzanis, K. K. (1998). Neurocognitive
a core feature of borderline personality disorder. Journal of deficit in schizophrenia: A quantitative review of the
Personality Disorders, 23, 20–28. evidence. Neuropsychology, 12, 426–445.
Goldin, P. R., McRae, K., Ramel, W., & Gross, J. J. (2008). The Henry, J. D., Bailey, P. E., von Hippel, C., Rendell, P. G., &
neural bases of emotion regulation: Reappraisal and Lane, A. (2010). Alexithymia in schizophrenia. Journal of
suppression of negative emotion. Biological Psychiatry, 63, Clinical and Experimental Neuropsychology, 32, 890–897.
577–586. Henry, J. D., Green, M. J., de Lucia, A., Restuccia, C.,
Gottesman, I. I., & Gould, T. D. (2003). The endophenotype McDonald, S., & O’Donnell, M. (2007). Emotion
concept in psychiatry: Etymology and strategic intentions. dysregulation in schizophrenia: Reduced amplification of
American Journal of Psychiatry, 160, 636–645. emotional expression is associated with emotional blunting.
Green, M. F., Horan, W. P., & Lee, J. (2015). Social cognition in Schizophrenia Research, 95, 197–204.
schizophrenia. Nature Reviews Neuroscience, 16, 620–631. Henry, J. D., Green, M. J., Restuccia, C., de Lucia, A., Rendell,
Green, M. F., Kern, R. S., Braff, D. L., & Mintz, J. (2000). P. G., McDonald, S., & Grisham, J. R. (2009). Emotion
Neurocognitive deficits and functional outcome in dysregulation and schizotypy. Psychiatry Research, 166, 116–124.
schizophrenia: Are we measuring the “right stuff”? Henry, J. D., Rendell, P. G., Green, M. J., McDonald, S., &
Schizophrenia Bulletin, 26, 119–136. O’Donnell, M. (2008). Emotion regulation in schizophrenia:
Green, M. F., Olivier, B., Crawley, J. N., Penn, D. L., & Silverstein, Affective, social, and clinical correlates of suppression and
S. (2005). Social cognition in schizophrenia: Recommendations reappraisal. Journal of Abnormal Psychology, 117, 473–478.
from the measurement and treatment research to improve Herbener, E. S., Rosen, C., Khine, T., & Sweeney, J. A. (2007).
cognition in schizophrenia new approaches conference. Failure of positive but not negative emotional valence to
Schizophrenia Bulletin, 31, 882–887. enhance memory in schizophrenia. Journal of Abnormal
Gross, J. J. (1998). Antecedent- and response-focused emotion Psychology, 116, 43–55.
regulation: Divergent consequences for experience, Horan, W. P., Hajcak, G., Wynn, J. K., & Green, M. F. (2013).
expression, and physiology. Journal of Personality and Impaired emotion regulation in schizophrenia: Evidence
Social Psychology, 74, 224–237. from event-related potentials. Psychological Medicine, 43,
Gross, J. J. (2002). Emotion regulation: Affective, cognitive, and 2377–2391.
social consequences. Psychophysiology, 39, 281–291. Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D. S.,
Gross, J. J., & John, O. P. (2003). Individual differences in two Quinn, K., . . . Wang, P. (2010). Research domain criteria
emotion regulation processes: Implications for affect, (RDoC): Toward a new classification framework for research
relationships, and well-being. Journal of Personality and Social on mental disorders. American Journal of Psychiatry, 167,
Psychology, 85, 348–362. 748–751.
Gross, J. J., & Levenson, R. W. (1997). Hiding feelings: The Jablensky, A. V., & Kalaydjieva, L. V. (2003). Genetic
acute effects of inhibiting negative and positive emotion. epidemiology of schizophrenia: Phenotypes, risk factors, and
Journal of Abnormal Psychology, 106, 95–103. reproductive behavior. American Journal of Psychiatry, 160,
Gruber, J., & Kring, A. M. (2008). Narrating emotional events in 425–429.
schizophrenia. Journal of Abnormal Psychology, 117, 520–533. John, O. P., & Gross, J. J. (2007). Individual differences in
Gur, R. E., Kohler, C. G., Ragland, J. D., Siegel, S. J., Lesko, K., emotion regulation strategies: Links to global trait, dynamic,
Bilker, W. B., & Gur, R. C. (2006). Flat affect in schizophrenia: and social cognitive constructs. In J. J. Gross (Ed.),
Relation to emotion processing and neurocognitive measures. Handbook of emotion regulation (pp. 351–372). New York,
Schizophrenia Bulletin, 32, 279–287. NY: Guilford Press.
Gyurak, A., Goodkind, M. S., Madan, A., Kramer, J. H., Miller, Jones, S. R., & Fernyhough, C. (2009). Rumination, reflection,
B. L., & Levenson, R. W. (2009). Do tests of executive intrusive thoughts, and hallucination-proneness: Towards a
functioning predict ability to downregulate emotions new model. Behaviour Research and Therapy, 47, 54–59.

Kendler, K. S. (2015). A joint history of the nature of genetic Meyer, E. C., Carrion, R. E., Cornblatt, B. A., Addington, J.,
variation and the nature of schizophrenia. Molecular Cadenhead, K. S., Cannon, T. D., . . . NAPLS group. (2014).
Psychiatry, 20, 77–83. The relationship of neurocognition and negative symptoms
Khoury, B., & Lecomte, T. (2012). Emotion regulation and to social and role functioning over time in individuals at
schizophrenia. International Journal of Cognitive Therapy, 5, clinical high risk in the first phase of the North American
67–76. Prodrome Longitudinal Study. Schizophrenia Bulletin, 40,
Kim, K. R., Song, Y. Y., Park, J. Y., Lee, E. H., Lee, M., Lee, 1452–1461.
S. Y., .
.
.
Kwon, J. S. (2013). The relationship between Milev, P., Beng-Choon, H., Arndt, S., & Andreasen, N. C.
psychosocial functioning and resilience and negative symptoms (2005). Predictive values of neurocognition and negative
in individuals at ultra-high risk for psychosis. Australian and symptoms on functional outcome in schizophrenia: A
New Zealand Journal of Psychiatry, 47, 762–771. longitudinal first-episode study with 7-year follow-pp.
Kimhy, D., Gill, K. E., Brucato, G., Vakhrusheva, J., Arndt, L., American Journal of Psychiatry, 162, 495–506.
Gross, J. J., & Girgis, R. R. (2016). The impact of emotion Moran, E. K., Culbreth, A. J., & Barch, D. M. (2017). Emotion
awareness and regulation on social functioning in individuals regulation predicts everyday emotion experience and social
at clinical high risk for psychosis. Psychological Medicine, 46, function in schizophrenia. Clinical Psychological Science, 6,
2907–2918. 271–279.
Kimhy, D., Vakhrusheva, J., Jobson-Ahmed, L., Tarrier, N., Mueser, K. T., Penn, D. L., Blanchard, J. J., & Bellack, A. S.
Malaspina, D., & Gross, J. J. (2012). Emotion awareness and (1997). Affect recognition in schizophrenia: A synthesis of
regulation in individuals with schizophrenia: Implications findings across three studies. Psychiatry, 60, 301–308.
for social functioning. Psychiatry Research, 200, 193–201. Myin-Germeys, I., Krabbendam, L., Delespaul, P. A., & Van Os,
Kohler, C. G., Walker, J. B., Martin, E. A., Healey, K. M., & J. (2003). Do life events have their effect on psychosis by
Moberg, P. J. (2010). Facial emotion perception in influencing the emotional reactivity to daily life stress?
schizophrenia: A meta-analytic review. Schizophrenia Psychological Medicine, 33, 327–333.
Bulletin, 36, 1009–1019. Myin-Germeys, I., Oorschot, M., Collip, D., Lataster, J.,
Kotov, R., Krueger, R. F., Watson, D., Achenbach, T. M., Althoff, Delespaul, P., & van Os, J. (2009). Experience sampling
R. R., Bagby, R. M., .
.
.Zimmerman, M. (2017). The research in psychopathology: Opening the black box of daily
Hierarchical Taxonomy of Psychopathology (HiTOP): A life. Psychological Medicine, 39, 1533–1547.
dimensional alternative to traditional nosologies. Journal of National Advisory Mental Health Council Workgroup on Tasks
Abnormal Psychology, 126, 454–477. and Measures for Research Domain Criteria. (2016).
Kring, A. M., Barrett, L. F., & Gard, D. E. (2003). On the broad Behavioral assessment methods for RDoC constructs. Bethesda,
applicability of the affective circumplex: Representations of MD: National Institute of Mental Health.
affective knowledge among schizophrenia patients. Psychological Nelson, B., Yuen, K., & Yung, A. R. (2011). Ultra high risk
Science, 14, 207–214. (UHR) for psychosis criteria: Are there different levels of
Kring, A. M., & Caponigro, J. M. (2010). Emotion in risk for transition to psychosis? Schizophrenia Research, 125,
schizophrenia: Where feeling meets thinking. Current 62–68.
Directions in Psychological Science, 19, 255–259. Nolen-Hoeksema, S. (2000). The role of rumination in
Kring, A. M., & Elis, O. (2013). Emotion deficits in people depressive disorders and mixed anxiety/depressive symptoms.
with schizophrenia. Annual Review of Clinical Psychology, Journal of Abnormal Psychology, 109, 504–511.
9, 409–433. Nusslock, R., & Alloy, L. B. (2017). Reward processing and
Kring, A. M., & Moran, E. K. (2008). Emotional response mood-related symptoms: An RDoC and translational
deficits in schizophrenia: Insights from affective science. neuroscience perspective. Journal of Affective Disorders,
Schizophrenia Bulletin, 34, 819–834. 216, 3–16.
Kring, A. M., & Werner, K. (2004). Emotion regulation and O’Driscoll, C., Laing, J., & Mason, O. (2014). Cognitive
psychopathology. In P. Philippot & R. S. Feldman (Eds.), emotion regulation strategies, alexithymia and dissociation
The regulation of emotion (pp. 359–385). New York, NY: in schizophrenia: A review and meta-analysis. Clinical
Lawrence Erlbaum Associates. Psychology Review, 34, 482–495.
Laloyaux, J., Dessart, G., Van der Linden, M., Lemaire, M., & Ortony, A., Clore, G. L., & Collins, A. (1990). The cognitive
Laroi, F. (2016). Maladaptive emotion regulation strategies structure of emotions. Cambridge, UK: Cambridge University
and stress sensitivity mediate the relation between adverse Press.
life events and attenuated positive psychotic symptoms. Pantelis, C., & Maruff, P. (2002). The cognitive neuropsychiatric
Cognitive Neuropsychiatry, 21, 116–129. approach to investigating the neurobiology of schizophrenia
Livingstone, K., Harper, S., & Gillanders, D. (2009). An and other disorders. Journal of Psychosomatic Research, 53,
exploration of emotion regulation in psychosis. Clinical 655–664.
Psychology and Psychotherapy, 16, 418–430. Parker, J. D. A., Taylor, G. J., & Bagby, R. M. (2001). The
Llerena, K., Strauss, G. P., & Cohen, A. S. (2012). Looking at the relationship between emotional intelligence and alexithymia.
other side of the coin: A meta-analysis of self-reported Personality and Individual Differences, 30, 107–115.
emotional arousal in people with schizophrenia. Schizophrenia Penn, D. L., Sanna, L. J., & Roberts, D. L. (2008). Social
Research, 142, 65–70. cognition in schizophrenia: An overview. Schizophrenia
Lopez, A. D., Mathers, C. D., Ezzati, M., Jamison, D. T., & Bulletin, 34, 408–411.
Murray, C. J. (2006). Global and regional burden of disease Perry, Y., Henry, J. D., & Grisham, J. R. (2011). The habitual use
and risk factors, 2001: Systematic analysis of population of emotion regulation strategies in schizophrenia. British
health data. Lancet, 367, 1747–1757. Journal of Clinical Psychology, 50, 217–222.

Phillips, M. L., Drevets, W. C., Rauch, S. L., & Lane, R. (2003a). Startup, H., Freeman, D., & Garety, P. A. (2007). Persecutory
Neurobiology of emotion perception I: The neural basis of delusions and catastrophic worry in psychosis: Developing
normal emotion perception. Biological Psychiatry, 54, 504–514. the understanding of delusion distress and persistence.
Phillips, M. L., Drevets, W. C., Rauch, S. L., & Lane, R. Behaviour Research and Therapy, 45, 523–537.
(2003b). Neurobiology of emotion perception II: Strauss, G. P. (2013). The emotion paradox of anhedonia in
Implications for major psychiatric disorders. Biological schizophrenia: Or is it? Schizophrenia Bulletin, 39, 247–250.
Psychiatry, 54, 515–528. Strauss, G. P., & Gold, J. M. (2012). A new perspective on
Piskulic, D., Addington, J., Cadenhead, K. S., Cannon, T. D., anhedonia in schizophrenia. American Journal of Psychiatry,
Cornblatt, B. A., Heinssen, R., . . . McGlashan, T. H. (2012). 169, 364–373.
Negative symptoms in individuals at clinical high risk of Strauss, G. P., Jetha, S. S., Ross, S. A., Duke, L. A., & Allen,
psychosis. Psychiatry Research, 196, 220–224. D. N. (2010). Impaired facial affect labeling and
Posner, J., Russell, J. A., & Peterson, B. S. (2005). The circumplex discrimination in patients with deficit syndrome
model of affect: An integrative approach to affective schizophrenia. Schizophrenia Research, 118, 146–153.
neuroscience, cognitive development, and psychopathology. Strauss, G. P., Kappenman, E. S., Culbreth, A. J., Catalano,
Developmental Psychopathology, 17, 715–734. L. T., Lee, B. G., & Gold, J. M. (2013). Emotion regulation
Purcell, S. M., Wray, N. R., Stone, J. L., Visscher, P. M., abnormalities in schizophrenia: Cognitive change strategies
O’Donovan, M. C., Sullivan, P. F., . . . Moran, J. L. (2009). fail to decrease the neural response to unpleasant stimuli.
Common polygenic variation contributes to risk of Schizophrenia Bulletin, 39, 872–883.
schizophrenia and bipolar disorder. Nature, 460, 748–752. Taylor, S. F., & Liberzon, I. (2007). Neural correlates of emotion
Read, J., van Os, J., Morrison, A. P., & Ross, C. A. (2005). regulation in psychopathology. Trends in Cognitive Science,
Childhood trauma, psychosis and schizophrenia: A literature 11, 413–418.
review with theoretical and clinical implications. Acta Thompson, R. A. (1990). Emotion and self-regulation. In
Psychiatrica Scandinavica, 112, 330–350. R. A. Thompson (Ed.), Nebraska symposium on motivation:
Reddy, L. F., Horan, W. P., & Green, M. F. (2015). Motivational Socioemotional development (Vol. 36, pp. 367–469). Lincoln,
deficits and negative symptoms in schizophrenia: Concepts NE: University of Nebraska Press.
and assessments. In E. H. Simpson & P. D. Balsam (Eds.), Thompson, R. A. (1994). Emotion regulation: A theme in search
Behavioral neuroscience of motivation (Vol. 27, pp. 357–373). of definition. Monographs of the Society for Research in Child
Cham, Switzerland: Springer International Publishing. Development, 59, 25–52.
Regier, D. A., Narrow, W. E., Rae, D. S., Manderscheid, R. W., Tso, I. F., Grove, T. B., & Taylor, S. F. (2010). Emotional
Locke, B. Z., & Goodwin, F. K. (1993). The de facto mental experience predicts social adjustment independent of
and addictive disorders service system. Epidemiologic neurocognition and social cognition in schizophrenia.
Catchment Area prospective 1-year prevalence rates of disorders Schizophrenia Research, 122, 156–163.
and services. Archives of General Psychiatry, 50, 85–94. Turetsky, B. I., Kohler, C. G., Indersmitten, T., Bhati, M. T.,
Ripke, S., Neale, B. M., Corvin, A., Walters, J. T. R., Farh, Charbonnier, D., & Gur, R. C. (2007). Facial emotion
K. H., Holmans, P. A., . . . O’Donovan, M. C. (2014). recognition in schizophrenia: When and why does it go
Biological insights from 108 schizophrenia-associated genetic awry? Schizophrenia Research, 94, 253–263.
loci. Nature, 511, 421–427. Valmaggia, L. R., Day, F., Garety, P., Freeman, D., Antley, A.,
Robinson, M. D., & Clore, G. L. (2002). Belief and feeling: Slater, M., . . . McGuire, P. (2015). Social defeat predicts
Evidence for an accessibility model of emotional self-report. paranoid appraisals in people at high risk for psychosis.
Psychological Bulletin, 128, 934–960. Schizophrenia Research, 168, 16–22.
Schlosser, D. A., Campellone, T. R., Biagianti, B., Delucchi, van der Gaag, M. (2006). A neuropsychiatric model of
K. L., Gard, D. E., Fulford, D., . . . Vinogradov, S. (2015). biological and psychological processes in the remission of
Modeling the role of negative symptoms in determining delusions and auditory hallucinations. Schizophrenia
social functioning in individuals at clinical high risk of Bulletin, 32, S113–S122.
psychosis. Schizophrenia Research, 169, 204–208. van der Meer, L., van’t Wout, M., & Aleman, A. (2009). Emotion
Serper, M., & Berenbaum, H. (2008). The relation between regulation strategies in patients with schizophrenia. Psychiatry
emotional awareness and hallucinations and delusions in Research, 170, 108–113.
acute psychiatric inpatients. Schizophrenia Research, 101, van der Velde, J., Opmeer, E. M., Liemburg, E. J., Bruggeman,
195–200. R., Nieboer, R., Wunderink, L., & Aleman, A. (2015).
Sitskoom, M. M., Aleman, A., Ebisch, S. J. H., Appels, Lower prefrontal activation during emotion regulation in
M. C. M., & Kahn, R. S. (2004). Cognitive deficits in subjects at ultrahigh risk for psychosis: An fMRI-study.
relatives of patients with schizophrenia: A meta-analysis. NPJ Schizophrenia, 1, 15026.
Schizophrenia Research, 71, 285–295. van der Velde, J., Swart, M., van Rijn, S., van der Meer, L.,
Skowron, E. A., Cipriano-Essel, E., Gatzke-Kopp, L. M., Teti, Wunderink, L., Wiersma, D., . . . Aleman, A. (2015).
D. M., & Ammerman, R. T. (2014). Early adversity, RSA, Cognitive alexithymia is associated with the degree of risk for
and inhibitory control: Evidence of children’s neurobiological psychosis. PLoS One, 10, e0124803.
sensitivity to social context. Developmental Psychobiology, 56, van Os, J., van der Steen, Y., Islam, M. A., Guloksuz, S., Rutten,
964–978. B. P., Simons, C. J., & GROUP Investigators. (2017).
Snitz, B. E., Macdonald, A. W., 3rd, & Carter, C. S. (2006). Evidence that polygenic risk for psychotic disorder is
Cognitive deficits in unaffected first-degree relatives of expressed in the domain of neurodevelopment, emotion
schizophrenia patients: A meta-analytic review of putative regulation and attribution of salience. Psychological Medicine,
endophenotypes. Schizophrenia Bulletin, 32, 179–194. 47, 2421–2437.

van Rijn, S., Aleman, A., Swaab, H., & Kahn, R. S. (2005). populations: A review and integrated model of cognitive
Neurobiology of emotion and high risk for schizophrenia: mechanisms. Schizophrenia Bulletin, 38, 683–692.
Role of the amygdala and the X-chromosome. Neuroscience Westermann, S., Kesting, M. L., & Lincoln, T. M. (2012). Being
and Biobehavioral Reviews, 29, 385–397. deluded after being excluded? How emotion regulation
van Rijn, S., Schothorst, P., van’t Wout, M., Sprong, M., deficits in paranoia-prone individuals affect state paranoia
Ziermans, T., van Engeland, H., .
.
.
Swaab, H. (2011). during experimentally induced social stress. Behavior Therapy,
Affective dysfunctions in adolescents at risk for psychosis: 43, 329–340.
Emotion awareness and social functioning. Psychiatry Westermann, S., & Lincoln, T. M. (2011). Emotion regulation
Research, 187, 100–105. difficulties are relevant to persecutory ideation. Psychological
Vos, T., Barber, R. M., Bell, B., Bertozzi-Villa, A., Bollinger, Psychotherapy, 84, 273–287.
B. S., Charlson, F., . . . Global Burden of Disease Study 2013 Westermann, S., Rief, W., & Lincoln, T. M. (2014). Emotion
Collaborators. (2013). Global, regional, and national regulation in delusion-proneness: Deficits in cognitive
incidence, prevalence, and years lived with disability for 301 reappraisal, but not in expressive suppression. Psychology and
acute and chronic diseases and injuries in 188 countries, Psychotherapy, 87, 1–14.
1990–2013: A systematic analysis for the global burden of Wielgus, M. D., Aldrich, J. T., Mezulis, A. H., & Crowell, S. E.
disease study. Lancet, 386, 743–800. (2016). Respiratory sinus arrhythmia as a predictor of self-
Walsh-Messinger, J., Ramirez, P. M., Wong, P., Antonius, D., injurious thoughts and behaviors among adolescents.
Aujero, N., McMahon, K., .
.
.
Malaspina, D. (2014). International Journal of Psychophysiology, 106, 127–134.
Impairment in emotional modulation of attention and memory Yuii, K., Suzuki, M., & Kurachi, M. (2007). Stress sensitization
in schizophrenia. Schizophrenia Research, 157, 63–69. in schizophrenia. In P. Csermely, T. Korcsmaros, & K. Sulyok
Waters, F., Allen, P., Aleman, A., Fernyhough, C., Woodward, (Eds.), Stress responses in biology and medicine: Stress of life in
T. S., Badcock, J. C., .
.
.
Laroi, F. (2012). Auditory molecules, cells, organisms, and psychosocial communities (Vol.
hallucinations in schizophrenia and nonschizophrenia 1113, pp. 276–290). Oxford, UK: Blackwell Publishing.

CH A PTE R
22 Emotion Dysregulation in Addiction
Eric L. Garland, Spencer Bell, Rachel M. Atchley, and Brett Froeliger
Abstract
Several decades of scientific research provide strong evidence that individuals who suffer from e motion
dysregulation, such as that observed in depression and anxiety, are more vulnerable to addictive
behavior. Furthermore, a growing body of studies indicates that chronic use of addictive substances
dysregulates emotional responding. Emerging research also suggests that recurrent drug use and addiction
are associated with deficits in the capacity to proactively regulate negative and positive emotions. This
chapter synthesizes evidence from clinical and neuroscientific studies on effects of addictive behavior
(including misuse of prescription opioids, addiction to cigarettes, and addiction to more powerful
stimulants) on emotion dysregulation to outline an integrative model of emotion dysregulation in
addiction. This model has implications for treatment development and further scientific investigation.
Keywords: emotion regulation, emotion dysregulation, addiction, opioids, stimulants
Introduction These forms of emotion dysregulation are e vident

For millennia, humans have consumed psychoactive in three of the most common forms of addictive be-
substances to alleviate emotional distress. The ancient havior: addiction to prescription opioids, cigarettes,
Greeks used opium to relieve dysphoria (Dormandy, and more powerful stimulants including cocaine
2012). In The Odyssey, Homer referred to such use in and methamphetamine. Prescription opioid misuse
the following passage: has reached epidemic levels in the United States,
largely stemming from ubiquitous use of opioid an-
Into the bowl in which their wine was mixed, she
algesics for chronic pain despite known health risks
slipped a drug that had the power of robbing grief
including overdose, dependence, and addiction
and anger of their sting and banishing all painful
(Chou et al., 2015). Misuse of prescription opioids
memories. No one who swallowed this dissolved in
has increased more than threefold over the past 20
their wine could shed a single tear that day, even for
years (Hall et al., 2008). It is estimated that more
the death of his mother or father.
than two million Americans are dependent on pre-
Indeed, squelching of negative emotions is often scription opioids (Saha et al., 2016), and approxi-
a driver of addictive behavior, insofar as individuals mately 25% of chronic pain patients misuse opioids
attempt to alleviate intense negative emotional (Vowles et al. 2015). Similarly, cigarette addiction is
states through substance use. A sizable body of clin- extremely prevalent and despite decades of inter-
ical and preclinical research indicates that recurrent vention efforts remains the leading preventable
use of many classes of addictive substances is asso- cause of death and disability in the United States
ciated with dysregulated emotional responding. (Centers for Disease Control, 2002). The effects of
Emerging research also suggests that chronic drug cigarette smoking on health expenditures and
use and addiction are associated with impaired abil- associated lost work productivity cost nearly $200
ity to proactively regulate emotions. billion each year (Roger et al., 2011). Costs of cocaine
313
and methamphetamine use include cardiovascular Howard, 2016; Goesling et al., 2015; Smith et al.,
disease and other major health consequences, 2015; Edlund et al., 2015; Scherrer, Salas, Lustman,
long-lasting impairment in neural systems that gen- Burge, & Schneider, 2015; Goldner, Lusted,
erate positive affect, incarceration, and crime (e.g., Roerecke, Rehm, & Fischer, 2014; Scherrer et al.,
Chang, Alicata, Ernst, & Volkow, 2007; Enns et al., 2014; Gros, Milanak, Brady, & Back, 2013; Merrill
2017). Given the high prevalence rates of and public et al., 2012; Grattan, Sullivan, Saunders, Campbell,
health effects of opioid, cigarette, and stimulant & Von Korff, 2012; Hooten, Shi, Gazelka, &
addiction, we synthesize evidence from extant stud- Warner, 2011; Fatséas et al., 20109). Early preva-
ies of these drugs and present an integrative model lence estimates indicated that 45% of individuals
of emotion dysregulation in addiction—one that with prescription opioid use disorders met full
yields tractable targets for future research and treat- Diagnostic and Statistical Manual of Mental Disorders,
ment efforts. fourth edition (DSM-IV) criteria for a depressive
or anxiety disorder (Sullivan, Edlund, Steffick, &
Dysregulated Emotions Increase Unutzer, 2005). A more recent survey of over
Vulnerability to Addictive Behavior 26,000 respondents indicated that approximately
Substance use is negatively reinforcing through 80% of individuals who engage in nonmedical use
temporary alleviation of distressing emotions of prescription opioids experience depression and
(Baker, Piper, McCarthy, Majeskie, & Fiore, 2004). anxiety (Green, Black, Grimes Serrano, Budman, &
Such down-regulation of negative affect may increase Butler, 2011). Notably, however, opioids themselves
risk of addictive behavior. An early articulation of have depressive effects, so without longitudinal data
this notion was outlined in the self-medication that include direct assessment of opioid use as a
hypothesis, which posits that individuals with dis- means of self-medication, it is difficult to discern
positional impairments in their capacity to regulate whether dependence and nonmedical use of opi-
psychological distress may be prone to relieve that oids are causes, correlates, or consequences of nega-
distress through substance use (Khantzian, 1997). tive affect.
The self-medication hypothesis posits that specific In the largest longitudinal investigation of this
forms of psychopathology are associated with topic to date, analysis of data from over 34,000
specific forms of drug use, matched according to the adult participants in Waves 1 and 2 of the National
pharmacologic profile of the psychoactive agent and Epidemiologic Survey on Alcohol and Related
putative receptor systems implicated in the disorder. Conditions (NESARC) revealed that baseline mood
Although such specificity lacks empirical support and anxiety disorders predicted the incidence of
(Lembke, 2012), numerous studies support the gen- nonmedical opioid use and opioid dependence sev-
eral notion that individuals use drugs to alleviate eral years later (Martins et al., 2012). These results
negative affect. In fact, onset of affective disorders converge with findings from a sample of prescrip-
often predicts later substance abuse and dependence tion opioid–dependent individuals in acute detoxi-
(e.g., Bolton, Robinson, & Sareen, 2009; Leeies, fication and long-term outpatient treatment, 94%
Pagura, Sareen, & Bolton, 2010; Robinson, Sareen, of whom reported frequent misuse of opioids to
Cox, & Bolton, 2011). This relation may be relieve negative affect (Garland, Hanley, Thomas,
explained in part by allostatic load models of
Knoll, & Ferraro, 2015). In a study of 115 chronic
addiction, which suggest that individuals compul- prescription opioid users, depressed mood was
sively seek and consume drugs to allay dysphoric associated with opioid craving, mediated by thought
mood states stemming from withdrawal and asso- suppression, indicating that attempts to suppress
ciated dysregulation of stress and reward circuitry in distressing and intrusive thoughts may lead to in-
the brain (see the section Drug Use Dysregulates creased craving among opioid users with depressive
Emotional Responding; Koob & Le Moal, symptoms (Garland, Brown, & Howard, 2016).
2001, 2008). These findings parallel research demonstrating that
maladaptive cognitive coping (e.g., catastrophizing)
Evidence from Studies of is associated with opioid misuse (Martel, Wasan,
Prescription Opioids Jamison, & Edwards, 2013) and opioid craving
Studies also demonstrate correspondence between (Martel, Jamison, Wasan, & Edwards, 2014) among
prescription opioid dependence and depression and patients with chronic pain, and that opioid craving
anxiety symptoms (Sullivan, 2016; Mayor, 2016; mediates associations between negative affect and
Scherrer et al., 2016; Arteta, Cobos, Hu, Jordan, & opioid misuse among pain patients (Martel, Dolman,
314 Emotion Dysregul ation in Addiction

Edwards, Jamison, & Wasan, 2014). Thus, above and exacerbate pre-existing dysregulated affective
and beyond motivation to obtain pain relief, indi- processes. In laboratory models of stress-related

viduals may experience an addictive propensity lapse behavior, stress leads abstinent smokers to
toward opioids when they attempt to suppress nega- reinitiate smoking sooner, take more puffs, and

tive mental states via opioid use. increase puff volume (McKee et al., 2011). Finally,
34% of individuals report that stress and negative
Evidence from Studies of Smoking affect are the primary triggers for smoking lapses
Although 20% of US adults without psychiatric (Shiffman et al., 1996, 1997). Stress- or negative
disorders smoke cigarettes (US Health and Human affect–induced smoking lapses are clinically mean-
Services, 2010), 41% of those with a psychiatric dis- ingful, since lapses among smokers who are at-
order do so (Lasser et al., 2000). Furthermore, tempting to quit predict full-blown relapse (see
smokers with affective disorders transition more McKee, 2009, for a review).
quickly to nicotine dependence (Khaled, Bulloch,
Williams, Lavorato, & Patten, 2011), report greater Neurocircuitry of Reward and
negative affect while abstaining from smoking Self-Regulation
(Kahler, Brown, Strong, Lloyd-Richardson, & Before discussing how drug use dysregulates emo-
Niaura, 2003), and are more likely to relapse fol- tional responding and proactive regulation of emo-
lowing attempts to quit (Glassman, 1993). Even tions, it is useful to consider how the neurocircuitry
among people who do not meet full criteria for a of reward relates to brain circuits of self-regulation.
psychiatric disorder, smoking and negative emo- Although different drugs of abuse initially bind to
tional processes are intertwined. Many smokers different receptors (e.g., nicotine binds to nicotinic
smoke in the face of negative affect and/or stress acetylcholine receptors, opiates bind to μ-opioid
(Shiffman & Waters, 2004), and many report that receptors, cocaine binds to dopamine transporter
smoking alleviates negative affect (Shiffman & receptors), they all modulate dopaminergic neuro-
Waters, 2004; Spielberger, 1986). A study among transmission in the mesocorticolimbic reward path-
nonsmoking adolescents found that self-reported way, which projects from the ventral tegmental area
difficulties with emotion regulation were associated (VTA) to the nucleus accumbens, as well as to various
with higher expectancies of social and affective regions of the prefrontal cortex (PFC) and amyg-
benefits of smoking (Dir, Banks, Zapolski, dala, to reinforce future drug use, leading to gluta-
McIntyre, & Hulvershorn, 2016). Thus, even sub- matergic neuroplasticity in cortico-limbic-striatal
clinical emotion dysregulation may increase risk for circuitry when drug use recurs over time (Kalivas
initiating smoking. and Volkow, 2005). Within this circuit, a number
It is also clear that smoking cessation increases of functional distinctions have been identified
negative affect (Parrott, Garnham, Wesnes, & (Haber & Knutson, 2010): (1) the striatum codes
Pincock, 1996) and exacerbates unpleasant mood for salience of incentives, (2) the dorsolateral pre-
states including anxiety, depression, and irritability frontal cortex helps modulate striatal responses to
(American Psychiatric Association [APA], 2000; incentives, (3) the orbitofrontal cortex (OFC)
Baker et al., 2004). These negative affective states interacts with the striatum to encode immediate
emerge soon after smoking ceases (Hendricks, versus distal reward outcomes, and (4) the amygdala
Ditre, Drobes, & Brandon, 2006) and can persist communicates with striatal brain regions through
for one month or longer (Gilbert et al., 1999; the bed nucleus of the stria terminalis to integrate
Gilbert et al., 2002). Cigarette addiction–related contextual information about rewards and punish-
disturbances in affective processes (APA, 2000; ments to adjust motivation levels.
Baker et al., 2004) that fail to resolve within a In contexts of addiction, compulsive
month of quitting (Gilbert et al., 2002) are most self-administration of drugs is mediated by dysregu-
pronounced among individuals with depressed lated neural communication within cortico-limbic-
affect (Gilbert et al., 1999) and contribute to main- striatal circuitry—including between regions in-
tenance of smoking (Shiffman, 2005). Additionally, volved in executive function and valuation of reward
elevated symptoms of depression prior to cessa- (e.g., PFC, OFC, anterior cingulate cortex [ACC]),
tion increase susceptibility to abstinence-induced negative reinforcement (e.g., striatum, amygdala),
increases in negative affect (Gilbert, McClernon, and reward processing (e.g., striatum, OFC)
et al., 2004). Taken together, these findings suggest (Goldstein & Volkow, 2002; Kalivas & Volkow,
that abstinence may potentiate negative affect 2005). Outside contexts of addiction, human
Garl and, Bell, Atchley, and Froeliger 315

neuroimaging research implicates these same with healthy controls, those who currently or
cortico-limbic-striatal circuits in basic self-regulation previously used opioids exhibit blunted emotional
and reward functions: regulation of both positive responses to positive stimuli relative to neutral stim-
and negative emotions depends on reciprocal com- uli (Arcos et al., 2008). Those who previously mis-
munication within a corticolimbic network (PFC/ used opioids also exhibit blunted parasympathetic
ACC and amygdala/insula; Kanske et al., 2011; nervous system (high-frequency heart rate variabil-
Ochsner & Gross, 2005), whereas regulation of ity [HRV]) responses to positive emotional stimuli,
adaptive goal-directed behavior and reward processing and less positive affect in general, compared to those
is mediated by neural communication in the cortico- who take opioids as prescribed (Garland, Bryan,
striatal network (PFC, ACC, striatum; S. H. Kim & Nakamura, Howard, & Froeliger, 2017). In this
Hamann, 2007; Mak, Hu, Zhang, Xiao, & Lee, study, the relation between opioid misuse and crav-
2009). Imbalances in either of these networks may ing was mediated by low positive affect in response
result in deficits in the ability to self-regulate nega- to viewing positive images, suggesting that opioid
tive affect and positive affect associated with reward misusers crave opioids when they experience
responding (Heatherton & Wagner, 2011). anhedonic responses to naturally rewarding stimuli.
This finding supports allostatic models (Shurman
Drug Use Dysregulates Emotional et al., 2010; Garland, Froeliger, Zeidan, Partin, &
Responding Howard, 2013; Elman & Borsook, 2016) that sug-
Chronic exposure to drugs is associated with dys- gest that opioid misuse leads to insensitivity to natural
regulation of neurobiological systems that subserve rewards, which in turn impels craving for opioids as
reward, emotional experience, and self-regulation a means of obtaining hedonic equilibrium.
(e.g., Volkow, Koob, & McLellan, 2016). Functional In another study (Garland, Froeliger, & Howard,
disruption of these systems can promote addiction, 2015b), opioid-treated chronic pain patients com-
relapse, and loss of control over substance use. pleted a dot probe task in which negative emotional
Neuroplastic alterations to the extended amygdala (pain-related) and positive emotional (natural reward)
and striatal circuitry induce allostatically mediated images were paired with neutral images and then
sensitization to emotional distress (Shurman, Koob, replaced by a target probe to which participants
& Gutstein, 2010) and insensitivity to reward, responded. During this task, HRV was assessed.
resulting in reduced hedonic capacity and dysphoria Prescription opioid misusers showed blunted HRV
(Koob & Le Moal, 2008). This allostatic shift in responses during attention to both negative and
reward sensitivity may then drive increased con- positive emotional stimuli relative to individuals
sumption of psychoactive substances as a means of who took opioids as prescribed—an autonomic
achieving hedonic equilibrium (Koob, 2015). The response difference that was most pronounced for
attempt to maintain hedonic homeostasis exacts a positive emotional stimuli. Consistent with this
cost: chronic substance use renders the individual finding, the non-misuser group exhibited an atten-
increasingly insensitive to positive affect from natu- tional bias to positive emotional stimuli, whereas
rally rewarding experiences yet increasingly sensitive the misuser group showed no such bias. Taken
to aversive states, including stress and negative emo- together, these findings suggest that chronic pain
tions (Koob & Le Moal, 2008). Thus, allostatic load patients who misuse prescription opioids exhibit
incurred from chronic drug use promotes neuroad- reward-processing deficits relative to chronic pain
aptations to drug effects and modulates sensitiza- patients who take opioids as prescribed. Although
tion to rewards and punishment, resulting in preclinical studies demonstrate effects of chronic
heightened negative affective responses and blunted pain on brain reward systems that parallel the
positive affective responses. These findings have clinical observation that chronic pain is accompa-
direct implications for emotion dysregulation. nied by anhedonia and loss of motivation to obtain
reward (Becker, Gandhi, & Schweinhardt, 2012),
Evidence of Dysregulated Emotional findings from Garland, Froeliger, et al. (2015)
Responding from Studies of Opioids suggest that prescription opioid misuse is associated
An emerging literature demonstrates reward dys- with reward deficits over and above those imbued
function and affect dysregulation among individuals by chronic pain.
who exhibit opioid misuse and addiction (Younger Prescription opioid–dependent patients who are in
et al., 2011; Bunce et al., 2015; Garland, Froeliger, & treatment (Huhn et al., 2016), compared with healthy
Howard, 2015a; Borsook et al., 2016). Compared controls, report more anhedonia and reduced positive

affective responses to positive emotional stimuli to positive emotional cues (Versace et al., 2014),
during affect-modulated startle. As measured by func- anticipating monetary rewards (Sweitzer et al.,
tional near-infrared spectroscopy, opioid-dependent 2016), and responding to a reward outcome (Wilson
patients also exhibit reduced neural activation in et al., 2014) all predict smoking lapses/relapses.
rostral and ventral PFC regions in response to food Nicotine addiction is also associated with
images, and reduced left ventrolateral PFC activa- heightened reactivity to negative emotional stimuli.
tion in response to images depicting positive social Greater emotional reactivity to physiological stress-
situations relative to controls. ors, for example, predicts poorer outcomes among
Such dysregulated emotional responding among smokers who are attempting to quit (Zvolensky,
opioid users may stem from long-term pharmaco- Feldner, Eifert, & Brown, 2001). Nicotine with-
logical effects of opioids on reward circuitry. In drawal is also associated with heightened emotional
support of this notion, a longitudinal neuroimaging reactivity, as evidenced by potentiated startle
study of opioid-naïve chronic pain patients who ini- responses to negative emotional pictures among

tiated a one-month course of opioid therapy found smokers in a state of abstinence compared to satiety
volumetric decreases in gray matter of the amygdala (Engelmann, Gewirtz, & Cuthbert, 2011). Functional
and orbitofrontal cortex from pre- to posttreatment magnetic resonance imaging (fMRI) studies show
via tensor-based morphometry that were main- that abstinent versus sated smokers exhibit greater
tained approximately six months after cessation of blood oxygen level–dependent (BOLD) responses
opioid administration (Younger et al., 2011). Given to negative emotional stimuli in the lateral PFC and
the role that the amygdala and orbitofrontal cortex dorsal ACC (Froeliger, Modlin, Kozink, Wang, &
play in reward processing, such neuropathology McClernon, 2012). Among abstinent smokers,
may be associated with the hedonic deficits ob- acute nicotine administration, compared to placebo,
served in this population. reduces BOLD responding in the lateral PFC during
Evidence is also emerging that prescription viewing of negative emotional images (Froeliger
opioid addiction is associated with heightened neg- et al., 2012). Nicotine administration in abstinent
ative emotional responding. Current opioid users smokers also reduces the magnitude of electrophys-
exhibit heightened emotional responses to negative iological correlates of negative emotional interfer-
stimuli compared to both abstinent users and ence on ongoing and subsequent attention processes,
healthy controls (Arcos et al., 2008). A study of suggesting that nicotine can reverse disruptions in
prescription opioid–dependent subjects identified attentional processing resulting from negative emo-
heightened subjective stress responses to the Trier tional stimuli (Gilbert et al., 2007).
Social Stress Test relative to healthy controls, and
increases in stress-related physiology were associated Addiction Impairs Volitional
with opioid cue-elicited physiological responses in a Regulation of Emotion
subsequently presented cue-reactivity paradigm Most central to the theme of this volume, addiction
(Back et al., 2015). Similarly, in a study of opioid- impairs volitional regulation of emotion. Substantial
treated chronic pain patients involving experimen- neuroscience research indicates that volitional emo-
tal pain induction via quantitative sensory testing, tion regulation occurs through interactions between
McHugh et al. (2016) found that opioid misuse was top-down cortical neural systems (e.g., dorsolateral
associated with inability to manage and regulate PFC, dorsal ACC, ventromedial PFC, ventrolateral
negative emotional states (distress intolerance), PFC) and bottom-up subcortical neural systems
which in turn was associated with increased anxiety (e.g., amygdala, striatum; ; S. H. Kim & Hamann,
and stress during psychophysical pain testing. 2007). Those with strong volitional emotion regula-
tion efficiently recruit frontal regions to downregu-
Evidence of Dysregulated Emotional late subcortically generated affect—a skill in which
Responding from Studies of Cigarettes those with poor emotion regulation are less profi-
Similar to opioid misusers, deficits in reward proc- cient at (see Beauchaine, 2015; Beauchaine &
essing are evident among smokers. Neuroimaging Zisner, 2017). Top-down engagement of emotion
research reveals that, compared to nonsmokers, regulatory processes to modulate bottom-up affec-
smokers exhibit blunted neural response in the tive impulses dampens effects of strong emotions on
striatum relative to non-drug-related reinforcers cognitive performance and goal attainment
(e.g., food cues; Jastreboff et al., 2015). Among (S. H. Kim & Hamann, 2007; Ochsner & Gross,
smokers, the magnitude of blunted striatal responses 2005;). In contrast, emotion dysregulation often

ensues when emotional experience and expression Fredrickson, 2015) and positive rumination
become dominated by bottom-up processes, or (Quoidback et al., 2010). Such deficiencies may
when cortical-subcortical connectivity is compro- stem from hypofrontality (blunted PFC activation)
mised (Heatherton & Wagner, 2011). or deficient frontostriatal connectivity, which medi-
During processing of affective experiences and ates motivation, reward seeking, and drug use
cues, individuals who suffer from addiction exhibit (Froeliger et al., 2015; Froeliger, McConnel, et al.,
hypoactivation in prefrontal circuitry (Asensio 2017). Decreased capacity of frontal executive sys-
et al., 2010; Diggs, Froeliger, Carlson, & Gilbert, tems to upregulate responses in the ventral striatum
2013; Froeliger et al., 2012; Sinha et al., 2005). to naturally rewarding stimuli may result in anhe-
Regardless of whether such functional deficits are donia characteristic of addiction (Garfield, Lubman,
due to pre-existing impairments that confer vulner- & Yuucel, 2014). Although considerable research
ability to addiction or reflect neuropathology of the links anhedonia to deficits in incentive processes
PFC resulting from acute exposure to drugs, indi- (e.g., Beauchaine & Zisner, 2017), there is a dearth
viduals with substance use disorders may be unable of direct research investigating effects of addictive
to effectively regulate negative affect when con- behavior on neural mechanisms that subserve posi-
fronted with stressful or negative emotional stimuli. tive emotion and its regulation. With respect to
Interestingly, emerging research indicates that sub- opioid, nicotine, and stimulant addiction specifi-
stance use itself impairs PFC function prospectively, cally, few studies have examined volitional emotion
and that structural abnormalities in the dorsolateral regulation. However, both direct and indirect evi-
PFC and OFC predict future substance use prob- dence support this notion, as outlined in the next
lems (e.g., Bava, Jacobus, Thayer, & Tapert, 2013; three sectinos.
Brumback, Castro, Jacobus, & Tapert., 2016).
Unlike healthy individuals who often regulate Evidence of Deficient Emotion Regulation
negative affect through proactive processes such as from Studies of Opioids
reappraisal, individuals with substance use disor- Recently, in a study of chronic pain patients who
ders are prone to engage in suppression of un- received extended opioid therapy, misusers evi-
wanted emotions and distressing thoughts (Moss denced deficits in performance on an emotion regu-
et al., 2015). When individuals with substance use lation task compared to patients who took opioids
disorders engage in suppression, the pendulum of as prescribed, as indicated by attenuated autonomic
prefrontal regulation swings from undercontrol regulation during reappraisal of negative emotional
to overcontrol, whereby attempts to suppress dys- stimuli and savoring of positive emotional stimuli
phoric emotion paradoxically lead to hyperaccessi- (Garland et al., 2017). Moreover, opioid dose was
bility of unwanted mental experiences, increasing associated inversely with positive emotion regula-
their frequency and intensity (Wegner & Erber, tion, such that patients who took comparatively
1992; Wegner, Schneider, Carter, & White, 1987; higher opioid doses were less able to proactively
Wenzlaff & Wegner, 2000). Neuroimaging research increase positive affect via savoring positive images
demonstrates that, unlike reappraisal of negative than patients who took low doses. Opioid-misusing
emotion, which involves heightened prefrontal re- chronic pain patients also report decreased reap-
sponding coupled with reduced amygdala activity praisal capacity relative to patients who take opioids
(Goldin, McRae, Ramel, & Gross, 2008), suppres- as prescribed (Garland et al., 2017), and reduced re-
sion slows deployment of prefrontal regulatory appraisal is associated with increased opioid craving.
resources (Goldin et al., 2008) and concurrently Opioid misusers further report favoring suppression
exacerbates amygdala reactivity to negative emo- over reappraisal as a means of emotion regulation
tional information (Vanderhasselt et al., 2013). (Mohajerin, Dolatshahi, Shahbaz, & Farhoudian,
Thus, although hypoactivation in prefrontal circuits 2013).
may result in inability to effectively downregulate
emotional responses, excessive and ill-timed hyper- Evidence of Deficient Emotion Regulation
activation during suppression of negative emotions from Studies of Smoking
can backfire and exacerbate emotion intensity. Attentional bias models of nicotine addiction (e.g.,
Moreover, those who suffer from addictive Gilbert, 1995) posit that nicotine reduces negative
disorders exhibit impairments in the ability to voli- affect by shifting attention away from negative
tionally upregulate positive emotions via strategies affect–provoking stimuli via nicotine-induced
such as savoring (see Garland, Farb, Goldin, & increases in frontally mediated top-down regulation

of emotion. Electroencephalography (Gilbert, Sugai, whereas frequent suppression predicts earlier smoking
et al., 2004) and fMRI (Froeliger, Modlin, Kozink, initiation (Magar, Phillips, & Hosie, 2008) and
Wang, & McClernon, 2012) studies provide sup- number of years smoking (Fucito, Juliano, & Toll,
port for this model by showing that PFC responses 2010). Greater tendencies among smokers to
to negative stimuli are disrupted during nicotine engage in suppression are correlated with greater
withdrawal. Across a series of fMRI studies, smokers attentional interference when presented with smok-
compared to nonsmokers exhibit dysregulated BOLD ing cues, whereas greater tendencies to implement
responding in prefrontal cognitive control circuitry reappraisal are associated with less cigarette con-
during affective processing (Diggs et al., 2013; sumption, less depression, and less expectation of
Froeliger et al., 2013), and withdrawal engenders negative reinforcement from smoking (Fucito et al.,
further disruption in prefrontally mediated neuro- 2010). When brief instructions are given to smokers
cognition (Froeliger, Beckham, Dennis, Kozink, & to reappraise as opposed to suppress, smoking
McClernon, 2012; Froeliger, Modlin, Wang, behavior and craving are reduced (Beadman et al.,
Kozink, & McClernon, 2012; Froeliger, Modlin, 2015), which is accompanied by decreases in dorsal
Kozink, et al., 2012; Kozink, Lutz, Rose, Froeliger, ACC activation (Zhao et al., 2012). This suggests
& McClernon, 2010). Moreover, magnitudes of that enhancing prefrontally mediated reappraisal
dysregulated BOLD responding (i.e., hyperre- strategies may present a viable avenue for treatment
sponding) in the PFC while sated smokers perform development. Overall, more research is needed
inhibitory control tasks predict both how soon they regarding neural mechanisms underlying relations
smoke ad lib in the laboratory and who goes on to between nicotine addiction, emotion regulation,
relapse in 10 weeks following a smoking cessation and specific regulatory strategies.
attempt (Froeliger et al., 2017).
With regard to emotion regulation, smokers Effects of Cocaine and Methamphetamine
report lower ability to regulate negative emotion on Emotion Dysregulation
than nonsmokers (Lyvers, Carlopio, Bothma, & Use of stimulants such as cocaine and methamphet-
Edwards, 2014). Consistent with use of nicotine to amine is also associated with altered emotional
self-medicate affect dysregulation (Gehricke et al., reactivity and dysregulation of negative emotions.
2007), high expectancies that smoking will reduce For example, Potenza et al. (2012) found that nega-
negative affect are related to increased smoking be- tive affect–inducing stimuli produced heightened
havior (Schleicher, Harris, Catley, & Nazir, 2009) corticolimbic reactivity among females with cocaine
and reduced anxiety following smoking (Juliano & use disorder relative to controls. Other studies indi-
Brandon, 2002). This suggests that nicotine is used cate hypoactivation in the dorsal ACC when c ocaine
by some individuals to promote/enhance volitional users process negative emotion (Sinha et al., 2005).
emotion regulation. Self-reported difficulties with Blunted electrocortical responses to negative and
emotion regulation mediate relations between nega- positive emotional cues are also observed among
tive affect and motivation to relieve negative affect cocaine users relative to healthy controls (Dunning
through smoking (Johnson & McLeish, 2016). et al., 2011), suggesting that cocaine use is associated
Moreover, among smokers with a psychiatric disor- with reduced affective reactivity.
der, difficulties with emotion regulation mediate In addition, Decker, Morie, Hunkele, Babuscio,
relation between symptoms and motivation to
and Carroll (2016) found that addiction severity
smoke for relief of negative affect (Short, Oglesby, among cocaine addicts was associated inversely with
Raines, Zvolensky, & Schmidt, 2015; Yang, use of reappraisal, whereas reappraisal use was
Zvolensky, & Leyro, 2017). Difficulties with emo- associated positively with lifetime months of

tion regulation among smokers also relate to greater cocaine abstinence. Cocaine-dependent individuals
perceived barriers to quitting (Gonzalez, Zvolensky, also report deficits in understanding and regulating
Vujanovic, Leyro, & Marshall, 2008), and smokers emotions when newly abstinent (Fox, Axelrod,
who experience emotion regulation difficulties Paliwal, Sleeper, & Sinha, 2007).
relapse sooner following attempts to quit (Farris, Studies that use performance-based measures
Zvolensky, & Schmidt, 2016). also show deficits in proactive regulation of emo-
Emotion dysregulation among smokers may tions among cocaine users. Albein-Urios and col-
manifest in a bias toward suppressive as opposed to leagues (2014) examined neural substrates of negative
reappraisal strategies. Individuals who report greater emotion regulation in cocaine-dependent individu-
reappraisal tendencies are less likely to be smokers, als using fMRI. Participants completed a reappraisal

task, in which they were instructed to observe, in emotion regulation compared to healthy controls.
maintain, or suppress their emotional reactions Whether or not such affective liabilities antedate or
(via reappraisal) while viewing neutral or negative are subsequent to onset of stimulant use disorders
images. Interaction seed-based analyses indicated is not yet clear. However, emotion regulation style
decreased functional coupling between the inferior predicts risk for onset of substance misuse. For
frontal gyrus and amygdala among cocaine depen- example, individuals who habitually use adaptive
dents relative to healthy controls during reappraisal, emotion regulation strategies such as reappraisal
suggesting that cocaine dependence is associated with show later age of initiation of stimulant use and
inability to engage top-down regulation of limbic fewer days of recent stimulant use than individuals
brain regions during negative emotional processing. who primarily rely on maladaptive forms of emo-
Altered emotional reactivity and processing are tion regulation such as suppression (Wong et al.,
also observed among methamphetamine addicts. 2013). Thus, as in opioid and nicotine addiction,
Methamphetamine users report heightened reac- relations between stimulant use and emotion dys-
tivity to negative emotions relative to controls regulation are likely bidirectional.
(Uhlmann et al., 2016). Differences in emotion
processing–related brain activation are also observed. Conclusion
Deactivation of the bilateral dorsolateral PFC and Taken together, findings from studies of opioid,
insula, paired with increased activation in the fusi- cocaine, and methamphetamine users, as well as
form gyrus, hippocampus, parahippocampal gyrus, smokers, suggest that addiction is closely linked
and posterior cingulate cortex, is observed in meth- with emotion dysregulation. Broadly speaking,
amphetamine users when they view negative emo- this linkage is evident in several domains. Initially,
tional images (Y. T. Kim et al., 2011). These patterns dysregulated emotional responses appear to foster
of hypoactivation and functional impairment rela- addictive behavior potentially as a means of coping
tive to controls suggest that emotion regulation is with heightened stress or blunted affect. Individuals
compromised in methamphetamine users when with a pre-existing propensity toward emotional
they process images that provoke fear and empathy. distress are more likely to engage in substance use,
Emotion dysregulation experienced by people perhaps due to shared neural vulnerabilities to affec-
who are dependent on methamphetamines may tive, impulse control, and substance use disorders.
be related to altered D2-type dopamine receptor When people chronically use substances to alleviate
signaling in the amygdala, a primary brain region negative emotions, such palliative coping may
involved in emotional processing ( Okita et al., strengthen addiction by means of negative rein-
2016). As further evidence for deficits in emotional forcement conditioning (Baker et al., 2004), result-
processing in this population, methamphetamine ing in continued substance use. Chronic use of
users exhibit difficulty understanding and verbalizing psychoactive substances may in turn further dys-
their emotions, a problem known as alexithymia, regulate emotional responding by allostatic/neuro-
which is associated with deactivation of the ventral plastic mechanisms, which rewire synaptic connec-
inferior frontal gyrus and increased aggression (Payer, tions (Koob & Le Moal, 2001, 2008). These
Lieberman, & London, 2011). neuroplastic changes underpin increased sensitivity
Research on proactive emotion regulation among to negative affect and blunted positive affective
methamphetamine users is sparse. Uhlmann and responding to natural reinforcers, resulting in

colleagues (2016) investigated cortical thickness as reward deficits that propel consummatory behavior
an indicator of emotion dysregulation issues in par- and dose escalation as a means of obtaining hedonic
ticipants who were dependent on methamphet- equilibrium. Finally, protracted substance use and
amines, as well as those with methamphetamine- addiction are presaged by and exacerbate deficits in
associated psychosis. Methamphetamine-dependent volitional emotion regulation, as manifested in a re-
participants with psychosis had thinner cortices in a duced ability to downregulate negative emotional
number of brain regions, including the fusiform responses using strategies such as reappraisal, and
gyrus, the inferior temporal gyrus, the OFC, the upregulate positive emotional responses using strat-
inferior frontal gyrus, the insula, and the hippocam- egies such as savoring. These emotion regulation
pus. Moreover, cortical thickness in some of these impairments may stem from attenuated prefrontal
brain areas was associated with difficulties in emotion activation or attenuated functional connectivity
regulation. However, methamphetamine users both between bottom-up, subcortical emotion generation
with and without psychosis reported impairments systems and top-down, cortical emotion regulation

systems. Regardless of their neural generators under review), autonomic (Garland et al., 2014),
and irrespective of whether or not such emotion electrocortical (Garland, Froeliger, & Howard, 2015),
regulation deficits are antecedent to or conse- and functional neural measures (Froeliger et al.,
quences of substance use disorders, reduced capac- 2017). Beyond stand-alone interventions, treatment
ity to regulate emotions sustains and exacerbates packages that combine behavioral, pharmacologi-
addiction, increasing dependence on substances cal, cognitive remediation, and brain stimulation
as a means of alleviating dysphoria and anxious therapies may be especially efficacious means of
arousal. regulating the dysphoria, anxiety, negative affec-
Although the outlines of a model of the role of tive reactivity, and anhedonia characteristic of
emotion dysregulation in addiction are emerging, addiction.
many unanswered questions remain. First, whether In conclusion, addiction may be conceptualized
emotion dysregulation is a cause, correlate, or con- as a set of hedonic dysregulatory processes through
sequence of addictive behavior remains largely which emotional responding is reorganized from
unknown. Longitudinal human studies in both
valuation of natural rewards to valuation of drug
laboratories and environments of adaptation are rewards. Over time, the reward value obtained from
needed to ascertain temporal dynamics of emotion both natural reinforcers and addictive drugs plum-
dysregulation among individuals who develop sub- mets, resulting in a deficit of positive affectivity.
stance use disorders. Studies involving fine-grained Concomitantly, drug-induced stress sensitization
ecological momentary assessments may be well exacerbates negative affective reactions that are
suited to conducting functional analyses of time- further magnified by an increasing inability to con-
lagged and cross-lagged relations between dysregu- sciously and proactively decrease negative emotions
lated emotional reactions, proactive attempts to reg- and increase positive emotions. As chronic exposure
ulate emotions, and substance use and craving. to psychoactive substances disrupts brain systems
With regard to effects on emotion dysregulation, it implicated in cognitive control, stress, and reward
is not yet known the extent to which the neuropsy- processing, the consequent inability to regulate the
chopharmacologic mechanisms of acute drug expo- emotional balance of rewarding and aversive experi-
sure can be disentangled from chronic changes that ences results in an overall hedonic deficit that drives
occur during addiction. Chronification of emotion a downward spiral of behavioral escalation toward
regulation deficits observed in contexts of full- compulsive drug use.
blown addiction may be distinct from transitory
forms of emotion dysregulation induced by acute Acknowledgments
pharmacological modulation of cortical and subcor- This work was supported by grant numbers R01DA042033 and
R61AT009296 from the National Institutes of Health awarded
tical circuits (as well as their autonomic, visceral,
to E.L.G, R01DA033459 and R01DA038700 awarded to B.F.,
and peripheral efferents). Furthermore, just as there and support from T32DA07288 to S.B.
are differential effects of various substances on emo-
tional responding (e.g., sedatives-hypnotics reduce
stress arousal, whereas stimulants increase arousal),
Conflict of Interest
The authors have no conflicts of interest to disclose.
different classes of drugs may exert different effects
on volitional emotion regulation and cause specific
forms of emotion regulatory deficits. Finally, research References
Albein-Urios, N., Verdejo-Román, J., Asensio, S., Soriano-Mas,
should identify therapies to ameliorate emotion C., Martínez-González, J. M., & Verdejo-García, A. (2014).
dysregulation in addiction. One promising therapy, Re-appraisal of negative emotions in cocaine dependence:
Mindfulness-Oriented Recovery Enhancement Dysfunctional corticolimbic activation and connectivity.
(MORE), targets emotion regulation deficits in ad- Addiction Biology, 19(3), 415–426.
diction through combined training in mindfulness,
statistical manual of mental disorders (4th ed., text revision).
reappraisal, and savoring. MORE decreases nega- Washington, DC: Author.
tive affective reactivity and stress arousal (Garland, Arcos, F. A., Verdejo-García, A., Ceverino, A., Montañez-Pareja,
Froeliger, & Howard, 2014; Garland, Roberts- M., López-Juárez, E., Sánchez-Barrera, M., . . . PEPSA Team.
Lewis, Tronnier, Kelley, & Graves, 2016), increases (2008). Dysregulation of emotional response in current and
abstinent heroin users: Negative heightening and positive
positive affective responses (Garland et al., 2016;
blunting. Psychopharmacology, 198, 159–166.
Garland et al., 2017), enhances reappraisal (Garland Arteta, J., Cobos, B., Hu, Y., Jordan, K., & Howard, K. (2016).
et al., 2014; Li, Garland, & Howard, 2018), and Evaluation of how depression and anxiety mediate the
increases savoring across self-report (Thomas et al., relationship between pain catastrophizing and prescription

opioid misuse in a chronic pain population. Pain Medicine, systematic review for a National Institutes of Health
17, 295–303. Pathways to Prevention Workshop. Annals of Internal
Asensio, S., Romero, M. J., Palau, C., Sanchez, A., Senabre, I., Medicine, 162, 276–286.
Morales, J. L., .
.
.
Romero, F. J. (2010). Altered neural Decker, S. E, Morie, K., Hunkele, K., Babuscio, T., & Carroll,
response of the appetitive emotional system in cocaine K. M. (2016). Emotion regulation strategies in individuals
addiction: An fMRI Study. Addiction Biology, 15, 504–516. with cocaine use disorder maintained on methadone.
Back, S. E., Gros, D., Price, M., LaRowe, S., Flanagan, J., Brady, American Journal on Addictions, 25, 529–532.
K., . . . McCauley, J. (2015). Laboratory-induced stress and Diggs, H., Froeliger, B., Carlson, J. M., & Gilbert, D. G. (2013).
craving among individuals with prescription opioid Smoker-nonsmoker differences in neural response to
dependence. Drug and Alcohol Dependence, 155, 60–67. smoking-related and affective cues: An fMRI investigation.
Baker, T. B., Piper, M. E., McCarthy, D. E., Majeskie, M. R., & Psychiatry Research: Neuroimaging, 211, 85–87.
Fiore, M. C. (2004). Addiction motivation reformulated: An Dir, A. L., Banks, D. E., Zapolski, T. C. B., McIntyre, E., &
affective processing model of negative reinforcement. Hulvershorn, L. A. (2016). Negative urgency and emotion
Psychological Review, 111, 33–51. regulation predict positive smoking expectancies in non-
Bava, S., Jacobus, J., Thayer, R. E., & Tapert, S. F. (2013). smoking youth. Addictive Behavior, 58, 47–52.
Longitudinal changes in white matter integrity among Dormandy, T. (2012). Opium: Reality’s dark dream. New Haven,
adolescent substance users. Alcoholism: Clinical and CT: Yale University Press.
Experimental Research, 37(s1). Dunning, J. P., Parvaz, M. A., Hajcak, G., Maloney, T., Alia-
Beadman, M., Das, R. K., Freeman, T. P., Scragg, P., West, R., & Klein, N., Woicik, P. A., . . . Goldstein, R. Z. (2011).
Kamboj, S. K. (2015). A comparison of emotion regulation Motivated attention to cocaine and emotional cues in
strategies in response to craving cognitions: Effects on abstinent and current cocaine users—An ERP study.
smoking behaviour, craving and affect in dependent smokers. European Journal of Neuroscience, 33, 1716–1723.
Behavior Research and Therapy, 69, 29–39. Edlund, M. J., Forman-Hoffman, V., Winder, C., Heller, D.,
Beauchaine, T. P. (2015). “Respiratory sinus arrhythmia: A Kroutil, L., Lipari, R., & Colpe, L. (2015). Opioid abuse and
transdiagnostic biomarker of emotion dysregulation and depression in adolescents: Results from the National Survey
psychopathology.” Current Opinion in Psychology 3, 43–47. on Drug Use and Health. Drug and Alcohol Dependence, 152,
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion 131–138.
regulation, and the latent structure of psychopathology: an Elman, I., & Borsook, D. (2016). Common brain mechanisms of
integrative and convergent historical perspective. chronic pain and addiction. Neuron, 89, 11–36.
International Journal of Psychophysiology, 119, 108–118. Engelmann, J. M., Gewirtz, J. C., & Cuthbert, B. N. (2011).
Becker, S., Gandhi, W., & Schweinhardt, P. (2012). Cerebral Emotional reactivity to emotional and smoking cues during
interactions of pain and reward and their relevance for smoking abstinence: Potentiated startle and P300
chronic pain. Neuroscience Letters, 520, 182–187. suppression. Psychophysiology, 48, 1656–1668.
Bolton, J. M., Robinson, J., & Sareen, J. (2009). Self-medication Enns, B., Krebs, E., DeBeck, K., Hayashi, K., Milloy, M.-J.,
of mood disorders with alcohol and drugs in the National Richardson, L., . . . Nosyk, B. (2017). The costs of crime
Epidemiologic Survey on Alcohol and Related Conditions. associated with stimulant use in a Canadian setting. Drug
Journal of Affective Disorders, 115, 367–375. and Alcohol Dependence, 180, 304–310.
Borsook, D., Linnman, C., Faria, V., Strassman, A. M., Becerra, L., Farris, S. G., Zvolensky, M. J., & Schmidt, N. B. (2016).
& Elman, I. (2016). Reward deficiency and anti-reward in Difficulties with emotion regulation and psychopathology
pain chronification. Neuroscience and Biobehavioral Reviews, interact to predict early smoking cessation lapse. Cognitive
68, 282–297. Therapy and Research, 40, 357–367.
Brumback, T., Castro, N., Jacobus, J., & Tapert, S. (2016). Fatséas, M., Denis, C., Lavie, E., & Auriacombe, M. (2010).
Effects of marijuana use on brain structure and function: Relationship between anxiety disorders and opiate
Neuroimaging findings from a neurodevelopmental dependence—A systematic review of the literature. Journal of
perspective. In International review of neurobiology (Vol. 129, Substance Abuse Treatment, 38, 220–230.
pp. 33–65). Academic Press. Fox, H. C., Axelrod, S. R., Paliwal, P., Sleeper, J., & Sinha, R.
Bunce, S. C., Harris, J. D., Bixler, E. O., Taylor, M., Muelly, E., (2007). Difficulties in emotion regulation and impulse
Deneke, E., . . . Meyer, R. E. (2015). Possible evidence for re- control during cocaine abstinence. Drug and Alcohol
regulation of HPA axis and brain reward systems over time in Dependence, 89, 298–301.
treatment in prescription opioid-dependent patients. Journal Froeliger, B., Beckham, J. C., Dennis, M. F., Kozink, R. V., &
of Addiction Medicine, 9, 53–60. McClernon, F. J. (2012). Effects of nicotine on emotional
Centers for Disease Control. (2002). Annual smoking- reactivity in PTSD and non-PTSD smokers: Results of a
attributable mortality, years of potential life lost, and pilot fMRI study. Advances in Pharmacological Sciences, 2012,
productivity losses—United States, 1995–1999. Morbidity 265724.
and Mortality Weekly Report, 51, 300–313. Froeliger, B., Mathew, A. R., McConnell, P. A., Eichberg, C.,
Chang, L., Alicata, D., Ernst, T., & Volkow, N. (2007). Saladin, M. E., Carpenter, M. J., & Garland, E. L. (2017).
Structural and metabolic brain changes in the striatum Restructuring reward mechanisms in nicotine addiction: A
associated with methamphetamine abuse. Addiction, 102, pilot fMRI study of mindfulness-oriented recovery
16–32. doi:10.1111/j.1360-0443.2006.01782.x enhancement for cigarette smokers. Evidence-Based
Chou, R., Turner, J. A., Devine, E. B., Hansen, R. N., Sullivan, Complementary and Alternative Medicine, 2017, 7018014.
S. D., Blazina, I., . . . Deyo, R. A. (2015). The effectiveness Froeliger, B., McConnell, P. A., Bell, S., Sweitzer, M., Kozink,
and risks of long-term opioid therapy for chronic pain: A R. V., Eichberg, C., . . . McClernon, F. J. (2017). Association

between baseline corticothalamic-mediated inhibitory prescription opioid misuse, and addiction: Cognitive,
control and smoking relapse vulnerability. JAMA Psychiatry, affective, and neuro-psychopharmacologic pathways.
74, 379–386. Neuroscience and Biobehavioral Reviews, 37, 2597–2607.
Froeliger, B., McConnell, P. A., Stankeviciute, N., McClure, Garland, E. L., Hanley, A. W., Thomas, E. A., Knoll, P., &
E. A., Kalivas, P. W., & Gray, K. M. (2015). The effects of Ferraro, J. (2015). Low dispositional mindfulness predicts
N-Acetylcysteine on frontostriatal resting-state functional self-medication of negative emotion with prescription
connectivity, withdrawal symptoms and smoking abstinence: opioids. Journal of Addiction Medicine, 9, 61–67.
A double-blind, placebo-controlled fMRI pilot study. Drug Garland, E. L., Manusov, E. G., Froeliger, B., Kelly, A., Williams,
and Alcohol Dependence, 156, 234–242. J. M., & Howard, M. O. (2014). Mindfulness-oriented
Froeliger, B., Modlin, L. A., Kozink, R. V., Wang, L., Garland, recovery enhancement for chronic pain and prescription
E. L., Addicott, M. A., & McClernon, F. J. (2013). opioid misuse: Results from an early-stage randomized
Frontoparietal attentional network activation differs between controlled trial. Journal of Consulting and Clinical Psychology,
smokers and nonsmokers during affective cognition. 82, 448–459.
Psychiatry Research, 211, 57–63. Garland, E. L., Roberts-Lewis, A., Tronnier, C. D., Graves, R., &
Froeliger, B., Modlin, L. A., Kozink, R. V., Wang, L., & Kelley, K. (2016). Mindfulness-Oriented Recovery
McClernon, F. J. (2012). Smoking abstinence and depressive Enhancement versus CBT for co-occurring substance
symptoms modulate the executive control system during dependence, traumatic stress, and psychiatric disorders:
emotional information processing. Addiction Biology, 17, Proximal outcomes from a pragmatic randomized trial.
668–679. Behaviour Research and Therapy, 77, 7–16.
Froeliger, B., Modlin, L., Wang, L., Kozink, R., & McClernon, F. Gehricke, J.-G., Loughlin, S. E., Whalen, C. K., Potkin, S. G.,
(2012). Nicotine withdrawal modulates frontal brain function Fallon, J. H., Jamner, L. D., . . . Leslie, F. M. (2007). Smoking
during an affective Stroop task. Psychopharmacology, 220, to self-medicate attentional and emotional dysfunctions.
707–718. Nicotine and Tobacco Research, 9, S523–S536.
Fucito, L. M., Juliano, L. M., & Toll, B. A. (2010). Cognitive Gilbert, D. G. (1995). Smoking: Individual difference,
reappraisal and expressive suppression emotion regulation psychopathology, and emotion. Washington, DC: Taylor and
strategies in cigarette smokers. Nicotine and Tobacco Research, Francis.
12, 1156–1161. Gilbert, D. G., McClernon, F. J., Rabinovich, N. E., Dibb,
Garfield, J. B., Lubman, D. I., & Yücel, M. (2014). Anhedonia W. D., Plath, L. C., Hiyane, S., . . . Gehlbach, B. A. (1999).
in substance use disorders: A systematic review of its nature, EEG, physiology, and task-related mood fail to resolve across
course and clinical correlates. Australian and New Zealand 31 days of smoking abstinence: Relations to depressive traits,
Journal of Psychiatry, 48, 36–51. nicotine exposure, and dependence. Experimental and
Garland, E. L., Brown, S. M., & Howard, M. O. (2016). Thought Clinical Psychopharmacology, 7, 427–443.
suppression as a mediator of the association between depressed Gilbert, D. G., McClernon, F. J., Rabinovich, N. E., Plath,
mood and prescription opioid craving among chronic pain L. C., Masson, C. L., Anderson, A. E., & Sly, K. F. (2002).
patients. Journal of Behavioral Medicine, 39, 128–138. Mood disturbance fails to resolve across 31 days of cigarette
Garland, E. L., Bryan, C. J., Finan, P. H., Thomas, E. A., Priddy, abstinence in women. Journal of Consulting and Clinical
S. E., Riquino, M. R., & Howard, M. O. (2017). Pain, Psychology, 70, 142–152.
hedonic regulation, and opioid misuse: Modulation of Gilbert, D. G., McClernon, J., Rabinovich, N., Sugai, C., Plath,
momentary experience by Mindfulness-Oriented Recovery L., Asgaard, G., . . . Botros, N. (2004). Effects of quitting
Enhancement in opioid-treated chronic pain patients. Drug smoking on EEG activation and attention last for more than
and Alcohol Dependence, 173, S65–S72. 31 days and are more severe with stress, dependence, DRD2
Garland, E. L., Bryan, C. J., Nakamura, Y., Froeliger, B., & A1 allele, and depressive traits. Nicotine and Tobacco Research,
Howard, M. O. (2017). Deficits in autonomic indices of 6, 249–267.
emotion regulation and reward processing associated with Gilbert, D. G., Sugai, C., Zuo, Y., Claire, N. E., McClernon,
prescription opioid use and misuse. Psychopharmacology, F. J., Rabinovich, N. E., . . . Radtke, R. (2004). Effects of
234, 621–629. nicotine on brain responses to emotional pictures. Nicotine
Garland, E. L., Froeliger, B., & Howard, M. O. (2014). Effects of and Tobacco Research, 6, 985–996.
Mindfulness-Oriented Recovery Enhancement on reward Gilbert, D. G., Sugai, C., Zuo, Y., Rabinovich, N. E.,
responsiveness and opioid cue-reactivity. Psychopharmacology, McClernon, F. J., & Froeliger, B. (2007). Brain indices of
231, 3229–3238. nicotine’s effects on attentional bias to smoking and
Garland, E. L., Froeliger, B., & Howard, M. O. (2015a). emotional pictures and to task-relevant targets. Nicotine and
Allostatic dysregulation of natural reward processing in Tobacco Research, 9, 351–363.
prescription opioid misuse: Autonomic and attentional Glassman, A. H. (1993). Cigarette smoking: Implications for
evidence. Biological Psychology, 105, 124–129. psychiatric illness. American Journal of Psychiatry, 150,
Garland, E. L., Froeliger, B., & Howard, M. O. (2015b). 546–553.
Neurophysiological evidence for remediation of reward Goesling, J., Henry, M., Moser, S., Rastogi, M., Hassett, A.,
processing deficits in chronic pain and opioid misuse Clauw, D., & Brummett, C. (2015). Symptoms of depression
following treatment with Mindfulness-Oriented Recovery are associated with opioid use regardless of pain severity and
Enhancement: Exploratory ERP findings from a pilot RCT. physical functioning among treatment-seeking patients with
Journal of Behavioral Medicine, 38, 327–336. chronic pain. Journal of Pain, 16, 844–851.
Garland, E. L., Froeliger, B., Zeidan, F., Partin, K., & Howard, Goldin, P. R., McRae, K., Ramel, W., & Gross, J. J. (2008). The
M. O. (2013). The downward spiral of chronic pain, neural bases of emotion regulation: Reappraisal and

suppression of negative emotion. Biological Psychiatry, 63, Kahler, C. W., Brown, R. A., Strong, D. R., Lloyd-Richardson,
577–586. E. E., & Niaura, R. (2003). History of major depressive
Goldner, E., Lusted, A., Roerecke, M., Rehm, J., & Fischer, B. disorder among smokers in cessation treatment: Associations
(2014). Prevalence of Axis-1 psychiatric (with focus on with dysfunctional attitudes and coping. Addictive Behavior,
depression and anxiety) disorder and symptomatology 28, 1033–1047.
among non-medical prescription opioid users in substance Kalivas, P. W., & Volkow, N. D. (2005). The neural basis of
use treatment: Systematic review and meta-analyses. addiction: A pathology of motivation and choice. American
Addictive Behaviors, 39, 520–531. Journal of Psychiatry, 162, 1403–1413.
Goldstein, R. Z., & Volkow, N. D. (2002). Drug addiction and Kanske, P., Heissler, J. Schonfelder, S., Bongers, A., & Wessa, M.
its underlying neurobiological basis: Neuroimaging evidence (2011). How to regulate emotion? Neural networks for
for the involvement of the frontal cortex. American Journal of reappraisal and distraction. Cerebral Cortex, 21, 1379–1388.
Psychiatry, 159, 1642–1652. Khaled, S. M., Bulloch, A. G., Williams, J. V. A., Lavorato,
Gonzalez, A., Zvolensky, M. J., Vujanovic, A. A., Leyro, T. M., D. H., & Patten, S. B. (2011). Major depression is a risk
& Marshall, E. C. (2008). An evaluation of anxiety factor for shorter time to first cigarette irrespective of the
sensitivity, emotional dysregulation, and negative affectivity number of cigarettes smoked per day: Evidence from a
among daily cigarette smokers: Relation to smoking motives national population health survey. Nicotine and Tobacco
and barriers to quitting. Journal of Psychiatry Research, 43, Research, 13, 1059–1067.
138–147. Khantzian, E. J. (1997). The self-medication hypothesis of
Grattan, A., Sullivan, M., Saunders, K., Campbell, C., & Von substance use disorders: A reconsideration and recent
Korff, M. (2012). Depression and prescription opioid misuse applications. Harvard Review of Psychiatry, 4, 231–244.
among chronic opioid therapy recipients with no history of Kim, S. H., & Hamann, S. (2007). Neural correlates of positive
substance abuse. Annals of Family Medicine, 10, 304–311. and negative emotion regulation. Journal of Cognitive
Green, T. C., Black, R., Grimes Serrano, J. M., Budman, S. H., Neuroscience, 19, 776–798.
& Butler, S. F. (2011). Typologies of prescription opioid use Kim, Y. T., Song, H. J., Seo, J. H., Lee, J. J., Lee, J., Kwon,
in a large sample of adults assessed for substance abuse D. H., . . . Chang, Y. (2011). The differences in neural network
treatment. PLoS ONE, 6, e27244. activity between methamphetamine abusers and healthy
Gros, D., Milanak, M., Brady, K., & Back, S. (2013). Frequency subjects performing an emotion-matching task: Functional
and severity of comorbid mood and anxiety disorders in MRI study. NMR in Biomedicine, 24, 1392–1400.
prescription opioid dependence. American Journal on Koob, G. F. (2015). The dark side of emotion: The addiction
Addictions, 22, 261–265. perspective. European Journal of Pharmacology, 753, 73–87.
Haber, S. N., & Knutson, B. (2010). The reward circuit: Koob, G. F., & Le Moal, M. (2001). Drug addiction, dysregulation
Linking primate anatomy and human neuroimaging. of reward, and allostasis. Neuropsychopharmacology, 24, 97–129.
Neuropsychopharmacology, 35, 4–26. Koob, G. F., & Le Moal, M. (2008). Addiction and the brain
Hall, A. J., Logan, J. E., Toblin, R. L., Kaplan, J. A., Kraner, antireward system. Annual Review of Psychology, 59, 29–53.
J. C., Bixler, D., . . . Paulozzi, L. J. (2008). Patterns of abuse Kozink, R. V., Lutz, A. M., Rose, J. E., Froeliger, B., &
among unintentional pharmaceutical overdose fatalities. McClernon, F. J. (2010). Smoking withdrawal shifts the
JAMA, 300, 2613–2620. spatiotemporal dynamics of neurocognition. Addiction
Heatherton, T. F., & Wagner, D. D. (2011). Cognitive Biology, 15, 480–490.
neuroscience of self-regulation failure. Trends in Cognitive Lasser, K., Boyd, J. W., Woolhandler, S., Himmelstein, D. U.,
Sciences, 15, 132–139. McCormick, D., & Bor, D. H. (2000). Smoking and mental
Hendricks, P. S., Ditre, J. W., Drobes, D. J., & Brandon, T. H. illness. JAMA, 284, 2606–2610.
(2006). The early time course of smoking withdrawal effects. Leeies, M., Pagura, J., Sareen, J., & Bolton, J. M. (2010). The use of
Psychopharmacology, 187, 385–396. alcohol and drugs to self-medicate symptoms of posttraumatic
Hooten, W. M., Shi, Y., Gazelka, H., & Warner, D. (2011). The stress disorder. Depression and Anxiety, 27, 731–736.
effects of depression and smoking on pain severity and opioid Lembke, A. (2012). Time to abandon the self-medication
use in patients with chronic pain. Pain, 152, 223–229. hypothesis in patients with psychiatric disorders. American
Huhn, A. S., Meyer, R. E., Harris, J. D., Ayaz, H., Deneke, E., Journal of Drug and Alcohol Abuse, 38, 524–529.
Stankoski, D. M., & Bunce, S. C. (2016). Evidence of Li, W., Garland, E. L., & Howard, M. O. (2018). Therapeutic
anhedonia and differential reward processing in prefrontal mechanisms of mindfulness-oriented recovery enhancement
cortex among post-withdrawal patients with prescription for internet gaming disorder: Reducing craving and addictive
opiate dependence. Brain Research Bulletin, 123, 102–109. behavior by targeting cognitive processes. Journal of Addictive
Jastreboff, A. M., Sinha, R., Lacadie, C. M., Balodis, I. M., Diseases, 1–9.
Sherwin, R., & Potenza, M. N. (2015). Blunted striatal Lyvers, M., Carlopio, C., Bothma, V., & Edwards, M. S. (2014).
responses to favorite-food cues in smokers. Drug and Alcohol Mood, mood regulation, and frontal systems functioning in
Dependence, 146, 103–106. current smokers, long-term abstinent ex-smokers, and never-
Johnson, A. L., & McLeish, A. C. (2016). The indirect effect of smokers. Journal of Psychoactive Drugs, 46, 133–139.
emotion dysregulation in terms of negative affect and smoking- Magar, E. C., Phillips, L. H., & Hosie, J. A. (2008). Self-
related cognitive processes. Addictive Behavior, 53, 187–192. regulation and risk-taking. Personality and Individual
Juliano, L. M., & Brandon, T. H. (2002). Effects of nicotine Differences, 45(2), 153–159.
dose, instructional set, and outcome expectancies on the Mak, A. K., Hu, Z. G., Zhang, J. X., Xiao, Z. W., & Lee, T. M.
subjective effects of smoking in the presence of a stressor. (2009). Neural correlates of regulation of positive and negative
Journal of Abnormal Psychology, 111, 88–97. emotions: An fMRI study. Neuroscience Letters, 457, 101–106.

Martel, M., Dolman, A., Edwards, R., Jamison, R., & Wasan, A. Potenza, M. N., Hong, K. I., Lacadie, C. M., Fulbright, R. K.,
(2014). The association between negative affect and Tuit, K. L., & Sinha, R. (2012). Neural correlates of stress-
prescription opioid misuse in patients with chronic pain: The induced and cue-induced drug craving: Influences of sex and
mediating role of opioid craving. Journal of Pain, 15, 90–100. cocaine dependence. American Journal of Psychiatry, 169,
Martel, M. O., Jamison, R. N., Wasan, A. D., & Edwards, R. R. 406–414.
(2014). The association between catastrophizing and craving Quoidback, J., Berry, E. V., Hansenne, M., & Mikolajczak, M.
in patients with chronic pain prescribed opioid therapy: A (2010). Positive emotion regulation and wellbeing: Comparing
preliminary analysis. Pain Medicine, 15, 1757–1764. the impact of eight savoring and dampening strategies.
Martel, M. O., Wasan, A. D., Jamison, R. N., & Edwards, R. R. Personality and Individual Differences, 49, 368–373.
(2013). Catastrophic thinking and increased risk for Roger, V. L., Go, A. S., Lloyd-Jones, D. M., Adams, R. J., Berry,
prescription opioid misuse in patients with chronic pain. J. D., Brown, T. M., . . . on behalf of the American Heart
Drug and Alcohol Dependence, 132, 335–341. Association Statistics Committee and Stroke Statistics
Martins, S. S., Fenton, M. C., Keyes, K. M., Blanco, C., Zhu, Subcommittee, J. (2011). Heart disease and stroke
H., & Storr, C. L. (2012). Mood and anxiety disorders and statistics—2011 update: A report from the American Heart
their association with non-medical prescription opioid use Association. Circulation, 123(4), e18–e209.
and prescription opioid-use disorder: Longitudinal evidence Robinson, J., Sareen, J., Cox, B. J., & Bolton, J. M. (2011). Role
from the National Epidemiologic Study on Alcohol and of self-medication in the development of comorbid anxiety
Related Conditions. Psychological Medicine, 42, 1261–1272. and substance use disorders: A longitudinal investigation.
Mayor, S. (2016). Long term opioid analgesic use is linked to Archives of General Psychiatry, 68, 800–807.
increased risk of depression, study shows. BMJ, 352, i134. Saha, T. D., Kerridge, B. T., Goldstein, R. B., Chou, S. P.,
McHugh, R. K., Weiss, R. D., Cornelius, M., Martel, M. O., Zhang, H., Jung, J., . . . Grant, B. F. (2016). Nonmedical
Jamison, R. N., & Edwards, R. R. (2016). Distress intolerance prescription opioid use and DSM-5 nonmedical prescription
and prescription opioid misuse among patients with chronic opioid use disorder in the United States. Journal of Clinical
pain. Journal of Pain, 17, 806–814. Psychiatry, 77, 772–780.
McKee, S. A. (2009). REVIEW: Developing human laboratory Scherrer, J. F., Salas, J., Copeland, L., Stock, E., Ahmedani, B.,
models of smoking lapse behavior for medication screening. Sullivan, M., . . . Lustman, P. (2016). Prescription opioid
Addiction Biology, 14, 99–107. duration, dose, and increased risk of depression in 3 large
McKee, S. A., Sinha, R., Weinberger, A. H., Sofuoglu, M., patient populations. Annals of Family Medicine, 14, 54–62.
Harrison, E. L., Lavery, M., & Wanzer, J. (2011). Stress Scherrer, J. F., Salas, J., Lustman, P., Burge, S., & Schneider, F. D.
decreases the ability to resist smoking and potentiates (2015). Change in opioid dose and change in depression in a
smoking intensity and reward. Journal of Psychopharmacology, longitudinal primary care patient cohort. Pain, 156, 348–355.
25, 490–502. Scherrer, J. F., Svrakic, D., Freedland, K., Chrusciel, T.,
Merrill, J. O., Von Korff, M., Banta-Green, C., Sullivan, M., Balasubramanian, S., Bucholz, K., . . . Lustman, P. (2014).
Saunders, K., Campbell, C., & Weisner, C. (2012). Prescribed Prescription opioid analgesics increase the risk of depression.
opioid difficulties, depression and opioid dose among Journal of General Internal Medicine, 29, 491–499.
chronic opioid therapy patients. General Hospital Psychiatry, Schleicher, H. E., Harris, K. J., Catley, D., & Nazir, N. (2009).
34, 581–587. The role of depression and negative affect regulation
Mohajerin, B., Dolatshahi, B., Shahbaz, A., & Farhoudian, A. expectancies in tobacco smoking among college students.
(2013). Differences between expressive suppression and Journal of American College of Health, 57, 507–512.
cognitive reappraisal in opioids and stimulant dependent Shiffman, S. (2005). Dynamic influences on smoking relapse
patients. International Journal of High Risk Behaviors and process. Journal of Personality, 73, 1715–1748.
Addiction, 2, 8–14. Shiffman, S., Hufford, M., Hickcox, M., Paty, J. A., Gnys, M.,
Moss, A. C., Erskine, J. A. K., Albery, I. P., Allen, J. R., & Kassel, J. D. (1997). Remember that? A comparison of real-
Georgiou, G. J. (2015). To suppress, or not to suppress? That time versus retrospective recall of smoking lapses. Journal of
is repression: Controlling intrusive thoughts in addictive Consulting and Clinical Psychology, 65(2), 292–300.
behaviour. Addictive Behaviors, 44, 65–70. Shiffman, S., Paty, J. A., Gnys, M., Kassel, J. A., & Hickcox, M.
Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of (1996). First lapses to smoking: Within-subjects analysis of
emotion. Trends in Cognitive Science, 9, 242–249. real-time reports. Journal of Consulting and Clinical
Okita, K., Ghahremani, D. G., Payer, D. E., Robertson, C. L., Psychology, 64(2), 366–379.
Dean, A. C., Mandelkern, M. A., & London, E. D. (2016). Shiffman, S., & Waters, A. J. (2004). Negative affect and
Emotion dysregulation and amygdala dopamine D2-type smoking lapses: A prospective analysis. Journal of Consulting
receptor availability in methamphetamine users. Drug and and Clinical Psychology, 72, 192–201.
Alcohol Dependence, 161, 163–170. Short, N. A., Oglesby, M. E., Raines, A. M., Zvolensky, M. J., &
Parrott, A. C., Garnham, N. J., Wesnes, K., & Pincock, C. Schmidt, N. B. (2015). Posttraumatic stress and emotion
(1996). Cigarette smoking and abstinence: Comparative dysregulation: Relationships with smoking to reduce negative
effects upon cognitive task performance and mood state over affect and barriers to smoking cessation. Comprehensive
24 hours. Human Psychopharmacology: Clinical and Psychiatry, 61, 15–22.
Experimental, 11, 391–400. Shurman, J., Koob, G. F., & Gutstein, H. B. (2010). Opioids,
Payer, D. E., Lieberman, M. D., & London, E. D. (2011). pain, the brain, and hyperkatifeia: A framework for the
Neural correlates of affect processing and aggression in rational use of opioids for pain. Pain Medicine, 11, 1092–1098.
methamphetamine dependence. Archives of General Sinha, R. (2007). The role of stress in addiction relapse. Current
Psychiatry, 68, 271–282. Psychiatry Reports, 9, 388–395.

Sinha, R., Lacadie, C., Skudlarski, P., Fulbright, R. K., Prequit fMRI responses to pleasant cues and cigarette-related
Rounsaville, B. J., Kosten, T. R., & Wexler, B. E. (2005). cues predict smoking cessation outcome. Nicotine and
Neural activity associated with stress-induced cocaine Tobacco Research, 16, 697–708.
craving: A functional magnetic resonance imaging study. Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016).
Psychopharmacology (Berl), 183, 171–180. Neurobiologic advances from the brain disease model
Smith, K., Mattick, R., Bruno, R., Nielsen, S., Cohen, M., of addiction. New England Journal of Medicine, 374(4),
Campbell, G., . . . Degenhardt, L. (2015). Factors associated 363–371.
with the development of depression in chronic non-cancer Vowles, K. E., McEntee, M. L., Julnes, P. S., Frohe, T., Ney, J. P.,
pain patients following the onset of opioid treatment for & van der Goes, D. N. (2015). Rates of opioid misuse, abuse,
pain. Journal of Affective Disorders, 184, 72–80. and addiction in chronic pain: A systematic review and data
Spielberger, C. D. (1986). Psychological determinants of smoking synthesis. PAIN, 156, 569–576.
behavior. In R. D. Tollinson (Ed.), Smoking and society: Wegner, D. M., & Erber, R. (1992). The hyperaccessibility of
Toward a more balanced assessment. Lexington, MA: Heath. suppressed thoughts. Journal of Personality and Social
Sullivan, M. D. (2016). Why does depression promote long-term Psychology, 63, 903–912.
opioid use? Pain, 157, 2395–2396. Wegner, D. M., Schneider, D. J., Carter, S. R., & White, T. L.
Sullivan, M. D., Edlund, M. J., Steffick, D., & Unutzer, J. (1987). Paradoxical effects of thought suppression. Journal of
(2005). Regular use of prescribed opioids: Association with Personality and Social Psychology, 53, 5–13.
common psychiatric disorders. Pain, 119, 95–103. Wenzlaff, R. M., & Wegner, D. M. (2000). Thought suppression.
Sweitzer, M. M., Geier, C. F., Denlinger, R., Forbes, E. E., Raiff, Annual Review of Psychology, 51, 59–91.
B. R., Dallery, J., . . . Donny, E. C. (2016). Blunted striatal Wilson, S. J., Delgado, M. R., McKee, S. A., Grigson, P. S.,
response to monetary reward anticipation during smoking MacLean, R. R., Nichols, T. T., & Henry, S. L. (2014). Weak
abstinence predicts lapse during a contingency-managed quit ventral striatal responses to monetary outcomes predict an
attempt. Psychopharmacology, 233, 751–760. unwillingness to resist cigarette smoking. Cognitive and
Thomas, E., Mijangos, J., White, S., Hansen, P., Reimers, C., Affective Behavioral Neuroscience, 14, 1196–1207.
Walker, D., . . . Garland, E. L. (under review). Mindfulness- Wong, C. F., Silva, K., Kecojevic, A., Schrager, S. M., Bloom,
oriented recovery enhancement restructures reward processing J. J., Iverson, E., & Lankenau, S. E. (2013). Coping and
and promotes interoceptive awareness in overweight cancer emotion regulation profiles as predictors of nonmedical
survivors: Results from a stage 1 RCT. prescription drug and illicit drug use among high-risk young
Uhlmann, A., Fouche, J. P., Koen, N., Meintjes, E. M., Wilson, adults. Drug and Alcohol Dependence, 132, 165–171.
D., & Stein, D. J. (2016). Fronto-temporal alterations and Yang, M. J., Zvolensky, M. J., & Leyro, T. M. (2017). The
affect regulation in methamphetamine dependence with and indirect effect of panic disorder on smoking cognitions via
without a history of psychosis. Psychiatry Research, 248, 30–38. difficulties in emotion regulation. Addictive Behavior, 72,
US Health and Human Services. (2010). Results from the 2009 126–132.
National Survey on Drug Use and Health: Volume I. Summary Younger, J. W., Chu, L. F., D’Arcy, N. T., Trott, K. E., Jastrzab,
of national findings. Retrieved from http://www.gmhc.org/ L. E., & Mackey, S. C. (2011). Prescription opioid analgesics
files/editor/file/a_pa_nat_drug_use_survey.pdf on 8/24/2017 rapidly change the human brain. PAIN, 152, 1803–1810.
Vanderhasselt, M.-A., Baeken, C., Van Schuerbeek, P., Luypaert, Zhao, L. Y., Tian, J., Wang, W., Qin, W., Shi, J., Li, Q., . . . Lu, L.
R., & De Raedt, R. (2013). Inter-individual differences in (2012). The role of dorsal anterior cingulate cortex in the
the habitual use of cognitive reappraisal and expressive regulation of craving by reappraisal in smokers. PLoS One, 7,
suppression are associated with variations in prefrontal e43598.
cognitive control for emotional information: an event related Zvolensky, M. J., Feldner, M. T., Eifert, G. H., & Brown, R. A.
fMRI study. Biological Psychology, 92, 433–439. (2001). Affective style among smokers: Understanding
Versace, F., Engelmann, J. M., Robinson, J. D., Jackson, E. F., anxiety sensitivity, emotional reactivity, and distress tolerance
Green, C. E., Lam, C. Y., . . . Cinciripini, P. M. (2014). using biological challenge. Addictive Behavior, 26, 901–915.

CH A PTE R
Emotion Dysregulation
23 and Eating Disorders
Sarah E. Racine and Sarah A. Horvath
Abstract
This chapter reviews evidence for the role of emotion dysregulation in the etiology and maintenance of
eating disorders. It examines theoretical models that describe functional relations between emotions
and eating disorder behaviors. Data from self-report questionnaire studies, ecological momentary
assessment, and experimental research designs are considered, with a focus on identifying similarities
and differences in emotion dysregulation across eating disorders. The chapter concludes by describing
a model in which stable (i.e., trait) emotion regulation difficulties increase the likelihood of using
maladaptive strategies, such as eating disorder behaviors, to regulate emotions. Future work must
identify factors that predict whether someone will express trait emotion dysregulation as an eating
disorder versus another psychiatric disorder, and whether emotion dysregulation maintains eating
disorders and can be targeted in treatment.
Keywords: emotion dysregulation, emotion regulation, eating disorders, self-report, ecological

momentary assessment, experimental research
Introduction ED, with greater prevalence in females than males

Eating disorders (EDs) are severe psychiatric illnesses and the peak period of risk being mid- to late
characterized by disturbances in eating behavior and adolescence (APA, 2013; Hudson, Hiripi, Pope, &
thoughts about body shape and weight. The primary Kessler, 2007; Stice, Marti, & Rohde, 2013). Beyond
EDs recognized by the Diagnostic and Statistical DSM-5 diagnoses, the occurrence of disordered
Manual of Mental Disorders, 5th edition (DSM-5; eating cognitions and behaviors is strikingly high; one
American Psychiatric Association [APA], 2013) are study found that 49% of college women endorsed
anorexia nervosa (AN), defined by persistent dietary one or more ED symptoms (e.g., Berg, Frazier, &
restriction and maintenance of a significantly low Sherr, 2009). EDs are linked to significant medical
body weight; bulimia nervosa (BN), involving re- consequences and mortality, functional impairment,
current binge eating episodes (i.e., consumption of and psychological distress (APA, 2013), highlighting
a large amount of food in a short period of time and the importance of understanding causal and main-
loss of control [LOC] over eating) and compensatory tenance factors for EDs.
behaviors (e.g., self-induced vomiting, dietary re- Like many psychiatric disorders, emotion
striction); and binge eating disorder (BED), charac- dysregulation is critically important in the etiology
terized by recurrent binge eating in the absence of and maintenance of EDs. Historically, emotion
compensatory behaviors. Other clinically significant dysregulation–ED work focused on BN, rather
eating disturbances are included under the DSM-5 than AN. Early theories described the role of nega-
category of “other specified or unspecified feeding and tive affect in triggering binge eating and purging, as
eating disorder” diagnoses (APA, 2013). Approximately well as the functional role of these behaviors in
5% to 10% of the population will have a lifetime regulating emotions (Hawkins & Clement, 1984;
327
Heatherton & Baumeister, 1991; Polivy & Herman, interpersonal problems then trigger binge eating
1993). Ecological momentary assessment (EMA) re- episodes in daily life, as individuals turn to binge
search largely supports the assertion that negative eating in an attempt to alleviate distress (Polivy &
affect increases prior to and decreases in the hours Herman, 1993). Negative affect reduction occurs
following binge eating and purging (Engel et al., because binge eating provides temporary comfort
2013; Smyth et al., 2007). More recently, scholars and distraction and also may displace distress onto
have posited that restrictive eating and thoughts overeating, with compensatory behaviors then used
about weight, shape, and eating in AN serve similar to undo the “problem” and its anticipated effects on
emotion regulation purposes and may also be used appearance (Hawkins & Clement, 1984). The affect
to prevent the onset of aversive emotions (Schmidt & regulation model is the basis for most research on
Treasure, 2006; Wildes, Ringham, & Marcus, 2010). reciprocal negative affect–ED behavior associations
Patients with AN have difficulty understanding and suggests that binge eating occurs in response to
emotions in others and show impaired emotional stressors in individuals with pre-existing characteris-
expression (Davies et al., 2016; Oldershaw et al., tics, such as emotionally labile temperament and
2011), which may affect their ability to engage in depressive tendencies.
emotion regulation. Broad emotion regulation dif-
ficulties are reported by individuals with EDs (e.g., Escape Model of Binge Eating/Bulimia
elevated scores on Difficulties in Emotion Regulation Nervosa
Scale [DERS] subscales), suggesting that ED behav- A related but distinct maintenance model of binge
iors may function to regulate emotions. eating is the escape model (Heatherton & Baumeister,
This chapter will critically review evidence for 1991). The escape model posits a specific mechanism
associations between emotion dysregulation and EDs. to account for reductions in negative affect during
We begin by describing theoretical models that a binge eating episode—escape from aversive
highlight functional relationships between emotions self-awareness. Individuals with binge eating are
and ED behaviors. We then review research that has hypothesized to self-impose unreasonably high

used self-report questionnaires, with a particular standards and are very aware of shortcomings in re-
focus on the DERS. We also discuss EMA research, lation to these standards. Perceived failures create
which tests tenets of theoretical models explicitly, negative affect, prompting an urge to escape un-
and research that has used experimental paradigms pleasant feelings. Eating provides an avenue for cog-
and laboratory designs to overcome limitations of nitive narrowing (e.g., by focusing on immediate
self-report and causal inference, respectively. We sensations related to the food), and binge eating
finish by synthesizing existing research into an inte- may ensue because the shift from higher to lower
grative framework regarding the role of emotion levels of awareness removes the normal inhibitions
dysregulation in the etiology and maintenance of of eating. However, once a binge episode ends,
EDs and present future directions. awareness returns and individuals experience previ-
ously unwanted thoughts and feelings (e.g., weight
Theoretical Models and shape concerns) that are then addressed through
Several theoretical models that posit functional rela- compensatory behaviors (Heatherton & Baumeister,
tionships between emotions and ED behaviors are 1991). Notably, the escape model is difficult to test
described. given that higher self-awareness is needed to report
on one’s emotions and binge eating (Haedt-Matt &
Affect Regulation Model of Binge Keel, 2011).
Eating/Bulimia Nervosa
The affect regulation model of binge eating has Emotion Avoidance Model of
two tenets: (1) negative mood is a precursor to binge Anorexia Nervosa
eating, and (2) binge eating results in reduction of The emotion avoidance model of AN posits that
distress (Haedt-Matt & Keel, 2011). Hawkins and disordered behaviors and cognitions are driven by a
Clement (1984) state that factors such as being desire to avoid expressing or experiencing physical
overweight, being unassertive, or having an emo- sensations, thoughts, urges, and behaviors related to
tionally labile temperament relate to a negative intense emotional states (Wildes et al., 2010; Wildes
self-image and lead individuals to become preoccu- & Marcus, 2011). Unlike the previously mentioned
pied with dieting and/or a fear of losing control models, the emotion avoidance model considers
over their eating. Stressors such as daily hassles or avoidance of both positive and negative emotional
328 Emotion Dysregul ation and Eating Disorders

states and focuses on the role of AN symptoms in habitual cognitions and behaviors related to emo-
preventing the onset of emotions, as well as reductions. The DERS is a multidimensional self-report
ing the intensity of emotional reactions after they questionnaire that evaluates several facets of emo-
have arisen. The desire to avoid emotions is due to tion dysregulation (Gratz & Roemer, 2004). The
individual features, such as personality traits and co- DERS is the most widely used measure in ED re-
morbid emotional disorders (Wildes et al., 2010), search and the focus of this section.
which result from both genetic vulnerabilities and
aversive childhood experiences (e.g., emotional DERS Model of Emotion Dysregulation
abuse; Racine & Wildes, 2015a). Similar hypotheses The DERS is a self-report measure of difficulties in
are put forth in the broader cognitive-interpersonal emotion regulation. Past researchers conceptualized
maintenance model of AN (Schmidt & Treasure, emotion regulation as the control of emotional ex-
2006); AN symptoms theoretically facilitate avoid- perience and reduction of emotional arousal (Cortez
ance of both emotions and interpersonal relationships & Bugental, 1994), while others stressed the adapt
that trigger strong emotions, leading to emotional ive nature of emotions and the utility of accurately
“numbing” (Schmidt & Treasure, 2006). Notably, understanding them (Thompson & Calkins, 1996).
an experimental treatment based on the emotion In an attempt to integrate these perspectives, Gratz
avoidance model, Emotion Acceptance Behavior and Roemer (2004) posited that emotion regula-
Therapy, shows promise in pilot testing with adults tion involves (1) awareness and understanding of
with AN (Wildes, Marcus, Cheng, McCabe, & emotions, (2) acceptance of emotions, (3) ability to
Gaskill, 2014). control impulsive behaviors and act in accordance
with desired goals when experiencing negative emo-
Transactional Model of Emotion tions, and (4) ability to use situation-appropriate
Dysregulation and Anorexia Nervosa emotion regulation strategies flexibly to modulate
Given that early research almost exclusively exam- emotional responses based on desired goals. The
ined emotion dysregulation in relation to binge DERS assesses deficits in the aforementioned do-
eating and BN, Haynos and Fruzzetti (2011) ex- mains of emotion regulation via six subscales and an
plored the evidence to support AN as a “disorder of overall total score.
emotion dysregulation.” These authors applied the Lavender et al. (2015) used the DERS model as a
transactional model of emotion regulation origi- framework to review empirical literature on emo-
nally developed for borderline personality disorder tion dysregulation in AN and BN. The authors as-
(Fruzzetti, Shenk, & Hoffman, 2005) to AN. serted that, due to its multidimensional nature, the
Temperamental levels of emotional vulnerability DERS is especially clinically relevant and captures
develop from a pervasive history of emotional in- both emotional and behavioral dysregulation in
validation and, when combined with state levels of EDs (Lavender et al., 2015). The review concluded
emotional vulnerability and emotional events and that those with AN and BN exhibit greater deficits
judgments about these events, result in heightened in emotion regulation than healthy controls across
emotional arousal. If emotional arousal is height- all DERS domains, although some differences be-
ened sufficiently, individuals may not be able to tween AN and BN may exist. Here, we will consider
engage in successful emotion regulation in the serv emotion dysregulation differences by ED diagnosis,
ice of long-term goals. For individuals with AN, relations with continuous assessments of eating
heightened emotional arousal may lead to ED be- symptoms, and effects of weight recovery and treat-
haviors in an attempt to provide temporary relief ment on emotion dysregulation in EDs.
from distress. Heightened arousal also may be asso-
ciated with inaccurate expression of emotions, re- DERS Scores Across Eating
sulting in invalidating responses from others and Disorder Diagnoses
perpetuating a cycle of emotional invalidation In general, patients with AN, BN, and BED evi-
(Haynos & Fruzzetti, 2011). Since the publication dence greater emotion dysregulation on the DERS
of this review, research that supports a role for emo- than healthy controls (Brockmeyer et al., 2014;
tion dysregulation in AN has accumulated. Harrison, Sullivan, Tchanturia, & Treasure, 2010;
Svaldi, Griepenstroh, Tuschen-Caffier, & Ehring,
Self-Report Questionnaire Research 2012; Wolz, Aguera, Granero, Jimenez-Murcia, &
Emotion dysregulation research using self-report Frank, 2015). Patients with BED exhibit more
questionnaires requires individuals to report on emotion dysregulation than both normal-weight
Racine and Horvath 329

and overweight controls, suggesting that binge eating whereas no associations between binge eating
rather than weight status is linked to emotion frequency and emotion dysregulation emerged.

dysregulation (Brockmeyer et al., 2014). However, Interestingly, patients with full-threshold BN had
elevated emotion dysregulation is not specific to greater emotion dysregulation than those with
EDs, with one study finding similar DERS scores subthreshold BN, despite nonsignificant EDE
in patients with EDs, major depressive disorder, Global score differences (Lavender et al., 2014).
and borderline personality disorder (Svaldi et al., Additional research is needed to determine whether
2012). This suggests that emotion dysregulation is a emotion dysregulation–ED symptom relationships
transdiagnostic feature of psychopathology. truly differ by diagnosis, or whether recruitment or
While most research suggests that individuals sample differences account for divergent findings.
with AN and BN are similarly impaired (Brockmeyer With regard to nonclinical samples, Cooper and
et al., 2014; Harrison et al., 2010; Svaldi et al., colleagues (2014) found that all DERS subscales,
2012), Wolz et al. (2015) found that patients with except lack of emotional awareness, related to over-
AN reported less emotion dysregulation than those all ED severity and ED behaviors. The DERS
with BN. Some literature indicates that BED is Awareness and Goals subscales uniquely predicted
characterized by less severe emotion dysregulation ED severity, while DERS Impulse uniquely
than AN and BN (Brockmeyer et al., 2014; Svaldi predicted the ED behavior composite. The unique
et al., 2012), although Wolz et al. (2015) did not effects of DERS Awareness in the Cooper et al.
find significant differences between BED and other (2014) and Racine and Wildes (2013) studies may
EDs. In contrast to these mixed findings, difficulties be an artifact of the low correlations between this
with impulse control in the presence of strong emo- and most other DERS subscales. In undergraduates,
tion differs consistently by AN subtype. Patients the DERS Total score accounted for significant ad-
with AN binge eating/purging subtype (AN-B/P) ditional variance in binge eating above and beyond
report greater DERS Impulse scores than patients sex, overvaluation of weight and shape, and food
with AN restricting subtype (AN-R; Brockmeyer restriction, with lack of emotional clarity and access
et al., 2014; Haynos, Roberto, Martinez, Attia, & to strategies uniquely associated with binge eating
Fruzzetti, 2014; Racine & Wildes, 2013; Svaldi et al., (U. Whiteside et al., 2007). A recent study of ours
2012). found that the combination of overeating and
LOC over eating was associated with the greatest
DERS Scores and Disordered emotion dysregulation, as compared to unique ef-
Eating Symptoms fects of overeating or LOC (Racine & Horvath,
Research in clinical and nonclinical samples sup- 2018). Finally, while most studies examine females,
ports an association between DERS scores and ED the DERS Total and subscale scores also relate to
symptom severity, and several studies have exam- disordered eating and body dissatisfaction in men
ined differential associations between facets of (Lavender & Anderson, 2010). Taken together,
emotion dysregulation and specific symptoms of greater emotion dysregulation is related to more
EDs. In a large sample of patients with AN receiv- severe eating pathology. Notably, inconsistent find-
ing intensive treatment (N = 192), Racine and ings regarding specific associations between DERS
Wildes (2013) found that ED cognitions (assessed subscales and ED symptoms may result partially
with the Eating Disorder Examination [EDE] from sample-specific intercorrelations among DERS
Global score) were related to almost all DERS subscales.
subscales, but lack of emotional awareness was the
only subscale that uniquely predicted ED cognitions. DERS Scores in Relation to Illness
In contrast to these broad associations, impulse Status and Treatment
control difficulties was the only facet related to It is important to know whether the emotion dys-
binge eating and purging in AN (Racine & Wildes, regulation that characterizes EDs is specific to the
2013). In patients with BN enrolled in a treatment illness state or, alternatively, reflects an enduring
trial (N = 80), Lavender et al. (2014) found that characteristic that predisposes to or maintains an
the EDE Global score was related to several facets ED. If emotion regulation difficulties improve
of emotion dysregulation (although not lack of naturally with weight gain or other symptoms, they
emotional awareness). Impairments in goal-directed may not need to be targeted separately; however,
behavior were positively related to frequency of if emotion dysregulation maintains EDs, treat-
driven exercise and negatively related to purging, ments should address these deficits. A handful of

cross-sectional and prospective studies have investi- Controlled studies are needed to test the independent
gated this question in AN. Harrison, Tchanturia, and interactive effects of these treatments to inform
and Treasure (2010) found that individuals with etiologic and maintenance models of emotion dys-
current AN had significantly higher DERS Total regulation and AN.
and subscale scores than those recovered from AN Although Rowsell et al. (2016) demonstrated
(defined as a body mass index [BMI] ≥ 18.5, normal that changes in emotion dysregulation and ED
menstruation, and nonclinical EDE-Q score), and symptoms were related, this study was unable to
recovered patients had similar emotion dysregulation address the direction of this association. In a
scores to controls. Similarly, Merwin et al. (2013) sample of women with AN receiving intensive
found that currently underweight patients with AN treatment, Racine and Wildes (2015b) used a mul-
endorsed greater difficulties with emotional clarity, tiwave longitudinal design (i.e., discharge and 3-,
awareness, nonacceptance, and access to strategies 6-, and 12-month follow-ups) to examine whether
than weight-restored patients. These findings point emotion dysregulation predicts the maintenance
to emotion dysregulation as a state versus trait char- of ED symptoms and/or whether ED symptoms
acteristic of AN. In contrast, Brockmeyer, Grosse, predict worsening emotion regulation. Emotion
Bents, and Kämmerer (2012) found that acute and dysregulation predicted change in ED symptoms,
recovered AN patients had greater DERS Total but the reverse was not true. Specifically, high
scores than healthy controls, and similar scores to emotion dysregulation predicted an increase and
clinical controls. Further, a positive association be- maintenance of ED symptoms, whereas low emotion
tween emotion dysregulation and BMI emerged in dysregulation predicted a decreasing ED symptom
the acute AN group; the authors posited that self- trajectory, with effects independent of BMI and
starvation and resulting low BMI may be a dysfunc- depressive symptoms. These results suggest that
tional strategy to mitigate elevated trait emotion emotion regulation deficits are involved in the
dysregulation in AN (Brockmeyer et al., 2012). maintenance of ED symptoms and provide sup-
Notably, these studies are limited by their port for targeting emotion dysregulation in treat-
cross-sectional design, as lower emotion dysregula- ments in an effort to improve long-term outcomes.
tion scores could contribute to improved recovery To our knowledge, comparisons of emotion
rates in AN. dysregulation in active versus remitted or recovered
Prospective studies of the same patients before patients with BN or BED have not been conducted.
and after treatment are also somewhat mixed. However, two treatment studies suggest that emo-
Inpatients with AN who were assessed at hospital ad- tion dysregulation may maintain ED symptoms in
mission and after weight restoration experienced these patients. In patients with BED receiving a
clinically relevant improvements in eating and inter- guided self-help version of dialectical behavior ther-
nalizing symptoms; however, changes in emotion apy, change in DERS Total score from pre- to post-
dysregulation were either nonsignificant or much treatment predicted abstinence from binge eating at
more modest (Haynos et al., 2014). These findings treatment completion and follow-up points (Wallace,
correspond with a trait account of emotion dysregu- Masson, Safer, & von Ranson, 2014). In patients
lation in AN, although short-term weight restoration with BN receiving either cognitive-behavioral ther-
may not sufficiently reverse the effects of the ED on apy (CBT) or integrative cognitive-affective therapy
emotion dysregulation. More recently, Rowsell, (ICAT; a treatment focused on improving emotion
MacDonald, and Carter (2016) examined changes in regulation; Wonderlich et al., 2014), improvements
emotion dysregulation in patients with AN receiving in emotion regulation predicted improvements in
a hybrid inpatient/day hospital treatment that in- EDE Global scores at the end of treatment and at
cluded therapy focused on emotion regulation skills. follow-up, as well as improvements in binge eating
Significant change in emotion dysregulation from at follow-up (Peterson et al., 2017). Additional re-
pre- to posttreatment was observed, although effects search on BN/BED is important to clarify how
became nonsignificant when controlling for weight emotion dysregulation changes in response to treat-
gain. In contrast, change in emotion dysregulation ment and recovery, independent of significant changes
was significantly related to change in ED symptoms, in weight.
independent of weight gain. Taken together with
Haynos et al. (2014), it may be that weight restoration Other Self-Report Research
and psychological treatment work in combination In addition to the DERS, other self-report scales
to improve emotion regulation in those with AN. have been used to examine emotion dysregulation

in EDs. Here, we review research on two constructs et al., 2016). Longitudinal research indicates that
that overlap with DERS subscales—alexithymia negative urgency prospectively predicts binge eating
and negative urgency—as well as work on specific onset (Pearson, Zapolski, & Smith, 2015) and
regulation strategies. differentiates adolescents who later develop binge
eating and purging (Pearson & Smith, 2015). Further,
Alexithymia negative urgency and binge eating share a large pro-
Alexithymia (i.e., difficulty identifying, distin- portion of genetic risk factors (Racine et al., 2013).
guishing, and/or describing emotions; Sifneos, Thus, negative urgency appears to be an etiologic
Apfel-Savitz, & Frankel, 1977) is similar to the factor for binge eating (and likely purging), but no
DERS Clarity subscale. Meta-analyses report that data exist to speak to maintenance.
alexithymia is more characteristic of individuals
with AN (Cohen’s d = 1.29) and EDs (d = 1.31) Use of Adaptive and Maladaptive
than healthy controls (Caglar-Nazali et al., 2014; Strategies
Oldershaw, Lavender, Sallis, Stahl, & Schmidt, While the DERS assesses perceived access to strate-
2015). While a recent review suggested that alexi- gies to regulate emotions, DERS research does not
thymia may be greater in patients with AN than inform us about specific emotion regulation strate-
BN (Nowakowski, McFarlane, & Cassin, 2013), gies commonly used or not used by patients with
meta-analytic findings suggest similar impairments EDs. A meta-analysis by Aldao, Nolen-Hoeksema,
in AN and BN, but lower alexithymia in BED and Schweizer (2010) found that ED symptoms
(Caglar-Nazali et al., 2014). Whether or not ele- were significantly negatively related to the adaptive
vated alexithymia is due to comorbid internalizing strategy of problem solving (r = −.29; but not cog-
psychopathology in those with EDs is unclear nitive reappraisal, r = −.05) and positively related to
(Nowakowski et al., 2013); some studies find that rumination, suppression, and avoidance (rs = .18–.36).
controlling for depression and anxiety symptoms Another meta-analysis found that those with AN
renders alexithymia–ED symptom associations were less likely to use adaptive strategies (i.e., positive
nonsignificant (e.g., Parling, Mortazavi, & Ghaderi, problem solving, reappraisal, acceptance; ds = −0.26
2010), whereas others continue to find elevated to 1.13) and more likely to use maladaptive strate-
alexithymia after accounting for depression (e.g., gies (i.e., avoidance, social comparison, rumination,
Beadle, Paradiso, Salerno, & McCormick, 2013). suppression; ds = 1.00–1.54), compared to healthy
Alexithymia scores appear to decrease significantly controls (Oldershaw et al., 2015). One study found
following ED treatment, although they remain similar levels of cognitive reappraisal and expressive
elevated after treatment compared to healthy con- suppression across ED diagnoses (as well as depres-
trols (e.g., de Groot, Rodin, & Olmsted, 1995). sion and borderline personality disorder; Svaldi
Finally, in a longitudinal study that followed ado- et al., 2012), another reported more suppression in
lescent females with AN (N = 60) for 18 months AN than BN (Danner, Sternheim, & Evers, 2014),
after hospitalization, alexithymia and ED severity while a third found more reappraisal in those with
were closely related over time, independent of de- restricting versus binge eating and purging (Danner,
pression, anxiety, and BMI (Courty, Godart, Evers, Stok, van Elburg, & de Ridder, 2012). Finally,
Lalanne, & Berthoz, 2015). a multiwave longitudinal study of 496 female
adolescents found reciprocal associations between
Negative Urgency rumination and bulimic symptoms; rumination
Negative urgency (i.e., the tendency to act rashly predicted increases in symptoms and onset of binge
when distressed; S. P. Whiteside & Lynam, 2001) is eating, and bulimic symptoms also predicted increases
similar to the DERS Impulse subscale. In a meta- in rumination (Nolen-Hoeksema, Stice, Wade, &
analysis conducted by Fischer, Smith, and Cyders Bohon, 2007). To our knowledge, there are no
(2008), negative urgency was the form of impulsivity other prospective studies on specific emotion regula-
most strongly related to bulimic symptoms (r = .38 tion strategies and EDs, but reciprocal relationships
vs. rs = .08–.16 for other impulsive traits). Although should be investigated further to clarify ED risk and
most negative urgency research has been done with maintenance processes.
nonclinical samples, patients with EDs character-
ized by binge eating and purging endorse higher Ecological Momentary Assessment Research
negative urgency than those with restriction only EMA has been used to test tenets of maintenance
(Claes, Vandereycken, & Vertommen, 2005; Culbert models of EDs that specify momentary affective

processes (e.g., affect regulation and emotion avoid- 2013). However, in the same sample, an increasing
ance models). EMA has advantages over the use of trajectory of negative affect in the hours prior to and
retrospective questionnaires, such as minimization a decreasing trajectory of negative affect in the hours
of recall biases, response in natural environment, following these behaviors was found. Haedt-Matt
and intensive repeated-measures assessment (Engel and Keel (2015) also reported different results based
et al., 2016). EMA is particularly well suited on analytic approach in 24 women with purging
to studying affective processes, given that affect disorder (i.e., regular purging behavior in the ab-
changes from moment to moment. Several smaller sence of objectively large binge eating episodes).
(Ns = ~20–40) EMA studies have examined Specifically, negative affect increased after purging
emotion-eating behavior associations in clinical episodes in proximal affect rating analyses, whereas
and nonclinical samples (e.g., Deaver, Miltenberger, trajectory analyses indicated decreasing negative affect
Smyth, Meidinger, & Crosby, 2003; Stein et al., following purging. Thus, analytic approach is an
2007). In addition, two large EMA studies have important consideration when conducting research
been conducted in patients with BN (N = 133; on the affective consequences of ED behaviors.
Smyth et al., 2007) and AN (N = 118; Engel et al., To further clarify reciprocal relations among
2013). negative affect, binge eating, and purging, Lavender
and colleagues (2016) applied a very different ana-
Affect Regulation, Binge Eating, lytic approach (i.e., autoregressive cross-lagged
and Purging models) to the large EMA study of women with
A meta-analysis of 36 EMA studies of participants BN. In this report, negative affect ratings later in
with BN, BED, and binge eating found that nega- the day positively predicted the occurrence of binge
tive affect was significantly elevated before binge eating at the next assessment point, and binge eating
eating episodes, relative to both average negative negatively predicted future negative affect ratings.
affect (effect size = .63) and negative affect prior to There was limited evidence of reciprocal relations
regular eating episodes (effect size = .68; Haedt- between negative affect and purging. Findings con-
Matt & Keel, 2011). Diagnosis and binge eating verge with those from trajectory analyses to suggest
definition significantly moderated this effect, with a that binge eating may effectively reduce negative
diagnosis of BED (vs. BN) and self-defined binge affect over a period of hours but, given proximal
eating (vs. DSM-defined binge eating) related to affect rating findings, there may be an initial in-
greater negative affect prior to binge eating. The crease in negative affect upon completion of the
binge eating definition finding may indicate that binge eating episode.
perceived LOC, often used to self-define binge eating,
is more strongly related to increases in negative affect Affect Regulation and Other Eating
than amount of food consumed (see Goldschmidt Disorder Behaviors
et al., 2012 for a study supporting this premise in In addition to binge eating and purging, EMA re-
obese adults with BED). In contrast to predictions search has examined the role of affect in triggering
from the affect regulation model, negative affect was and maintaining other ED behaviors. Within the
further elevated after binge eating episodes, com- large AN study, negative affect rose linearly before
pared to prebinge levels (effect size = .50). Given weighing behavior, but did not significantly change
this, the authors concluded that reductions in nega- after weighing. Although negative affect was signifi-
tive affect may not actually maintain binge eating. cantly lower immediately after exercise and drink-
Conclusions from this meta-analysis contrast ing fluids to curb appetite, there was no significant
with the two large EMA studies of BN and AN; change in negative affect in the hours surrounding
both found decreasing trajectories of negative affect these behaviors (Engel et al., 2013). Results for
in the hours following binge eating and LOC eating affect–restrictive eating associations in women with
episodes, respectively (Engel et al., 2013; Smyth AN again depend on analytic approach and AN
et al., 2007). As first demonstrated by Engel and subtype. In proximal affect rating analyses, negative
colleagues (2013), the discrepancy appears to result affect increased prior to restrictive and nonrestric-
partially from differences in analytic approach. In tive eating episodes and remained stable afterward;
women with AN, negative affect increased follow- positive affect was stable prior to and significantly
ing LOC eating, purging, and their combination decreased following both eating episode types
when examining the single affect ratings immedi- (Fitzsimmons-Craft et al., 2015). Trajectory analyses
ately before and after the behaviors (Engel et al., revealed no relation between changes in global

negative affect and restrictive eating episodes, while antecedents and consequences of ED behaviors. In
positive affect decreased prior to restrictive eating in the large EMA study of BN, Berg et al. (2013) found
women with AN-R and increased prior to restrictive that all four facets of negative affect (i.e., fear, guilt,
eating in women with AN-B/P (Haynos et al., hostility, and sadness) increased prior to, and de-
2017). These findings suggest that positive affect decreased following, binge eating and purging events.
creases may trigger restrictive eating in women with However, guilt was highest immediately prior to
AN-R, whereas planning restrictive eating episodes these events and was the only facet significantly re-
may increase positive affect in women with AN-B/P lated to ED behaviors after controlling for other
(Haynos et al., 2017). Finally, when examining negative affect facets. Similarly, in a sample of 50
affect averaged across the day, Haynos et al. (2015) adults with obesity, global negative affect and guilt
reported that average negative and positive affect (but not the other facets) increased prior to and de-
did not differ on days characterized by high versus creased following binge eating episodes (Berg et al.,
low or no restriction, contrary to the assertion that 2015). Haynos et al. (2017) also found that guilt in-
restriction numbs affective experience (Wildes et al., creased prior to and decreased following restrictive
2010). As with assessments of binge eating in EMA eating episodes in the AN EMA sample. As with
research, a limitation is that participants were asked global positive affect, the association between posi-
to classify eating episodes as restrictive (i.e., en- tive affect facets and restrictive eating differed by
dorsement of “I ate as little as possible”), as opposed AN subtype: joviality and self-assurance decreased
to episodes being defined based on objective caloric before, and self-assurance increased after, restrictive
intake. eating in AN-R, whereas self-assurance increased
In an interesting EMA study of disorder-specific prior to and remained stable following restrictive
rumination in patients with AN and healthy con- eating in AN-B/P. A study using the BN EMA sample
trols, time-lag analyses revealed that negative affect examined contextual precipitants of negative affect
did not predict subsequent disorder-specific rumi- that then trigger ED behaviors (Goldschmidt et al.,
nation, but rumination about weight predicted greater 2014). Interpersonal stress, daily hassles, and stress
negative affect at the following time point (Seidel appraisal uniquely predicted increases in negative
et al., 2016). These findings indicate that disorder- affect, which then predicted the occurrence of binge
specific thoughts may not effectively reduce negative eating and purging. In contrast, work and environ-
affect, as would be suggested by the emotion avoid- mental stressors were not independently related to
ance model of AN. Finally, one study examined co- increases in negative affect prior to ED behaviors. In
variation among negative and positive affect, drive sum, findings across diverse samples to date suggest
for thinness, urge to engage in physical activity, that guilt is the most important precipitant of ED
and actual physical activity in inpatients with an behaviors, and these behaviors serve to effectively
ED (Vansteelandt, Rijmen, Pieters, Probst, & regulate guilt. More data are needed on positive
Vanderlinden, 2007). Negative emotional state affect facets, as well as positive, yet stressful, life
did not predict urge to be physically active after events and ED behaviors.
controlling for drive for thinness, but those with
chronically elevated negative affect were more Emotion Dysregulation and
likely to report urge to engage in physical activity Eating Disorder Behaviors
during times of high state drive for thinness. Thus, EMA data have also been used to explicitly examine
individuals with EDs may view exercise as a mech- indices of emotion dysregulation and relations with
anism to cope with high trait levels of negative affect ED behaviors. In the BN dataset, Selby et al. (2012)
and momentary drives to be thin. Given a growing reported that variability in negative affect (defined
interest in compulsive exercise and EDs (Meyer as the standard deviation of negative emotion rat-
et al., 2016), additional EMA research on problem- ings on a given day) was greater on days with versus
atic exercise as a maladaptive emotion regulation without binge eating or purging episodes. Berner
strategy is needed. et al. (2017) extended these findings by examining
two indices of affective instability and temporal re-
Affective Facets and Contexts and Eating lations with binge eating and/or purging episodes.
Disorder Behaviors Both the probability of acute increases in negative
To gain a more fine-grained understanding of affect and the mean squared successive difference
affect–ED behavior associations, specific facets of (MSSD) between consecutive ratings of negative
negative and positive affect have been examined as affect were greater on days with, versus without,

bulimic episodes. Interestingly, whereas the proba- days, with rates of behaviors on high-negative-affect
bility of an acute increase in negative affect was less days similar across negative urgency levels. Moreover,
likely after a bulimic episode than before it, average across the day, women with high negative urgency
instability in negative affect (MSSD) was greater experienced greater negative affect, and thus smaller
after than before bulimic behaviors. These same two changes in negative affect prior to binge eating
indices of emotion dysregulation were similarly ele- and purging, compared to women with low nega-
vated in patients with BN, borderline personality tive urgency. Findings reveal how negative urgency
disorder, and posttraumatic stress disorder, as com- influences real-world behavior in response to mo-
pared to healthy controls (Santangelo et al., 2014), mentary shifts in emotion and suggest that reduc-
again supporting the transdiagnostic nature of emo- ing overall negative affect and behavioral responses
tion dysregulation. In the AN sample, instability in to negative affect will aid treatment. Examining
both negative and positive emotional experiences, as state–trait emotion interactions is a key direction
well as the interaction between negative and positive for future research, as theoretical models of EDs
emotional instability, predicted greater total fre- describe the use of ED behaviors to regulate emo-
quency of weight loss activities (Selby et al., 2015). tions among those with pre-existing vulnerabilities.
Finally, in a one-week EMA study that examined
“pulse” (i.e., variability in affect intensity) and “spin” Experimental Research
(i.e., variability in affect quality) from the interper- Given that patients with EDs report difficulties
sonal circumplex, patients with AN-R had similar with clarity and awareness of their own emotions
mean levels of affective valence and intensity, but (Lavender et al., 2015), the ability to accurately
lower spin values, than patients with AN-B/P and report on other aspects of emotion regulation may
BN (Vansteelandt, Probst, & Pieters, 2013). Thus, be compromised. Experimental research on socio-
variability in affect type may differentiate EDs emotional processing and emotion dysregulation
characterized by binge eating and/or purging versus has supplemented self-report data to better under-
restriction. In sum, initial EMA findings converge stand the nature and degree of emotion dysregula-
with questionnaire data to suggest that EDs are tion in EDs. The following section will discuss (1)
characterized by affective dysregulation. Additional objectively evaluated impairments in emotion rec-
research that directly compares ED subtypes and ognition and expression, (2) behavioral and psycho-
includes healthy and psychiatric control groups physiological evidence for emotion dysregulation,
could identify facets of emotion dysregulation that and (3) effects of laboratory manipulations of mood
may be unique to different EDs. and emotion regulation on eating behavior.
State–Trait Emotion Interactions Socioemotional Processing and

Surprisingly few studies have tested the hypothesis Eating Disorders
that ED behaviors regulate emotions among those Most ED research that has examined socioemotional
with pre-existing emotion regulation deficits, a core processing, such as emotion recognition and expres-
tenet of most theoretical models. An early study by sion, has been conducted in AN. Individuals who
Engel and colleagues (2007) examined whether those develop AN are thought to have premorbid traits
with BN who were high on impulsivity (assessed via associated with negative emotionality and poor social
the Barratt Impulsiveness Scale) were more likely to functioning, and starvation may serve to dampen
engage in binge eating and purging in response to emotional responses but exacerbate problems in so-
anger, relative to those low on impulsivity. The in- cioemotional communication (Schmidt & Treasure,
teraction between anger level and impulsivity was 2006). In a systematic review of AN socioemotional
trend-level significant, and the interaction between processing, the authors found that patients with AN
anger variability and impulsivity significantly pre- have more difficulty recognizing basic emotions
dicted the probability of a binge eating episode (e.g., in faces; small to medium effect) and complex
(Engel et al., 2007). More recently, Culbert et al. emotions (e.g., in eyes; large effect) compared to
(2016) examined whether individuals with AN high healthy controls (Oldershaw et al., 2011). Similar
on negative urgency are more likely to engage in emotion recognition impairments have been de-
binge eating and purging in response to increasing tected in voices (Kucharska-Pietura, Nikolaou,
levels of negative affect. Contrary to predictions, Masiak, & Treasure, 2004) and in a body motion
women with high versus low negative urgency paradigm (K. Lang et al., 2015). Some studies report
engaged in more behaviors on low-negative-affect

emotion recognition difficulties in people with BN

(Medina-Pradas, Navarro, Alvarez-Moya, Grau, & used more negative words when describing a sad
Obiols, 2012), although null results exist (Kenyon autobiographical event; no differences in positive
et al., 2012; Tapajóz, Soneira, Aulicino, & Allegri, words were reported (Brockmeyer, Grosse, Bents,
2013). A review of positive emotions in EDs con- Herzog, & Friederich, 2013). Interestingly, there
cluded that there are not case-control differences in was a significant positive correlation between nega-
recognizing basic positive emotions, while data for tive emotion word retrieval and body weight in the
complex positive emotion recognition are mixed AN sample, consistent with the notion that low-
(Tchanturia, Dapelo, Harrison, & Hambrook, 2015). weight status may facilitate emotion avoidance
Poor emotion recognition may relate to difficulty (Brockmeyer et al., 2013). In sum, despite similar
with emotion naming; indeed, one study reported self-reported difficulties in emotional clarity and
alexithymia, but not ED symptoms, correlated with awareness in AN and BN, poor emotion recogni-
emotion recognition deficits in patients with EDs tion and expression appear to be more characteristic
and controls matched for alexithymia (Brewer, of AN than BN, potentially contributing to greater
Cook, Cardi, Treasure, & Bird, 2015). social difficulties in AN (Harrison, Mountford, &
With regard to emotion expression, a meta- Tchanturia, 2014). Given findings in the recovered
analysis of studies that used film clips to evoke emo- state and associations with BMI, socioemotional
tions and facial coding systems to measure expres- processing deficits may at least partially result from
sion indicated that patients with AN demonstrate starvation and other illness features in AN.
less positive (large effect) and negative (medium
effect) facial expressions relative to controls (Davies Behavioral and Psychophysiological
et al., 2016). These findings were partially confirmed Evidence of Emotion Dysregulation in
in a recent study that applied computerized auto- Eating Disorders
matic facial recognition software to a pooled data A small number of studies have used behavioral and
set of published and unpublished studies (Leppanen psychophysiological paradigms to examine emotion
et al., 2017). Patients with AN demonstrated less regulation and dysregulation in EDs. The emotional
happiness when viewing a humorous film clip, but conflict task, a variant of the Stroop task that in-
no differences while viewing a sad film clip, relative cludes trials with matching and nonmatching emo-
to recovered AN and healthy controls. Reduced tional faces and words, was used to investigate im-
positive emotion expression may be specific to the plicit emotion regulation in patients with BED at
illness state and relate to the greater emotional baseline and after receiving treatment (Robinson,
avoidance and suppression of patients with current Safer, Austin, & Etkin, 2015). Facets of BED symp-
versus past AN (Oldershaw et al., 2015). toms were related to task performance at baseline, as
An interesting set of studies measured emotion well as change in task performance from baseline to
expression using automatic emotion detection soft- posttreatment. There were no statistically significant
ware while participants played a video game de- differences in performance between patients with
signed to train emotion regulation. Despite greater BED at baseline and posttreatment and healthy
self-reported anger, patients with EDs displayed less controls, although posttreatment scores more closely
anger during the video game than controls, suggest- resembled those of healthy controls. The Paced
ing intentional suppression of anger expression Auditory Serial Addition Task-Computer version,
(Claes et al., 2012; Tárrega et al., 2014). However, an unpleasant task that assesses the ability to persist
contrary to findings of reduced positive emotion ex- in the face of negative emotions, was used as a be-
pression in AN, those with active BN displayed havioral measure of emotion dysregulation in col-
more expressions of joy than controls and recovered lege students with versus without binge eating
BN participants (Tárrega et al., 2014). Additional (Eichen, Chen, Boutelle, & McCloskey, 2017). As
research must establish whether methodological or expected, participants with binge eating were more
true diagnostic differences account for these diver- likely to desist early and report more frustration and
gent findings. In terms of verbal emotional expres- irritation after the task than those without binge
sion, one study reported that participants with AN eating. Quitting early was correlated with DERS
used fewer overall words and fewer positive-affect Total scores, indicating convergence of self-report
words when describing personal experiences; there and behavioral indices of emotion dysregulation.
were no differences between patients with BN and Thus, cognitive and behavioral dyscontrol in the
controls (Davies, Swan, Schmidt, & Tchanturia, presence of strong emotion may be particularly rel-
2012). Another study found that patients with AN evant for binge eating, but the small number of

studies and exclusive focus on binge eating/BED affect is causally related to increases in ED symptoms.
point to the need for future behavioral research. A meta-analysis revealed a significant effect of
The emotion-modulated startle paradigm (EMSP) negative mood (relative to neutral mood) on food
has been employed to examine psychophysiological consumption, with stronger effects in those with
indices of motivational responding to emotional restrained eating or subthreshold/threshold BED

stimuli, as well as regulation of these responses, in compared to obese and healthy control groups
EDs. Participants experience loud startle probes (Cardi, Leppanen, & Treasure, 2015). Similarly, a
while viewing images that vary on emotional valence systematic review that included additional studies
and arousal; the magnitude of the startle eye-blink excluded from the meta-analysis concluded that
response is potentiated during aversive images, and negative affect triggers increased food consumption
attenuated during pleasant images, relative to neu- and/or other indices of binge eating (e.g., desire to
tral images (P.J. Lang, Bradley, & Cuthbert, 1990). eat, eating rate) in BED but not among those with
In the first EMSP study in EDs, patients with AN obesity (Leehr et al., 2015). In contrast, one experi-
and BN demonstrated enhanced startle blink re- mental study in AN found that negative affect in-
sponses to positive images, relative to neutral creased self-reported ED symptoms but not caloric
images, unlike the attenuated response seen in con- intake (Wildes, Marcus, Bright, & Dapelo, 2012).
trols (Friederich et al., 2006). This same finding was Findings are consistent with EMA research in sug-
reported in an adult AN sample (Racine et al., gesting that negative emotions increase behavioral
2016), but not in adolescents with AN (Reichel, dyscontrol when participants with binge eating are
Schneider, Grünewald, & Kienast, 2014). In an- confronted with food.
other study, patients with acute AN, chronic AN, Extending these results, laboratory studies have
and long-term recovered AN failed to demonstrate examined whether brief training on adaptive (e.g.,
the typical emotional modulation of the startle cognitive reappraisal, acceptance) versus maladaptive
blink reflex seen in healthy controls (Erdur, Weber, emotion regulation strategies (e.g., suppression,
Zimmermann-Viehoff, Rose, & Deter, 2017). rumination) produces differences in mood and

Finally, a recent study by our group used the EMSP eating behavior. Several studies report reduced food
to investigate voluntary emotion regulation abilities intake and drive to eat after participants use cognitive
in AN (Racine et al., 2016). In healthy controls, reappraisal versus expressive suppression. Using a
cues to enhance emotional responses to affective within-subjects design, Svaldi, Caffier, and Tuschen-
pictures increase, whereas cues to suppress emo- Caffier (2010) reported that drive to binge eat in-
tional responses decrease startle blink magnitudes, creased from baseline to postfilm when participants
relative to cues to maintain emotional responses with BED were asked to suppress emotional response
(Dillon & LaBar, 2005; Jackson, Malmstadt, Larson, to a sad film clip, whereas no increase was found in
& Davidson, 2000). However, patients with AN the reappraise condition. No increase in drive to
demonstrated the ability to enhance, but not sup- binge eat was found in overweight controls in either
press, emotional responses to aversive (and food) condition. A similar finding emerged in a study of
images and the ability to suppress, but not enhance, restrained and unrestrained eaters (Svaldi, Tuschen-
emotional responses to pleasant images, as indexed Caffier, Lackner, Zimmermann, & Naumann, 2012).
by startle blink magnitudes. Essentially, patients However, this latter study also demonstrated that
with AN were successful at employing emotion reg- acceptance was unexpectedly associated with in-
ulation strategies to worsen, but not improve, their creased drive to eat in restrained eaters, which the
affect. Findings converge with questionnaire studies authors suggest may reflect a temporary increase in
indicating greater use of maladaptive, and reduced awareness of internal states, such as hunger. Another
use of adaptive, emotion regulation strategies in study found that food intake after a sad film was
patients with AN versus controls (Oldershaw et al., greater in participants with BED than overweight
2015). controls, and greater in participants assigned to
expressive suppression versus cognitive reappraisal,
Laboratory Studies of Mood Manipulation but there was no significant Group × Strategy inter-
and Instructed Emotion Regulation in action (Svaldi, Tuschen-Caffier, Trentowska, Caffier,
Eating Disorders & Naumann, 2014).
Experimental laboratory studies that involve a con- Recent laboratory studies have examined addi-
trolled mood induction and measurement of eating tional adaptive and maladaptive emotion regulation
behavior have been used to test whether negative strategies with particular relevance for EDs. Indeed,

compared to healthy controls, participants with AN (Cardi et al., 2015; Engel et al., 2013; Haedt-Matt
and BN were more likely to report state levels of & Keel, 2015; Smyth et al., 2007). The fact that
rumination and suppression, and less likely to maladaptive behaviors such as binge eating and
report state levels of acceptance, after watching a sad purging occur in response to negative emotions
film clip, whereas no differences for cognitive reap- and are used to try to decrease negative emotion is
praisal were found (Naumann, Tuschen-Caffier, itself behavioral evidence of emotion dysregulation
Voderholzer, & Svaldi, 2016). In a study designed to in EDs.
induce body dissatisfaction in patients with BED, Second, despite similarities in most dimensions
assignment to a rumination condition was associ- of self-reported emotion dysregulation across ED
ated with worse mood over time (but had no effect diagnoses, AN appears to be associated with greater
on body dissatisfaction), compared to an acceptance impairment in socioemotional processing than other
condition (Svaldi & Naumann, 2014). In addition, ED diagnoses. Objectively observed difficulties with
rumination after a sad film clip led to significant emotion recognition and expression in AN may at
increases in sadness and a greater drive to abstain in least partially result from the illness state and may
patients with AN and drive to binge in patients with contribute to interpersonal difficulties (Schmidt &
BN; no such changes were found in the distraction Treasure, 2006). Restrictive eating and repetitive
condition (Naumann, Tuschen-Caffier, Voderholzer, thoughts about shape/weight are posited to numb
Caffier, & Svaldi, 2015). Taken together, laboratory emotional experiences in AN (Wildes et al., 2010);
studies of induced negative affect and instructed initial EMA data suggest that restrictive eating may
emotion regulation confirm that negative affect be less closely tied to changes in negative affect than
triggers binge eating and that maladaptive emotion binge eating and purging, but lower negative affect
regulation strategies worsen mood and eating be- in response to restrictive eating or disorder-specific
havior. Despite advantages of laboratory studies for rumination has not been found (Haynos et al.,
minimizing confounds and increasing causal inter- 2015; Haynos et al., 2017; Seidel et al., 2016).
pretations, these designs are limited to short-term Alexithymia and emotional avoidance in AN may
effects of emotion regulation training on eating bias self-report EMA data, pointing to the importance
behavior in nonnaturalistic settings. Moreover, to of using objective methods for testing emotional
our knowledge, studies have failed to investigate avoidance hypotheses in AN.
whether trait emotion regulation and dysregulation Based on our review of the literature, we propose
moderate effects of instructed emotion regulation an integrative model in which trait emotion
on eating and mood outcomes; it is important to dysregulation represents a vulnerability factor that
know whether emotion regulation training can im- increases the likelihood of using maladaptive
prove behavioral control in those most vulnerable to behaviors, such as ED symptoms, to regulate emo-
emotion-induced dysregulated eating. tions during times of elevated emotional arousal.
Although few of the reviewed studies implicate
Synthesis, Integrative Model, and emotion dysregulation in the etiology of EDs, the
Future Directions broader research literature suggests that high emo-
From our review of the literature on emotion dys- tional arousal and poor emotion regulation are pre-
regulation and EDs, we can draw several conclusions. morbid risk factors for EDs. Individuals with EDs
First, there is strong converging evidence that EDs have higher levels of emotion-related personality
characterized by binge eating and purging are asso- traits (e.g., neuroticism, harm avoidance, negative
ciated with difficulties controlling behavior in the urgency) and greater comorbidity with disorders
presence of strong emotions. DERS Impulse and involving emotional difficulties (e.g., major depres-
negative urgency scores tend to be greater in pa- sion, anxiety disorders, borderline personality dis-
tients with EDs that involve binge eating and purg- order; APA, 2013). Neuroticism appears to precede
ing versus restriction only and correlate with these and predict the onset of an ED (see Culbert,
ED behaviors. Initial behavioral data point to Racine, & Klump, 2015 for a review), and emotional
problems with task persistence when distressed in traits and disorders share a significant proportion
those with versus without binge eating (Eichen et al., of their genetic risk factors with ED symptoms
2017). Consistent with theory (Hawkins & Clement, (Livesley, Jang, & Thordarson, 2004; Racine et al.,
1984), EMA and experimental laboratory studies 2013; Slane, Burt, & Klump, 2011). In individuals
find that increases in negative affect precede binge who have pre-existing difficulties managing high
eating and purging behaviors across ED diagnoses emotional arousal, ED symptoms may develop as a

potentially effective, yet maladaptive, emotion Peterson et al., 2017 for treatment studies of BED
regulation strategy. Notably, the extent to which and BN, respectively). Thus, there is a need for ad-
emotional arousal impairs emotion regulation and ditional research to establish that emotion dysregu-
leads to maladaptive strategies, such as ED behaviors, lation is a viable maintenance mechanism to target
likely varies based on individual difference factors in ED treatment. Further, research that considers
(see the Culbert et al., 2016 EMA study). Thus, to how pretreatment levels of emotion dysregulation
empirically test the proposed model, it is critical to relate to outcomes from treatments that do and do
continue to examine interactions between state and not explicitly attempt to improve emotion regula-
trait emotion-related variables in EMA and experi- tion may help the field move toward more personal-
mental studies to identify those individuals who are ized treatment approaches (see Accurso et al., 2016
most likely to experience ED behaviors during times for a study that examined personality traits as mod-
of high emotional arousal, and thus most likely to erators of outcome of CBT versus ICAT for BN).
benefit from emotion regulation training. Patients characterized by emotional and behavioral
As highlighted throughout the chapter and dysregulation tend to have poorer outcomes in tra-
evidenced by the topic of this handbook, emotion ditional ED treatments (e.g., Wildes et al., 2011),
dysregulation is associated with multiple forms of which highlights the importance of designing treat-
psychopathology. Thus, in addition to gaining a ments that specifically address factors maintaining
better understanding of the transdiagnostic emotion ED behaviors in this subpopulation.
dysregulation construct(s) at the biological, behav-
ioral, and environmental levels of analysis, it is References
Accurso, E. C., Wonderlich, S. A., Crosby, R. D., Smith, T. L.,
important to identify the factors that lead an
Klein, M. J., Mitchell, J. E., . . . Peterson, C. B. (2016).
individual with elevated emotion dysregulation to Predictors and moderators of treatment outcome in a
develop one psychiatric condition versus another. randomized clinical trial for adults with symptoms of bulimia
Recent studies by our group have found that classic nervosa. Journal of Consulting and Clinical Psychology, 84,
178–184.
sociocultural and behavioral risk factors for EDs
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion-
(e.g., appearance pressures, body dissatisfaction) regulation strategies across psychopathology: A meta-analytic
interact with negative urgency to predict binge review. Clinical Psychology Review, 30, 217–237.
eating, but not depressive symptoms or problematic American Psychiatric Association. (2013). Diagnostic and statistical
alcohol use (Racine & Martin, 2016). These risk manual of mental disorders (5th ed.). Arlington, VA: Author.
Beadle, J. N., Paradiso, S., Salerno, A., & McCormick, L. M.
factors appear to specifically enhance the genetic,
(2013). Alexithymia, emotional empathy, and self-regulation
rather than environmental, sharing between negative in anorexia nervosa. Annals of Clinical Psychiatry, 25, 107–120.
urgency and binge eating, such that the genetically Berg, K. C., Crosby, R. D., Cao, L., Peterson, C. B., Engel,
mediated tendency to act impulsively when upset S. G., Mitchell, J. E., & Wonderlich, S. A. (2013). Facets of
may be most likely to be expressed as binge eating in negative affect prior to and following binge-only, purge-only,
and binge/purge events in women with bulimia nervosa.
the context of these sociocultural and behavioral
Journal of Abnormal Psychology, 122, 111–118.
risk factors (Racine et al., 2017). Both of these studies Berg, K. C., Crosby, R. D., Crow, S. J., Engel, S. G., Wonderlich,
used cross-sectional data, and there is a need to ex- S. A., & Peterson, C. B. (2015). Negative affect prior to and
amine whether interactions between transdiagnostic following overeating-only, loss of control eating-only, and
and disorder-specific factors predict the onset of EDs binge eating episodes in obese adults. International Journal of
Eating Disorders, 122, 641–654.
prospectively versus other forms of psychopathology.
Berg, K. C., Frazier, P., & Sherr, L. (2009). Eating behaviors
Research that includes multiple patient groups and/ change in eating disorder attitudes and behavior in college
or psychiatric outcomes can help identify factors women: Prevalence and predictors. Eating Behaviors, 10,
that relate to divergent psychopathology trajectories 137–142.
in the context of high emotion dysregulation. Berner, L. A., Crosby, R. S., Cao, L., Engel, S. G., Lavender,
J. M., Mitchell, J. E., & Wonderlich S. A. (2017). Temporal
Finally, establishing that emotion dysregulation
associations between affective instability and dysregulated
is involved in the maintenance of EDs and can be eating behavior in bulimia nervosa. Journal of Psychiatric
effectively targeted in treatment is critical. Although Research, 81, 183–390.
treatments that target emotion dysregulation have Brewer, R., Cook, R., Cardi, V., Treasure, J., & Bird, G. (2015).
been designed for or applied to ED populations, Emotion recognition deficits in eating disorders are
explained by co-occurring alexithymia. Royal Society Open
there is limited data examining emotion dysregula-
Science, 2, 1–12.
tion in the maintenance of EDs over extended time Brockmeyer, T., Grosse, M., Bents, H., Herzog, W., &
periods (see Racine & Wildes, 2015b for a naturalis- Friederich, H. (2013). Lower body weight is associated with
tic study in AN, as well as Wallace et al., 2014 and less negative emotions in sad autobiographical memories of

patients with anorexia nervosa. Psychiatry Research, 210, review and meta-analysis. Neuroscience and Biobehavioral
548–552. Reviews, 64, 252–271.
Brockmeyer, T., Grosse, M., Bents, H., & Kämmerer, A. (2012). Deaver, C. M., Miltenberger, R. G., Smyth, J., Meidinger,
Starvation and emotion regulation in anorexia nervosa. A. M. Y., & Crosby, R. (2003). An evaluation of affect and
Comprehensive Psychiatry, 53, 496–501. binge eating. Behavior Modification, 27, 578–599.
Brockmeyer, T., Skunde, M., Wu, M., Bresslein, E., Rudofsky, de Groot, J. M., Rodin, G., & Olmsted, M. P. (1995).
G., Herzog, W., & Friederich, H. (2014). Difficulties in Alexithymia, depression, and treatment outcome in bulimia
emotion regulation across the spectrum of eating disorders. nervosa. Comprehensive Psychiatry, 36, 53–60.
Comprehensive Psychiatry, 55, 565–571. Dillon, D. G., & Labar, K. S. (2005). Startle modulation during
Caglar-Nazali, H. P., Corfield, F., Cardi, V., Ambwani, S., conscious emotion regulation is arousal-dependent.
Leppanen, J., Olabintan, O., .
.
.
Treasure, J. (2014). A Behavioral Neuroscience, 119, 1118–1124.
systematic review and meta-analysis of “Systems for Social Eichen, D. M., Chen, E., Boutelle, K. N., & McCloskey, M. S.
Processes” in eating disorders. Neuroscience and Biobehavioral (2017). Behavioral evidence of emotion dysregulation in
Reviews, 42, 55–92. binge eaters. Appetite, 111, 1–6.
Cardi, V., Leppanen, J., & Treasure, J. (2015). The effects of Engel, S. G., Boseck, J. J., Crosby, R. D., Wonderlich, S. A.,
negative and positive mood induction on eating behaviour: Mitchell, J. E., Smyth, J., .
.
.
Steiger, H. (2007). The
A meta-analysis of laboratory studies in the healthy relationship of momentary anger and impulsivity to bulimic
population and eating and weight disorders. Neuroscience and behavior. Behavior Research and Therapy, 45, 437–447.
Biobehavioral Reviews, 57, 299–309. Engel, S. G., Crosby, R. D., Thomas, G., Bond, D., Lavender,
Claes, L., Jiménez-Murcia, S., Santamaría, J. J., Moussa, M. B., J. M., Mason, T., . . . Wonderlich, S. A. (2016). Ecological
Sánchez, I., Forcano, L., . . . Fernández-Aranda, F. (2012). The momentary assessment in eating disorder and obesity
facial and subjective emotional reaction in response to a research: A review of the recent literature. Current Psychiatry
video game designed to train emotional regulation. European Reports, 18, 1–9.
Eating Disorders Review, 20, 484–489. Engel, S. G., Wonderlich, S. A., Crosby, R. D., Mitchell, J. E.,
Claes, L., Vandereycken, W., & Vertommen, H. (2005). Crow, S., Peterson, C. B., . . . Gordon, K. H. (2013). The role
Impulsivity-related traits in eating disorder patients. of affect in the maintenance of anorexia nervosa: Evidence
Personality and Individual Differences, 39, 739–749. from a naturalistic assessment of momentary behaviors and
Cooper, J. L., O’Shea, A. E., Atkinson, M. J., & Wade, T. D. emotion. Journal of Abnormal Psychology, 122, 709–719.
(2014). Examination of the difficulties in emotion regulation Erdur, L., Weber, C., Zimmermann-Viehoff, F., Rose, M., &
scale and its relation to disordered eating in a young female Deter, H. C. (2017). Affective responses in different stages of
sample. International Journal of Eating Disorders, 47, 630–639. anorexia nervosa: Results from a startle-reflex paradigm.
Cortez, V. L., & Bugental, D. B. (1994). Children’s visual European Eating Disorders Review, 25, 114–122.
avoidance of threat: A strategy associated with low social Fischer, S., Smith, G. T., & Cyders, M. A. (2008). Another look
control. Merrill-Palmer Quarterly, 40, 82–97. at impulsivity: A meta-analytic review comparing specific
Courty, A., Godart, N., Lalanne, C., & Berthoz, S. (2015). dispositions to rash action in their relationship to bulimic
Alexithymia, a compounding factor for eating and social symptoms. Clinical Psychology Review, 28, 1413–1425.
avoidance symptoms in anorexia nervosa. Comprehensive Fitzsimmons-Craft, E. E., Accurso, E. C., Ciao, A. C.,
Psychiatry, 56, 217–228. Crosby, R. D., Cao, L., Pisetsky, E. M., . . . Wonderlich, S. A.
Culbert, K. M., Lavender, J. M., Crosby, R. D., Wonderlich, S. A., (2015). Restrictive eating in anorexia nervosa: Examining
Engel, S. G., Peterson, C. B., . . . Fischer, S. (2016). Associations maintenance and consequences in the natural environment.
between negative affect and binge/purge behaviors in women International Journal of Eating Disorders, 48, 923–932.
with anorexia nervosa: Considering the role of negative Friederich, H. C., Kumari, V., Uher, R., Riga, M., Schmidt, U.,
urgency. Comprehensive Psychiatry, 66, 104–112. Campbell, I. C., . .
.
Treasure, J. (2006). Differential
Culbert, K. M., Racine, S. E., & Klump, K. L. (2015). Research motivational responses to food and pleasurable cues in
Review: What have we learned about the causes of eating anorexia and bulimia nervosa: A startle reflex paradigm.
disorders—A synthesis of sociocultural, psychological, and Psychological Medicine, 36, 1327–1335.
biological research. Journal of Child Psychology and Psychiatry, Fruzzetti, A. E., Shenk, C., & Hoffman, P. D. (2005). Family
56, 1141–1164. interaction and the development of borderline personality
Danner, U. N., Evers, C., Stok, F. M., van Elburg, A. A., & de disorder: A transactional model. Development and
Ridder, D. T. D. (2012). A double burden: Emotional eating Psychopathology, 17, 1007–1030.
and lack of cognitive reappraisal in eating disordered women. Goldschmidt, A. B., Engel, S. G., Wonderlich, S. A., Crosby,
European Eating Disorders Review, 20, 490–495. R. S., Peterson, C. B., Le Grange, D., . . . Mitchell, J. E.
Danner, U. N., Sternheim, L., & Evers, C. (2014). The (2012). Momentary affect surrounding loss of control and
importance of distinguishing between the different eating overeating in obese adults with and without binge eating
disorder (sub)types when assessing emotion regulation disorder. Obesity, 20, 1206–1211.
strategies. Psychiatry Research, 215, 727–732. Goldschmidt, A. B., Wonderlich, S. A., Crosby, R. D., Engel,
Davies, H., Swan, N., Schmidt, U., & Tchanturia, K. (2012). An S. G., Lavender, J. M., Peterson, C. B., . . . Mitchell, J. E.
experimental investigation of verbal expression of emotion in (2014). Ecological momentary assessment of stressful events
anorexia and bulimia nervosa. European Eating Disorders and negative affect in bulimia nervosa. Journal of Consulting
Review, 20, 476–483. and Clinical Psychology, 82, 30–39.
Davies, H., Wolz, I., Leppanen, J., Fernandez-Aranda, F., Gratz, K. L., & Roemer, L. (2004). Multidimensional
Schmidt, U., & Tchanturia, K. (2016). Facial expression to assessment of emotion regulation and dysregulation. Journal
emotional stimuli in non-psychotic disorders: A systematic of Psychopathology and Behavioral Assessment, 26, 41–54.

Haedt-Matt, A., & Keel, P. K. (2011). Revisiting the affect Exploring emotion recognition in adults and adolescents
regulation model of binge eating: A meta-analysis of studies with anorexia nervosa using a body motion paradigm.
using ecological momentary assessment. Psychological Bulletin, European Eating Disorders Review, 23, 262–268.
137, 660–681. Lavender, J. M., & Anderson, D. A. (2010). Contribution of
Haedt-Matt, A. A., & Keel, P. K. (2015). Affect regulation and emotion regulation difficulties to disordered eating and body
purging: An ecological momentary assessment study in purging dissatisfaction in college men. International Journal of Eating
disorder. Journal of Abnormal Psychology, 124, 399–411. Disorders, 43, 352–358.
Harrison, A., Mountford, V. A., & Tchanturia, K. (2014). Social Lavender, J. M., Happel, K., Antestis, M. D., Tull, M. T., &
anhedonia and work and social functioning in the acute and Gratz, K. L. (2014). The interactive role of distress tolerance
recovered phases of eating disorders. Psychiatry Research, 218, and eating expectancies in bulimic symptoms among
187–194. substance abusers. Eating Behaviors, 16, 79–91.
Harrison, A., Sullivan, S., Tchanturia, K., & Treasure, J. (2010). Lavender, J. M., Utzinger, L. M., Wonderlich, S. A., Engel,
Emotional functioning in eating disorders: Attentional bias, S. G., Mitchell, J. E., & Crosby, R. D. (2016). Reciprocal
emotion recognition, and emotion regulation. Psychological associations between negative affect, binge eating, and
Medicine, 40, 1887–1897. purging in the natural environment in women with bulimia
Harrison, A., Tchanturia, K., & Treasure, J. (2010). Attentional nervosa. Journal of Abnormal Psychology, 125, 381–386.
bias, emotion recognition, and emotion regulation in Lavender, J. M., Wonderlich, S. A., Engel, S. G., Gordon, K. H.,
anorexia: State or trait? Biological Psychiatry, 68, 755–761. Kaye, W. H., & Mitchell, J. E. (2015). Dimensions of
Hawkins, R. C., & Clement, P. F. (1984). Binge eating: emotion dysregulation in anorexia nervosa and bulimia
Measurement problems and a conceptual model. In nervosa: A conceptual review of the empirical literature.
R. C. Hawkins, W. J. Fremouw, & P. F. Clement (Eds.), The Clinical Psychology Review, 40, 111–122.
binge-purge syndrome: Diagnosis, treatment, and research Lavender, J. M., Wonderlich, S. A., Peterson, C. B., Crosby,
(pp. 229–253). New York, NY: Springer. R. D., Engel, S. G., Mitchell, J. E, . . . Berg, K. C. (2014).
Haynos, A. F., Berg, K. C., Cao, L., Crosby, R. D., Lavender, Dimensions of emotion dysregulation in bulimia nervosa.
J. M., Utzinger, L. M., . . . Crow, S. J. (2017). Trajectories of European Eating Disorders Review, 22, 212–216.
higher- and lower-order dimensions of negative and positive Leehr, E. J., Krohmer, K., Schag, K., Dresler, T., Zipfel, S., &
affect relative to restrictive eating in anorexia nervosa. Journal Giel, K. E. (2015). Emotion regulation model in binge eating
of Abnormal Psychology, 126, 494–505. disorder and obesity—A systematic review. Neuroscience and
Haynos, A. F., Crosby, R. D., Engel, S. G., Lavender, J. M., Biobehavioral Reviews, 49, 125–134.
Wonderlich, S. A., Mitchell, J. E., . . . Le Grange, D. (2015). Leppanen, J., Dapelo, M. M., Davies, H., Lang, K., Treasure, J.,
Initial test of an emotional avoidance model of restriction in & Tchanturia, K. (2017). Computerised analysis of facial
anorexia nervosa using ecological momentary assessment. emotion expression in eating disorders. PLoS ONE, 12,
Journal of Psychiatric Research, 68, 134–139. e0178972.
Haynos, A. F., & Fruzzetti, A. E. (2011). Anorexia nervosa as a Livesley, W. J., Jang, K. L., & Thordarson, D. S. (2004).
disorder of emotion dysregulation: Evidence and treatment Etiological relationships between eating disorder symptoms
implications. Clinical Psychology: Science and Practice, 18, and dimensions of personality disorder. Eating Disorders: The
183–203. Journal of Treatment and Prevention, 13, 23–35.
Haynos, A. F., Roberto, C. A., Martinez, M. A., Attia, E., & Medina-Pradas, C., Navarro, J. B., Álvarez-Moya, E. M., Grau,
Fruzzetti, A. E. (2014). Emotion regulation difficulties in A., & Obiols, J. E. (2012). Emotional theory of mind in
anorexia nervosa before and after inpatient weight restoration. eating disorders. International Journal of Clinical and Health
International Journal of Eating Disorders, 47, 888–891. Psychology, 12, 189–202.
Heatherton, T. F., & Baumeister, R. F. (1991). Binge eating as Merwin, R. M., Moskovich, A. A., Wagner, H. R., Ritschel,
escape from self-awareness. Psychological Bulletin, 110, 85–108. L. A., Craighead, L. W., & Zucker, N. L. (2013). Emotion
Hudson, J. I., Hiripi, E., Pope, H. G., & Kessler, R. C. (2007). regulation difficulties in anorexia nervosa: Relationship to
The prevalence and correlates of eating disorders in the self-perceived sensory sensitivity. Cognition and Emotion, 27,
National Comorbidity Survey Replication. Biological Psychiatry, 441–453.
61, 348–358. Meyer, C., Plateau, C. R., Taranis, L., Brewin, N., Wales, J., &
Jackson, D. C., Malmstadt, J. R., Larson, C. L., & Davidson, R. J. Arcelus, J. (2016). The Compulsive Exercise Test: Confirmatory
(2000). Suppression and enhancement of emotional responses factor analysis and links with eating psychopathology among
to unpleasant pictures. Psychophysiology, 37, 515–522. women with clinical eating disorders. Journal of Eating
Kenyon, M., Samarawickrema, N., Dejong, H., Startup, H., Disorders, 4, 1–9.
Lavender, A., & Goodman-Smith, E. (2012). Theory of Naumann, E., Tuschen-Caffier, B., Voderholzer, U., Caffier, D.,
mind in bulimia nervosa. International Journal of Eating & Svaldi, J. (2015). Rumination but not distraction increases
Disorders, 45, 377–384. eating-related symptoms in anorexia and bulimia nervosa.
Kucharska-Pietura, K., Nikolaou, V., Masiak, M., & Treasure, J. Journal of Abnormal Psychology, 124, 412–420.
(2004). The recognition of emotion in the faces and voice of Naumann, E., Tuschen-Caffier, B., Voderholzer, U., & Svaldi, J.
anorexia nervosa. International Journal of Eating Disorders, (2016). Spontaneous emotion regulation in anorexia
35, 42–47. and bulimia nervosa. Cognitive Therapy and Research, 40,
Lang, P. J., Bradley, M. M., & Cuthbert, B. N. (1990). Emotion, 304–313.
attention, and the startle reflex. Psychological Review, 97, Nolen-Hoeksema, S., Stice, E., Wade, E., & Bohon, C. (2007).
377–395. Reciprocal relations between rumination and bulimic,
Lang, K., Dapelo, M. M., Khondoker, M., Morris, R., substance abuse, and depressive symptoms in female
Surguladze, S., Treasure, J., & Tchanturia, K. (2015). adolescents. Journal of Abnormal Psychology, 116, 198–207.

Nowakowski, M. E., McFarlane, T., & Cassin, S. (2013). Racine, S. E., & Wildes, J. E. (2015b). Dynamic longitudinal
Alexithymia and eating disorders: A critical review of the relations between emotion regulation difficulties and anorexia
literature. Journal of Eating Disorders, 1, 1–14. nervosa symptoms over the year following intensive
Oldershaw, A., Hambrook, D., Stahl, D., Tchanturia, K., treatment. Journal of Consulting and Clinical Psychology, 83,
Treasure, J., & Schmidt, U. (2011). The socio-emotional 785–795.
processing stream in anorexia nervosa. Neuroscience and Reichel, V. A., Schneider, N., Grünewald, B., & Kienast, T.
Biobehavioral Reviews, 35, 970–988. (2014). “Glass fairies” and “bone children”: Adolescents and
Oldershaw, A., Lavender, T., Sallis, H., Stahl, D., & Schmidt, U. young adults with anorexia nervosa show positive reactions
(2015). Emotion generation and regulation in anorexia towards extremely emaciated body pictures measured by the
nervosa: A systematic review and meta-analysis of self-report startle reflex paradigm. Psychophysiology, 51, 168–177.
data. Clinical Psychology Review, 39, 83–95. Robinson, A., Safer, D. L., Austin, J. L., & Etkin, A. (2015).
Parling, T., Mortazavi, M., & Ghaderi, A. (2010). Eating Does implicit emotion regulation in binge eating disorder
behaviors alexithymia and emotional awareness in anorexia matter? Eating Behaviors, 18, 186–191.
nervosa: Time for a shift in the measurement of the concept? Rowsell, M., MacDonald, D. E., & Carter, J. C. (2016). Emotion
Eating Behaviors, 11, 205–210. regulation difficulties in anorexia nervosa: Associations with
Pearson, C. M., & Smith, G. T. (2015). Bulimic symptom onset improvements in eating psychopathology. Journal of Eating
in young girls: A longitudinal trajectory analysis. Journal of Disorders, 4, 1–10.
Abnormal Psychology, 124, 1003–1013. Santangelo, P., Reinhard, I., Mussgay, L., Steil, R., Sawitzki, G.,
Pearson, C. M., Zapolski, T. C. B., & Smith, G. T. (2015). Klein, C., . . . & Ebner-Priemer, U. W. (2014). Specificity of
A longitudinal test of impulsivity and depression pathways affective instability in patients with borderline personality
to early binge eating onset. International Journal of Eating disorder compared to posttraumatic stress disorder, bulimia
Disorders, 48, 230–237. nervosa, and healthy controls. Journal of Abnormal Psychology,
Peterson, C. B., Berg, K. C., Crosby, R. D., Lavender, J. M., 123, 258–272.
Accurso, E. C., Ciao, A. C., . . . Wonderlich, S. A. (2017). The Schmidt, U., & Treasure, J. (2006). Anorexia nervosa: Valued
effects of psychotherapy treatment outcome in bulimia and visible. A cognitive-interpersonal maintenance model
nervosa: Examining indirect effects through emotion and its implications for research and practice. British Journal
regulation, self-directed behavior, and self-discrepancy in the of Clinical Psychology, 45, 343–366.
mediation model. International Journal of Eating Disorders, Seidel, M., Petermann, J., Diestel, S., Ritschel, F., Boehm, I.,
50, 636–647. King, J. A., . . . Ehrlich, S. (2016). A naturalistic examination
Polivy, J., & Herman, P. (1993). Etiology of binge eating: of negative affect and disorder-related rumination in
Psychobiological mechanisms. In C. G. Fairburn (Ed.), Binge anorexia nervosa. European Child and Adolescent Psychiatry,
eating: Nature, assessment, and treatment (pp. 173–205). 25, 1207–1216.
New York, NY: Guilford Press. Selby, E. A., Cornelius, T., Fehling, K. B., Kranzler, A., Panza,
Racine, S. E., Forbush, K. T., Wildes, J. E., Hagan, K. E., E. A., Lavender, J. M., . . . & Crow, S. J. (2015). A perfect
Pollack, L. O., & May, C. (2016). Voluntary emotion regulation storm: Examining the synergistic effects of negative and
in anorexia nervosa: A preliminary emotion-modulated startle positive emotional instability on promoting weight loss
investigation. Journal of Psychiatric Research, 77, 1–7. activities in anorexia nervosa. Frontiers in Psychology, 6, 1–33.
Racine, S. E., & Horvath, S. A. (2018). Emotion dysregulation Selby, E. A., Doyle, P., Crosby, R. D., Wonderlich, S. A., Engel,
across the spectrum of pathological eating: Comparisons S. G., Mitchell, J. D., & Le Grange, D. (2012). Momentary
among women with binge eating, overeating, and loss of emotion surrounding bulimic behaviors in women with
control eating over eating. Eating Disorders: The Journal of bulimia nervosa and borderline personality disorder. Journal
Treatment and Prevention, 26, 13–25. of Psychiatric Research, 46, 1492–1500.
Racine, S. E., Keel, P. K., Burt, S. A., Sisk, C. L., Neale, M., Sifneos, P. E., Apfel-Savitz, R., & Frankel, F. H. (1977). The
Boker, S., & Klump, K. L. (2013). Exploring the relationship phenomenon of ‘alexithymia’. Psychotherapy and Psychosomatics,
between negative urgency and dysregulated eating: Etiologic 28, 47–57.
associations and the role of negative affect. Journal of Slane, J. D., Burt, S. A., & Klump, K. L. (2011). Genetic and
Abnormal Psychology, 122, 433–444. environmental influences on disordered eating and depressive
Racine, S. E., & Martin, S. J. (2016). Exploring divergent symptoms. International Journal of Eating Disorders, 44,
trajectories: Disorder-specific moderators of the association 605–611.
between negative urgency and dysregulated eating. Appetite, Smyth, J. M., Wonderlich, S. A., Heron, K. E., Sliwinski, M. J.,
103, 45–53. Crosby, R. D., Mitchell, J. E., & Engel, S. G. (2007). Daily
Racine, S. E., VanHuysse, J. L., Keel, P. K., Burt, S. A., Neale, and momentary mood and stress are associated with binge
M. C., Boker, S., & Klump, K. L. (2017). Eating disorder- eating and vomiting in bulimia nervosa patients in the
specific risk factors moderate the relationship between natural environment. Journal of Consulting and Clinical
negative urgency and binge eating: A behavioral genetic Psychology, 75, 629–638.
investigation. Journal of Abnormal Psychology, 126, 481–494. Stein, R. I., Kenardy, J., Wiseman, C. V., Dounchis, J. Z.,
Racine, S. E., & Wildes, J. E. (2013). Emotion dysregulation and Arnow, B. A., & Wilfley, D. E. (2007). What’s driving the
symptoms of anorexia nervosa: The unique roles of lack of binge in binge eating disorder? A prospective examination of
emotional awareness and impulse control difficulties when precursors and consequences. International Journal of Eating
upset. International Journal of Eating Disorders, 46, 713–721. Disorders, 40, 195–203.
Racine, S. E., & Wildes, J. E. (2015a). Emotion dysregulation Stice, E., Marti, C. N., & Rohde, P. (2013). Prevalence, incidence,
and anorexia nervosa: An exploration of the role of childhood impairment, and course of the proposed DSM-5 eating
abuse. International Journal of Eating Disorders, 48, 55–59. disorder diagnoses in an 8-year prospective community

study of young women. Journal of Abnormal Psychology, 122, Wallace, L. M., Masson, P. C., Safer, D. L., & von Ranson,
445–457. K. M. (2014). Change in emotion regulation during the
Svaldi, J., Caffier, D., & Tuschen-Caffier, B. (2010). Emotion course of treatment predicts binge abstinence in guided self-
suppression but not reappraisal increases desire to binge in help dialectical behavior therapy for binge eating disorder.
women with binge eating disorder. Psychotherapy and Journal of Eating Disorders, 2, 1–9.
Psychosomatics, 79, 188–190. Whiteside, U., Chen, E., Neighbors, C., Hunter, D., Lo, T., &
Svaldi, J., Griepenstroh, J., Tuschen-Caffier, B., & Ehring, T. Larimer, M. (2007). Difficulties regulating emotions: Do
(2012). Emotion regulation deficits in eating disorders: binge eaters have fewer strategies to modulate and tolerate
A marker of eating pathology or general psychopathology? negative affect? Eating Behaviors, 8, 162–169.
Psychiatry Research, 197, 103–111. Whiteside, S. P., & Lynam, D. R. (2001). The Five Factor Model
Svaldi, J., & Naumann, E. (2014). Effects of rumination and and impulsivity: Using a structural model of personality to
acceptance on body dissatisfaction in binge eating disorder. understand impulsivity. Personality and Individual Differences,
European Eating Disorders Review, 22, 338–345. 30, 669–689.
Svaldi, J., Tuschen-Caffier, B., Lackner, H. K., Zimmermann, S., Wildes, J. E., & Marcus, M. D. (2011). Development of emotion
& Naumann, E. (2012). The effects of emotion regulation acceptance behavior therapy for anorexia nervosa: A case
on the desire to overeat in restrained eaters. Appetite, 59, series. International Journal of Eating Disorders, 44, 421–427.
256–263. Wildes, J. E., Marcus, M. D., Bright, A. C., & Dapelo, M.
Svaldi, J., Tuschen-Caffier, B., Trentowska, M., Caffier, D., & (2012). Emotion and eating disorder symptoms in patients
Naumann, E. (2014). Differential caloric intake in overweight with anorexia nervosa: An experimental study. International
females with and without binge eating: Effects of a Journal of Eating Disorders, 45, 876–882.
laboratory-based emotion-regulation training. Behaviour Wildes, J. E., Marcus, M. D., Cheng, Y., McCabe, E. B., &
Research and Therapy, 56, 39–46. Gaskill, J. A. (2014). Emotion acceptance behavior therapy
Tapajóz, P. S. F., Soneira, S., Aulicino, A., & Allegri, R. F. for anorexia nervosa: A pilot study. International Journal of
(2013). Theory of mind in eating disorders and their Eating Disorders, 47, 870–874.
relationship to clinical profile. European Eating Disorders Wildes, J. E., Marcus, M. D., Crosby, R. D., Ringham, R. M.,
Review, 21, 479–487. Dapelo, M. M., Gaskill, J. A., & Forbush, K. T. (2011). The
Tárrega, S., Fagundo, A. B., Jiménez-Murcia, S., Granero, R., clinical utility of personality subtypes in patients with
Giner-Bartolomé, C., Forcano, L., . . . & Konstantas, D. anorexia nervosa. Journal of Consulting and Clinical Psychology,
(2014). Explicit and implicit emotional expression in bulimia 79, 665–674.
nervosa in the acute state and after recovery. PloS One, 9, 1–7. Wildes, J. E., Ringham, R. M., & Marcus, M. D. (2010).
Tchanturia, K., Dapelo, M. A. M., Harrison, A., & Hambrook, Emotion avoidance in patients with anorexia nervosa: Initial
D. (2015). Why study positive emotions in the context of test of a functional model. International Journal of Eating
eating disorders? Current Psychiatry Reports, 17, 1–12. Disorders, 43, 398–404.
Thompson, R. A., & Calkins, S. D. (1996). The double-edged Wolz, I., Agüera, Z., Granero, R., Jiménez-Murcia, S., & Frank, S.
sword: Emotional regulation for children at risk. Development (2015). Emotion regulation in disordered eating: Psychometric
and Psychopathology, 8, 163–182. properties of the difficulties in emotion regulation scale
Vansteelandt, K., Probst, M., & Pieters, G. (2013). Assessing among Spanish adults and its interrelations with personality
affective variability in eating disorders: Affect spins less in and clinical severity. Frontiers in Psychology, 6, 1–13.
anorexia nervosa of the restrictive type. Eating Behaviors, 14, Wonderlich, S. A., Peterson, C. B., Crosby, R. D., Smith, T. L.,
263–268. Klein, M. H., Mitchell, J. E., & Crow, S. J. (2014). A
Vansteelandt, K., Rijmen, F., Pieters, G., Probst, M., & randomised controlled comparison of integrative cognitive-
Vanderlinden, J. (2007). Drive for thinness, affect regulation affect therapy (ICAT) and enhanced cognitive-behavioral
and physical activity in eating disorders: A daily life study. therapy (CBT-E) for bulimia nervosa. Psychological Medicine,
Behaviour Research and Therapy, 45, 1717–1734. 44, 543–553.

CH A PTE R
24 Self-Inflicted Injury
Erin A. Kaufman and Sheila E. Crowell
Abstract
Leading theories and an increasingly large body of empirical work each implicate emotion dysregulation
as a central contributor to the emergence and maintenance of a range of self-injurious behaviors. In
fact, self-inflicted injury (SII) often serves as a maladaptive emotion regulation strategy. In this chapter,
we review shared biological and contextual contributors to both conditions, and discuss mutually
reinforcing influences on their development. Available evidence indicates that emotion dysregulation
and SII are particularly likely to emerge when biologically vulnerable individuals are reared in specific
developmental contexts. However, we cannot yet accurately predict which affective patterns mark
imminent risk for SII. Although research on links between emotion dysregulation and SII has burgeoned
in recent years and associations between these conditions are well established, mediating and moderating
pathways require further exploration. We review recent findings, current methodological barriers, and
directions for future research.
Keywords: self-inflicted injury, suicide, emotion dysregulation, affective variability, etiology
Introduction maintenance of SII (e.g., Anestis, Bagge, Tull,

Self-inflicted injury (SII)—including both n
onsuicidal & Joiner, 2011; Ammerman, Kleiman, Uyeji, Knorr,
self-harm and suicide attempts—is a topographi- & McCloskey, 2015; Law, Khazem, & Anestis, 2015;
cally diverse condition with various etiological Linehan, 1993). Emotion dysregulation is a common
influences (Crowell, Derbidge, & Beauchaine, developmental precursor to initiation of nonsuicidal
2014). Such behavior can be understood as deliber- self-injury (NSSI; e.g., cutting, burning, etc., without
ate and self-induced destruction of bodily tissue any intent to die), a well-replicated maintaining
for nonculturally sanctioned purposes (American factor for NSSI (e.g., Klonsky, 2007, 2009), and a
Psychiatric Association [APA], 2013). SII may occur proximal risk factor for suicide attempts (Ammerman
once in a person’s life, yet often becomes repetitive et al., 2015; Andover & Morris 2014; Armey,
and more severe over time (Andrews, Martin, Crowther, & Miller, 2011; Bagge, Littlefield, &
Hasking, & Page, 2013; Brezo et al., 2008; Nock, Glenn, 2017). In longitudinal studies, affective in-
2010). Historically, scientists thought of SII as stability (defined as frequent and unpredictable
a symptom or consequence of other psychiatric emotional changes, moodiness, low threshold for
diagnoses. However, the behavior is better con- emotional arousal, high emotional intensity, irri-
ceptualized as transdiagnostic, since it is observed tability, and impatience with a low threshold for
in numerous psychiatric disorders (Hoertel et al., annoyance) differentiates nonattempters from
2015; National Institute of Mental Health one-time suicide attempters (Brezo et al., 2008).
[NIMH], 2011). Furthermore, children who exhibit severe emotion
Leading theories implicate emotion dysregulation dysregulation are more likely to develop SII and
as a key etiological factor in the emergence and suicidal ideation by adolescence compared with
345
peers (e.g., Deutz, Geeraerts, Baar, Deković, & much remains to be learned, as indicated in sections
Prinzie, 2016). Studies consistently find higher where we discuss recent findings, methodological
emotional intensity, deficits in emotional expressivity, barriers to improved understanding of etiology, and
and greater difficulty tolerating emotional distress directions for future research.
among individuals who engage in SII compared
with those without such histories (Iancu et al., 1999; Terms and Concepts
Klonsky, 2009; Muehlenkamp, Peat, Claes, & Smits Self-Inflicted Injury
2012; Nock & Mendes, 2008; Rajappa, Gallagher, Historically, research on SII has been hampered by
& Miranda, 2012). overlapping, vague, and sometimes contradictory
Notably, SII itself often serves as a maladaptive definitions of key constructs (Silverman, Berman,
emotion regulation strategy (Houben et al., 2017; Sanddal, O’Carroll, & Joiner, 2007a, 2007b). Even
Linehan, 1993; Nock & Prinstein, 2004). The most today, few if any terms enjoy universal acceptance.
frequently endorsed reason for engaging in self-harm This has led to significant confusion within the field,
is to escape, circumvent, or otherwise cope with and to difficulties generalizing findings across diverse
aversive affective states (Baetens, Claes, Willem, clinical populations. A key consideration is intent,
Muehlenkamp, & Bijttebier, 2011; Edmondson, defined by the level of conscious desire an individual
Brennan, & House, 2016; Jacobson, Batejan, has to escape from or end his or her life, and the
Kleinman, & Gould, 2013; Chapman, Gratz, & degree to which he or she has resolved to do so
Brown, 2006; Klonsky, 2007; Van Orden et al., (Silverman et al., 2007a). Self-injury can occur both
2015). Retrospective self-report and data collected with and without a desire to die, so separate terms
using real-time sampling indicate that high arousal have evolved to demarcate intent. The term NSSI
and negatively valenced affective states increase refers to acts of bodily harm without conscious intent
prior to, and gradually decrease following, SII to die, whereas ambivalent SII refers to destruction of
(Armey et al., 2011; Claes, Klonsky, Muehlenkamp, bodily tissue associated with uncertain intent to die.
Kuppens, & Vandereycken, 2010; Klonsky, 2009; In contrast, suicide attempts, which may or may not
Nock, Prinstein, & Sterba, 2009). result in death, vary widely from any nonzero level of
Although temporarily effective in regulating intent to certain intention to die. Table 24.1 presents
negative affect, those who engage in SII typically these and additional common SII-related terms.
experience significant deterioration in emotional SII is a deliberately broad term that captures a
state only minutes following an episode (Favazza & continuum of self-injurious behaviors, ranging
Conterio, 1989; Houben et al., 2017; Kamphuis, from NSSI to attempted and completed suicide.
Ruyling, & Reijntjes, 2007). Moreover, SII exacer- Including all self-injurious acts under a general de-
bates emotion dysregulation deficits over time scription has benefits and limitations. Historically,
(Andrews et al., 2013; Gratz & Tull, 2010). In con- important distinctions between various SII behav-
trast, improved emotion regulation contributes to iors were often overlooked (see Linehan, 1997;
SII cessation (see, e.g., Duggan, Heath, & Hu, Muehlenkamp & Gutierrez, 2004), and suicidal
2015; Gratz, Bardeen, Levy, Dixon-Gordon, & Tull, self-harm and NSSI were assumed to serve identical
2015; Slee, Spinhoven, Garnefski, & Arensman, functions, which may or may not be the case
2008; Whitlock, Prussien, & Pietrusza, 2015). (Simpson, 1950; Zilboorg, 1936a, 1936b). For the
Following from these and other findings, many re- past several decades, researchers have sought to
searchers conceptualize SII as a specific manifestation divide SII into meaningful subtypes based on level
of a broader deficit in adaptive emotion regulation of intent, associated function(s), lethality of method,
(Chapman et al., 2006; Gratz & Roemer, 2004; and physical outcomes associated with self-harm
Linehan, 1993). (e.g., Beautrais, Joyce, & Mulder, 1996; Linehan
In this chapter, we review biological and contex- et al., 2006; Zlotnick, Mattia, & Zimmerman, 1999).
tual contributors to emotion dysregulation and SII, Of note, classifying by physical outcome can be prob-
and discuss mutually reinforcing influences on lematic because people who use the same means with
development of these transdiagnostic vulnerabilities similar intent may incur very different results. For
to psychopathology. As demonstrated in the sections example, two individuals may ingest the same dose
to follow, emotion dysregulation and SII emerge of the same harmful substance, with little or no
when vulnerable individuals are reared in specific physical damage incurred by one who is d iscovered
developmental contexts. Although much has been by a relative or friend, versus very serious damage or
learned about these phenomena in recent years, death incurred by another who is not discovered.
346 Emotion Dysregul ation and Self-Inflicted Injury

Table 24.1. Self-Inflicted Injury–Related Terms (Silverman et al., 2007a, 2007b)
Term Definition
Intent Level of conscious desire an individual has to escape from or end his or her life
and the degree to which he or she has resolved to do so.
Self-inflicted injury/self-harm Nonaccidental actions that result in some destruction of bodily tissue or have a
potential effect on bodily functioning.
Nonsuicidal self-injury (NSSI) Self-induced destruction of bodily tissue without any intention to die.
Ambivalent self-inflicted injury Self-induced destruction of bodily tissue and/or deliberate engagement in behaviors
(SII) that place the individual at risk for injury/death (e.g., walking into traffic,
playing roulette with a loaded gun) with uncertain intention to die.
Suicide attempt Self-induced destruction of bodily tissue and/or deliberate engagement in
behaviors that place the individual at risk for injury/death with any nonzero
level of intention to die.
Suicide Intentional self-inflicted injury that results in death.
Thwarted suicide attempt An interrupted suicide attempt, through either discovery by others or losing
access to means of causing injury.
Suicidal threat A verbal or written communication regarding some desire to die and some
degree of intention to act on such desires. This term has fallen out of favor with
many in the field due to its implied associations with manipulation and coercion
(which are frequently unfounded and pejorative).
Suicidal gesture An action communicating some desire to die and some degree of intention to act
on such desires. Typically, such actions are low-lethality behaviors and unlikely
to result in serious damage to bodily tissue. This term has fallen out of favor with
many in the field due to its implied associations with manipulation and coercion
(which are frequently unfounded and pejorative).
Parasuicide An outdated term for nonfatal suicide attempt or NSSI. This term has fallen
out of favor due to implications that parasuicidal behaviors occur due to some
suicidal intent, which is often not the case.
Suicide-related ideations Thoughts about ending one’s life, which may or may not be accompanied by intent.
Passive suicide-related ideations Thoughts about ending one’s life or death without conscious intent or planning
to do so. Often experienced as “unprompted” and without intent.
Suicide-related communications Verbal or written communication regarding some desire to die and some degree
of intention to act on such desires.
Lethality The degree of risk of death associated with specific SII behaviors.
Lethality of means The degree of risk of death associated with specific SII methods/means.
Outcome The level of physical damage resulting from SII.
To complicate matters further, many infer level are sought, and obscure the dimensional nature of
of suicidal intent from the lethality of the method lethality and intent. Moreover, certain populations
selected, even though these are not necessarily related (e.g., youth) may frequently misunderstand which
(Linehan et al., 2006). Many studies also include means are most risky.
people who engaged in low-lethality behaviors On balance, most research has been conducted
such as repetitive cutting, burning, or bruising (e.g., with artificially restricted samples—limiting our
Simpson, 1975), lumping them together with others understanding of continuities in severity of SII and
who engage in more lethal means. Other studies how severity may differ across clinical populations
restrict their samples to participants based on be- (Crowell et al., 2014; Derbidge & Beauchaine,
haviors such as hanging, drowning, and shooting 2014). Those who study personality, mood, and
(e.g., Seiden, 1978). Although neither is necessarily psychotic disorders often examine SII only within
wrong, these sampling strategies can introduce their respective diagnostic group (e.g., Dworkin,
unwanted variability when homogeneous samples 1994; Heisel, Conwell, Pisani, & Duberstein, 2011;
Kaufman and Crowell 347

Large, Nielssen, & Babidge, 2010; Reutfors et al., (e.g., Cole, Martin, & Dennis, 2004). Throughout
2010). Although distinguishing among subtypes of this volume, we adopt this functionalist perspective
SII events has proved helpful, many researchers also and define emotion regulation by processes through
attempt to categorize people as either suicidal or which emotional experience and/or expression
nonsuicidal self-injurers. Recent studies frequently are shaped in the service of adaptive behavior
recruit based on these narrow phenotypes (e.g., those (Thompson, 1990). Notably, such processes may be
who have exclusively engaged in either NSSI or volitional or automatic (see Cole, Hall, & Hajal,
suicide attempts) and thus fail to capture how in- 2017) and occur through a range of attentional,
dividuals may move across the spectrum of self- cognitive, social, and behavioral mechanisms (see
injurious behaviors. Assessment measures often focus Aldao, Nolen-Hoeksema, & Schweizer, 2010).
on one category or another, despite evidence for We also take a functionalist perspective on emo-
common vulnerabilities and risk factors, and data tion dysregulation, which can be defined as patterns
showing that many who exhibit NSSI go on to of emotional experience and expression that impede
engage in both suicidal and nonsuicidal self-harm. goal-directed, adaptive behavior (see Beauchaine,
In fact, a history of NSSI is the single best predictor 2015; Beauchaine, Gatzke-Kopp, & Mead, 2007).
of eventual completed suicide (Hamza, Stewart, & In SII and many associated forms of psychopathology,
Willoughby, 2012; Klonsky, May, & Glenn, 2013). certain emotions, including anxiety, panic, and
In fact, longitudinal research shows that baseline sadness, are experienced too intensely or too pro-
rates of NSSI are a stronger predictor of suicidal tractedly to be adaptive. This definition contrasts
thoughts and attempts than baseline suicide attempts with some early conceptualizations, which defined
themselves (Asarnow et al., 2011; Guan, Fox, & emotion dysregulation solely by the absence of ef-
Prinstein, 2012). Such findings have important impli- fective volitional control over negative emotions.
cations for prevention efforts and clinical practice, yet Research on emotion dysregulation also reveals a
many therapists may be unaware that NSSI and number of dimensions to the construct. Gratz and
suicide attempts are so closely tied (Wilkinson, 2011). Roemer (2004) were the first to fully articulate this
In apparent contrast to these findings, the when they published the Difficulties in Emotion
Diagnostic and Statistical Manual for Mental Regulation Scale (DERS). The DERS was derived
Disorders, fifth edition (DSM-5; APA, 2013) now from factor analysis, which revealed six core emotion
classifies nonsuicidal self-injury disorder and sui- regulation difficulties: nonacceptance of emotional
cidal behavior disorder as distinct diagnoses in a responses (nonacceptance), difficulties engaging in
new section labeled “Conditions for Further Study.” goal-directed behavior (goals), impulse control
If adopted, these diagnoses will further reify artificial difficulties (impulse), lack of emotional awareness
distinctions among people who engage in self-injury. (awareness), limited access to emotion regulation
Categorical conceptualizations of SII may also strategies (strategies), and lack of emotional clarity
impede identification of individuals on high-risk (clarity). Current empirical work examines how
developmental trajectories and obscure important these specific emotion dysregulation dimensions
areas of overlap and divergence in biological vulner- may differentiate various SII behaviors (see later).
abilities and psychosocial risk factors associated with
various forms of SII (Crowell et al., 2014). We argue Theoretical Perspectives
that focusing on underlying individual differences Scientists are continually moving toward interactive,
that give rise to broad classes of behavior (such as multiple-levels-of-analysis approaches to better
emotion dysregulation) will improve our understand- understand mechanisms underlying stability and
ing of all forms of SII, both suicidal and nonsuicidal. change in psychopathology (Beauchaine & McNulty,
2013; Cicchetti & Blender, 2004; Crowell &
Emotion Dysregulation Kaufman, 2016; NIMH, 2011, National Advisory
Emotion regulation was once viewed as a unidimen- Mental Health Council Workgroup on Tasks and
sional process ranging from adaptive to maladaptive Measures for Research Domain Criteria 2016).
control over disruptive emotions (Thompson, 1994). Predominant etiological theories suggest that emo-
Since then, more differentiated theories have emerged. tion dysregulation and SII are most likely to develop
Emotion regulation researchers often focus on how among biologically vulnerable youth who are reared
individuals use emotion-related inputs and strategies in stressful caregiving environments—especially
to adapt to their environments and/or change contexts of invalidation, abuse, and neglect (see,
their emotional experiences or related behaviors e.g., Crowell, Beauchaine, & Linehan, 2009;

Guendelman, Owens, Galan, Gard, & Hinshaw, (Gray & McNaughton, 2000), externalizing
2016; Hinshaw et al., 2012). Although traditional presentations are more typically characterized by
models often placed greater emphasis on social dysregulated anger, aggression, and/or impulsivity
mechanisms, it is now well established that affect and have neural substrates in the mesolimbic
dysregulation and SII are byproducts of complex dopamine (DA) system (see Beauchaine, 2015;

transactions between neurobiological vulnerabilities Zisner & Beauchaine, 2016b). Generally, low striatal
and environmental risk factors across development DA activity and reactivity to incentives are associ-
(Beauchaine, Klein, Crowell, Derbidge, & Gatzke- ated with anhedonia and irritability (Forbes &
Kopp, 2009). These transactions begin as early as Dahl, 2012; Luking, Pagliaccio, Luby, & Barch,
conception and include intergenerational influences 2016; Zisner & Beauchaine, 2016a), whereas high
(Crowell & Kaufman, 2016). Here, we present a tonic levels of DA within mesolimbic structures are
brief overview of research indicating that identifiable associated with contentment and other pleasurable
temperamental vulnerabilities predispose to devel- affective states (e.g., Ashby, Isen, & Turken, 1999;
opment of emotion dysregulation. In turn, SII may Berridge, 2003; Berridge & Robinson, 2003;
eventually develop when combined with interper- Sharot, Shiner, Brown, Fan, & Dolan, 2009).
sonal stressors, depleted resources for effective regu- Although neural vulnerabilities in early-maturing
lation, and behavioral contingencies that reinforce bottom-up subcortical brain regions confer risk for
extreme affective displays. Commonalities between emotion dysregulation, top-down cortical brain
theories of emotion dysregulation and SII develop- networks are implicated in volitional self-regulation
ment are discussed. (see Beauchaine, 2015; Beauchaine & McNulty,
As described earlier, emotion dysregulation is a 2013). The prefrontal cortex (PFC) and its intercon-
common developmental precipitant of SII spectrum nections with subcortical structures are involved in
behaviors (Crowell et al., 2009). Linehan’s (1993) managing anxiety (e.g., through lateral PFC inhibi-
theory suggests that individuals with high baseline tion of amygdalar activity/reactivity) and impulsiv-
sensitivity to emotional stimuli, intense reactivity to ity (e.g., through orbitofrontal and dorsolateral
emotions, and a slow return to emotional baseline PFC inhibition of striatal activity/reactivity; see
are particularly vulnerable. Although shaped through- Davidson, 2002; Heatherton, 2011; Heatherton &
out the lifespan, these characteristics appear to be Wagner, 2011). Inadequate medial PFC control of
mediated by biological mechanisms—especially the amygdala and reduced connectivity between
early in development. For example, early environ- the amygdala and the orbitofrontal cortex are also
mental stressors appear to shape multiple biological implicated in emotional lability and deficient
systems, including genes involved in monoamine self-regulation (see Churchwell, Morris, Heurtelou,
neurotransmitter functioning (via epigenetic mech- & Kesner, 2009; Hilt, Hanson, & Pollak, 2011).
anisms), neurobiological stress systems, immune As noted previously, mounting evidence suggests
functioning, inflammatory processes, and more that these and other neural vulnerabilities interact
(e.g., Beauchaine et al., 2011; Conradt et al., in with environmental adversity—particularly within
press). Such biological adaptations shape lifelong interpersonal relationships—to potentiate emotion
patterns of emotion regulation when they interact dysregulation (see, e.g., Beauchaine & Zisner,
with core social affiliative processes (e.g., Doyle & 2017; Beauchaine et al., 2007). The caregiver–child
Cicchetti, 2017). relationship is the most formative postnatal context
for temperamentally vulnerable infants (Hughes,
A Developmental Model of Crowell, Uyeji, & Coan, 2012; Stepp, Whalen,
Emotion Dysregulation Pilkonis, Hipwell, & Levine, 2012). Early transac-
Propensities toward negative affectivity, emotional tions between parents and their children have last-
sensitivity, and emotional reactivity can be identified ing effects on youths’ affective and self-regulatory
by infancy and confer vulnerability to later emotion behaviors through a host of mechanisms (Diamond,
dysregulation (Beauchaine, 2001; Kagan, 2017). Fagundes, & Butterworth, 2012; Essex et al., 2013;
Temperamental or trait affectivity is mediated in part Laurent, 2014). For example, caregiver stress and
by heritable individual differences in neurological associated behaviors influence youth neurodevel-
functioning (see Beauchaine, 2015). Whereas in- opment in prefrontal brain regions responsible
ternalizing presentations characterized by excessive for social affiliation, executive function, and emotion
anxiety, panic, and melancholy are linked to vari- regulation (e.g., Hanson et al., 2010; Hughes
ations in septohippocampal system functioning et al., 2012; Pollak, 2015). The parent–child

context is also the primary training ground for (Beauchaine & McNulty, 2013; Coplan, Bowker, &
self-regulatory strategies (e.g., Bernier, Carlson, & Cooper, 2003; Molfese et al., 2010; Sidor, Fischer,
Whipple, 2010; Cipriano & Stifter, 2010). & Cierpka, 2017).
Early in development, children’s emotional and As such vulnerable children mature into tod-
physiological responses are often coregulated by dlerhood and preschool, they are often exposed to
primary caregivers (e.g., Fonagy, Gergely, & Target, social relationship dynamics that promote and
2007; Skowron, Cipriano-Essel, Benjamin, Pincus, maintain emotion dysregulation directly (Patterson,
& Van Ryzin, 2013). Parents facilitate emotion 1976, 1982; Linehan, 1993). Considerable research
regulation acquisition by accurately labeling their implicates harsh, inconsistent, and invalidating
child’s emotional expressions, validating their child’s parenting as key mediating mechanisms between
emotional experiences, and providing strategies to neurobiological vulnerability and both emotion
modulate emotional arousal within the relational dysregulation and SII (Crowell et al., 2005, 2009,
context (e.g., providing effective soothing when the 2013). Invalidating caregivers ignore, minimize, and/
infant is distressed; Fox, 1998). Effective coregula- or reject their children’s emotional expressions,
tion requires parents to appraise and respond to while intermittently reinforcing extreme emotional
moment-to-moment changes in infants’ emotional displays. Across development, family members esca-
states (Fonagy et al., 2007). Infants learn to associate late aversive behaviors and negative affect over thou-
their own regulation with contingent and responsive sands of interactions in attempt to get their needs
parental behaviors. As they mature, these skills met (see Crowell et al., 2009; Grove & Crowell, in
become integrated into their own behavioral rep- press; Linehan, 1993). Such escalations negatively
ertoires, facilitating autonomous self-regulation reinforce emotional lability and affect dysregulation
(see Calkins & Dedmon, 2000; Calkins, Graziano, because they effectively terminate dyadic interac-
Berdan, Keane, & Degnan, 2008). Thus, supportive tions that both parties wish to escape (hence the
parenting environments facilitate emotional and term “escape conditioning”; see Beauchaine &
behavioral stability and effective, reciprocal social Zalewski, 2016; Snyder, Schrepferman, & St. Peter,
skills (Ainsworth, 1989; Sroufe & Rutter, 1984). 1997). Over time, such escalations become more
Those who suffer early compromises in coregula- frequent and intense, resulting in physiological
tion—including those who experience abusive and arousal, poor emotional and behavioral control, and
neglectful parenting—fail to develop effective poor conflict resolution skills (Berman, Jobes, &
emotion regulation strategies, which renders them Silverman, 2006; Bongar, 2002; Kuo & Linehan,
vulnerable to both internalizing and externalizing 2009). SII may emerge as one strategy to reduce
psychopathology (Creaven, Skowron, Hughes, emotional distress (Nock, 2009). Prominent models
Howard, & Loken, 2013; Eisenberg, Spinrad, & of SII highlight emotional distress and interpersonal
Eggum, 2011; Hughes et al., 2012). difficulties as catalysts of the behavior (e.g., Joiner,
Youth are both affected by and actively influence 2005; Klonsky, 2007, 2009; Linehan, 1993). Of
their parents’ behavior. Infants with difficult tem- note, emotion regulation deficits mediate relations
peramental predispositions including high nega- between young adults’ feelings of alienation in both
tive emotionality are more challenging to parent parent and peer relationships and NSSI (Yurkowski
and at the same time more susceptible to harsh et al., 2015). Once established, emotion dysregula-
and nonsupportive caregiving (Belsky, Bakermans- tion and self-injury are exceedingly difficult to treat
Kranenburg, & van Ijzendoorn, 2007; Oddi, (e.g., Asarnow et al., 2011).
Murdock, Vadnais, Bridgett, & Gartstein, 2013). Interactive effects of trait vulnerabilities and
These relationship dynamics tax parents, who can social risk factors for emotion dysregulation can be
become overwhelmed. In turn, overwhelmed detected at the autonomic nervous system level.
mothers endorse fewer positive feelings about Studies have used respiratory sinus arrhythmia
their children and are less perceptive of and re- (RSA) as a measure of early emotional sensitivity
sponsive to their children’s behavioral cues (Crnic, and later emotional lability (Beauchaine, 2001,
Greenberg, Ragozin, Robinson, & Basham, 1983). 2015). RSA captures heart rate variability across the
Thus, aversive bidirectional relationship dynamics respiratory cycle and is an established index of
can emerge in which children’s temperamental at- vagally mediated parasympathetic influences on

tributes induce parental stress. This affects parenting cardiac activity (Berntson et al., 1994; Cacioppo
in ways that further compromise children’s socio- et al., 1994). Resting RSA appears to serve as a
emotional development and affect regulation skills biomarker of emotion regulation capacity, whereas

RSA reactivity is associated with in-the-moment were exposed to an algometer that exerted steady
regulation (Beauchaine, 2015). Like neurologically focal pressure on the tip of a finger. Those assigned
mediated affective instability, patterns of RSA re- to distraction were instructed to listen to and write
sponding also appear to be partially heritable down a series of neutral words. Controls sat alone
(Boomsma, Van Baal, & Orlebeke, 1990; Livesley quietly. All participants rated their positive and neg-
& Jang, 2008; Neijts et al., 2015). Theoretical and ative mood every 20 seconds. Those in the control
empirical evidence suggests that high RSA is generally condition did not experience mood improvement,
protective, whereas low RSA increases vulnerability whereas those in the distraction condition did.
to emotion dysregulation (Crowell et al., 2009; Those in the pain condition also reported mood im-
Porges, 1995, 2007; Thayer & Lane, 2009). For provement, but only if they were also highly
example, research with self-injuring adolescents has self-critical. In contrast, those who scored low on
identified a profile characterized by low RSA and a self-criticism felt significantly worse. Although the
negative slope on RSA reactivity during emotional predictive validity of such experiments is unknown,
and interpersonal stress (Crowell, Baucom, et al., results suggest that nonpainful distraction may be a
2014; Crowell et al., 2005). Taken together, multi- promising tactic for emotion regulation, yet also
ple methods of assessment indicate that emotion point to the importance of addressing self-criticism
dysregulation and SII often develop through common among affected individuals.
biological and environmental mechanisms. As reviewed earlier, key theories of self-harm
conceptualize emotion dysregulation as a vulnera-
Why Is Self-Inflicted Injury Effective? bility to SII, which then functions as a regulation
There are competing theoretical perspectives on strategy (e.g., Linehan, 1993). Notably, however,
why SII functions to regulate aversive affective states correlates of SII may not fully explain its emergence.
(McKenzie & Gross, 2014). Clarifying precise Vulnerabilities and risk factors precede outcomes
mechanisms could lead to more effective and and offer some degree of prospective prediction.
targeted treatments. According to the pain-offset Emotion dysregulation is sometimes treated as a
relief hypothesis, inflicting and then removing causal risk factor. However, we should be circum-
physical pain can produce emotional relief, as spect about such claims since it characterizes most
overlapping brain regions process both affective and forms of psychopathology, only some of which are
bodily pain signals (see Eisenberger, 2012; Franklin associated with SII (see Beauchaine, 2015). As re-
et al., 2013). Self-harm may also be used as a means viewed previously, by itself emotion dysregulation is
of self-punishment (Itzhaky, Shahar, Stein, & Fennig, likely not sufficient for development of SII. Rather,
2015; McKenzie & Gross, 2014). Individuals it potentiates SII in the presence of other vulnerabil-
who engage in NSSI exhibit greater levels of self- ities (Beauchaine et al., 2009; Crowell et al., 2009).
derogation compared to individuals who do not Nevertheless, improving emotion dysregulation is
(Klonsky & Muehlenkamp, 2007). Other lines of imperative in treating SII given its clear maintaining
research highlight social communicative functions of role in expression of the behavior (Linehan, 1993).
SII, suggest that physical pain may refocus attention Despite numerous empirical findings and re-
and thereby improve mood (see McKenzie & Gross, views linking emotion dysregulation and SII, a
2014), and/or release endogenous o pioids with asso- recent meta-analysis surveying the past 50 years of
ciated analgesic effects (e.g., Stanley et al., 2010). research did not support an association between
Laboratory research has produced mixed results emotion dysregulation and suicide-related thoughts
depending on samples, which may suggest that SII and behaviors (Franklin et al., 2017). These authors
serves different functions at different times for dif- examined risk and protective factors for SII by col-
ferent people (McKenzie & Gross, 2014). For exam- lapsing 4,084 reported effect sizes into 16 categories.
ple, a recent study of individuals who engaged in Effect sizes related to emotion dysregulation were
moderate to severe NSSI over the previous year ex- included under internalizing psychopathology, in-
amined how distraction, pain, and self-criticism including anxiety disorders, mood disorders, hope-
teracted to influence mood (Fox, Toole, Franklin, & lessness, and sleep disturbance. Surprisingly, no risk
Hooley, 2016). Participants were randomly assigned factor category or subcategory emerged as a stronger
to pain, distraction, and control conditions, and predictor than any other. Furthermore, no unique
negative mood was induced by asking them to reset of vulnerabilities/risk factors predicted specific
flect on an occasion when they failed or let them- SII outcomes (e.g., suicide ideation, suicide plan,
selves down. For the pain condition, participants suicide attempt, or suicide death). Internalizing

psychopathology, demographics, externalizing psy- for identifying and describing patterns through
chopathology, and social factors were the most which contextual factors influence participants’
commonly examined risk factors reported in the SII thoughts, emotions, and actions (Bolger, Davis, &
literature. Most vulnerability/risk factor categories— Rafaeli, 2003). By selecting appropriate event sam-
including emotion dysregulation—were weak pre- ples (e.g., those of high, moderate, and low risk for
dictors of suicidal thoughts and actions. Aggression SII based on current etiological theories), EMA can
and impulsivity were similarly weak predictors, in elucidate how proximal risk factors may interact
spite of being common to etiological theories of SII with distal and/or chronic risk and vulnerabilities to
(e.g., Crowell et al., 2009). predict a range of SII-related outcomes (Armey,
Franklin and colleagues (2017) speculated that 2012; see Chapter 29). Because of the naturalistic
their results could be attributable to methodological and longitudinal nature of this methodology, EMA
limitations observed across SII studies. Existing provides a unique opportunity to explore proximal
research has evaluated restricted ranges of vulnera- factors that elicit SII.
bilities and risk factors over long follow-ups with EMA has already begun to refine our under-
few data collection points, and usually in isolation standing of relations between emotional experiences
rather than in combination. In addition, and as and SII, to help identify possible intervention tar-
noted earlier, contributors to SII and suicidal be- gets, and to establish timelines for SII precipitants
haviors do not confer large main effects, but rather and action. For example, Muehlenkamp et al. (2009)
interact to maximize risk. For example, in our past examined self-reported affect preceding, during,
research on SII (Crowell et al., 2005, 2008), neither and following episodes of SII among participants
adolescent serotonin levels nor dyadic interaction with bulimia nervosa. Participants who endorsed
quality (including dysregulated emotion) with parents NSSI during the assessment period described their
predicted appreciable variance in self-harm events. self-harm episodes as preceded by both an increase
In contrast, their interaction accounted for 64% of in negative affect and a decrease in positive affect.
observed variance in self-harm. Had we not evaluated Following NSSI, participants reported decreases in
the interaction, we would have concluded that negative affect and increased positive affect.
neither serotonin levels nor dysregulation in dyadic Although long theorized in the literature (e.g.,
exchanges with mothers plays a role in the etiology Linehan, 1993), this study provided direct evidence
of SII. Main-effects models are therefore limited for demonstrating that NSSI may function to negative
studying SII given the complex multiply deter- affect. Others have extended this work by identify-
mined nature of the behaviors (Crowell et al., 2014). ing which forms of negative affect are most closely
tied to SII urges and actions. Nock and colleagues
Current Methods and Findings (2009) found that adolescents endorsed using
A number of novel methods are currently being self-harm in efforts to reduce negative affect for
applied in studies of SII. In particular, ecological 65% of their NSSI episodes, and that feelings of
momentary assessment (EMA) and investigations of sadness, anger, and being overwhelmed were par-
mediating and moderating mechanisms are contin- ticularly likely to precipitate self-harm.
ually refining our understanding of relations be- Armey et al. (2011) and Armey, Nugent, and
tween SII and emotion dysregulation (e.g., Fox Crowther (2014) have used dispositional measures
et al., 2016). Researchers are also beginning to ex- in combination with EMA-measured self-reported
amine associations between specific dimensions of affect to predict the presence and severity of NSSI.
emotion dysregulation and diverse forms of SII. EMA measures of negative emotional experiences
contributed incrementally to predicting NSSI sever-
Ecological Momentary Assessment ity, above and beyond pretest measures. Consistent
When using EMA, participants report on their ex- with the Muehlenkamp et al. (2009) findings,
periences as they happen in day-to-day life. EMA is Armey found that negative affect increased prior to
usually implemented through use of computerized NSSI events, peaked during these episodes, and
personal diaries, through which participants dis- faded gradually in the hours following self-harm.
cretely complete assessments multiple times over This pattern was only observed among participants
days or even weeks. Sampling can occur on a fixed who engaged in NSSI during the course of the
schedule, on a random schedule, as experiences of study, and was absent for individuals with a history
interest occur naturally, or some combination of of self-injury but no self-harm while enrolled (Armey
these approaches. EMA is particularly well suited et al., 2011). Although SII is often conceptualized as

an impulsive action (Mann, Waternaux, Haas, & Forty percent of the sample belonged to a class
Malone, 1999), Armey et al. (2014) reported that who reported relatively low mean levels of intensity
changes in negative affect associated with eventual and frequency of feeling hostile, alone, and afraid—
NSSI were often detectable up to 8 hours prior to both the day before and day of their suicide attempt,
SII events. These findings suggest that SII may be with a significant increase in the hours just prior to
predictable—and therefore potentially prevented— their self-harm. Twenty-two percent of the sample re-
through careful evaluation of changing affective ported high mean levels of negative affect the day pre-
experiences. In addition to being less biased than ceding their suicide attempt with even higher negative
retrospective self-reports, EMA can help to identify affect the day of and a spike during the hours just
precipitants of SII that lie outside of participants’ prior to SII. Twenty-one percent of the sample re-
awareness. In fact, Armey et al. observed a funda- ported drastic shifts in affective experience, with low
mental disconnect between participants’ awareness to moderate intensity the day before and moderate to
of their affective experiences and their subjective high intensity on the day of their suicide attempt.
perception of why SII occurs. Those affected by SII Finally, a mixed subset emerged in which some types
may not be aware of how accumulating affective of affect were high (dissatisfied with self and alone)
changes contribute to self-injury, and instead place over the 48 hours before their attempts, whereas
disproportionate emphasis on acute stressors that others remained relatively low in magnitude (hostile
immediately precede the events. and fear). Although these results highlight how un-
Finally, EMA demonstrates that SII may derstanding within-person affective experience may
ultimately increase negative affect. Houben and be important for suicide prevention, we should take
colleagues (2017) used experience sampling among care not to reify subgroups as distinct from one an-
30 inpatients with high borderline personality other. Indeed, effect sizes separating groups were
disorder symptoms. Elevated negative affect pre- modest, and longitudinal latent class analysis is known
dicted a higher probability of subsequent NSSI; to extract classes from continuously distributed data
however, the authors did not observe indications (Bauer & Curran, 2003). Nevertheless, results suggest
of emotional relief following self-harm. In fact, that one-size-fits-all approaches to understanding re-
participants reported a further increase of negative lations between a ffective states and SII are likely insuf-
emotionality and decrease in positive affect within ficient for deterring suicide.
hours of NSSI. Thus, SII may act to increase the
frequency of negative affect overall. Body regard
Another important factor that influences relations
Moderating and Mediating Influences between emotion dysregulation and SII is body
Affective variability regard—how people perceive, experience, and care
Mood shifts often precede SII (especially increases for their bodies (Muehlenkamp, Bagge, Tull, &
in rage, anger, guilt, loathing, and anxiety/agita- Gratz, 2013). Those with low body regard are often
tion; e.g., Ammerman et al., 2015; Armey et al., detached from bodily experiences, tend to devalue
2011; Nock et al., 2009; Rudd et al., 2006). their bodies, and show ambivalence toward protect-
However, these affective experiences and general ing or taking care of their bodies (Muehlenkamp
mood lability are common experiences among et al., 2013). Negative body image and body dissat-
those at highest risk—making it difficult to iden- isfaction are associated prospectively with suicidal
tify which specific individual is in imminent ideation and behavior across sexes and cultures
danger following which specific event. Thus, al- (e.g., Kim & Kim, 2009; Rodriguez-Cano, Beato-
though recognizing emotional precipitants to SII Fernandez, & Llario, 2006) and are associated con-
is undoubtedly beneficial, affective warning signs sistently with NSSI (Muehlenkamp & Brausch,
are subject to both inter- and intraindividual 2012; Nelson & Muehlenkamp, 2012; Ross, Heath,
variability. Research using timeline follow-back & Toste, 2009). Muehlenkamp and colleagues
methods suggests variability among suicide at- (2013) found that emotion regulation was associ-
tempters based on specific affective patterns lead- ated with NSSI only among those who reported low
ing to SII (Bagge et al., 2017). Self-dissatisfaction, levels of body regard. Furthermore, emotion dys-
hostility, feeling alone, and feeling afraid increased regulation, borderline personality disorder, and gen-
across their full sample of hospitalized individuals eral negative affect were not related to NSSI when
in the 6 hours preceding suicide attempts. the authors controlled for body regard, suggesting it
However, four classes of attempters emerged. may be a core moderator of NSSI.

In another study, Muehlenkamp et al. (2005) and perceived limited access to emotion regulation
found an indirect effect of negative body image on strategies. Taken together, results suggest that clini-
NSSI among college women via depressive symp- cians may see the most incremental benefit from
toms. Thus, a combination of emotional distress teaching self-harming individuals more adaptive
and body image problems may help explain self- and nonavoidant methods of responding to their
harm engagement (Muehlenkamp et al., 2005). emotions and skills needed to accurately identify,
Others have reported that emotion dysregulation label, and differentiate among emotional states.
mediates relations between negative body image
and NSSI among men and women (Duggan, Toste, Theoretical Synthesis and
& Heath, 2013). Taken together, results indicate Future Directions
that negative affect surrounding body image may be Leaders in the field have devoted considerable
a critical risk factor for NSSI. effort and resources to SII prevention for decades.
Yet we have not witnessed an observable reduction
Specific Emotion Dysregulation Dimensions in suicide rates, and prediction remains diffi-
and Self-Inflicted Injury cult—as with all low-base-rate behaviors. Despite
Researchers have begun to examine whether some these struggles, effective treatments such as dialec-
aspects of emotion dysregulation are stronger cortical behavior therapy (Linehan, 1993) have
relates of SII than others. DERS total scores, as well emerged, and sophisticated assessment techniques
as lack of access to effective emotion regulation such as EMA are refining our understanding of
strategies, emotional nonacceptance, and lack of when and how to intervene most effectively
emotional clarity, are associated with NSSI above (Armey, 2012). Each suggests high potential bene-
and beyond other common correlates such as sub- fit for targeting emotion dysregulation as a core
stance use, familial discord, borderline personality vulnerability to SII.
disorder symptoms, trauma, and childhood mal- Etiological theories and empirical findings indi-
treatment (Adrian, Zeman, Erdley, Lisa, & Sim, cate that affective instability and deficient problem
2011; Anderson & Crowther, 2012; Gratz & Tull, solving in the face of aversive emotional states (1)
2010; Muehlenkamp, Kerr, Bradley, & Adams-Larsen, emerge earlier in development than SII, (2) are
2010; Sim, Adrian, Zeman, Cassano, & Friedrich, often core features of caregiving contexts, and (3)
2009). Gratz and Roemer (2008) found that lim- potentiate SII engagement among temperamentally
ited access to effective emotion regulation strategies vulnerable individuals. Thus, early family interven-
and a lack of emotional clarity were both associated tions may be needed to most effectively prevent SII
with SII histories among college women, and ac- and related conditions. It may be critical to provide
counted for unique variance in self-harm frequency, support to at-risk families, beginning as early as in-
above and beyond the other risk factors in their fancy, when known vulnerabilities and risk factors
models. for emotion dysregulation first emerge. As already
In another study, substance users with SII histories demonstrated (David, David, & Dobrean, 2014;
reported significantly higher levels of overall emo- Miller, Rathus, & Linehan, 2007), helping parents
tion dysregulation and specific problems with to learn flexibility in responding to their children,
emotional nonacceptance, limited access to effective to differentiate and communicate their emotional
emotion regulation strategies, and difficulties in en- experiences, and to model adaptive emotion regula-
gaging in goal-directed behaviors when distressed tion techniques can shift aversive family dynamics
compared to substance users who never engaged in and encourage effective regulation skills among
SII. These findings held when controlling for other children (see Crowell et al., 2017). Decades of re-
key risk factors that are typically associated with SII search show how difficult it can be to raise a tem-
and emotion dysregulation (e.g., child abuse, sub- peramentally vulnerable child (e.g., Fox & Stifter,
stance use severity, posttraumatic stress disorder, 1989; Degnan et al., 2015). Negative affectivity and
and personality pathology). Rajappa and colleagues high reactivity evoke parental distress, aggression,
(2012) examined whether specific emotion dysregu- ambivalence, withdrawal, and self-perceptions of
lation dimensions distinguished individuals with parenting incompetence. Given that early child-
differing histories of suicidality. They found that hood is a critical stage for emotion regulation skill
participants with multiple suicide attempts differed acquisition, it is also a critical point for prevention
from those without suicidal ideation and no past at- of SII and suicide prevention. Relative to costly
tempts on nonacceptance of emotional responses and intensive adulthood treatments for SII, such

as emergency room utilization and inpatient Andrews, T., Martin, G., Hasking, P., & Page, A. (2013).
psychiatric hospitalization especially, providing
Predictors of continuation and cessation of nonsuicidal self-
injury. Journal of Adolescent Health, 53, 40–46.
emotion regulation–focused therapy to children Anestis, M. D., Bagge, C. L., Tull, M. T., & Joiner, T. E. (2011).
and families is cost-effective and has high potential Clarifying the role of emotion dysregulation in the
to divert pain and suffering (Crowell & Kaufman, interpersonal-psychological theory of suicidal behavior in an
2016). Research is needed to assess whether parental undergraduate sample. Journal of Psychiatric Research, 45,
emotion-focused training is an effective means of 603–611.
Armey, M. F. (2012). Ecological momentary assessment and
reducing child emotion regulation difficulties and intervention in nonsuicidal self-injury: A novel approach to
later SII (Stepp et al., 2012). treatment. Journal of Cognitive Psychotherapy, 26, 299–317.
Although associations between emotion dys- Armey, M. F., Crowther, J. H., & Miller, I. W. (2011). Changes
regulation and SII are well established, research in ecological momentary assessment reported affect
indicates many mediating and moderating associated with episodes of nonsuicidal self-injury. Behavior
Therapy, 42, 579–588.
pathways that require further exploration. A one- Armey, M. F., Nugent, N. R., & Crowther, J. H. (2014). An
size-fits-all approach to SII prediction will likely exploratory analysis of situational affect, early life stress, and
not be optimal. Ultimately, the field needs to non-suicidal self-injury in college students. Journal of Child
develop methods for identifying typical affective and Adolescent Trauma, 5, 327–343.
patterns among self-injuring persons, as well as Asarnow, J. R., Porta, G., Spirito, A., Emslie, G., Clarke, G.,
Wagner, K. D., . . . Brent, D. A. (2011). Suicide attempts and
strategies for detecting within-person changes nonsuicidal self-injury in the Treatment of Resistant
that accurately predict acute SII risk. Similarly, Depression in Adolescents: Findings from the TORDIA
research examining specific emotion dysregula- study. Journal of the American Academy of Child and Adolescent
tion facets suggests that teaching emotional dif- Psychiatry, 50, 772–781.
ferentiation and nonavoidant emotion regulation Ashby, F. G., Isen, A. M., & Turken, A. U. (1999). A
neuropsychological theory of positive affect and its influence
strategies may hold the greatest universal benefit. on cognition. Psychological Review, 106, 529–550.
Yet clinicians would do well to carefully assess Baetens, I., Claes, L., Willem, L., Muehlenkamp, J., & Bijttebier,
each client’s unique struggles and create personal- P. (2011). The relationship between non-suicidal self-injury
ized treatment plans to address specific emotion and temperament in male and female adolescents based on
regulation gaps. child- and parent-report. Personality and Individual
Differences, 50, 527–530.
Bagge, C. L., Littlefield, A. K., & Glenn, C. R. (2017).
Acknowledgment Trajectories of affective response as warning signs for suicide
The authors would like to acknowledge Dr. Mitch Prinstein for attempts: An examination of the 48 hours prior to a recent
his valuable consultation on this chapter. suicide attempt. Clinical Psychological Science, 5, 259–271.
Bauer, D. J., & Curran, P. J. (2003). Distributional assumptions
References of growth mixture models: Implications for overextraction of
Adrian, M., Zeman, J., Erdley, C., Lisa, L., & Sim, L. (2011). latent trajectory classes. Psychological Methods, 8, 338–363.
Emotional dysregulation and interpersonal difficulties as risk Beauchaine, T. P. (2001). Vagal tone, development, and Gray’s
factors for nonsuicidal self-injury in adolescent girls. Journal motivational theory: Toward an integrated model of
of Abnormal Child Psychology, 39, 389–400. autonomic nervous system functioning in psychopathology.
Ainsworth, M. S. (1989). Attachments beyond infancy. American Development and Psychopathology, 13, 183–214.
Psychologist, 44, 709–716. Beauchaine, T. P. (2015). Future directions in emotion
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). dysregulation and youth psychopathology. Journal of Clinical
Emotion regulation strategies and psychopathology: A meta- Child and Adolescent Psychology, 44, 875–896.
analysis. Clinical Psychology Review, 30, 217–237. Beauchaine, T. P., Gatzke-Kopp, L., & Mead, H. K. (2007).
American Psychiatric Association. (2013). Diagnostic and Polyvagal theory and developmental psychopathology:
statistical manual of mental disorders (5th ed.). Arlington, VA: Emotion dysregulation and conduct problems from
Author. preschool to adolescence. Biological Psychology, 74, 174–184.
Ammerman, B. A., Kleiman, E. M., Uyeji, L. L., Knorr, A. C., & Beauchaine, T. P., Klein, D. N., Crowell, S. E., Derbidge, C.,
McCloskey, M. S. (2015). Suicidal and violent behavior: The & Gatzke-Kopp, L. M. (2009). Multifinality in the
role of anger, emotion dysregulation, and impulsivity. development of personality disorders: A Biology × Sex ×
Personality and Individual Differences, 7, 957–962. Environment interaction model of antisocial and
Anderson, N. L., & Crowther, J. H. (2012). Using the experiential borderline traits. Development and Psychopathology, 21,
avoidance model of non-suicidal self-injury: Understanding 735–770.
who stops and who continues. Archives of Suicide Research, Beauchaine, T. P., & McNulty, T. (2013). Comorbidities and
16, 124–134. continuities as ontogenic processes: Toward a developmental
Andover, M. S., & Morris, B. W. (2014). Expanding and spectrum model of externalizing psychopathology.
clarifying the role of emotion regulation in nonsuicidal self- Development and Psychopathology, 25, 1505–1528.
injury. The Canadian Journal of Psychiatry/La Revue Beauchaine, T. P., Neuhaus, E., Zalewski, M., Crowell, S. E., &
Canadienne De Psychiatrie, 59, 569–575. Potapova, N. (2011). The effects of allostatic load on neural

systems subserving motivation, mood regulation, and social Chapman, A. L., Gratz, K. L., & Brown, M. Z. (2006). Solving
affiliation. Development and Psychopathology, 23, 975–999. the puzzle of deliberate self-harm: The experiential avoidance
Beauchaine, T. P., & Zalewski, M. (2016). Physiological and model. Behaviour Research and Therapy, 44, 371–394.
developmental mechanisms of emotional lability in coercive Churchwell, J. C., Morris, A. M., Heurtelou, N. M., & Kesner,
relationships. In T. J. Dishion & J. J. Snyder (Eds.), The R. P. (2009). Interactions between the prefrontal cortex and
Oxford handbook of coercive relationship dynamics (pp. 39–52). amygdala during delay discounting and reversal. Behavioral
New York, NY: Oxford University Press. Neuroscience, 123, 1185–1196.
Beauchaine, T. P., & Zisner, A. (2017). Motivation, emotion Cicchetti, D., & Blender, J. A. (2004). A multiple-levels-of-
regulation, and the latent structure of psychopathology: analysis approach to the study of developmental processes in
An integrative and convergent historical perspective. maltreated children. Proceedings of the National Academy of
International Journal of Psychophysiology. Advance online Sciences, 101, 17325–17326.
publication. Cipriano, E., & Stifter, C. (2010). Predicting preschool effortful
Beautrais, A. L., Joyce, P. R., & Mulder, R. T. (1996). Risk factors control from toddler temperament and parenting behavior.
for serious suicide attempts among youths aged 13 through Journal of Applied Developmental Psychology, 31, 221–230.
24 years. Journal of the American Academy of Child & Claes, L., Klonsky, E. D., Muehlenkamp, J., Kuppens, P., &
Adolescent Psychiatry, 35, 1174–1182. Vandereycken, W. (2010). The affect-regulation function of
Belsky, J., Bakermans-Kranenburg, M. J., & van IJzendoorn, nonsuicidal self-injury in eating-disordered patients:
M. H. (2007). For better and for worse: Differential Which affect states are regulated? Comprehensive Psychiatry,
susceptibility to environmental influences. Current Directions 51, 386–392.
in Psychological Science, 16, 300–304. Cole, P. M., Hall, S. E., & Hajal, N. J. (2017). Emotion
Berman, A. L., Jobes, D. A., & Silverman, M. M. (2006). dysregulation as a vulnerability to psychopathology. In
Adolescent suicide: Assessment and intervention (2nd ed.). T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent
Washington, DC: American Psychological Association. psychopathology (3rd ed., pp. 346–386). Hoboken, NJ: Wiley.
Bernier, A., Carlson, S. M., & Whipple, N. (2010). From Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion
external regulation to self-regulation: Early parenting regulation as a scientific construct: Methodological challenges
precursors of young children’s executive functioning. Child and directions for child development research. Child
Development, 81, 326–339. Development, 75, 317–333.
Berntson, G. G., Cacioppo, J. T., Binkley, P. F., Uchino, B. N., Conradt, E., Adkins, D. E., Crowell, S. E., Raby, K. L.,
Quigley, K. S., & Fieldstone, A. (1994). Autonomic cardiac Diamond, L. M., & Ellis, B. (in press). Incorporating
control: III. Psychological stress and cardiac response in epigenetic mechanisms to advance prenatal programming
autonomic space as revealed by pharmacological blockades. theories. Development and Psychopathology.
Psychophysiology, 31, 599–608. Coplan, R. J., Bowker, A., & Cooper, S. M. (2003). Parenting
Berridge, K. C. (2003). Pleasures of the brain. Brain and daily hassles, child temperament and social adjustment in
Cognition, 52, 106–128. preschool. Early Childhood Research Quarterly, 18, 376–395.
Berridge, K. C., & Robinson, T. E. (2003). Parsing reward. Creaven, A. M., Skowron, E. A., Hughes, B., Howard, S., &
Trends in Neuroscience, 26, 507–513. Loken, E. (2013). Dyadic concordance in mother and
Bolger, N., Davis, A., & Rafaeli, E. (2003). Diary methods: preschooler resting cardiovascular function varies by risk
Capturing life as it is lived. Annual Review of Psychology, 54, status. Developmental Psychobiology, 56, 142–152.
579–616. Crnic, K. A., Greenberg, M. T., Ragozin, A. S., Robinson,
Bongar, B. (2002). The suicidal patient: Clinical and legal N. M., & Basham, R. B. (1983). Effects of stress and social
standards of care (2nd ed.). Washington, DC: American support on mothers and premature and full-term infants.
Psychological Association. Child Development, 54, 209–217.
Boomsma, D. I., Van Baal, G. C., & Orlebeke, J. F. (1990). Crowell, S. E., Baucom, B. R., McCauley, E., Potapova, N. V.,
Genetic influences on respiratory sinus arrhythmia across Fitelson, M., Barth, H., . . . Beauchaine, T. P. (2013).
different task conditions. Acta Geneticae Medicae Et Mechanisms of contextual risk for adolescent self-injury:
Gemellologiae: Twin Research, 39, 181–191. Emotional invalidation and conflict escalation in mother-
Brezo, J., Paris, J., Hébert, M., Vitaro, F., Tremblay, R., & child interactions. Journal of Clinical Child and Adolescent
Turecki, G. (2008). Broad and narrow personality traits as Psychology, 42, 467–480.
markers of one-time and repeated suicide attempts: A Crowell, S. E., Baucom, B. R., Yaptangco, M., Bride, D.,
population-based study. BMC Psychiatry, 8, 15. Hsiao, R., McCauley, E., & Beauchaine, T. P. (2014).
Cacioppo, J. T., Uchino, B. N., & Berntson, G. G. (1994). Emotion dysregulation and dyadic conflict in depressed
Individual differences in the autonomic origins of heart rate and typical adolescents: Evaluating concordance across
reactivity: The psychometrics of respiratory sinus arrhythmia psychophysiological and observational measures. Biological
and preejection period. Psychophysiology, 31, 412–419. Psychology, 98, 50–58.
Calkins, S. D., & Dedmon, S. A. (2000). Physiological and Crowell, S. E., Beauchaine, T. P., & Linehan, M. M. (2009). A
behavioral regulation in two-year-old children with biosocial developmental model of borderline personality:
aggressive/destructive behavior problems. Journal of Elaborating and extending Linehan’s theory. Psychological
Abnormal Child Psychology, 28, 103–118. Bulletin, 135, 495–510.
Calkins, S. D., Graziano, P. A., Berdan, L. E., Keane, S. P., & Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C.,
Degnan, K. A. (2008). Predicting cardiac vagal regulation Stevens, A. L., & Sylvers, P. D. (2005). Psychological,
in early childhood from maternal-child relationship physiological, and serotonergic correlates of parasuicidal
quality during toddlerhood. Developmental Psychobiology, behavior among adolescent girls. Development and
50, 751–766. Psychopathology, 17, 1105–1127.

Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C. J., Edmondson, A. J., Brennan, C. A., & House, A. O. (2016).
Vasilev, C. A., & Stevens, A. L. (2008). Parent–child Non-suicidal reasons for self-harm: A systematic review of
interactions, peripheral serotonin, and self-inflicted injury in self-reported accounts. Journal of Affective Disorders, 191,
adolescents. Journal of Consulting and Clinical Psychology, 76, 109–117.
15–21. Eisenberger, N. I. (2012). Broken hearts and broken bones: A
Crowell, S. E., Butner, J. E., Wiltshire, T. J., Munion, A. K., neural perspective on the similarities between social and
Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating physical pain. Current Directions in Psychological Science, 21,
emotional and biological sensitivity to maternal behavior 42–47.
among self-injuring and depressed adolescent girls using Eisenberg, N., Spinrad, T. L., & Eggum, N. D. (2011). Emotion-
nonlinear dynamics. Clinical Psychological Science, 5, 272–285. related self-regulation and its relation to children’s
Crowell, S. E., Derbidge, C. A., & Beauchaine, T. P. (2014). The maladjustment. Annual Review of Clinical Psychology, 6,
development of suicidal and self-injurious behaviors. In 495–525.
M. K. Nock (Ed.), The Oxford handbook of suicide and self- Essex, M. J., Boyce, W. T., Hertzman, C., Lam, L. L., Armstrong,
injury. New York, NY: Oxford University Press. J. M., Neumann, S. A., & Kobor, M. S. (2013). Epigenetic
Crowell, S. E., & Kaufman, E. A. (2016). Development of self- vestiges of early developmental adversity: Childhood stress
inflicted injury: Comorbidities and continuities with exposure and DNA methylation in adolescence. Child
borderline and antisocial personality traits. Development and Development, 84, 58–75.
Psychopathology, 28, 1071–1088. Favazza, A. R., & Conterio, K. (1989). Female habitual self-
David, O. A., David, D., & Dobrean, A. (2014). Efficacy of the mutilators. Acta Psychiatrica Scandinavica, 79, 283–289.
Rational Positive Parenting Program for child externalizing Fonagy, P., Gergely, G., & Target, M. (2007). The parent-infant
behavior: Can an emotion-regulation enhanced cognitive- dyad and the construction of the subjective self. Journal of
behavioral parent program be more effective than a standard Child Psychology and Psychiatry, 48, 288–328.
one? Journal of Evidence-Based Psychotherapies, 14, 159–178. Forbes, E. E., & Dahl, R. E. (2012). Altered reward function in
Davidson, R. J. (2002). Anxiety and affective style: Role of adolescent depression. What, when, and how? Journal of
prefrontal cortex and amygdala. Biological Psychiatry, 51, Child Psychology and Psychiatry, 53, 3–15.
68–80. Fox, N. A. (1998). Temperament and regulation of emotion in
Degnan, K. A., Hane, A. A., Henderson, H. A., Walker, O. L., the first years of life. Pediatrics, 102, 1230–1235.
Ghera, M., & Fox, N. A. (2015). Emergent patters of risk for Fox, N. A., & Stifter, C. A. (1989). Biological and behavioral
psychopathology: The influence of infant temperament and differences in infant reactivity and regulation. In
maternal caregiving on trajectories of social reticent. G. A. Kohnstamm, J. Bates, & M. K. Rothbart (Eds.),
Development and Psychopathology, 27, 1163–1178. Handbook of temperament in childhood (pp. 169–183).
Derbidge, C., & Beauchaine, T. P. (2014). A developmental New York, NY: Wiley.
model of self-inflicted injury, borderline personality, and Fox, K. R., Toole, K. E., Franklin, J. C., & Hooley, J. M. (2016).
suicide risk. In M. Lewis & K. Rudolph (Eds.), Handbook Why does nonsuicidal self-injury improve mood? A
of developmental psychopathology (3rd ed., pp. 521–542). preliminary test of three hypotheses. Clinical Psychological
New York, NY: Springer. Science, 5, 111–121.
Deutz, M. F., Geeraerts, S. B., Baar, A. L., Deković, M., & Franklin, J. C., Puzia, M. E., Lee, K. M., Lee, G. E., Hanna,
Prinzie, P. (2016). The Dysregulation Profile in middle E. K., Spring, V. L., & Prinstein, M. J. (2013). The nature of
childhood and adolescence across reporters: Factor structure, pain offset relief in nonsuicidal self-injury: A laboratory
measurement invariance, and links with self-harm and study. Clinical Psychological Science, 1, 110–119.
suicidal ideation. European Child and Adolescent Psychiatry, Franklin, J. C., Ribeiro, J. D., Fox, K. R., Bentley, K. H.,
25, 431–442. Kleiman, E. M., Huang, X., . . . Nock, M. K. (2017). Risk
Diamond, L. M., Fagundes, C. P., & Butterworth, M. R. factors for suicidal thoughts and behaviors: A meta-
(2012). Attachment style, vagal tone, and empathy during analysis of 50 years of research. Psychological Bulletin, 143,
mother–adolescent interactions. Journal of Research on 187–232.
Adolescence, 22, 165–184. Gratz, K. L., Bardeen, J. R., Levy, R., Dixon-Gordon, K. L., &
Doyle, C., & Cicchetti, D. (2017). From the cradle to the grave: Tull, M. T. (2015). Mechanisms of change in an emotion
The effect of adverse caregiving environments on attachment regulation group therapy for deliberate self-harm among
and relationships throughout the lifespan. Clinical Psychology: women with borderline personality disorder. Behaviour
Science and Practice, 24, 203–217. Research and Therapy, 65, 29–35.
Duggan, J., Heath, N., & Hu, T. (2015). Non-suicidal self-injury Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment
maintenance and cessation among adolescents: A one-year of emotion regulation and dysregulation: Development,
longitudinal investigation of the role of objectified body factor structure, and initial validation of the Difficulties in
consciousness, depression and emotion dysregulation. Child Emotion Regulation Scale. Journal of Psychopathology and
and Adolescent Psychiatry and Mental Health, 9, 21. Behavioral Assessment, 26, 41–54.
Duggan, J. M., Toste, J. R., & Heath, N. L. (2013). An Gratz, K. L., & Roemer, L. (2008). The relationship between
examination of the relationship between body image factors emotion dysregulation and deliberate self-harm among
and non-suicidal self-injury in young adults: The mediating female undergraduate students at an urban commuter
influence of emotion dysregulation. Psychiatry Research, 206, university. Cognitive Behaviour Therapy, 37, 14–25.
256–264. Gratz, K. L., & Tull, M. T. (2010). The relationship between
Dworkin, R. H. (1994). Pain insensitivity in schizophrenia: A emotion dysregulation and deliberate self-harm among
neglected phenomenon and some implications. Schizophrenia inpatients with substance use disorders. Cognitive Therapy
Bulletin, 20, 235–248. and Research, 34, 544–553.

Gray, J. A., & McNaughton, N. (2000). The neuropsychology of Itzhaky, L., Shahar, G., Stein, D., & Fennig, S. (2015). In eating-
anxiety: An enquiry into the functions of the septo-hippocampal disordered inpatient adolescents, self-criticism predicts
system (2nd ed.). New York, NY: Oxford University Press. nonsuicidal self-injury. Suicide and Life-Threatening Behavior,
Grove, J. G., & Crowell, S. E. (in press). Invalidating 46, 385–397.
environments and the development of borderline personality Jacobson, C., Batejan, K., Kleinman, M., & Gould, M. (2013).
disorder. In M. Swales (Ed.), The Oxford handbook of Reasons for attempting suicide among a community sample
dialectical behaviour therapy. New York, NY: Oxford of adolescents. Suicide and Life-Threatening Behavior, 43,
University Press. 646–662.
Guan, K., Fox, K. R., & Prinstein, M. J. (2012). Nonsuicidal Joiner, T. E. (2005). Why people die by suicide. Cambridge, MA:
self-injury as a time-invariant predictor of adolescent suicide Harvard University Press.
ideation and attempts in a diverse community sample. Kagan, J. (2017). Brain and emotion. Emotion Review. Advance
Journal of Consulting and Clinical Psychology, 80, 842–849. online publication.
Guendelman, M., Owens, E. B., Galan, C., Gard, A., & Hinshaw, Kamphuis, J. H., Ruyling, S. B., & Reijntjes, A. H. (2007).
S. P. (2016). Early adult correlates of maltreatment in girls Testing the emotion regulation hypothesis among self-
with ADHD: Increased risk for internalizing problems and injuring females: Evidence for differences across mood states.
suicidality. Development and Psychopathology, 28, 1–14. Journal of Nervous and Mental Disease, 195, 912–918.
Hamza, C. A., Stewart, S. L., & Willoughby, T. (2012). Kim, D., & Kim, H. (2009). Body-image dissatisfaction as a
Examining the link between nonsuicidal self-injury and predictor of suicidal ideation among Korean boys and girls in
suicidal behavior: A review of the literature and an integrated different stages of adolescence: A two-year longitudinal
model. Clinical Psychology Review, 32, 482–495. study. Journal of Adolescent Health, 45, 47–54.
Hanson, J. L., Chung, M. K., Avants, B. B., Shirtcliff, E. A., Klonsky, E. D. (2007). The functions of deliberate self-injury:
Gee, J. C., . . . Pollak, S. D. (2010). Early stress is associated A review of the evidence. Clinical Psychology Review, 27,
with alterations in the orbitofrontal cortex: A tensor-based 226–239.
morphometry investigation of brain structure and behavioral Klonsky, E. D. (2009). The functions of self-injury in young
risk. Journal of Neuroscience, 30, 7466–7472. adults who cut themselves: Clarifying the evidence for affect-
Heatherton, T. F. (2011). Neuroscience of self and self-regulation. regulation. Psychiatry Research, 166, 260–268.
Annual Review of Psychology, 62, 363–390. Klonsky, E. D., May, A. M., & Glenn, C. R. (2013). The
Heatherton, T. F., & Wagner, D. D. (2011). Cognitive relationship between nonsuicidal self-injury and attempted
neuroscience of self-regulation failure. Trends in Cognitive suicide: Converging evidence from four samples. Journal of
Sciences, 15, 132–139. Abnormal Psychology, 122, 231–237.
Heisel, M. J., Conwell, Y., Pisani, A. R., & Duberstein, P. R. Klonsky, E. D., & Muehlenkamp, J. J. (2007). Self-injury: A
(2011). Concordance of self- and proxy-reported suicide research review for the practitioner. Journal of Clinical
ideation in depressed adults 50 years of age or older. The Psychology, 63, 1045–1056.
Canadian Journal of Psychiatry/La Revue Canadienne De Kuo, J. R., & Linehan, M. M. (2009). Disentangling emotion
Psychiatrie, 56, 219–226. processes in borderline personality disorder: Physiological
Hilt, L. M., Hanson, J. L., & Pollak, S. D. (2011). Emotion and self-reported assessment of biological vulnerability,
dysregulation. In B. B. Brown & M. J. Prinstein (Eds.), baseline intensity, and reactivity to emotionally evocative
Encyclopedia of adolescence (Vol. 3, pp. 160–169). New York, stimuli. Journal of Abnormal Psychology, 118, 531–544.
NY: Elsevier. Large, M. M., Nielssen, O. B., & Babidge, N. (2010). Self-
Hinshaw, S. P., Owens, E. B., Zalecki, C., Huggins, S. P., mutilation is strongly associated with schizophrenia, but not
Montenegro-Nevado, A. J., Schrodek, E., & Swanson, E. N. with bipolar disorder. Australian and New Zealand Journal of
(2012). Prospective follow-up of girls with attention-deficit/ Psychiatry, 44, 677.
hyperactivity disorder into early adulthood: Continuing Laurent, H. K. (2014). Clarifying the contours of emotion
impairment includes elevated risk for suicide attempts and regulation: Insights from parent–child stress research. Child
self-injury. Journal of Consulting and Clinical Psychology, 80, Development Perspectives, 8, 30–35.
1041–1051. Law, K. C., Khazem, L. R., & Anestis, M. D. (2015). The role of
Hoertel, N., Franco, S., Wall, M. M., Oquendo, M. A., Kerridge, emotion dysregulation in suicide as considered through the
B. T., Limosin, F., & Blanco, C. (2015). Mental disorders ideation to action framework. Current Opinion in Psychology,
and risk of suicide attempt: A national prospective study. 3, 30–35.
Molecular Psychiatry, 20, 718–726. Linehan, M. M. (1993). Cognitive-behavioral treatment of
Houben, M., Claes, L., Vansteelandt, K., Berens, A., Sleuwaegen, borderline personality disorder. New York, NY: Guilford Press.
E., & Kuppens, P. (2017). The emotion regulation function Linehan, M. M. (1997). Behavioral treatments of suicidal
of nonsuicidal self-injury: A momentary assessment study in behaviors. Definitional obfuscation and treatment outcomes.
inpatients with borderline personality disorder features. Annals New York Academy of Sciences, 836, 302–328.
Journal of Abnormal Psychology, 126, 89–95. Linehan, M. M., Comtois, K. A., Murray, A. M., Brown, M. Z.,
Hughes, A. E., Crowell, S. E., Uyeji, L., & Coan, J. A. (2012). A Gallop, R. J., Heard, H. L., . . . Lindenboim, N. (2006). Two-
developmental neuroscience of borderline pathology: year randomized controlled trial and follow-up of dialectical
Emotion dysregulation and social baseline theory. Journal of behavior therapy vs therapy by experts for suicidal behaviors
Abnormal Child Psychology, 40, 21–33. and borderline personality disorder. Archives of General
Iancu, I., Horesh, N., Offer, D., Dannon, P. N., Lepkifker, E., & Psychiatry, 63, 757–766.
Kotler, M. (1999). Alexithymia, affect intensity and Livesley, W. J., & Jang, K. L. (2008). The behavioral genetics of
emotional range in suicidal patients. Psychotherapy and personality disorder. Annual Review of Clinical Psychology, 4,
Psychosomatics, 68, 276–280. 247–274.

Luking, K. R., Pagliaccio, D., Luby, J. L., & Barch, D. M. Nock, M. K. (2010). Self-injury. Annual Review of Clinical
(2016). Reward processing and risk for depression across Psychology, 6, 339–363.
development. Trends in Cognitive Sciences, 20, 456–468. Nock, M. K., & Mendes, W. B. (2008). Physiological arousal,
Mann, J. J., Waternaux, C., Haas, G. L., & Malone, K. M. distress tolerance, and social problem-solving deficits among
(1999). Toward a clinical model of suicidal behavior in adolescent self-injurers. Journal of Consulting and Clinical
psychiatric patients. American Journal of Psychiatry, 156, Psychology, 76, 28–38.
181–189. Nock, M. K., & Prinstein, M. J. (2004). A functional approach
McKenzie, K. C., & Gross, J. J. (2014). Nonsuicidal self- to the assessment of self-mutilative behavior. Journal of
injury: An emotion regulation perspective. Psychopathology, Consulting and Clinical Psychology, 72, 885–890.
47, 207–219. Nock, M. K., Prinstein, M. J., & Sterba, S. K. (2009). Revealing
Miller, A. L., Rathus, J. H., & Linehan, M. M. (2007). Dialectical the form and function of self-injurious thoughts and
behavior therapy with suicidal adolescents. New York, NY: behaviors: A real-time ecological assessment study among
Guilford Press. adolescents and young adults. Journal of Abnormal Psychology,
Molfese, V. J., Rudasill, K. M., Beswick, J. L., Jacobi-Vessels, 118, 816–827.
J. L., Ferguson, M. C., & White, J. M. (2010). Infant Oddi, K. B., Murdock, K. W., Vadnais, S., Bridgett, D. J., &
temperament, maternal personality, and parenting stress as Gartstein, M. A. (2013). Maternal and infant temperament
contributors to infant developmental outcomes. Merrill- characteristics as contributors to parenting stress in the first
Palmer Quarterly, 56, 49–79. year postpartum. Infant and Child Development, 22, 553–579.
Muehlenkamp, J. J., Bagge, C. L., Tull, M. T., & Gratz, K. L. Patterson, G. R. (1976). The aggressive child: Victim and
(2013). Body regard as a moderator of the relation between architect of a coercive system. In E. J. Mash,
emotion dysregulation and nonsuicidal self-injury. Suicide L. A. Hamerlynck, & L. C. Handy (Eds.), Behavior
and Life-Threatening Behavior, 43, 479–493. modification and families (pp. 267–316). New York, NY:
Muehlenkamp, J. J., & Brausch, A. M. (2012). Body image as a Brunner/Mazel.
mediator of non-suicidal self-injury in adolescents. Journal of Patterson, G. R. (1982). Coercive family processes. Eugene, OR:
Adolescence, 35, 1–9. Castalia.
Muehlenkamp, J. J., Engel, S. G., Wadeson, A., Crosby, R. D., Pollak, S. D. (2015). Multilevel developmental approaches to
Wonderlich, S. A., Simonich, H., & Mitchell, J. E. (2009). understanding the effects of child maltreatment: Recent
Emotional states preceding and following acts of non- advances and future challenges. Development and
suicidal self-injury in bulimia nervosa patients. Behaviour Psychopathology, 27, 1387–1397.
Research and Therapy, 47, 83–87. Porges, S. W. (1995). Orienting in a defensive world: Mammalian
Muehlenkamp, J. J., & Gutierrez, P. M. (2004). An investigation modifications of our evolutionary heritage. A polyvagal
of differences between self-injurious behavior and suicide theory. Psychophysiology, 32, 301–318.
attempts in a sample of adolescents. Suicide and Life- Porges, S. W. (2007). The polyvagal perspective. Biological
Threatening Behavior, 34, 12–23. Psychiatry, 74, 116–143.
Muehlenkamp, J. J., Kerr, P. L., Bradley, A. R., & Larsen, M. A. Rajappa, K., Gallagher, M., & Miranda, R. (2012). Emotion
(2010). Abuse subtypes and nonsuicidal self-injury: dysregulation and vulnerability to suicidal ideation and
Preliminary evidence of complex emotion regulation patterns. attempts. Cognitive Therapy and Research, 36, 833–839.
Journal of Nervous and Mental Disease, 198, 258–263. Reutfors, J., Bahmanyar, S., Jönsson, E. G., Ekbom, A.,
Muehlenkamp, J. J., Peat, C. M., Claes, L., & Smits, D. (2012). Nordström, P., Brandt, L., & Ösby, U. (2010). Diagnostic
Self-injury and disordered eating: Expressing emotion profile and suicide risk in schizophrenia spectrum disorder.
dysregulation through the body. Suicide and Life-Threatening Schizophrenia Research, 123, 251–256.
Behavior, 42, 416–425. Rodríguez-Cano, T., Beato-Fernández, L., & Llario, A. B.
Muehlenkamp, J. J., Swanson, J. D., & Brausch, A. M. (2005). (2006). Body dissatisfaction as a predictor of self-reported
Self-objectification, risk taking, and self-harm in college suicide attempts in adolescents: A Spanish community
women. Psychology of Women Quarterly, 29, 24–32. prospective study. Journal of Adolescent Health, 38, 684–688.
National Advisory Mental Health Council Workgroup on Tasks Ross, S., Heath, N. L., & Toste, J. R. (2009). Non-suicidal self-
and Measures for Research Domain Criteria. (2016). injury and eating pathology in high school students.
Behavioral assessment methods for RDoC constructs. Bethesda, American Journal of Orthopsychiatry, 79, 83–92.
MD: National Institute of Mental Health. Rudd, M. D., Berman, A. L., Joiner, T. J., Nock, M. K.,
National Institute of Mental Health. (2011). NIMH research Silverman, M. M., Mandrusiak, M., . . . Witte, T. (2006).
domain criteria (RDoC). Retrieved August 17, 2017, from Warning signs for suicide: Theory, research, and clinical
http://www.nimh.nih.gov/research-priorities/rdoc/index. applications. Suicide and Life-Threatening Behavior, 36,
shtml. 255–262.
Neijts, M., van Lien, R., Kupper, N., Boomsma, D., Willemsen, Seiden, R. H. (1978). Where are they now? A follow-up study of
G., & de Geus, E. C. (2015). Heritability and temporal suicide attempters from the Golden Gate Bridge. Suicide and
stability of ambulatory autonomic stress reactivity in Life-Threatening Behavior, 8, 1–13.
unstructured 24-hour recordings. Psychosomatic Medicine, Sharot, T., Shiner, T., Brown, A. C., Fan, J., & Dolan, R. J.
77, 870–881. (2009). Dopamine enhances expectation of pleasure in
Nelson, A., & Muehlenkamp, J. J. (2012). Body attitudes and humans. Current Biology, 19, 2077–2080.
objectification in non-suicidal self-injury: Comparing males Sidor, A., Fischer, C., & Cierpka, M. (2017). The link between
and females. Archives of Suicide Research, 16, 1–12. infant regulatory problems, temperament traits, maternal
Nock, M. K. (2009). Why do people hurt themselves? Current depressive symptoms and children’s psychopathological
Directions in Psychological Science, 18, 78–83. symptoms at age three: A longitudinal study in a German

at-risk sample. Child and Adolescent Psychiatry and Mental Thayer, J. F., & Lane, R. D. (2009). Claude Bernard and the
Health, 11, 10. heart-brain connection: Further elaboration of a model of
Simpson, G. (1950). Methodological problems in determining the neurovisceral integration. Neuroscience and Biobehavioral
aetiology of suicide. American Sociological Review, 15, 658–663. Reviews, 33, 81–88.
Simpson, M. A. (1975). The phenomenology of self-mutilation Thompson, R. A. (1990). Emotion and self-regulation. In
in a general hospital setting. Canadian Psychiatric Association R. A. Thompson (Ed.), Nebraska Symposium on Motivation:
Journal, 20, 429–434. Vol. 36. Socioemotional development (pp. 383–483). Lincoln,
Silverman, M. M., Berman, A. L., Sanddal, N. D., O’Carroll, NE: University of Nebraska Press.
P. W., & Joiner, T. J. (2007a). Rebuilding the Tower of Babel: Thompson, R. A. (1994). Emotion regulation: A theme in search
A revised nomenclature for the study of suicide and suicidal of definition. Monographs of the Society for Research in Child
behaviors: Part 1: Background, rationale, and methodology. Development, 59, 25–52.
Suicide and Life-Threatening Behavior, 37, 248–263. Van Orden, K. A., Wiktorsson, S., Duberstein, P., Berg, A. I.,
Silverman, M. M., Berman, A. L., Sanddal, N. D., O’Carroll, Fässberg, M. M., & Waern, M. (2015). Reasons for attempted
P. W., & Joiner, T. J. (2007b). Rebuilding the Tower of Babel: suicide in later life. American Journal of Geriatric Psychiatry,
A revised nomenclature for the study of suicide and suicidal 23, 536–544.
behaviors: Part II: Suicide-related ideations, communications Whitlock, J., Prussien, K., & Pietrusza, C. (2015). Predictors of
and behaviors. Suicide and Life-Threatening Behavior, 37, self-injury cessation and subsequent psychological growth:
264–277. Results of a probability sample survey of students in eight
Sim, L., Adrian, M., Zeman, J., Cassano, M., & Friedrich, W. N. universities and colleges. Child and Adolescent Psychiatry and
(2009). Adolescent deliberate self-harm: Linkages to emotion Mental Health, 9, 19.
regulation and family emotional climate. Journal of Research Wilkinson, P. O. (2011). Nonsuicidal self-injury: A clear marker
on Adolescence, 19, 75–91. for suicide risk. Journal of the American Academy of Child and
Skowron, E. A., Cipriano-Essel, E. A., Benjamin, L. S., Pincus, Adolescent Psychiatry, 50, 741–743.
A. L., & Van Ryzin, M. (2013). Cardiac vagal tone and Yurkowski, K., Martin, J., Levesque, C., Bureau, J., Lafontaine,
quality of parenting show concurrent and time-ordered M., & Cloutier, P. (2015). Emotion dysregulation mediates
associations that diverge in abusive, neglectful, and non- the influence of relationship difficulties on non-suicidal self-
maltreating mothers. Couple and Family Psychology: Research injury behavior in young adults. Psychiatry Research, 228,
and Practice, 2, 95–115. 871–878.
Slee, N., Spinhoven, P., Garnefski, N., & Arensman, E. (2008). Zilboorg, G. (1936a). Considerations on suicide, with particular
Emotion regulation as mediator of treatment outcome in reference to that of the young. Journal of Orthopsychiatry, 7,
therapy for deliberate self-harm. Clinical Psychology and 15–31.
Psychotherapy, 15, 205–216. Zilboorg, G. (1936b). Differential diagnostic types of suicide.
Snyder, J., Schrepferman, L., & St. Peter, C. (1997). Origins of Archives of General Psychiatry, 35, 270–291.
antisocial behavior: Negative reinforcement and affect Zisner, A., & Beauchaine, T. P. (2016a). Neural substrates of trait
dysregulation of behavior as socialization mechanisms in impulsivity, anhedonia, and irritability: Mechanisms of
family interaction. Behavior Modification, 21, 187–215. heterotypic comorbidity between externalizing disorders and
Sroufe, L. A., & Rutter, M. (1984). The domain of developmental unipolar depression. Development and Psychopathology, 28,
psychopathology. Child Development, 55, 17–29. 1179–1210.
Stanley, B., Sher, L., Wilson, S., Ekman, R., Huang, Y., & Mann, Zisner, A. R., & Beauchaine, T. P. (2016b). Psychophysiological
J. J. (2010). Nonsuicidal self-injurious behavior, endogenous methods and developmental psychopathology. In
opioids, and monoamine neurotransmitters. Journal of D. Cicchetti, D. Cicchetti (Eds.), Developmental
Affective Disorders, 124, 134–140. psychopathology: Developmental neuroscience (pp. 832–884).
Stepp, S. D., Whalen, D. J., Pilkonis, P. A., Hipwell, A. E., & Hoboken, NJ, US: John Wiley & Sons Inc.
Levine, M. D. (2012). Children of mothers with borderline Zlotnick, C., Mattia, J. I., & Zimmerman, M. (1999). Clinical
personality disorder: Identifying parenting behaviors as correlates of self-mutilation in a sample of general
potential targets for intervention. Personality Disorders: psychiatric patients. Journal of Nervous And Mental Disease,
Theory, Research, and Treatment, 3, 76–91. 187, 296–301.

CH A PTE R
25 Borderline Personality Disorder
Katherine L. Dixon-Gordon, Lauren A. Haliczer, and Lindsey C. Conkey
Abstract
Emotion dysregulation has been theorized to either directly or indirectly drive many of the symptoms
associated with borderline personality disorder. In this chapter, several current controversies in this
body of work are reviewed. The chapter presents the role of emotion dysregulation in theories of the
development and maintenance of borderline personality disorder. Further, it reviews the state of
research on emotional responding in borderline personality disorder, focusing on any evidence of
emotional sensitivity, reactivity, and time course. Building on this review, the chapter summarizes
recent advances in the study of difficulties in emotion regulation capacities and strategies in the
context of this disorder. In addition, it outlines the links between emotion dysregulation and other
problems in borderline personality disorder. Finally, this chapter highlights the limitations and future
directions in this line of work.
Keywords: borderline personality disorder, emotion, emotion dysregulation, emotion regulation,

emotional responding
Introduction According to many researchers, emotional in-

Borderline personality disorder (BPD) is a debilitating stability or dysregulation is at the heart of BPD
mental health disorder. Those suffering from (Livesley, Jackson, & Schroeder, 1992; Siever &
BPD tend to have persistent unemployment Davis, 1991; Skodol et al., 2002; Trull, Tomko,
(Zimmerman, Martinez, Young, Chelminski, & Brown, & Scheiderer, 2010). This emotional insta-
Dalrymple, 2012), poor interpersonal functioning bility is reflected directly in the diagnostic criteria
(Tomko, Trull, Wood, & Sher, 2014), numerous of inappropriate anger and affective instability
co-occurring disorders, and extremely high rates of (American Psychiatric Association, 2013). In addi-
intentional self-harm (Bolton & Robinson, 2010; tion, emotional instability is thought to underlie
Zanarini et al., 2008). Approximately one-fifth of many of the other diagnostic criteria (Linehan,
all suicides have been attributed to BPD (Bolton & 1993), including an unstable identity, stormy in-
Robinson, 2010). As a result, BPD is associated terpersonal relationships, emotion-dependent cog-
with high rates of treatment use, disability, and nitive distortions such as dissociation or paranoia,
loss of productivity (Bender et al., 2001; Hörz, and frequent engagement in impulsive, potentially
Zanarini, Frankenburg, Reich, & Fitzmaurice, self-damaging behaviors (American Psychiatric
2010; van Asselt, Dirksen, Arntz, & Severens, 2007). Association, 2013). Although endorsement of the
Given the tremendous personal and societal costs affective instability criterion is not required for a
associated with this disorder, we need a better un- diagnosis (only five of the nine criteria are re-
derstanding of mechanisms underlying BPD to quired), one study found that 90% of adults with
inform prevention and treatment efforts. BPD endorsed affective instability at baseline, and
361
50% of the sample continued to endorse this demands (Gratz & Roemer, 2004). In other words,
criterion six years later (Zanarini, Frankenburg,
emotion dysregulation is characterized by a pattern
Hennen, & Silk, 2003). Thus, emotional dysfunction of emotional expressions or experiences that inter-
appears to be a critical component of BPD. fere with appropriate goal-directed behaviors.
In this chapter, we define relevant terms and Consequently, emotion dysregulation confers
concepts and review theoretical perspectives on vulnerability to a range of internalizing and exter-
emotion dysregulation in BPD. We also discuss cur- nalizing behavior problems (Beauchaine, 2015).
rent controversies in the literature on emotion dys- We can look at emotion regulation and dysregu-
regulation and BPD and present empirical evidence lation from two perspectives. Drawing on the process
supporting each perspective. After synthesizing the model (Gross, 1998), much of the research on emo-
literature and pointing to possible explanations for tion regulation describes the state use of different
discrepancies, we conclude with suggestions for types of emotion modulation strategies, implemented
future research on emotion dysregulation and BPD. at different times across the emotional response.
From this strategy-based approach, specific emotion
Defining Emotions, Emotion Regulation, regulation strategies, such as emotional acceptance,
Emotion Dysregulation, and Related cognitive reappraisal, and problem solving, have
Concepts typically been classified as adaptive in light of their
Two criteria for BPD—affective instability and negative associations with psychopathology symp-
anger—directly reflect disturbances in emotions. These toms (Aldao, Nolen-Hoeksema, & Schweizer, 2010;
emotions, such as fear, anger, shame, and sadness, Garnefski, Kraaij, & Spinhoven, 2001; Gross, 1998).
can be described as short-lived, loosely coordinated Conversely, strategies such as self-criticism, worry,
responses across experiential, physiological, and rumination, suppression, and avoidance are consid-
behavioral domains to a stimulus (Ekman, 1992). ered maladaptive since they tend to be positively as-
Although in typical populations these emotions are sociated with psychopathology (Aldao et al., 2010;
generally adaptive (i.e., by rapidly signaling and Aldao & Nolen-Hoeksema, 2010; Garnefski, Kraaij,
facilitating responses to situational demands), when & Spinhoven, 2001).
these emotions fail to align with situational demands Expanding beyond a focus on strategies, we can
and goals, they require regulation. also focus on dispositional emotion regulation abili-
Before exploring the role of emotion dysregulation ties (Tull & Aldao, 2015). Although we distinguish
in BPD, it is helpful to define emotion regulation. here between emotional responses and regulation,
Despite numerous definitions of emotion regulation, we acknowledge that these are related. We can
most descriptions share several commonalities. consider excessive negative emotionality to be a

Generally, emotion regulation is defined as a multi- consequence of underuse of emotion regulation
faceted construct that involves modulation of strategies, selection of inappropriate strategies, or
emotional experiences and/or expressions (Cole, ineffective use of regulation strategies (Linehan,
Michel, & Teti, 1994; Gross, 1998), alterations to the 1993; Maffei & Fusi, 2016). Conversely, we can also
intensity and/or duration of emotions (Thompson, view intense emotionality as requiring more effective
1994), and regulation of problematic behaviors or extensive regulatory resources. Both excessive
associated with emotions (Cole et al., 1994; Gratz & emotional responding and difficulties modulating
Tull, 2010). This process of emotion regulation fa- emotions are present in BPD, and thus we explore
cilitates goal-directed behavior, even in the context both of these conceptually related yet distinct do-
of strong negative emotions (Gottman & Katz, mains in hopes of better understanding emotion
1989; Linehan, 1993). dysregulation in BPD more broadly.
In contrast, emotion dysregulation involves diffi-
culties in these domains. One prominent multidi- Theoretical Perspectives on Emotion
mensional model suggests that emotion dysregulation Dysregulation and Borderline
can be broadly construed as (1) a lack of emotional Personality Disorder
awareness, understanding, or acceptance of emotions; Across multiple developmental theories of BPD,
(2) difficulties controlling impulsive behaviors in emotion dysregulation is viewed as a critical early
accordance with desired goals when distressed; and etiological mechanism. One prominent model, the
(3) limited access to situationally appropriate emo- biosocial theory, regards emotion dysregulation as
tion regulation strategies to modulate emotional essential, contributing directly to the development
responses in order to meet goals and situational and maintenance of BPD (Linehan, 1993). According
362 Emotion Dysregul ation and BPD

to Linehan’s theory, BPD arises from a transaction reciprocal transactions between child and caregiver
over time between a biologically based emotional may lead to a disorganized/ambivalent attachment
vulnerability and an early rearing environment that style that persists across development. From this
is experienced as invalidating. Children with this perspective, the patient’s hypersensitivity toward
biological vulnerability may have higher emotional interpersonal signals intensifies, while the patient
sensitivity (i.e., a low threshold to elicit an emo- increasingly inhibits his or her interpersonal needs.
tional response), emotional reactivity (i.e., a high- These interpersonal processes may contribute directly
magnitude response), and a slow return to one’s to relationship problems and may also escalate
baseline. Elaborating on this model, Crowell and emotion dysregulation (Crowell, 2016). This model
colleagues proposed that the biological vulnerability implies that emotion dysregulation in BPD may be
for BPD consisted of both temperamental emo- particularly evident in interpersonal contexts.
tional vulnerability and a propensity for impulsivity The mentalization-based approach to under-
(Crowell, Beauchaine, & Linehan, 2009). In the standing BPD also highlights emotion dysregulation
context of an invalidating environment, children as a critical mechanism underlying BPD (Bateman
with this emotional vulnerability may get the message & Fonagy, 2004). Akin to other perspectives, this
that their emotional reactions are not warranted, model emphasizes transactions between child and
justified, or valid. Consequently, over time these caregiver as a central etiological process in BPD. In
individuals learn to mistrust their emotions, and the context of nonresponsive or incongruent mir-
do not acquire effective strategies for managing roring of the child’s experiences by a caretaker, the
emotions. Across multiple, reciprocal interactions child may not learn to label his or her internal expe-
between these temperamental vulnerabilities and riences appropriately, which in turn intensifies these
environmental risk factors, emotion dysregulation experiences. Ultimately, an insecure attachment
intensifies and becomes more entrenched. More between child and caregiver develops. This sets the
specifically, this process exacerbates frequent, in- stage for both a failure to develop emotion regula-
tense, and prolonged emotional responses; low tion abilities and a failure to foster developmentally
emotional clarity, awareness, or acceptance; limited appropriate mentalization or the social cognitive
access to adaptive emotion regulation strategies; and capacity to make sense of one’s own and others’ in-
poor behavioral control in the presence of intense ternal experiences. Over time, in the context of
distress. In the context of this intense distress, emotionally charged interpersonal relationships, the
emotion-dependent information processing deficits patient experiences mentalization failures. From
emerge. These individuals may therefore resort to this vantage point, mentalization difficulties and
maladaptive ways of avoiding emotions, such as emotion dysregulation remain intertwined, such
self-harm or substance use. As such, an implication that one may evoke the other. Similar to the
of this model is that many problematic behaviors Gene–Environment interaction theory of BPD
associated with BPD, such as self-injury or sub- (Gunderson & Lyons-Ruth, 2008), this model also
stance use, are a direct consequence of emotion dys- suggests that emotion dysregulation would be
regulation (Gratz & Roemer, 2004; Gratz & Tull, exacerbated in interpersonal contexts. Another

2010; Muehlenkamp, Peat, Claes, & Smits, 2012). implication of this model is that emotion dysregula-
Beyond this biological propensity for emotional tion in BPD may be, in part, associated with failures
vulnerability and impulsivity, a Gene–Environmental to accurately identify one’s emotional experience.
interaction theory also emphasizes the role of inter- Taken together, prevailing theories of the devel-
personal vulnerability factors in the development of opment of BPD share a number of commonalities.
BPD (Gunderson & Lyons-Ruth, 2008). In partic- First, all authors acknowledge a biological basis for
ular, biologically based interpersonal hypersensitivity, intense emotionality that predates a formal diagno-
alongside propensities for emotional vulnerability sis of BPD. Second, this biological propensity likely
and impulsivity, is thought to (1) heighten emotional reciprocally transacts in a dynamic manner over
reactivity in interpersonal contexts and (2) disrupt time with environmental risk factors. Third, early
development of securely attached relationships be- interpersonal interactions, especially with caregivers,
tween the child and caregiver. While caregivers may constitute an important environmental risk factor.
contribute to these transactions with their own inse- These interactions may be characterized by a mis-
cure attachment or psychopathology, a child prone match in responses to the child’s experiences of
to distress and interpersonal sensitivity may also emotions, perceived invalidation of such emotions, or
elicit less responsive caregiver behaviors. Ultimately, insufficient support of emotion regulation capacities,
Dixon-Gordon, Haliczer, and Conkey 363

and may be influenced by the child’s biological pro- Current Methods and Findings Related to
pensity to emotion regulation difficulties. Fourth, Emotion Dysregulation in Borderline
this transaction potentiates more severe emotion Personality Disorder
dysregulation, which manifests as a range of ineffec- Emotion Responding in Borderline
tive interpersonal and risky behaviors. Thus, across Personality Disorder
models, emotion dysregulation is one critical mech- Since we consider emotions to be dynamic, short-
anism underlying the emergence and maintenance lived responses to discrete stimuli (Ekman, 1992),
of BPD symptoms. observed differences in emotional responding could
emerge in several ways. Specifically, people could
Unresolved Controversies Surrounding the differ in terms of (1) emotional sensitivity, such that
Role of Emotion Dysregulation in their emotions are more easily elicited by lower
Borderline Personality Disorder threshold stimuli, or specific types of stimuli; (2)
Despite a theoretical consensus that emotion dys- emotional reactivity, or the magnitude/intensity of
regulation is a key feature of BPD, several contro- an emotional response once it unfolds; (3) duration
versies remain. One unresolved debate revolves of response, with some people demonstrating a
around emotional responding among individuals slower return to baseline; or (4) regulation of the ex-
with the diagnosis. Although most theories point periences or expressions of an emotion. Although
to a predominance of negative emotions in BPD, these distinct aspects of an emotional response are
it is unclear which aspects of emotional responding dissociable in theory, it is difficult to disentangle
are impaired. For instance, whereas some research emotional sensitivity, reactivity, time course, and
points to emotional hyperreactivity to emotional regulation in daily life. The onset of an emotional
stimuli (Dixon-Gordon, Chapman, Lovasz, & response is thought to reflect sensitivity, whereas the
Walters, 2011; Weinberg, Klonsky, & Hajcak, offset is thought to reflect one type of emotion
2009), other studies have either failed to find group regulation (Koole, 2009). However, against the

differences or have found evidence of hyporeactivity backdrop of differences in “baseline” emotionality,
(Herpertz, Kunert, Schwenger, & Sass, 1999; Jacob determining the onset and offset of an emotional
et al., 2009; Kuo & Linehan, 2009). This discrep- response is difficult. Moreover, few studies include
ancy may stem from multiple factors. For instance, frequent enough measurements across multiple
it is possible that emotional responding in BPD is emotions to permit fine-grained discrimination of
only atypical in response to specific stressors, emo- these components in a single study.
tions, or domains. Whereas some theories of emotion
dysregulation in BPD suggest that dysregulation is Emotional Sensitivity
pervasive (Linehan, 1993), other approaches focus Some have proposed that perhaps rather than in-
on the unique dysregulation that may occur in re- creased reactivity to emotional stimuli, individuals
sponse to interpersonal stressor factors (Gunderson with BPD are initially more sensitive to emotional
& Lyons-Ruth, 2008). cues and events in their surrounding environments.
Another major controversy in the literature in- Of particular relevance to BPD, several studies
volves whether BPD is associated with differential support a negative bias in detecting social cues. For
use of emotion regulation strategies. For instance, it instance, empirical evidence suggests that individuals
is unclear whether individuals with BPD have fewer with BPD demonstrate a heightened ability to detect
emotion regulation strategies in their repertoire, im- emotional (i.e., angry and happy) facial stimuli
plement strategies ineffectively, or require different compared to healthy controls (Schulze, Domes,
strategies than typical controls. Although we might Koppen, & Herpertz, 2013). Relatedly, those with
theorize that those with BPD have fewer emotion BPD endorse being more sensitive to rejection than
regulation strategies in their repertoires, and there- healthy controls or socially anxious participants on
fore underutilize putatively “adaptive” strategies, there questionnaires (Staebler, Helbing, Rosenbach, &
is little evidence to support this notion. Furthermore, Renneberg, 2011), as well as on behavioral measures
although it is conceivable that individuals with BPD (Domsalla et al., 2014). To further examine rejection
overuse maladaptive strategies, there is also some sensitivity behaviorally, several studies used a com-
evidence to suggest that these strategies may have puterized ball-tossing game (Cyberball) containing
differential consequences for individuals with BPD. inclusion blocks (in which the participant received
Specific research findings supporting both claims an equal number of computerized “tosses” of a ball
are presented in the following section. as other fictional players) and exclusion blocks (in

which, after an introductory period, the participant to personally relevant emotional sounds (Rosenthal
was not tossed the ball; Domsalla et al., 2014). In et al., 2016), social rejection stressors (Dixon-
this paradigm, participants with BPD reported feel- Gordon et al., 2011; Reichenberger et al., 2017), an
ing more excluded than healthy controls across abuse-themed film clip (Lobbestael & Arntz, 2010),
blocks (Domsalla et al., 2014; Staebler, Renneberg, and a frustrating math task (Weinberg et al., 2009).
et al., 2011), although some work suggests that this In response to social-evaluative video clips that in-
difference only emerged in the inclusion block volved an actor making rejecting remarks, individu-
(Domsalla et al., 2014). For instance, participants als with BPD reported greater negative emotional
with BPD showed comparable activation to healthy reactivity (relative to a neutral baseline condition)
controls in a brain region thought to serve as a social compared to healthy controls. In contrast, partici-
exclusion alarm (the dorsal anterior cingulate) in re- pants with BPD reported less positive emotional re-
sponse to exclusion (Domsalla et al., 2014). In the activity in response to viewing video clips involving
inclusion condition, however, participants with praise (Reichenberger et al., 2017). Thus, subjective
BPD exhibited elevated activation in this region emotional reactivity in BPD may be circumscribed
compared to healthy controls. to negative emotions.
Despite theoretical reasons to suppose that Data on physiological measures of emotional
heightened emotional sensitivity in BPD may be reactivity in BPD are similarly heterogeneous. In
unique to BPD-salient stimuli, such as rejection, terms of sympathetic activity, participants with
the evidence is far from clear. Several studies found BPD or high BPD features show greater skin con-
some bias for negative emotional stimuli that were ductance response reactivity to personally relevant
theoretically linked with BPD, such as powerlessness sounds (Rosenthal et al., 2016), abuse-related stimuli
or malevolence (vs. stinginess; Sieswerda, Arntz, & (Lobbestael & Arntz, 2010; Schmahl, Elzinga, et al.,
Kindt, 2007). Other work, however, found an at- 2004), and social rejection stressors (Dixon-Gordon
tentional bias for negative emotional content more et al., 2011), compared to non-BPD or low-BPD
generally, but not specific to BPD-related content, controls. In addition, those with BPD evidence
among participants with BPD relative to controls higher blood pressure (Lobbestael & Arntz, 2010).
(Sieswerda et al., 2007). Meta-analyses likewise sug- In terms of parasympathetic reactivity, patients with
gest that participants with BPD show greater atten- BPD tend to show stable (Weinberg et al., 2009) or
tional bias for negative emotional content, and also decreasing (Fitzpatrick & Kuo, 2015) parasympa-
suggest that this effect is stronger for BPD-relevant thetic activity in response to stressors, relative to
stimuli (Kaiser, Jacob, Domes, & Arntz, 2017). controls. Emotional hyperreactivity is also seen in
Nevertheless, this bias is not apparent early on in the brain imaging studies. Several studies find that indi-
perceptual process. In affective priming (Donges, viduals with BPD show greater neural activation in
Dukalski, & Suslow, 2016) and Stroop (Sieswerda regions associated with emotional arousal, particu-
et al., 2007) paradigms with brief (<17 ms) or “sub- larly the amygdala, in response to emotional stimuli
liminal” stimulus presentations, no affective bias such as emotional faces (Donegan et al., 2003) and
was observed among participants with BPD relative unpleasant images (Hazlett et al., 2012) compared
to healthy controls. to healthy control participants. One meta-analysis
of 19 studies revealed that BPD participants demon-
Emotional Reactivity and Time Course strated hyperactivation of the left amygdala and
Evidence from trait-like self-report measures suggests posterior cingulate cortex, and attenuated activa-
elevated self-reported affective instability among tion of the dorsolateral prefrontal cortex (Schulze,
participants with BPD compared with other per- Schmahl, & Niedtfeld, 2016).
sonality disorders (Henry et al., 2001) and between On the other hand, several studies have failed to
individuals with higher (vs. lower) levels of BPD find evidence of emotional hyperreactivity in
features (Tragesser & Robinson, 2009). Findings BPD, and in some cases, have even indicated hypo-
from laboratory-based studies of emotional reactiv- reactivity. For instance, despite showing amygdala
ity and prolonged responding in BPD, however, are hyperreactivity, participants with BPD rated un-
more mixed, pointing to both emotional hyperreac- pleasant images as less unpleasant than healthy
tivity and hypoactivity in BPD. Consistent with controls in one study (Hazlett et al., 2012). In some
claims of emotional hyperreactivity, several studies cases, those with BPD report higher negative emo-
have found evidence of subjective emotional reactions at baseline (e.g., anger, sadness, anxiety, shame,
tivity in BPD relative to healthy controls, including annoyance, aversive tension; Jacob et al., 2009;

Kuo & Linehan, 2009; Reitz et al., 2012), but not context or type of emotional cue may be an impor-
greater emotional reactivity than healthy controls. tant factor to consider in understanding emotional
In addition, there is evidence that individuals with reactivity in BPD.
BPD demonstrate reduced sympathetic arousal in Given the dynamic nature of emotions, it is pos-
terms of skin conductance response (Herpertz et al., sible that these mixed findings regarding emotional
1999) and heart rate reactivity (Baschnagel, Coffey, reactivity reflect differences in the effect of BPD as
Hawk, Schumacher, & Holloman, 2013) to emo- emotions unfold. Emerging evidence paints a pic-
tional images compared to controls, as well as de- ture of prolonged emotional responses in BPD. For
creased amygdala activation during an emotional example, although participants with BPD did not
Stroop task (Malhi et al., 2013) and decreased acti- report greater emotional reactivity in terms of aver-
vation of the anterior cingulate cortex and orbitofron- sive tension to a stress induction (involving a stress-
tal cortex in response to trauma-related memories, ful math task in conjunction with emotionally
compared with controls (Schmahl, Vermetten, evocative images) than healthy controls, they did
Elzinga, & Bremner, 2004). A meta-analysis of 11 report a longer return to their emotional baseline
studies found that BPD participants show hyperac- (Reitz et al., 2012). Although another study revealed
tivation of the insula and posterior cingulate cortex no delay in self-reported emotional recovery to fear,
in response to negative emotions, but deactivation anger, or sadness film clips among those with BPD
of the amygdala and anterior cingulate and dorso- versus social anxiety, or healthy controls, there were
lateral prefrontal cortex compared to controls differences between groups in parasympathetic re-
(Ruocco, Amirthavasagam, Choi-Kain, & McMain, sponding (Fitzpatrick & Kuo, 2015). In particular,
2013). These findings of hyporeactivity stand in both participants with BPD and social anxiety ex-
sharp contrast to theory and self-report research hibited decreases in parasympathetic responding
suggesting emotional hyperreactivity in BPD. (i.e., respiratory sinus arrhythmia, an index of emo-
Several existing theories would also suggest that tion dysregulation) following a stressor, whereas
individuals with BPD may demonstrate particular healthy controls showed stable trajectories. Likewise,
emotional reactivity in response to interpersonal participants with BPD showed increasing sympa-
stressors. Many of the studies that found evidence thetic activity across the duration of a stressor,
for emotional hyperreactivity in BPD did use stim- whereas this pattern did not emerge among control
uli involving BPD-salient themes (e.g., rejection, participants (Weinberg et al., 2009). BPD has also
abuse, self-harm; Hazlett et al., 2007; Limberg, been linked with greater prolonged responses to on-
Barnow, Freyberger, & Hamm, 2011; Lobbestael & going stressors. For instance, participants with BPD
Arntz, 2010; C. Sauer, Arens, Stopsack, Spitzer, & reported prolonged experiences of specific emo-
Barnow, 2014) or interpersonally based stressors tions, such as anger, following a shame induction
(Chapman, Walters, & Dixon-Gordon, 2014; relative to healthy controls (Scheel et al., 2013), and
Dixon-Gordon et al., 2011; C. Sauer et al., 2014; shame after receiving negative feedback after a
Scott et al., 2017). In addition, there is some indica- stressful math task compared to healthy controls or
tion that emotional hyperreactivity may only be clinical controls without personality disorders (Gratz,
present in response to personally relevant stimuli Rosenthal, Tull, Lejuez, & Gunderson, 2010).
(Rosenthal et al., 2016). Whereas some experimen- Although participants with BPD or high BPD
tal work reveals greater shame reactivity to social features did not report differential immediate sub-
versus academic stressors among participants high jective reactivity to laboratory stressors, they did
in BPD features (Chapman et al., 2014), this find- report greater prolonged anxiety/fear responding
ing was not replicated in a comparison of social relative to depressed and nondepressed/BPD controls
versus another feedback-related stressful math task (Dixon-Gordon, Weiss, et al., 2015). This focus on
(Chapman, Dixon-Gordon, Butler, & Walters, prolonged emotional responses to an ongoing stres-
2015). It may be that emotional responding in BPD sor may better approximate emotional experiences
is more about a context-specific sensitivity, rather as they occur in patients’ lives.
than reactivity. As reviewed, individuals with BPD
seem to be more sensitive to ambiguous social Emotional Responding in Daily Life
stressors. However, once a clear stressor is detected The intense negative emotionality reported by those
and an emotional response occurs, the magnitude with BPD may not be solely, or even mostly, due to
of the response is comparable across groups. elevated reactivity. Rather, the environments of
Nevertheless, this pattern of findings suggests that those with BPD may actually be more stressful, or

these individuals may be more sensitive to stressors sponding in BPD found evidence of amygdala deac-
that exist in their daily environments. Generally tivation (Ruocco et al., 2013), another meta-analysis
speaking, studies that employ ecological momen- revealed hyperactivation of the left amygdala
tary assessment (EMA) methods find that partici- (Schulze et al., 2016). This latter meta-analysis
pants with BPD have an overall greater negative found that use of medications seems to attenuate
emotional state, or affective “home base,” and the link between BPD and amygdala hyperactiva-
greater variability in daily distress than healthy con- tion (Schulze et al., 2016). Thus, the numerous and
trols (Ebner-Priemer et al., 2015; Santangelo et al., heterogeneous medications prescribed to those with
2016; see Santangelo, Bohus, & Ebner-Priemer, BPD (Sansone, Rytwinski, & Gaither, 2003) may
2014 for a review). Relative to healthy controls, obscure findings of emotional reactivity.
those with BPD tend to report more frequent, in- Co-occurring symptoms may also cloud the pic-
tense, and persistent negative emotional responses ture of emotional responding in BPD. Several stud-
(Ebner-Priemer & Sawitzki, 2007; Ebner-Priemer ies suggest that posttraumatic stress symptoms and
et al., 2007; Reisch, Ebner-Priemer, Tschacher, state dissociation may attenuate emotional respond-
Bohus, & Linehan, 2008; Stiglmayr et al., 2005; ing in BPD. For instance, dissociation may mask
Trull et al., 2008) and greater emotional reactivity startle responses (Ebner-Priemer et al., 2005) and is
to negative social interactions in daily life (Sadikaj, associated with less amygdala activation (Hazlett
Russell, Moskowitz, & Paris, 2010). Indeed, BPD et al., 2012) among participants with BPD. Along
features were linked to more triggers, such as rejec- similar lines, posttraumatic stress symptoms attenu-
tion and betrayal, in daily life, and the link between ated cortisol reactivity to a laboratory stressor
these triggers and symptoms was stronger for those among participants with high BPD features (Dixon-
higher in BPD features (Miskewicz et al., 2015). Gordon, Gratz, & Tull, 2013). Likewise, PTSD can
They also report greater polarity (e.g., feeling all lead to elevated instability in fear and anxiety in
good vs. all bad) in affect and relational experiences daily life among those with BPD (Scheiderer et al.,
in their daily life, which intensifies during times of 2016). With the high rate of co-occurring psychiat-
heightened interpersonal stress (Coifman, Berenson, ric disorders seen in BPD (Zanarini, Frankenburg,
Rafaeli, & Downey, 2012). A recent EMA study also Hennen, Reich, & Silk, 2004), further work is
found that BPD symptoms predicted greater anger needed to disentangle the effects of these diagnoses
and shame reactivity to instances of perceived rejec- on emotional responding in BPD.
tion in daily life (Scott et al., 2017). It is unclear, Finally, methodological differences in the nature
however, to what extent individuals with BPD dem- and assessment of stressors may further complicate
onstrate greater emotional instability in daily life this literature. More consistent findings of emo-
relative to other psychiatric samples. For instance, tional reactivity in BPD tend to be found in studies
participants with BPD exhibited comparable emo- that utilize subjective assessment of emotions
tional intensity to those with mood disorders (Dixon-Gordon et al., 2011; Gratz et al., 2010), as
(Scheiderer, Wang, Tomko, Wood, & Trull, 2016) compared to studies that utilize behavioral (e.g.,
and comparable emotional variability to participants Arntz, Appels, & Sieswerda, 2000) or physiological
with other personality disorders (Farmer, Nash, & (Kuo & Linehan, 2009) measures. Even in terms of
Dance, 2004), posttraumatic stress, panic disorder, psychophysiological findings, measures of baseline
major depression, and bulimia nervosa (Santangelo responding versus reactivity could help explain dis-
et al., 2016). parate patterns of effects. For instance, most studies
that found evidence of hyperreactivity in BPD ex-
Resolving Controversies amined phasic increases from baseline, such as skin
Various possible explanations exist for these discrep- conductance responses (Dixon-Gordon et al., 2011;
ant findings. One factor that may account for con- Lobbestael & Arntz, 2010; Rosenthal et al., 2016;
flicting findings is medication use among partici- Schmahl, Elzinga, et al., 2004) or startle responses
pants with BPD. Indeed, in one study, over 85% of (Ebner-Priemer et al., 2005; Hazlett et al., 2007).
participants with BPD were taking prescribed psy- In addition, abnormalities in the time course of
chotropic medications (Rosenthal et al., 2016). emotional responses in BPD may be more accu-
There is some evidence that use of psychotropic rately captured by research that uses more frequent
medications may moderate findings of emotional assessment points. For instance, more frequent sam-
hyperreactivity in BPD. For instance, whereas one pling in EMA studies seems to better capture emo-
meta-analysis of neural correlates of emotional re- tional variability and instability in BPD than less

frequent sampling (Ebner-Priemer & Sawitzki, Investigations of emotion regulation strategies in
2007). Furthermore, there are theoretical reasons to response to specific stressors paint a muddier pic-
believe that BPD may be linked with hyperreactiv- ture of emotion regulation in BPD. Although
ity to particular classes of emotional cues. It is also theory might suggest that individuals with BPD
possible that emotional reactivity in BPD may be have fewer emotion regulation strategies in their
emotion specific, such that hyperreactivity is pres- repertoire, several studies indicate that this may not
ent when it comes to certain emotions (e.g., anger, be the case. In one laboratory study, there were no
shame, anxiety), yet not others (Fitzpatrick & Kuo, differences between individuals with BPD and de-
2015; Gratz, Rosenthal, Tull, Lejuez, & Gunderson, pressed or healthy participants in terms of sponta-
2010; Scott et al., 2017). Taken together, the hetero- neous use of emotion regulation strategies in re-
geneity of study designs complicates interpretation sponse to low-intensity and high-intensity emotional
across mixed findings, and also points to important images (C. Sauer et al., 2016). In a study of under-
areas for future research. graduate students, those classified as high regulators
(i.e., high use of all emotion regulation strategies)
Emotion Regulation Difficulties in and maladaptive regulators (i.e., high use of mala-
Borderline Personality Disorder daptive emotion regulation strategies) reported
Emotional Awareness and Clarity greater BPD symptoms than those classified as low
BPD symptoms have been associated with a self- regulators (Dixon-Gordon, Aldao, & De Los Reyes,
reported lack of emotional clarity (Salsman & 2015). Similarly, in another study, participants with
Linehan, 2012; Vine & Aldao, 2014), low emotional high BPD features reported using more emotion
awareness (Leible & Snell, 2004), and difficulties regulation strategies (i.e., distraction, cognitive re-
identifying and labeling specific emotions (Modestin, appraisal, emotion suppression) in response to a
Furrer, & Malti, 2004; Wolff, Stiglmayr, Bretz, lab-based stressor than those with low BPD features
Lammers, & Auckenthaler, 2007). Furthermore, (Chapman, Dixon-Gordon, & Walters, 2013). Of
when asked to describe their emotional experiences, note, those individuals high in BPD features en-
individuals with BPD emphasize valence (i.e., dorsed less spontaneous use of emotional accept
whether an emotion is pleasant or unpleasant) over ance in response to a laboratory stressor. Likewise,
arousal (whether an emotion is more calm or low in BPD severity has been shown to predict greater
arousal vs. highly arousing; Suvak, Litz, & Sloan, spontaneous use of avoidance in response to labora-
2011). Additionally, research suggests that individu- tory stressors (Evans, Howard, Dudas, Denman, &
als with BPD demonstrate poorer negative emotion Dunn, 2013). It is unclear whether individuals with
differentiation in their everyday lives relative to BPD are using certain emotion regulation strategies
controls (Zaki, Coifman, Rafaeli, Berenson, & ineffectively or are overutilizing all of their strategies
Downey, 2013) and report greater undifferentiated in a frantic attempt to reduce distressing emotions.
negative affect (across fear, hostility, and sadness It is also possible that certain emotion regulation
measures) than those with a depressive disorder in strategies function differently among individuals
daily life (Tomko et al., 2015). with BPD. In particular, a growing literature sug-
gests that individuals with BPD underrecruit brain
Emotion Regulation Strategies regions associated with cognitive control when
BPD has been linked with a tendency toward mala- using the emotion regulation strategy of reappraisal,
daptive emotion regulation strategies. For example, compared with their healthy counterparts
BPD features have been associated with thought (Mauchnik & Schmahl, 2010). When instructed to
avoidance (Rosenthal, Cheavens, Lejuez, & Lynch, use reappraisal, individuals with BPD have less acti-
2005), self-criticism, emotional suppression, alcohol vation in regions associated with cognitive control,
use, depressive and anger rumination (Aldao & specifically prefrontal cortex regions (Lang et al.,
Dixon-Gordon, 2014; Baer & Sauer, 2011), and 2012) such as the left orbitofrontal cortex (Schulze
emotional suppression (Beblo, Fernando, & Kamper, et al., 2011), compared with controls. Similarly,
2013). BPD symptoms are also associated with when viewing social-emotional stimuli and using
limited access to emotion regulation strategies, even psychological distancing (i.e., a type of cognitive re-
after controlling for affect intensity and reactivity appraisal), individuals with BPD showed different
(Glenn & Klonsky, 2009; Salsman & Linehan, neural dynamics in brain regions associated with
2012). These studies, however, largely relied on ret- cognitive control (e.g., less reactivity in the dorsal
rospective recall of emotion regulation strategies. anterior cingulate cortex and intraparietal sulcus;

greater activation in the superior temporal sulcus emotional acceptance (Chapman et al., 2017).
and superior frontal gyrus), and also those regions Similarly, participants with BPD reported that
related to emotional responding (i.e., less deactiva- they felt less effective in implementing reappraisal
tion in the amygdala), compared to healthy controls and distraction strategies than healthy participants
(Koenigsberg et al., 2010). With emotional suppres- (C. Sauer et al., 2016). However, whereas healthy
sion, however, individuals with BPD did not differ participants did not exhibit any differences in
from controls in brain activation or self-reported physiological responding when they accepted versus
affect (Ruocco, Medaglia, Ayaz, & Chute, 2010). suppressed emotions in response to a laboratory
Individuals with BPD also show differences when stressor, participants with BPD showed a different
preparing for emotional experiences. One study pattern (Dixon-Gordon, Turner, Rosenthal, &
found less activation in regions associated with cog- Chapman, 2017). In particular, participants with
nitive control during anticipation of emotional BPD who were assigned to accept their emotions
stimuli (Scherpiet et al., 2014). Thus, it may be that exhibited increased parasympathetic responding
those with BPD use less cognitive control regions in compared to those who suppressed their emotions.
their implementation of some emotion regulation Therefore, despite reported distress and perceived
strategies. ineffectiveness in implementing putatively adaptive
Emotion regulation strategies typically considered strategies, individuals with BPD appear to benefit
“maladaptive” may have both adverse and beneficial physiologically from some adaptive emotion regu-
consequences for individuals with BPD. For in- lation strategies.
stance, one putatively maladaptive strategy, rumina-
tion, has problematic effects in BPD relative to Emotion-Dependent Behaviors
other strategies. Namely, participants with BPD Another aspect of emotion dysregulation is a fail-
who were instructed to ruminate reported greater ure to inhibit emotion-dependent behaviors, or to
negative affect and showed less persistence in a frus- have difficulties engaging in goal-directed behavior
trating task than participants who were instructed when distressed. Several studies suggest that indi-
to engage in mindful self-focus (S. E. Sauer & Baer, viduals with BPD or high BPD features may strug-
2012). Other strategies typically considered mal- gle to inhibit impulsive behaviors when distressed.
adaptive, however, such as suppression, may be For instance, one study found that individuals
more effective among those with BPD. Although high in BPD features engaged in more impulsive
some work suggests that BPD severity does not responses on a behavioral measure of impulsivity
affect short-term effects of emotional suppression (a passive avoidance learning task) after a fear in-
on subjective experiences of distress (Evans et al., duction, whereas this was not the case among indi-
2013), other studies suggest that suppression may viduals low in BPD features (Chapman, Dixon-
actually be more effective for individuals with BPD. Gordon, Layden, & Walters, 2010). Similarly,
For instance, participants with high BPD features participants with BPD show decreased ability to
reported more positive emotions and lower urges to learn from punishment after an emotion induction,
engage in impulsive behavior on days when they whereas this pattern was not seen in participants
were instructed to suppress their emotions com- without BPD (Dixon-Gordon, Hackel, Tull, &
pared to days when they were instructed to simply Gratz, 2018). Using behavioral measures, BPD is
observe their emotions in a daily diary study also associated with decreased willingness to tolerate
(Chapman et al., 2009). Similar findings were found emotional distress to pursue goal-directed behav-
among participants with BPD when instructed to iors (Bornovalova et al., 2008; Gratz, Rosenthal,
suppress versus accept their emotions in daily life Tull, Lejuez, & Gunderson, 2006). Furthermore,
(Chapman, Rosenthal, Dixon-Gordon, Turner, & following a negative emotion induction, individu-
Kuppens, 2017). These data suggest that individuals als high in BPD features came up with fewer rele-
with BPD may perceive hedonic benefits from using vant solutions and more inappropriate solutions to
maladaptive strategies, despite their behavioral con- interpersonal problems; of note, increases in nega-
sequences. tive emotion were found to mediate the relationship
Although implementation of putatively adaptive between BPD features and reduced social problem-
strategies may be more helpful for individuals with solving performance (Dixon-Gordon et al., 2011).
BPD, it may simultaneously be more challenging. Thus, elevated state distress may account for some
For instance, in daily life, individuals with BPD of the problems engaging in goal-directed tasks
reported having greater distress when practicing among those with BPD.

Emotion Regulation as a Mechanism emotional stimuli, this bias was normalized in a
of Change small sample of recovered patients after three years of
Despite significant advances in treatment of BPD, intensive treatment (Sieswerda et al., 2007). Although
less is known about the mechanisms of change in other theoretically relevant candidate mediators war-
these treatments. Theoretically, if emotion dysregu- rant consideration, including mentalization ability
lation underlies many of the problems seen in BPD, (Fonagy & Bateman, 2006) or therapeutic alliance
effective treatments may enact change by improving (Bedics, Atkins, Harned, & Linehan, 2015), emerging
emotion dysregulation. Because most intervention work points to the importance of emotion regulation
studies are not designed to examine mechanisms of in the treatment of BPD.
change, however, there is a relative scarcity of mech-
anistic research on BPD treatments (Gratz, Moore, Resolving Controversies
& Tull, 2016). To truly establish that a variable is a Although individuals with BPD report having lim-
mechanism of a specific treatment, participants ited access to effective emotion regulation strategies
must be randomly assigned to the treatment, and (Glenn & Klonsky, 2009; Salsman & Linehan,
both the putative mechanisms and outcome vari- 2012), there is little evidence to suggest that indi-
ables must be measured at multiple occasions over viduals high in BPD features actually employ fewer
time to establish that the mechanism drives subse- strategies in response to discrete stressors. To the
quent change, rather than the other way around contrary, some research suggests that individuals
(Kazdin, 2007). Despite the dearth of research in high in BPD features report that they are in fact
this area, several studies suggest that aspects of emo- using more emotion regulation strategies when dis-
tion regulation may be candidate mechanisms of tressed (Dixon-Gordon, Aldao, et al., 2015). It is
change in the treatment of BPD. Generally, patients possible that individuals with BPD are indeed using
with BPD show improvements in reported disposi- more strategies but are implementing these strate-
tional emotion dysregulation after treatment gies ineffectively. There is some indication, for in-
(Goodman et al., 2014), such as dialectical behavior stance, that individuals with BPD differ from con-
therapy (DBT; Linehan, 1993). For instance, among trols in their recruitment of regions of the prefrontal
patients with BPD undergoing DBT, improvements cortex when using reappraisal (Mauchnik &
in coping strategies accounted for improvements in Schmahl, 2010). It is also possible that individuals
depression, suicide, and anger control (Neacsiu, with BPD are more indiscriminant in their use of
Rizvi, & Linehan, 2010). In addition, improve- strategies. Specifically, these individuals may be
ments in emotion dysregulation contributed to im- using several strategies, but the strategies may be
provements in cognitive and affective symptoms of poorly matched to contextual demands of the situa-
BPD in patients undergoing an emotion regulation tion. Thus, they may lack emotion regulation flexibil-
group treatment (Gratz, Bardeen, Levy, Dixon- ity, or the ability to vary their use of strategies to
Gordon, & Tull, 2015). meet the demands of the present context (Aldao,
Treatment has also been shown to result in Sheppes, & Gross, 2015).
changes in regions of the brain associated with Individuals with BPD may also differ from other
emotional experiencing and emotion regulation. groups in their definition of effective emotion regu-
Decreased amygdala activity in response to viewing lation. From context to context, people may vary in
emotional images was seen in patients after DBT their emotion regulation goals. At work, someone
(Goodman et al., 2014). Beyond changes in the may have the goal to reduce emotional intensity
amygdala, whereas females with BPD showed greater enough to permit attention to the present task. In
activity than controls in the anterior cingulate one conversation with a significant other, a person
cortex in response to negative emotional stimuli, ac- might have the goal of attending to his or her part-
tivity in this region normalized after treatment ner’s emotions; in another conversation, that same
(Schnell & Herpertz, 2007). This reduction in ante- person may hope to elicit support for him- or her-
rior cingulate activity may be linked to changes in self. Thus, if individuals with BPD are defining
effects of emotion regulation strategies. In particu- their end goal differently or less flexibly than healthy
lar, treatment responders showed decreased anterior individuals, this could account for discrepancies in
cingulate activity while distracting from emotional reported access to effective strategies—perhaps the
stimuli following treatment completion (Winter strategies are working the same way for those with
et al., 2017). Furthermore, whereas at baseline and without BPD, but were less likely to match the
patients with BPD showed an attentional bias for intended goal for those with BPD. In particular, it

seems likely that individuals with BPD implement whether individuals with BPD over- or underutilize a
emotion regulation strategies with the end goal of range of emotion regulation strategies, there is some
avoiding or escaping their emotions. To the extent indication that these individuals underuse emotional
that this goal is inflexible across contexts, this may acceptance, underrecruit cognitive control regions in
be one key source of emotion dysregulation. regulating emotions, and perceive their own emotion
regulation as less effective. Fifth, there is evidence to
Theoretical Synthesis of the Literature on suggest that negative emotional intensity may con-
Emotion Dysregulation in Borderline tribute to many of the problems seen in BPD, includ-
Personality Disorder ing impulsive behaviors, difficulty learning, and poor
Accumulating evidence suggests that BPD is charac- interpersonal problem solving. Finally, although re-
terized by emotion dysregulation. Although research search in this area is preliminary, emotion dysregula-
relying on self-report trait measures consistently re- tion may be one important mechanism (potentially
veals greater negative emotionality in BPD relative to of several) of change in treatments for BPD. These
healthy controls, results from laboratory studies are findings align with many of the aforementioned
far less conclusive. Several consistent themes emerge theories of emotion dysregulation in BPD (Bateman
from this literature (see Figure 25.1). First, individu- & Fonagy, 2004; Crowell et al., 2009; Gunderson &
als with BPD appear to have an elevated bias toward Lyons-Ruth, 2008; Linehan, 1993), and in particular
emotional stimuli. Second, individuals with BPD point to the need to examine the interaction of inter-
typically have more baseline negative emotions. personal dysfunction and emotion dysregulation in
Third, although the findings regarding emotional this disorder.
reactivity remain inconclusive, there seems to be
somewhat greater consistency in emotional reactivity Future Directions of Research on
to interpersonal or trauma/abandonment-themed Emotion Dysregulation and
stressors, particularly anger, shame, or anxiety reac- Borderline Personality Disorder
tivity. In addition, there is reason to believe that emo- Despite the tremendous strides toward understand-
tional responding may be exaggerated later on in the ing emotion dysregulation in BPD over the past two
emotional response. Fourth, although it is unclear decades, several critical steps are needed to enhance
Normative
BPD
Emotional Intensity
E. Regulation
A. Baseline Difficulties regulating.
Higher baseline – Less awareness
negative A B C D E – Less acceptance
emotionality. – Lower perceived
effectiveness
Time – Less cognitive
control
B. Sensitivity C. Acute Reactivity D. Prolonged

Lower threshold for Mixed evidence. Response
emotional response. Moderated by: Emerging evidence.
Attentional bias to – domain May indicate poor
self-referential, – type of emotion regulation.
trauma, and social – co-occuring
stimuli. symptoms
Figure 25.1 Graphical depiction of emotion dysregulation in borderline personality disorder.

our understanding of the assessment and treatment American Psychiatric Association. (2013). Diagnostic and
of BPD. Against the backdrop of the emerging re- statistical manual of mental disorders (5th ed.). Arlington, VA:
American Psychiatric Publishing.
search base examining emotional responding in Arntz, A., Appels, C., & Sieswerda, S. (2000). Hypervigilance in
BPD, the field could benefit from more nuanced borderline disorder: A test with the emotional Stroop
laboratory-based studies. For instance, the use of paradigm. Journal of Personality Disorders, 14, 366–373.
multiple fine-grained assessments across the time Baer, R. A., & Sauer, S. E. (2011). Relationships between
course of emotional responses may pinpoint where depressive rumination, anger rumination, and borderline
personality features. Personality Disorders: Theory, Research,
those with BPD diverge from healthy individuals. and Treatment, 2, 142–150.
In addition, the inconsistent results regarding emo- Baschnagel, J. S., Coffey, S. F., Hawk, L. W., Schumacher, J. A.,
tional reactivity in BPD underscore the need to & Holloman, G. (2013). Psychophysiological assessment
better understand the conditions under which this of emotional processing in patients with borderline
reactivity may be evident. It will also be important personality disorder with and without comorbid substance
use. Personality Disorders: Theory, Research, and Treatment, 4,
to examine how emotional responding interacts 203–213.
with other key domains of impairment in BPD, in- Bateman, A. W., & Fonagy, P. (2004). Mentalization-based
cluding interpersonal dysfunction (Lazarus, Cheavens, treatment of BPD. Journal of Personality Disorders, 18, 36–51.
Festa, & Rosenthal, 2014). Routine integration of Beauchaine, T. P. (2015). Future directions in emotion
behavioral outcomes into laboratory paradigms dysregulation and youth psychopathology. Journal of Clinical
Child and Adolescent Psychology, 44, 875–896.
would permit a clearer evaluation of the adaptiveness Beblo, T., Fernando, S., & Kamper, P. (2013). Increased attempts
of specific emotion regulation strategies, beyond to suppress negative and positive emotions in borderline
merely their hedonic effects. Furthermore, despite personality disorder. Psychiatry Research, 210, 505–509.
the mixed research on emotion regulation strategy Bedics, J. D., Atkins, D. C., Harned, M. S., & Linehan, M. M.
use in BPD, one consistent finding is the perceived (2015). The therapeutic alliance as a predictor of outcome
in dialectical behavior therapy versus nonbehavioral
ineffectiveness of emotion regulation for these indi- psychotherapy by experts for borderline personality disorder.
viduals. It is possible that those with BPD diverge Psychotherapy, 52, 67–77.
from healthy controls in their emotion regulation Bender, D. S., Dolan, R. T., Skodol, A. E., Sanislow, C. A.,
goals (e.g., to avoid or escape distress) rather than in Dyck, I. R., McGlashan, T. H., . . . Gunderson, J. G. (2001).
their use of specific strategies. Another important Treatment utilization by patients with personality disorders.
American Journal of Psychiatry, 158, 295–302.
avenue for future research is a concerted focus on Bolton, J. M., & Robinson, J. (2010). Population-attributable
examining which aspects of emotional dysfunction fractions of Axis I and Axis II mental disorders for suicide
are unique to BPD, especially given that the pres- attempts: Findings from a representative sample of the adult,
ence of co-occurring disorders is the norm, rather noninstitutionalized US population. American Journal of
than the exception, in BPD (Zanarini et al., 2004). Public Health, 100, 2473–2480.
Bornovalova, M. A., Gratz, K. L., Daughters, S. B., Nick, B.,
Furthermore, although preliminary findings suggest Delany-Brumsey, A., Lynch, T. R., Kosson, D.,. . . Lejuez,
that emotion dysregulation may be one candidate C. W. (2008). A multimodal assessment of the relationship
mechanism of change in treatment, we must examine between emotion dysregulation and borderline personality
emotion dysregulation alongside other candidate disorder among inner-city substance users in residential
mechanisms. Finally, it is important to examine treatment. Journal of Psychiatric Research, 42, 717–726.
Chapman, A. L., Dixon-Gordon, K. L., Butler, S. M., & Walters,
whether emotion dysregulation is a specific mech- K. N. (2015). Emotional reactivity to social rejection versus a
anism for some treatments for BPD or whether it is frustration induction among persons with borderline
an important target across different types of inter- personality features. Personality Disorders: Theory, Research,
ventions. and Treatment, 6, 88–96.
Chapman, A. L., Dixon-Gordon, K. L., Layden, B. K., &
Walters, K. N. (2010). Borderline personality features
References moderate the effect of a fear induction on impulsivity.
Aldao, A., & Dixon-Gordon, K. L. (2014). Broadening the Personality Disorders: Theory, Research, and Treatment, 1,
scope of research on emotion regulation strategies and 139–152.
psychopathology. Cognitive Behaviour Therapy, 43, 22–33. Chapman, A. L., Dixon-Gordon, K. L., & Walters, K. N. (2013).
Aldao, A., & Nolen-Hoeksema, S. (2010). Specificity of cognitive Borderline personality features moderate emotional reactivity
emotion regulation strategies: A transdiagnostic examination. and emotion regulation in response to a laboratory stressor.
Behaviour Research and Therapy, 48, 974–983. Journal of Experimental Psychopathology, 4, 451–470.
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Chapman, A. L., Rosenthal, M. Z., Dixon-Gordon, K. L.,
Emotion-regulation strategies across psychopathology: A Turner, B. J., & Kuppens, P. (2017). Borderline personality
meta-analytic review. Clinical Psychology Review, 30, 217–237. disorder and the effects of instructed emotional avoidance or
Aldao, A., Sheppes, G., & Gross, J. J. (2015). Emotion regulation acceptance in daily life. Journal of Personality Disorders, 31,
flexibility. Cognitive Therapy and Research, 39, 263–278. 483–502.

Chapman, A. L., Rosenthal, M. Z., & Leung, D. W. (2009). and self-other relevance information. Psychopathology, 49,
Emotion suppression in borderline personality disorder: An 116–123.
experience sampling study. Journal of Personality Disorders, Ebner-Priemer, U. W., Badeck, S., Beckmann, C., Wagner, A.,
23, 29–47. Feige, B., Weiss, I., . . . Bohus, M. (2005). Affective dysregulation
Chapman, A. L., Walters, K. N., & Dixon-Gordon, K. L. (2014). and dissociative experience in female patients with borderline
Emotional reactivity to social rejection and negative personality disorder: A startle response study. Journal of
evaluation among persons with borderline personality Psychiatric Research, 39, 85–92.
features. Journal of Personality Disorders, 28, 720–733. Ebner-Priemer, U. W., Kuo, J. R., Kleindienst, N., Welch, S. S.,
Coifman, K. G., Berenson, K. R., Rafaeli, E., & Downey, G. Reisch, T., Reinhard, I., . . . Bohus, M. (2007). State affective
(2012). From negative to positive and back again: Polarized instability in borderline personality assessed by ambulatory
affective and relational experience in borderline personality monitoring. Psychological Medicine, 37, 961–970.
disorder. Journal of Abnormal Psychology, 121, 668–679. Ebner-Priemer, U. W., Santangelo, P. S., Kleindienst, N.,
Cole, P. M., Michel, M. K., & Teti, L. O. (1994). The Tuerlinckx, F., Oravecz, Z., Bohus, M., & Kuppens, P.
development of emotion regulation and dysregulation: A (2015). Unraveling affective dysregulation in borderline
clinical perspective. Monographs of the Society for Research in personality disorder: A theoretical model and empirical
Child Development, 59, 73–100. evidence. Journal of Abnormal Psychology, 124, 186–198.
Crowell, S. E. (2016). Biting the hand that feeds: Current opinion Ebner-Priemer, U. W., & Sawitzki, G. (2007). Ambulatory
on the interpersonal causes, correlates, and consequences of assessment of affective instability in borderline personality
borderline personality disorder. F1000Research, 5, 2796. disorder: The effect of the sampling frequency. European
Crowell, S. E., Beauchaine, T. P., & Linehan, M. M. (2009). Journal of Psychological Assessment, 23, 238–247.
A biosocial developmental model of borderline personality: Ekman, P. (1992). Are there basic emotions? Psychological Review,
Elaborating and extending Linehan’s theory. Psychological 99, 550–553.
Bulletin, 135, 495–510. Evans, D., Howard, M., Dudas, R., Denman, C., & Dunn,
Dixon-Gordon, K. L., Aldao, A., & De Los Reyes, A. (2015). B. D. (2013). Emotion regulation in borderline personality
Repertoires of emotion regulation: A person-centered disorder: Examining the consequences of spontaneous and
approach to assessing emotion regulation strategies and links instructed use of emotion suppression and emotion
to psychopathology. Cognition and Emotion, 29, 1314–1325. acceptance when viewing negative films. Journal of
Dixon-Gordon, K. L., Chapman, A. L., Lovasz, N., & Walters, Experimental Psychopathology, 4, 546–565.
K. N. (2011). Too upset to think: The interplay of borderline Farmer, R. F., Nash, H. M., & Dance, D. (2004). Mood patterns
personality features, negative emotions, and social problem and variations associated with personality disorder pathology.
solving in the laboratory. Personality Disorders: Theory, Comprehensive Psychiatry, 45, 289–303.
Research, and Treatment, 2, 243–260. Fitzpatrick, S., & Kuo, J. R. (2015). A comprehensive examination
Dixon-Gordon, K. L., Gratz, K. L., & Tull, M. T. (2013). of delayed emotional recovery in borderline personality
Multimodal assessment of emotional reactivity in borderline disorder. Journal of Behavior Therapy and Experimental
personality pathology: The moderating role of posttraumatic Psychiatry, 47, 51–59.
stress disorder symptoms. Comprehensive Psychiatry, 54, Fonagy, P., & Bateman, A. W. (2006). Mechanisms of change in
639–648. mentalization-based treatment of BPD. Journal of Clinical
Dixon-Gordon, K. L., Hackel, L. M., Tull, M. T., & Gratz, K. L. Psychology, 62, 411–430.
(2018). The influence of emotional state on reinforcement Garnefski, N., Kraaij, V., & Spinhoven, P. (2001). Negative life
learning in borderline personality disorder. Journal of events, cognitive emotion regulation and emotional problems.
Personality Disorders. 32, 433–446. Personality and Individual Differences, 30, 1311–1327.
Dixon-Gordon, K. L., Turner, B. J., Rosenthal, M. Z., & Glenn, C. R., & Klonsky, E. D. (2009). Emotion dysregulation
Chapman, A. L. (2017). Emotion regulation in borderline as a core feature of borderline personality disorder. Journal of
personality disorder: An experimental investigation of the Personality Disorders, 23, 20–28.
effects of instructed acceptance and suppression. Behavior Goodman, M., Carpenter, D., Tang, C. Y., Goldstein, K. E.,
Therapy, 48, 750–764. Avedon, J., Fernandez, N., .
.
.
Hazlett, E. A. (2014).
Dixon-Gordon, K. L., Weiss, N. H., Tull, M. T., DiLillo, D., Dialectical behavior therapy alters emotion regulation and
Messman-Moore, T., & Gratz, K. L. (2015). Characterizing amygdala activity in patients with borderline personality
emotional dysfunction in borderline personality, major disorder. Journal of Psychiatric Research, 57, 108–116.
depression, and their co-occurrence. Comprehensive Gottman, J. M., & Katz, L. F. (1989). Effects of marital discord
Psychiatry, 62, 187–203. on young children’s peer interaction and health effects of
Domsalla, M., Koppe, G., Niedtfeld, I., Vollstädt-Klein, S., marital discord on young children’s peer interaction and
Schmahl, C., Bohus, M., & Lis, S. (2014). Cerebral health. Developmental Psychology, 25, 373–381.
processing of social rejection in patients with borderline Gratz, K. L., Bardeen, J. R., Levy, R., Dixon-Gordon, K. L., &
personality disorder. Social Cognitive and Affective Neuroscience, Tull, M. T. (2015). Mechanisms of change in an emotion
9, 1789–1797. regulation group therapy for deliberate self-harm among
Donegan, N. H., Sanislow, C. A., Blumberg, H. P., Fulbright, women with borderline personality disorder. Behaviour
R. K., Lacadie, C., Skudlarski, P., . . . Wexler, B. E. (2003). Research and Therapy, 65, 29–35.
Amygdala hyperreactivity in borderline personality disorder: Gratz, K. L., Moore, K. E., & Tull, M. T. (2016). The role
Implications for emotional dysregulation. Biological of emotion dysregulation in the presence, associated
Psychiatry, 54, 1284–1293. difficulties, and treatment of borderline personality disorder.
Donges, U. S., Dukalski, B., & Suslow, T. (2016). Borderline Personality Disorders: Theory, Research, and Treatment,
personality disorder and automatic processing of valence 7, 344–353.

Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment Koole, S. L. (2009). The psychology of emotion regulation: An
of emotion regulation and dysregulation: Development, integrative review. Cognition & Emotion, 23, 4–41.
factor structure, and initial validation of the Difficulties in Kuo, J. R., & Linehan, M. M. (2009). Disentangling emotion
Emotion Regulation Scale. Journal of Psychopathology and processes in borderline personality disorder: Physiological
Behavioral Assessment, 26, 41–54. and self-reported assessment of biological vulnerability,
Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., & baseline intensity, and reactivity to emotionally evocative
Gunderson, J. G. (2006). An experimental investigation of stimuli. Journal of Abnormal Psychology, 118, 531–544.
emotion dysregulation in borderline personality disorder. Lang, S., Kotchoubey, B., Frick, C., Spitzer, C., Grabe, H. J., &
Journal of Abnormal Psychology, 115, 850–855. Barnow, S. (2012). Cognitive reappraisal in trauma-exposed
Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., & women with borderline personality disorder. NeuroImage,
Gunderson, J. G. (2010). An experimental investigation of 59, 1727–1734.
emotional reactivity and delayed emotional recovery in Lazarus, S. A., Cheavens, J. S., Festa, F., & Rosenthal, M. Z.
borderline personality disorder: The role of shame. (2014). Interpersonal functioning in borderline personality
Comprehensive Psychiatry, 51, 275–285. disorder: A systematic review of behavioral and laboratory-
Gratz, K. L., & Tull, M. T. (2010). The relationship between based assessments. Clinical Psychology Review, 34, 193–205.
emotion dysregulation and deliberate self-harm among Leible, T. L., & Snell, W. E. (2004). Borderline personality
inpatients with substance use disorders. Cognitive Therapy disorder and multiple aspects of emotional intelligence.
and Research, 34, 544–553. Personality and Individual Differences, 37, 393–404.
Gross, J. J. (1998). The emerging field of emotion regulation: An Limberg, A., Barnow, S., Freyberger, H. J., & Hamm, A. O.
integrative review. Review of General Psychology, 2, 271–299. (2011). Emotional vulnerability in borderline personality
Gunderson, J. G., & Lyons-Ruth, K. (2008). BPD’s inter disorder is cue specific and modulated by traumatization.
personal hypersensitivity phenotype: A gene-environment- Biological Psychiatry, 69, 574–582.
developmental model. Journal of Personality Disorders, 22, Linehan, M. M. (1993). Cognitive-behavioral treatment of
22–41. borderline personality disorder. New York, NY: Guilford Press.
Hazlett, E. A., Speiser, L. J., Goodman, M., Roy, M., Carrizal, M., Livesley, W. J., Jackson, D. N., & Schroeder, M. L. (1992).
Wynn, J. K., . . . New, A. S. (2007). Exaggerated affect- Factorial structure of traits delineating personality disorders
modulated startle during unpleasant stimuli in borderline in clinical and general population samples. Journal of
personality disorder. Biological Psychiatry, 62, 250–255. Abnormal Psychology, 101, 432–440.
Hazlett, E. A., Zhang, J., New, A. S., Zelmanova, Y., Goldstein, Lobbestael, J., & Arntz, A. (2010). Emotional, cognitive and
K. E., Haznedar, M. M., . . . Chu, K.-W. (2012). Potentiated physiological correlates of abuse-related stress in borderline
amygdala response to repeated emotional pictures in borderline and antisocial personality disorder. Behaviour Research and
personality disorder. Biological Psychiatry, 72, 448–456. Therapy, 48, 116–124.
Henry, C., Mitropoulou, V., New, A. S., Koenigsberg, H. W., Maffei, C., & Fusi, V. (2016). Emotion dysregulation in
Silverman, J., & Siever, L. J. (2001). Affective instability and borderline personality disorder: A literature review.
impulsivity in borderline personality and bipolar II disorders: Phenomenology and Mind, 11, 210–220.
Similarities and differences. Journal of Psychiatric Research, Malhi, G. S., Tanious, M., Fritz, K., Coulston, C. M., Bargh,
35, 307–312. D. M., Phan, K. L., .
.
.
Das, P. (2013). Differential
Herpertz, S. C., Kunert, H. J., Schwenger, U. B., & Sass, H. engagement of the fronto-limbic network during emotion
(1999). Affective responsiveness in borderline personality processing distinguishes bipolar and borderline personality
disorder: A psychophysiological approach. American Journal disorder. Molecular Psychiatry, 18, 1247–1248.
of Psychiatry, 156, 1550–1556. Mauchnik, J., & Schmahl, C. (2010). The latest neuroimaging
Hörz, S., Zanarini, M. C., Frankenburg, F. R., Reich, D. B., & findings in borderline personality disorder. Current Psychiatry
Fitzmaurice, G. (2010). Mental health service use of patients Reports, 12, 46–55.
with borderline personality disorder and Axis II comparison Miskewicz, K., Fleeson, W., Arnold, E. M., Law, M. K.,
participants: A 10-year follow-up study. Psychiatric Services, Mneimne, M., & Furr, R. M. (2015). A contingency-
61, 612–616. oriented approach to understanding borderline personality
Jacob, G. A., Hellstern, K., Ower, N., Pillmann, M., Scheel, disorder: Situational triggers and symptoms. Journal of
C. N., Rusch, N., . . . Lieb, K. (2009). Emotional reactions Personality Disorders, 29, 486–502.
to standardized stimuli in women with borderline Modestin, J., Furrer, R., & Malti, T. (2004). Study on alexithymia
personality disorder: Stronger negative affect, but no in adult non-patients. Journal of Psychosomatic Research, 56,
differences in reactivity. Journal of Nervous and Mental 707–709.
Disease, 197, 808–815. Muehlenkamp, J. J., Peat, C. M., Claes, L., & Smits, D. (2012).
Kaiser, D., Jacob, G. A., Domes, G., & Arntz, A. (2017). Self-injury and disordered eating: Expressing emotion
Attentional bias for emotional stimuli in borderline personality dysregulation through the body. Suicide and Life-Threatening
disorder: A meta-analysis. Psychopathology, 49, 383–396. Behavior, 42, 416–425.
Kazdin, A. E. (2007). Mediators and mechanisms of change in Neacsiu, A. D., Rizvi, S. L., & Linehan, M. M. (2010). Dialectical
psychotherapy research. Annual Review of Clinical Psychology, behavior therapy skills use as a mediator and outcome of
3, 1–27. treatment for borderline personality disorder. Behaviour
Koenigsberg, H. W., Fan, J., Ochsner, K., Liu, X., Guise, K. G., Research and Therapy, 48, 832–839.
Pizzarello, S., . . . Siever, L. J. (2010). Neural correlates of the Reichenberger, J., Eibl, J. J., Pfaltz, M., Wilhelm, F. H.,
use of psychological distancing to regulate responses to Voderholzer, U., Hillert, A., & Blechert, J. (2017). Don’t
negative social cues: A study of patients with borderline praise me, don’t chase me: Emotional reactivity to positive
personality disorder. Biological Psychiatry, 66, 854–877. and negative social-evaluative videos in patients with

borderline personality disorder. Journal of Personality Scheel, C. N., Schneid, E.-M., Tuescher, O., Lieb, K., Tuschen-
Disorders, 31, 75–89. Caffier, B., & Jacob, G. A. (2013). Effects of shame induction
Reisch, T., Ebner-Priemer, U. W., Tschacher, W., Bohus, M., & in borderline personality disorder. Cognitive Therapy and
Linehan, M. M. (2008). Sequences of emotions in patients Research, 37, 1160–1168.
with borderline personality disorder. Acta Psychiatrica Scheiderer, E. M., Wang, T., Tomko, R. L., Wood, P. K., &
Scandinavica, 118, 42–48. Trull, T. J. (2016). Negative affect instability among
Reitz, S., Krause-Utz, A., Pogatzki-Zahn, E. M., Ebner-Priemer, individuals with comorbid borderline personality disorder
U. W., Bohus, M., & Schmahl, C. (2012). Stress regulation and posttraumatic stress disorder. Clinical Psychological
and incision in borderline personality disorder—A pilot Science, 4, 67–81.
study modeling cutting behavior. Journal of Personality Scherpiet, S., Bruhl, A. B., Opialla, S., Roth, L., Jancke, L., &
Disorders, 26, 605–615. Herwig, U. (2014). Altered emotion processing circuits
Rosenthal, M. Z., Cheavens, J. S., Lejuez, C. W., & Lynch, T. R. during the anticipation of emotional stimuli in women with
(2005). Thought suppression mediates the relationship borderline personality disorder. European Archives of
between negative affect and borderline personality disorder Psychiatry and Clinical Neuroscience, 264, 45–60.
symptoms. Behaviour Research and Therapy, 43, 1173–1185. Schmahl, C. G., Elzinga, B. M., Ebner-Priemer, U. W.,
Rosenthal, M. Z., Neacsiu, A. D., Geiger, P. J., Fang, C., Ahn, Simms, T., Sanislow, C., Vermetten, E., . . . Bremner, J. D.
R., & Larrauri, J. (2016). Emotional reactivity to personally- (2004). Psychophysiological reactivity to traumatic and
relevant and standardized sounds in borderline personality abandonment scripts in borderline personality and
disorder. Cognitive Therapy and Research, 40, 314–327. posttraumatic stress disorders: A preliminary report. Psychiatry
Ruocco, A. C., Amirthavasagam, S., Choi-Kain, L. W., & Research, 126, 33–42.
McMain, S. F. (2013). Neural correlates of negative Schmahl, C. G., Vermetten, E., Elzinga, B. M., & Bremner, J. D.
emotionality in borderline personality disorder: An (2004). A positron emission tomography study of memories
activation-likelihood-estimation meta-analysis. Biological of childhood abuse in borderline personality disorder.
Psychiatry, 73, 153–160. Biological Psychiatry, 55, 759–765.
Ruocco, A. C., Medaglia, J. D., Ayaz, H., & Chute, D. L. (2010). Schnell, K., & Herpertz, S. C. (2007). Effects of dialectic-
Abnormal prefrontal cortical response during affective behavioral-therapy on the neural correlates of affective
processing in borderline personality disorder. Psychiatry hyperarousal in borderline personality disorder. Journal of
Research, 182, 117–122. Psychiatric Research, 41, 837–847.
Sadikaj, G., Russell, J. J., Moskowitz, D. S., & Paris, J. (2010). Schulze, L., Domes, G., Koppen, D., & Herpertz, S. C. (2013).
Affect dysregulation in individuals with borderline Enhanced detection of emotional facial expressions in
personality disorder: Persistence and interpersonal triggers. borderline personality disorder. Psychopathology, 46, 217–224.
Journal of Personality Assessment, 92, 490–500. Schulze, L., Schmahl, C., & Niedtfeld, I. (2016). Neural
Salsman, N. L., & Linehan, M. M. (2012). An investigation of correlates of disturbed emotion processing in borderline
the relationships among negative affect, difficulties in personality disorder: A multimodal meta-analysis. Biological
emotion regulation, and features of borderline personality Psychiatry, 79, 97–106.
disorder. Journal of Psychopathology and Behavioral Assessment, Schulze, L., Domes, G., Kruger, A., Berger, C., Fleischer, M.,
34, 260–267. Prehn, K., Schmahl, C., Grossman, A., Hauenstein, K., &
Sansone, R. A., Rytwinski, D., & Gaither, G. A. (2003). Herpertz, S. C. (2011). Neural correlates of cognitive
Borderline personality and psychotropic medication reappraisal in borderline patients with affective instability.
prescription in an outpatient psychiatry clinic. Comprehensive Biological Psychiatry, 69, 564-573.
Psychiatry, 44, 454–458. Scott, L. N., Wright, A. G. C., Beeney, J. E., Lazarus, S. A.,
Santangelo, P. S., Bohus, M., & Ebner-Priemer, U. W. (2014). Pilkonis, P. A., & Stepp, S. D. (2017). Borderline personality
Ecological momentary assessment in borderline personality disorder symptoms and aggression: A within-person process
disorder: A review of recent findings and methodological model. Journal of Abnormal Psychology, 126, 429–440.
challenges. Journal of Personality Disorders, 28, 1–22. Sieswerda, S., Arntz, A., & Kindt, M. (2007). Successful
Santangelo, P. S., Limberger, M. F., Stiglmayr, C., Houben, M., psychotherapy reduces hypervigilance in borderline
Coosemans, J., Verleysen, G., . . . Ebner-Priemer, U. W. personality disorder. Behavioural and Cognitive Psychotherapy,
(2016). Analyzing subcomponents of affective dysregulation 35, 387–402.
in borderline personality disorder in comparison to other Siever, L. J., & Davis, K. L. (1991). A psychobiological perspective
clinical groups using multiple e-diary datasets. Borderline on the personality disorders. American Journal of Psychiatry,
Personality Disorder and Emotion Dysregulation, 3, 5–18. 148, 1647–1658.
Sauer, C., Arens, E. A., Stopsack, M., Spitzer, C., & Barnow, S. Skodol, A. E., Gunderson, J. G., McGlashan, T. H., Dyck, I. R.,
(2014). Emotional hyper-reactivity in borderline personality Stout, R. L., Bender, D. S., . . . Oldham, J. M. (2002).
disorder is related to trauma and interpersonal themes. Functional impairment in patients with schizotypal,
Psychiatry Research, 220, 468–476. borderline, avoidant, or obsessive-compulsive personality
Sauer, C., Sheppes, G., Lackner, H. K., Arens, E. A., Tarrasch, R., disorder. American Journal of Psychiatry, 159, 276–283.
& Barnow, S. (2016). Emotion regulation choice in female Staebler, K., Helbing, E., Rosenbach, C., & Renneberg, B.
patients with borderline personality disorder: Findings from (2011). Rejection sensitivity and borderline personality
self-reports and experimental measures. Psychiatry Research, disorder. Clinical Psychology & Psychotherapy, 18, 275–283.
242, 375–384. Staebler, K., Renneberg, B., Stopsack, M., Fiedler, P., Weiler, M.,
Sauer, S. E., & Baer, R. A. (2012). Ruminative and mindful self- & Roepke, S. (2011). Facial emotional expression in reaction
focused attention in borderline personality disorder. Personality to social exclusion in borderline personality disorder.
Disorders: Theory, Research, and Treatment, 3, 433–441. Psychological Medicine, 41, 1929–1938.

Stiglmayr, C., Grathwol, T., Linehan, M. M., Ihorst, G., Vine, V., & Aldao, A. (2014). Impaired emotional clarity and
Fahrenberg, J., & Bohus, M. (2005). Aversive tension in psychopathology: A transdiagnostic deficit with symptom-
patients with borderline personality disorder: A computer- specific pathways through emotion regulation. Journal of
based controlled field study. Acta Psychiatrica Scandinavica, Social and Clinical Psychology, 33, 319–342.
111, 372–379. Weinberg, A., Klonsky, E. D., & Hajcak, G. (2009). Autonomic
Suvak, M. K., Litz, B. T., & Sloan, D. M. (2011). Emotional impairment in borderline personality disorder: A laboratory
granularity and borderline personality disorder. Journal of investigation. Brain and Cognition, 71, 279–286.
Abnormal Psychology, 120, 414–426. Winter, D., Niedtfeld, I., Schmitt, R., Bohus, M., Schmahl, C.,
Thompson, R. A. (1994). Emotion regulation: A theme in search & Herpertz, S. C. (2017). Neural correlates of distraction in
of definition. Monographs of the Society for Research in Child borderline personality disorder before and after dialectical
Development, 59, 25–52. behavior therapy. European Archives of Psychiatry and Clinical
Tomko, R. L., Lane, S. P., Pronove, L. M., Treloar, H. R., Brown, Neuroscience, 267, 1–12.
W. C., Solhan, M. B., . . . Trull, T. J. (2015). Undifferentiated Wolff, S., Stiglmayr, C., Bretz, H. J., Lammers, C.-H., &
negative affect and impulsivity in borderline personality and Auckenthaler, A. (2007). Emotion identification and tension
depressive disorders: A momentary perspective. Journal of in female patients with borderline personality disorder.
Abnormal Psychology, 124, 740–753. British Journal of Clinical Psychology, 46, 347–360.
Tomko, R. L., Trull, T. J., Wood, P. K., & Sher, K. J. (2014). Zaki, L. F., Coifman, K. G., Rafaeli, E., Berenson, K. R., &
Characteristics of borderline personality disorder in a Downey, G. (2013). Emotion differentiation as a protective
community sample: Comorbidity, treatment utilization, and factor against nonsuicidal self-injury in borderline personality
general functioning. Journal of Personality Disorders, 28, disorder. Behavior Therapy, 44, 529–540.
734–750. Zanarini, M. C., Frankenburg, F. R., Hennen, J., Reich, D. B.,
Tragesser, S. L., & Robinson, R. J. (2009). The role of affective & Silk, K. R. (2004). Axis I comorbidity in patients with
instability and UPPS impulsivity in borderline personality borderline personality disorder: 6-year follow-up and
disorder features. Journal of Personality Disorders, 23, 370–383. prediction of time to remission. American Journal of
Trull, T. J., Solhan, M. B., Tragesser, S. L., Jahng, S., Wood, Psychiatry, 161, 2108–2114.
P. K., Piasecki, T. M., & Watson, D. (2008). Affective Zanarini, M. C., Frankenburg, F. R., Hennen, J., & Silk, K. R.
instability: Measuring a core feature of borderline personality (2003). The longitudinal course of borderline
disorder with ecological momentary assessment. Journal of psychopathology: 6-year prospective follow-up of the
Abnormal Psychology, 117, 647–661. phenomenology of borderline personality disorder. American
Trull, T. J., Tomko, R. L., Brown, W. C., & Scheiderer, E. M. Journal of Psychiatry, 160, 274–283.
(2010). Borderline personality disorder in 3-D: Dimensions, Zanarini, M. C., Frankenburg, F. R., Reich, D. B., Fitzmaurice,
symptoms, and measurement challenges. Social and G., Weinberg, I., & Gunderson, J. G. (2008). The 10-year
Personality Psychology Compass, 4, 1057–1069. course of physically self-destructive acts reported by
Tull, M. T., & Aldao, A. (2015). Editorial overview: New borderline patients and axis II comparison subjects. Acta
directions in the science of emotion regulation. Current Psychiatrica Scandinavica, 117, 177–184.
Opinion in Psychology, 3, iv–x. Zimmerman, M., Martinez, J. H., Young, D., Chelminski, I., &
van Asselt, A. D. I., Dirksen, C. D., Arntz, A., & Severens, J. L. Dalrymple, K. (2012). Sustained unemployment in
(2007). The cost of borderline personality disorder: Societal psychiatric outpatients with bipolar depression compared to
cost of illness in BPD-patients. European Psychiatry, 22, major depressive disorder with comorbid borderline
354–361. personality disorder. Bipolar Disorders, 14, 856–862.

CH A PTE R
Behavioral Assessment of
26 Emotion Dysregulation
Molly Adrian and Michele Berk
Abstract
Behavioral assessment of emotion dysregulation involves systematic measurement of observable behavioral

events and associated emotional responses. Behavioral assessment has been widely used to index the
dimensions of emotional dysregulation, individual differences in emotional dysregulation, and contextual
contributors to emotion dysregulation. The primary objective of this chapter is to review the range of
behavioral assessment strategies commonly used for measuring emotion dysregulation. First, the chapter
reviews the theoretical basis for the use of behavioral assessment strategies for evaluating emotion
dysregulation processes, including both behavioral observation and standardized computerized tasks.
Next, it provides an overview of the specific experimental paradigms and techniques that have been
used in research. It concludes with future directions for the measurement of emotional dysregulation
to contribute to the understanding of vulnerability to and maintenance of psychopathology.
Keywords: behavioral assessment, structured observation, computerized behavioral tasks, behavioral

methods, analog observation tasks, naturalistic observation
Introduction (parent, teacher, peer), (3) physiological/biological

Emotion dysregulation is a transdiagnostic construct indicators, (4) observational approaches, and
with prospective and concurrent associations with (5) behavioral tasks (for reviews, see Adrian, Zeman,
psychopathology, including both internalizing and & Veits, 2011; Beauchaine, 2015; Morris, Robinson,
externalizing spectrum disorders, and other clinical & Eisenberg, 2006; Weiss, Thomson, & Chan, 2014;
problems such as self-injurious behaviors, substance Zeman, Klimes-Dougan, Cassano, & Adrian, 2007).
abuse, and eating disorders (Cole, Hall, & Hajal, This chapter will focus on describing the latter two
2017; Chapters 1 and 7, this volume). Although measurement strategies, grouped together under the
specific emotions associated with these conditions term “behavioral assessment.” Observational and
vary, all are characterized by emotional reactions behavioral task strategies are critical for assessment
that are either too intense or too enduring to be of emotion dysregulation. These approaches can
adaptive (e.g., Beauchaine, 2015). Our goal in writing help elucidate dynamic, temporal associations while
this chapter is to review the range of behavioral avoiding some limitations of other measurement
assessment strategies commonly used for identify- strategies. Much previous research in this area has
ing emotion dysregulation as measurement deci- been reliant on self- or other-report measurement
sions affect how scientific inquiry is interpreted of emotionality and emotion dysregulation (Morris,
and understood. Silk, Steinberg, Terranova, & Kithakye, 2010;
Researchers interested in studying emotion Rothbart & Bates, 2007). Sole reliance on self-report
dysregulation have measured the construct primarily of emotion processes may be problematic, given
in five ways: (1) self-report, (2) other informant evidence that inaccuracy is higher among those with
377
high levels of distress (Smith, Leffingwell, & Ptacek, behave differently in a context with others
1999; Stone et al., 1998). Similarly, research using (e.g., parent, teacher, spouse). Despite these limita-
both self-report and observational strategies has tions, behavioral observations provide a powerful
illustrated that self-reports are frequently inaccurate measurement strategy for studying emotion
due to information processing biases combined dysregulation—especially when combined with

with the automaticity of overlearned processes effective experimental manipulations (see Cole
(Hawes, Dadds, & Pasalich, 2013; Stone et al., 1998). et al., 2017).
That is, when behaviors are repeated frequently,
they are more likely to occur outside of awareness Theoretical Perspectives
and, in combination with the interpretation of be- Measurement decisions in emotion research can be
haviors, may lead to systematic biases in self-report. linked directly to underlying theoretical issues.
For example, parental observation of their children Emotion dysregulation comprises a set of complex,
is repeated frequently over years, and implicit biases multidimensional, and multilevel processes that are
related to their children may influence parents’ difficult to define and even more difficult to quan-
description of their children’s behaviors. Research tify (Cole et al., 2004, 2017; Zeman, Cassano,
on parenting attributions and practices supports the Perry-Parrish, & Stegall, 2006). Three complemen-
notion that there are biases in the parent report of tary perspectives are presented with an emphasis on
their children. In video-recall procedures, parents how they inform behavioral assessment strategies.
frequently rate their children’s behavior as negative
when observers coded the same behaviors as neutral or Dynamic
positive (e.g., Lorber, O’Leary, & Kendziora, 2003). Emotion dysregulation encompasses a broad range
The contrasting of parent-rated and neutral observer- of processes occurring both discretely (excessive im-
rated codings suggests that parental self-report mediate emotional arousal) and longitudinally (in-
measures would not have captured the phenomenon stability of emotional state over time). Individuals
accurately. Thus, even the best-designed self-report who are dysregulated exhibit patterns of responding
measures are limited by self-perceptions. whereby a mismatch occurs between sociocultural
Behavioral observations and tasks minimize contextual demands and the person’s goals, responses,
limitations inherent to self-report by capturing and/or modes of expression. Finding measurement
behavior objectively and in real time. Trained ob- approaches that sufficiently characterize the com-
servers or automated computer algorithms code plexity of emotion dynamics has proved challenging
behaviors without the perceptual or emotional biases given that individuals have a variety of emotion
that may affect participant reports of emotion regulation strategies and can apply them to different
dysregulation. Despite the advantages of behavioral situations toward achieving their goals. For example,
observation, including flexibility in capturing be- Gross and Jazarieri (2014) highlight problematic
haviors relevant to one’s research question, it is not emotional patterns of intensity, duration, frequency,
without drawbacks. Observational approaches re- and type in the context of the individual’s emotional
quire significant investment of time and resources awareness, emotion-related goals, and strategies.
to design systems with high external validity and From this perspective, capturing the dynamic nature,
generalizability, obtain behavior samples, train coders, flexibility, and pattern of emotion dysregulation
and conduct coding to reliability. Furthermore, de- over time is an essential component of the assess-
pending on the nature of events, desired behaviors ment of emotion dysregulation (e.g., Gross &
may not occur, despite being primed. Because of Jazarieri, 2014; Chow et al., 2005).
variability in individual thresholds for emotional
responses, the need for regulation may vary greatly Functional
within and across individuals (e.g., Cole et al., Researchers must determine whether the primary
2017). If an individual fails to show emotion, we purpose of assessment is to determine the structure
may incorrectly assume that the individual elicited or function of emotion. Although it is not surpris-
emotional control over expressions rather than ing that psychologists would seek to learn what an
concluding that the stimulus was insufficiently emotion is (a structural theory addressing the nature
provocative for emotion elicitation (Cole, Martin, of emotion; e.g., Russell, 1980), researchers and cli-
& Dennis, 2004). Similarly, an individual may nicians also have great interest in what an emotion
regulate emotions effectively in the context of a does. According to functionalist approaches (e.g.,
laboratory setting with an unknown examiner but Barrett & Campos, 1987), a core focus is how
378 Behavioral Assessment of Emotion Dysregul ation

emotions organize behaviors in relationship with of gratitude so as to not hurt her aunt’s feelings.
their environment. A key difference between The ability to dissemble emotions also highlights
functionalist and previous theories of emotion is the importance of measuring aspects of the experi-
that emotions are seen as organizers of behavior— mental setting that may influence children’s overt
with well-regulated emotions accomplishing func- expression of emotion. Children as young as 4 years
tional outcomes—particularly social outcomes. old report expressing emotions differently and ex-
Although measurement decisions can address pecting different contingent responses from the
both structural and functional questions, it is help- environment depending on their social audience
ful for researchers to consider their key questions (Zeman, Penza, Shipman, & Young, 1997). Thus,
with respect to their theoretical perspectives. what may seem to be a trivial consideration when
developing observational paradigms (e.g., having a
Developmental parent in the room during a child observation) may
A third theoretical perspective that is complementary unintentionally introduce a significant confound.
with the other perspectives highlighted relates to the In addition, being observed in a laboratory by a
lifespan perspective of emotional dysregulation. stranger may increase the likelihood of emotional
That is, emotion dysregulation is developmentally dissemblance, limiting the validity of observational
defined. Developmental issues are a paramount data. Overall, measurement decisions related to ob-
consideration when deploying a system to evaluate servational methods need to attend to developmental
emotion dysregulation. Early in development, status, goals of the individual, and demands of the
fundamental biological and attentional processes social context (Barrett & Campos, 1987). These de-
are likely to be the best indices of emotion dysregu- velopmental considerations have informed analog
lation (e.g., Porges, 2011), whereas among older observations (e.g., Saarni’s disappointing gift task,
children, emotion awareness and appraisal may peer confederate tasks) that probe for social demand
be more important (Suveg, Morelen, Brewer, & characteristics and require emotional control.
Thomassin, 2010). Indeed, there have been several
calls for emotion dysregulation tasks that can be de- Unresolved Controversies
ployed across childhood, adolescence, and adult- Two core unresolved controversies are noted in
hood to capture continuity and discontinuities over behavioral assessments of emotion dysregulation.
time. However, given different capabilities across First, a significant unresolved controversy concerns
developmental epochs, such calls are difficult and agreement on the definition of emotion dysregula-
perhaps impossible to heed (see also Beauchaine, tion. Multiple components of adaptive emotion
2015). Inferring emotion dysregulation becomes in- regulation have been proposed, including the
creasingly challenging as children develop more ad- abilities to identify emotions, generate new emo-
vanced emotion regulation strategies. As a result, tional experiences, selectively deploy attention, re-
observational methods and longitudinal designs interpret potentially distressing cognitions, modify
have been used more frequently with the infant and potentially distressing situations, and modulate re-
preschool age groups, whereas self-report has been sponse (e.g., Aldao, Nolen-Hoeksema, & Schweizer,
used more frequently with older children, and pre- 2010; Eisenberg & Spinrad, 2004; Gross &
dominantly among adolescents (Adrian et al., 2011). Thompson, 2007; Gross & Jazaieri, 2014). Core
Clearly, some of these methodological choices re- processes involved in emotion dysregulation include
flect children’s developmental status, particularly emotional reactivity and failed regulatory efforts.
with respect to the validity of young children’s However, a lack of consistent definition across
self-report (Durbin, 2010; Reynolds, 1993) and the studies results in various measurement systems with
skills of adolescents to dissemble emotional displays limited ability to compare results across studies.
and report more accurately on their internal states Driven primarily by the lack of definitional consen-
(Klimes-Dougan & Zeman, 2007). By school age, sus, the field lacks reliable and valid behavioral
children become skilled at emotional dissemblance measures of emotion dysregulation that can be used
(i.e., masking their internal feelings by a different across contexts and age groups, which has led some
display of emotion), which makes assessment of authors to suggest that physiological data be col-
emotion as distinct from its regulation nearly im- lected along with behavioral data to triangulate on
possible (Campos, Frankel, & Camras, 2004). For inferences about emotion regulation and dysregula-
example, a child disappointed by a gift from a be- tion (see Beauchaine, 2015; Zisner & Beauchaine,
loved aunt may respond with exuberant expressions 2016). Explicit definitions with measurement
Adrian and Berk 379

approaches for key components of emotion Two primary forms of behavioral assessment are
dysregulation assessments would help to communi- considered: behavioral observation (including natu-
cate across studies. ralistic, structured, and analog) and lab-based be-
Another area of unresolved controversy for havioral tasks.
emotion dysregulation research is how to integrate
and connect measurements of emotion dysregulation Behavioral Observation
at each level of analysis to understand how com- Behavioral observation—systematic recording of
ponents of emotion dysregulation affect other behavior by an observer—is often cited as gold-
self-regulation processes. Emotion dysregulation is a standard behavioral assessment (Haynes & O’Brien,
multilevel phenomenon expressed at neural, cogni- 2003). Behavioral observation involves classifying
tive, behavioral, and social levels, and discrepancies and quantifying verbal and nonverbal behavioral
based on different reporters or levels of analyses may events, irrespective of participants’ reports or per-
shed light on the processes involved in emotional ceptions (Hawes et al., 2013). Procedures designed
dysregulation. Future research is challenged to to maximize the collection of valid and reliable data
distinguish activation of systems that are measured allow for systematic observations of important be-
and integrate multiple levels of analysis of emotion haviors. Facial expressions, words, tone of voice,
dysregulation as well as to determine the nature of and body gestures relay critical information about
the connection to other broader self-regulation human emotions. Accordingly, there is a long scien-
processes including executive functioning and at- tific tradition using observational methods to exam-
tentional and inhibitory control (see Beauchaine, ine various aspects of emotional expression, regula-
2015). Clarity of core constructs and their relationship tion, and dysregulation among children and adults
with one another at methodological levels would (e.g., Darwin, 1872; Ekman, Friesen, & Tomkins,
serve to integrate findings and advance the concep- 1971; Izard & Malatesta, 1987). Consequently, there
tualization of emotional dysregulation. is a plethora of observational methods and coding
systems used in emotion research (see Table 26.1).
Current Methods and Findings Behavioral observation is often applied in emotion
Behavioral assessment emphasizes empirically dysregulation research to (1) index dimensions
supported, multimethod, and multi-informant of emotions associated with specific disorders,
evaluations of specific, observable behaviors and (2) reveal contextual dynamics of functional impor-
contemporaneous causal variables in natural or tance to these disorders, and/or (3) examine indi-
laboratory environments (e.g., Haynes & O’Brien, vidual differences (e.g., child temperament) impli-
2003). In behavioral assessment paradigms, sys- cated in developmental pathways to dysfunctional
tematic measurement of precisely defined, directly emotional processes. Although few would dispute
observable and verifiable behaviors in a time series the importance of observational methods, ap-
can provide valid, rich, detailed, and clinically proaches vary considerably depending on develop-
useful data. Behavioral assessment provides data mental stage, social context, and the emotion(s) as-
about how and when a behavior occurs, how long it sessed. Because observational measures do not
lasts, and consequences of the behavior on what is access private events, behavioral observation of
obtained or avoided as a result. Behavioral assessment emotion dysregulation cannot disentangle emo-
plays a key role in the scientific study of emotion tional elicitation and reactivity from regulatory ef-
dysregulation, including investigations of the forts unless combined with other assessment tools
development of emotion dysregulation, the relation (see Chapter 2, this volume; Cole et al., 2004, 2017).
between emotion dysregulation and psychopathol-
ogy, and the effects of treatment on emotion dys- Naturalistic observation
regulation processes. The vast array of existing In the strictest sense, naturalistic observations in-
methods of behavioral assessment of emotion dys- volve watching individuals conduct their daily ac-
regulation allow for creative, flexible, and elegant tivities. More typically, constrained or structured
solutions to answer pressing questions of how emo- naturalistic observations are used, optimizing the
tion dysregulation develops and manifests across the potential for eliciting emotional content (e.g.,
lifespan. In this section, we illustrate some of the family mealtime, a cleanup task). Assuming the par-
paradigms researchers use to assess individual differ- ticipant’s awareness of/reactivity to being observed
ences in emotion dysregulation, including interper- can be minimized, naturalistic observation ap-
sonal interactions and emotion elicitation paradigms. proaches provide an ecologically valid method for

Table 26.1. Behavioral Assessment by Strategy, Age, and Method
Assessment Strategy Age Range Observation Methods Examples in Research Construct Assessment
Naturalistic observation Infant Infant at home Tonyan (2005) Assess infant emotion regulation (ER) in
home setting
Infant Playroom and high chair J. A. Crowell and Feldman (1988); Evaluates infant regulatory styles with
structured and semistructured Miller, McDonough, Rosenblum, and mother when placed in high chair with low
activities Sameroff (2002); Zeanah et al. (1997) and high challenge tasks
Toddler/preschool Free play alone, with teacher, J. A. Crowell and Feldman (1988); Coping with naturalistic emotional events,
with parent Denham et al. (2003); Eisenberg et al. emotional responses are coded, coding
(1995); Fabes and Eisenberg (1992); interactive behavior (CIB) system
Feldman and Greenbaum (1997)
Toddler/preschool Sibling interactions Volling, McElwain, and Miller (2002) Regulating distress and positive play
b ehavior when distressed
School age Best friend free play Leary and Katz (2005) Assess affective quality, cooperation,
conversational repair skills, etc.
Structured observation Infant Brazelton Neonatal Assessment Brazelton (1973) State regulation, distress, irritability
System
Infant Bayley Scales of Infant Bayley (1993) Negative affect, frustration, and flexibility
Development
Analog Infant Infant Emotional Challenge Malone, Gunnar, and Fisch (1985) Ability to self-soothe and use others for ER
efforts
Infant Behavior Response Paradigm Garcia-Coll et al. (1988) Latency of cry as presented stimuli become
more intrusive
Infant Still-face paradigm Cohn and Tronick (1983) Infant’s ER to maternal lack of facial
emotional expression
Infant Infant stranger paradigm Mangelsdorf, Shapiro, and Marzolf (1995) Aversion, self-soothe, distraction, avoidance
Infant/toddler/preschool Frustration tasks Buss and Goldsmith (1998); Calkins, Assess infant emotion regulatory responses
Dedmon, Gill, Lomax, and Johnson to frustration (barrier, arm restraint, maternal
(2002); Goldsmith and Rothbart (1999); prohibition) self-soothing, orient, redirect,
Stifter and Braungart (1995) communicate
Infant Mother-infant interaction Feldman, Eidelman, and Play time; maternal touch, affect, talk,
Rotenberg (2004) intrusiveness, adaptation; infant state
(continued )
Table 26.1. Continued
Infant High chair task Goldsmith and Rothbart (1996); Assess child’s ability to regulate negative
Graziano, Keane, and Calkins (2010) affect; code using LAB-TAB
Toddler/preschool Frustrating paradigm; negative Cummings (1987); Maughan and Frequency and effectiveness of distraction
emotion barrier Cicchetti (2002) as strategy
Toddler/preschool Disappointment paradigm Cole, Zahn-Waxler, and Danielle (1994); ER efforts when disappointed in presence of
Saarni (1979) audience figure or alone
Toddler/preschool Inhibition of positive emotion Carlson and Wang (2007) Evaluate child’s ability to keep a secret
(inhibit emotion) about an emotionally
positive valence event
Toddler/preschool Separation/strange situation task Ainsworth, Blehar, Waters, and Wall Assess emotionality and ability to regulate
(1978); Ainsworth and Wittig (1969) arousal
Toddler/preschool Delay of gratification, waiting Block and Block (1980); Grolnick, Code emotion regulation strategies: active
task, and separation from de- Bridges, and Connell (1996); Kochanska, distraction, focus on object, passive waiting,
sired object paradigms Murray, and Harlan (2000); information gathering, seeking physical
Marvin (1977) comfort
Toddler/preschool Anger induction: transparent Goldsmith and Rothbart (1999) Assess ability to regulate anger
box procedure
Toddler/preschool Mood induction stimulus for Cole, Jordan, & Zahn-Waxler (1990) Categories based on facial coding system:
children inexpressive, modulated expressive, highly
expressive
Toddler/preschool Entry task with peer Putallaz (1983) ER strategies coded during peer group entry
failure
Toddler/preschool “Beat the Bell” competitive task Cassidy, Parke, Butkovsky, and Braungart Children’s ER when losing a game
(1992); Lütkenhaus, Grossmann, and
Grossmann (1985)
Toddler/preschool Puppet task Cole, Dennis, Smith-Simon, and Assess understanding and elicitation of ER
Cohen (2009) strategies
Toddler/preschool Peer interactions Denham et al. (2001) Evaluated child’s response to a focal child
who expressed emotion
School age Induced distress Fabes, Eisenberg, Karbon, Troyer, and Evaluate child’s response to distress in other
Switzer (1994) (time spent talking, turning speaker off,
facial and vocal distress)
School age Affect regulation in the family Klinnert, McQuaid, McCormick, Examine quality of ER of child and with
Adinoff, and Bryant (2000); Lindahl, mother using positive emotion tasks,
Clements, and Markman (1993) frustrating tasks, conflict discussion
School age Anticipatory disappointment Guttentag and Ferrell (2008) Assess effects of expectations on
and regret disappointment and regret
School age Sadness induction Rice, Levine, and Pizarro (2007) Assess ability to disengage emotionally from
memory for event
School age Peer provocation computer Underwood and Hurley (1999) Assess display rules while playing computer
game game with peer
School age Peer rejection task Reijntjes, Stegge, Terwogt, Kamphuis, Assess ER strategies following peer rejection
and Telch (2006) in a rigged computer game and effect on
subsequent mood
School age Parent–child anger/frustration Melnick and Hinshaw (2000) Assess ER ability to manage anger in face of
induction frustration with parents present
School age Competitive puzzle task Hinshaw and Melnick (1995) Told to mask anger in task with peer
School age Mother–child conflict Melby and Conger (2001) Code positive and negative emotion using
resolution task Iowa family interaction rating system
School age Parent–child emotion Shipman and Zeman (1999) Examine ER in terms of parental validating
interaction task and invalidating response and child’s
response to parent
School age Parent–child interaction task Eisenberg et al. (2005); Suveg et al. Child’s ER strategies were assessed within
(2008) discussion task and coded as (1) cognitive
and behavioral problem-solving approaches
or (2) maladaptive responses
Adolescent Mother–teen problem solving Kobak, Cole, Ferenz-Gillies, Fleming, and Support, communication, dysfunctional
Gamble (1993) anger, avoidance
Adolescent Revealed differences task Strodtbeck (1951) Triadic interaction to resolve differences of
Hauser et al., 1984) opinion; code with Constraining and
Enabling Coding System
Adolescent Mother–teen “talk show” Zimmermann, Mohr, and Spangler Stimulate social evaluative context and elicit
(2009) emotional arousal; code for ER
Adolescent Mother–child interaction Allen et al. (1994) Autonomy and relatedness scales
Beijersbergen, Bakermans-Kranenburg,
Van IJzendoorn, and Juffer (2008)
(continued )
Table 26.1. Continued
Adolescent Parent–child interaction Yap, Allen, and Ladouceur (2008) LIFE coding system: Aversive, Dysphoric,
Positive Interpersonal
Adolescent Video recall procedures Ehrmantrout, Allen, Leve, Davis, and Recorded problem-solving task followed by
Sheeber (2011) teen identification of parental emotion in
20-second intervals
Computerized behavioral Adolescent Emotional go/no go Schulz et al. (2007) Emotional modulation of inhibition
tasks
Adolescent Mirror tracing persistence task Renna et al. (2017) Distress tolerance/persistence
Adolescent Paced auditory series Brown, Kahler, and Strong (2002); Distress tolerance/persistence
addition tasks Gronwall (1977); Lejuez, Kahler, and
Brown (2003)
Adolescent Distress tolerance task Nock and Mendes (2008) Distress tolerance/persistence
observing emotion dysregulation in context. This such assessments are conducted in an artificial setting
method provides the most flexibility because there such as a laboratory, although such observations may
are a wide array of settings and paradigms through be conducted in home or school settings. Typically,
which observations can take place. However, this cost, convenience, and control drive decisions to
high degree of flexibility and strength in ecological conduct observations in lab or clinic settings. The
validity for capturing behavior in the setting in strengths of analog observations include the ability
which it naturally occurs is offset by a low level of to have a standard observational setting with a high
experimental control. Given that neutral affect is degree of consistency across participants. Consistency
predominant throughout the day, research using and control standards allow researchers to contrast
observational approaches typically capitalizes on situational contexts (e.g., the strange situation para-
settings and paradigms that accentuate the chance digm measures child behavior with and without a
that emotional content will emerge with sufficient stranger present to observe parent–child interactions
frequency, intensity, and/or duration to obtain in two contexts; Ainsworth, Blehar, Waters, & Wall,
meaningful results. 1978) to examine the effects of specific stimuli or
events on participant behavior. Analog observation
Structured observation tasks involves the use of experimental paradigms that elicit
Researchers who study infants and preschoolers emotional responses and simulate common events.
often use structured observations during emotion Because ethical concerns arise when inducing strong
elicitation tasks to elicit emotion dysregulation. Out negative emotional states in children, these para-
of 13 tasks reviewed by Rothbart, Posner, & Kieras digms typically assess children’s responses to low to
(2006), 11 were suitable to be used with children moderate levels of stressors. We review a few of the
younger than 5 years of age. The most widely used most common analog observation paradigms for as-
structured observational systems are the Brazelton sessing emotion and emotion dysregulation.
Neonatal Behavioral Assessment Scale (BNBAS;
Brazelton & Nugent, 1995) and the Bayley Scales of Strange situation paradigm
Infant Development (Bayley, 1993). The BNBAS The strange situation is a classic paradigm that has
elicits behavioral and reflex responses, recorded with been used to assess parent–child attachment systems
criterion-referenced scoring. Most relevant research since the 1960s (Ainsworth and Wittig, 1969).
from this scale has focused on a range of state This 20-minute procedure exposes the infant to a
clusters and regulation of state clusters to create a series of contexts in which the parent and child are
“proneness to distress” or a “difficultness” factor that together alone, a stranger approaches, the parent
reflects both negative affect and components of separates from the infant, the parent and infant are
emotion dysregulation (Rothbart & Ahadi, 1994). reunited, the parent leaves the infant alone for the
Although assessment of these dimensions varies second separation episode, the stranger enters when
across studies, the construct appears to be relatively the infant is alone, and the parent and infant reunite
robust and stable over the first few months and even for a second time. During the task, the infant’s ex-
into later infancy. Kaye (1978) used the Brazelton ploration behaviors, reactions to caregiver departure
Neonatal Behavioral Assessment Scale to identify and reunion, and behavior toward the stranger alone
a single negative reactivity factor that included are used to categorize the infant’s attachment relation-
three dimensions: irritability to stimuli, rapidity ship with the caregiver as secure, anxious avoidant,
of buildup of negative emotion, and peak of ex- anxious ambivalent, or disorganized. The procedure
citement (i.e., level of distress). The Bayley Scales was designed for infants 8 to 18 months of age and
of Infant Development (Bayley, 2006) is another has been modified for use with older preschool
structured observational measure that includes a children (see Belsky et al., 1994). From the lens of
social-emotional scale. A strength of the Bayley is emotion dysregulation, the task can be deployed to
that the structured observation also has a normative evaluate the ability to regulate arousal and emotional
sample to compare a child’s performance with his or intensity in response to separation, parental sensitiv-
her same-age peers. ity, and parent–child interactions (Cole et al., 2017;
Guo, Leu, Barnard, Thompson, & Spieker, 2015).
Analog observations
Analog behavioral observation involves assessment Face-to-face still-face paradigm
in a contrived environment/circumstance to elicit The face-to-face still-face paradigm is a standardized
emotional reactions and associated processes. Usually, observational strategy designed for infants and their
Adrian and Berk 385

caregiver. The infants are required to cope with a in the evaluation process, with different results
stressful interaction as their caregiver provides a supported as a function of the child being alone,
neutral face expression and is vocally and gesturally with an unknown adult, or with a caregiver. Current
unresponsive. The task typically consists of 2 min- literature indicates that adults support positive
utes of typical face-to-face interaction in which the displays in the presence of a desirable gift and in-
caregiver is instructed to play with the infant as hibit relationship-damaging displays of negative
he or she typically would, followed by a 2-minute affect in response to an undesirable gift (Tobin &
episode where the caregiver is instructed to keep a Graziano, 2011).
still face and look at the infant but not smile, talk,
or touch the infant. This is followed by a second Conflict discussion task
2-minute normal reunion in which the caregiver One of the most common approaches used with
and infant resume play. Studies using the paradigm school-age children, adolescents, and adults is a con-
have revealed differences in the behavior of infants flict discussion paradigm (Robin & Foster, 1984).
and mothers as well as in the dyadic qualities of in- After reporting on areas of disagreement or conflict,
teractions between depressed and/or anxious moth- dyads are instructed to discuss and/or attempt to
ers and their infants, prematurely born infants and resolve issues of high conflict within a set period of
their mothers, and high- and low-risk groups (Frick time. Emotions and interpersonal responses may
& Adamson, 2003; Tronick, 1989). also be observed during interchanges with others in-
cluding peers, fathers, teachers, or experimenters, or
Frustration tasks even in the context of the larger unit where individu-
Several tasks have been used to elicit frustration in als are observed in their attempt to resolve conflicts
infant and toddler populations. The arm restraint and report on their emotion processes. A wide array
task is perhaps the most widely used task to assess of studies employing this approach have advanced
infants’ responses to frustration from 5 to 10 months our understanding of how emotion dysregulation
old. In this task, caregivers or research assistants are may appear, influence, and be reinforced in various
instructed to gently restrain their infants by holding social interactions including with families, with peers,
their infants’ arms down to their sides while main- and in romantic relationships (e.g., S. E. Crowell,
taining a neutral facial expression and to refrain Beauchaine, McCauley, et al., 2008; Fosco &
from verbally interacting with their infants. After 2 Grych, 2013; Whalen et al., 2014; Yap, Allen, &
minutes of arm restraint or 10 to 20 seconds of hard Ladouceur, 2008).
crying, caregivers are cued to release their infants’
arms but to continue their neutral, noninteractive Competitive game with peer
posture for 1 minute. Caregivers subsequently soothe confederates
their infant if necessary using any method they A confederate may be used to simulate a stressor
deem appropriate. This task has been utilized to within a highly controlled situation. To determine
identify infant responses to frustration, how the expressive emotion differences in children with
intensity of negative reactivity affects the develop- varying sociometric status (i.e., rejected vs. average),
ment of emotion dysregulation, dyadic regulation Hubbard (2001) observed child dyads composed of
of frustration, and caregiver behaviors in response a confederate and a child playing a standardized
to infant frustration (Braugnart-Rieker & Stifter, competitive game that induced frustration and
1996; Jahromi, Putnam, & Stifter, 2004; Stifter & coded facial, verbal intonation, and nonverbal mo-
Braungart, 1995). dalities. In some cases, a range of tasks were assessed
in an effort to estimate more enduring qualities of
Disappointing gift paradigm emotion, as illustrated by specific approaches used
The “disappointment paradigms” involve giving a to assess dispositional or temperament constructs
child rank-ordering possible toys he or she would and their relation to emotion dysregulation pro-
like to receive and then the child receiving a low- cesses (e.g., Goldsmith, 1993).
ranked/undesirable toy when he or she was expect-
ing to receive a more pleasing gift. This approach Video recall procedures
typically elicits negative emotion in preschool- and In a cleverly designed study to assess emotion dys-
early-elementary-school-age children (Cole, 1986; regulation, Ehrmantrout, Allen, Leve, Davis, and
Saarni, 1984). In addition to the task, experimental Sheeber (2011) videotaped depressed adolescents
control also varies depending on who is included and their parents in problem-solving interactions and

coded the affect expressed by parents. Adolescents 1998. Adaptations to these systems have recently
also viewed these recordings in a video-mediated been made to optimize microanalytic techniques,
recall procedure in which they were asked to iden- with focus placed on emotion features that are most
tify their parents’ emotions in 20-second intervals. relevant to the researcher (Ekman & Rosenberg,
By analyzing discrepancies between adolescents’ 1997; Lewis & Granic, 2000). Microanalytic ap-
subjective ratings of parent affect and the independ- proaches have also been used to evaluate use of
ently coded observations of affect, Ehrmantrout emotion language (e.g., Zahn-Waxler, Ridgeway,
et al. (2011) were able to identify emotion recogni- Denham, Usher, & Cole, 1993) and to test rein-
tion deficits that characterized these adolescents and forcement theories of emotion dysregulation (e.g.,
account for both behavioral aspects of emotion dys- S. E. Crowell et al., 2013). There are well-developed
regulation and perceptions of emotion processes. systems for capturing facial and behavioral aspects
These tandem processes would have been obscured of emotional displays; however, there are few relia-
without pairing methods. ble tools for evaluating emotional prosody (voice
inflections) or subtleties of indirect and nonverbal
Other emotion induction paradigms means of expressing emotion. These aspects of emo-
Other common paradigms place less emphasis on tion may be particularly relevant for research with
interpersonal emotion elicitation. These include seven adolescents and young adults. For example, some of
common emotion induction procedures used to the subtle aspects of contempt (e.g., eye rolling,
examine reactivity and regulatory efforts in the lab: sighing) that predict the dissolution of a marriage in
self-generated imagery, emotional stories, evocative adults (Gottman & Levenson, 1999) may be more
images (faces depicting emotion, video clips), distress- normative of adolescent–parent interactions. These
ing stimuli (like noise or air puffs), and recollections types of behaviors have been examined within re-
of emotions/rumination (see Brenner, 2000 for a search that addresses covert aggression and peer
review). Rarely do these approaches involve in vivo deviancy training (Dishion, Nelson, Winter, &
interpersonal interactions, yet they may use emotional Bullock, 2004; Underwood, 2003), with some using
stimuli relevant to social interactions (e.g., a depiction microanalytic coding systems designed to evaluate
of a threatening face, recollections of worry). These real-time processes.
methods provide considerable experimental control Global emotion coding systems provide an alter-
and are particularly effective when used in combina- native approach to microanalytic coding. Coding sys-
tion with assessments of internal emotional experi- tems may evaluate emotion displayed within longer
ence or psychophysiological indicators of reactivity. time segments (e.g., emotion displayed within
5-minute segments), a broader range of emotion in-
Coding systems dicators (tone of voice, facial expressions), or a crit-
Capturing, classifying, and quantifying emotion ical aspect of emotion dysregulation (e.g., dominant
requires observational coding strategies to analyze emotion expressed, use of a range of emotions).
data. Use of reliable and valid coding systems is Though global coding seeks to collapse a great
critical to enhancing our understanding of emotion amount of information into digestible units of anal-
and emotion dysregulation. Two predominant ap- ysis, it requires more inference on the part of the
proaches appear in the literature: micro (molecular) coder to make summary ratings. For example, if a
coding approaches that provide fine-grained, behav- child fails to show emotion during an observation
ioral units of analysis and molar (global) coding period, we may incorrectly assume that he or she is
approaches that provide more broad and inclusive controlling his or her emotional expressions rather
behavioral categories. There is a well-established than concluding that the stimulus was insufficiently
tradition of using microanalytic coding systems to provocative to elicit the emotion. Global coding
evaluate discrete emotions as expressed through systems are often appreciated for speed and simplic-
facial musculature, body postures, and verbal state- ity to adopt them, whereas microcoding systems are
ments with minimal inference (Coan & Allen, 2007; appreciated for the rich sources of information and
Ekman & Rosenberg, 1997; Izard & Dougherty, sequential relations of events that can be extracted
1982; Jones, Carrere, & Gottman, 2005). Because from a brief interaction.
infants and very young children are not able to
convey internal feelings verbally, researchers use these Computerized Behavioral Tasks
methods to infer emotional states (e.g., Infant and Brief behavioral tasks to assess emotion dysregula-
Caregiver Engagement Phases; Weinberg & Tronick, tion have grown in popularity as an economical and
Adrian and Berk 387

efficient way to measure aspects of emotion dysreg- mouse; however, the mouse is programmed to move
ulation. These tasks rely on measuring persistence the red dot in the reverse direction (i.e., if the par-
with a distressing task as the primary measure of ticipant moved the mouse to the left, the red dot
emotion dysregulation. A strength of computerized would move to the right, etc.). To further increase
behavioral tasks is the ease of standardized adminis- difficulty (and resultant frustration), moving the red
tration. These tasks require fewer resources, given dot outside of the lines of the star or stalling for
easy access to computers and programs, and the more than 2 seconds causes a loud buzz and the
costs related to training and implementation are red dot returns to the starting position. Participants
low. Primary criticisms of computerized behavioral are informed that although they may end the task at
tasks are the questions of external validity and the any time by pressing any key on the computer, their
need to upgrade software periodically. performance influences how much money they re-
ceive. After receiving instructions, participants begin
Paced auditory serial addition task the task and work independently until they finish or a
The paced auditory serial addition task (PASAT; 5-minute maximum duration is reached. Participants
Gronwall, 1977) has been deployed to measure are not informed of the maximum duration prior to
emotion dysregulation in that the task has been beginning. Willingness to tolerate emotional distress
shown to produce elevated levels of emotional dis- is indexed by latency in seconds to termination. The
tress (Lejuez, Kahler, & Brown, 2003). For this MTPT has good construct validity and is correlated
task, numbers are typically flashed sequentially on a with the PASAT (Daughters et al., 2013). Moreover,
computer screen and participants are instructed to unwillingness to tolerate emotional distress on the
add the presented number to the previously pre- MTPT predicts early treatment dropout among
sented number before the subsequent number ap- inner-city substance users in residential treatment
pears on the screen (using the computer mouse to (Daughters et al., 2013).
click on the correct answer). Numbers presented
typically range from 0 to 20, with no sum greater Emotional go/no-go
than 20, in order to not confound mathematical The emotional go/no-go (Hare et al., 2008) task
ability. Participants increase their score for correct was developed to examine emotional reactivity and
answers. Level of difficulty varies typically begin- regulation in the form of behavioral inhibition. This
ning with a 5-second latency for low level of diffi- emotional go/no-go task involves continuously pre-
culty and decreasing latency for difficult trials. sented series of stimuli composed of frequent “go”
Participants have training tasks and then are in- cues to which subjects respond as rapidly as possible
formed that once the final level begins, they can ter- and infrequent “no go” cues to which subjects should
minate exposure to the task at any time by clicking not respond. The frequency of go cues (≥75%)
a button on the computer screen labeled “Quit creates a prepotent tendency to respond that must
Task.” However, the amount of money they make then be inhibited for no-go cues, thereby providing
at the end of the session depends on their perfor- a measure of the ability to inhibit a prepotent
mance on the task. Willingness to tolerate emo- response. The emotional go/no-go task yields the
tional distress is indexed by latency in seconds to same measure of inhibition, but substitution of af-
task termination. In support of its construct validity, fective stimuli for letters or pictorial stimuli permits
the PASAT induces emotional distress in the form analysis of performance in response to cues of differ-
of anxiety, anger, frustration, and irritability among ent emotional valence (e.g., happy, sad). Thus, the
diverse samples (e.g., Lejuez et al., 2003). The PASAT task provides a measure not only of behavioral inhi-
appears to have good predictive validity, with PASAT bition but also of emotional modulation of this in-
scores predicting early treatment dropout among hibition (Drevets & Raichle, 1998).
inner-city substance users in residential treatment The emotional go/no-go task has been used
(Daughters, Gorka, Magidson, MacPherson, & extensively to test emotional processing in both

Seitz-Brown, 2013). healthy adults and patients with affective disorders.
A series of studies that used a go/no-go task with
Mirror tracing persistence task affective words as stimuli found mood-congruent
The computerized mirror tracing persistence task response biases in both manic and depressed patients,
(MTPT) is used widely to elicit emotion dysregula- such that manic patients made faster responses to
tion. In this task, participants are required to trace happy words on go trials, whereas depressed pa-
a red dot along lines of a star using the computer tients made faster responses to sad words (Murphy

et al., 1999). The lack of comparable performance advancements in conceptualizing and defining the
differences on no-go trials suggests that these complex construct of emotion dysregulation in
emotional biases do not extend to inhibitory
novel and creative ways, as reflected by the vast array
mechanisms. Rather, manic patients had difficulty of measurement strategies employed to understand
inhibiting responses on no-go trials regardless of emotion processes.
emotional valence, suggesting a general deficit in With such a broad conceptualization, it is diffi-
behavioral inhibition (Murphy et al., 1999). Research cult to characterize the state of the literature suc-
suggests that moderate convergence of performance cinctly and neatly and summarize the measurement
measures across emotional and nonemotional ver- tools used in all of emotion dysregulation research.
sions of the same go/no-go task supports the con- This chapter attempted to illustrate some exemplar
struct validity of behavioral inhibition and suggests paradigms and tasks that illustrate measurement
that the basic constructs of the original go/no-go choices reflective of emotional dysregulation pro-
task are preserved in the emotion adaptation (Schulz cesses. Behavioral assessment is powerful; however,
et al., 2007). we anticipate improvement in the strategies for
integrating multiple measurements that are hetero-
Distress tolerance test geneous with respect to their sources of error to fa-
(Nock & Mendes, 2008). The distress tolerance test cilitate more reliable and valid aggregates of emotional
(DTT) is a behavioral measure of distress tolerance dysregulation (Zinbarg, Suzuki, Uliaszek, & Lewis,
that uses an alternative form of the Wisconsin Card 2010). Additionally, there is much to be accom-
Sort Test (Grant & Berg, 1948; Heaton & PAR plished with respect to the reliability, validity, and
Staff, 1993). In this task, participants are presented utility of behavioral assessment of emotion dysregu-
with a pile of 64 cards, each of which features an lation. Empirical data are lacking regarding the
image that varies by shape, color, and number. stability of emotion dysregulation variables, their
Participants are told to sort the cards under one of developmental specificity, and mean level changes
four sample cards but are not given a sorting rule. across development. It will be important to under-
Scripted instructions indicate that the first 20 cards stand the developmental precursors of more mature
must be sorted but that the participant is free to stop emotion regulation mechanisms and the trajectory
after that. With each attempted sort, the participant of emotion dysregulation processes over time in
is told whether or not the attempt was correct. well-characterized samples. In addition, several tasks
Unlike the original Wisconsin Card Sort Test, how- have been developed for other self-regulation pro-
ever, there is no correct order in which to sort the cesses (e.g., peg tapping; Cameron-Ponitz et al.,
cards. Regardless of where cards are placed, partici- 2008; Diamond & Taylor, 1996; Ponitz et al., 2008)
pants are told that the first three sorts are correct. that have promise in providing useful information
After this, the next seven sorts are said to be incor- about emotion dysregulation if paired with mood
rect. The 11th sort is said to be correct. After this, all induction tasks. Latent variables, especially those
subsequent sorts are said to be incorrect. Distress constructed on the basis of several observational
tolerance is measured by the number of cards par- measures, may provide more robust and reliable
ticipants sort before ending the task. To our knowl- estimates of emotion dysregulation and its relation
edge, this measure has been used in one published to other self-regulation processes. Finally, because of
study, which supported its construct validity. Lower the contextual significance in determining emotion
levels of distress tolerance predicted greater physio- dysregulation, the evaluation of construct validity
logical reactivity to the task and greater likelihood and its equivalence across populations is needed.
of presenting with a history of nonsuicidal self-injury The next critical steps in the field are to bolster the
(Nock & Mendes, 2008). empirical evidence that indicates that emotion
dysregulation exists in a manner that can be relia-
Summary and Future Directions bly and validly measured and has incremental pre-
Over the past two decades, there has been much dictive power.
progress in measurement of behavioral aspects of
emotion dysregulation and its relationship to psy-
chopathology (Gross, 2015). Emotion dysregulation References
Adrian, M., Zeman, J., & Veits, G. (2011). Methodological
has become a central construct as a transdiagnostic implications of the affect revolution: A 35-year review of
mechanism implicated in the development of psy- emotion regulation assessment in children. Journal of
chopathology. Researchers have made important Experimental Child Psychology, 110, 171–197.
Adrian and Berk 389

Ainsworth, M. D., & Wittig, B. (1969). Attachment, exploration, Campos, J. J., Frankel, C. B., & Camras, L. (2004). On the
and separation: Illustrated by the behavior of one-year-olds nature of emotion regulation. Child Development, 75,
in a strange situation. Determinants of Infant Behaviour, 4, 377–394.
113–136. Carlson, S. M., & Wang, T. S. (2007). Inhibitory control and
Ainsworth, M. D. S., Blehar, M. C., Waters, E., & Wall, S. N. emotion regulation in preschool children. Cognitive
(1978). Patterns of attachment: A psychological study of the Development, 22, 489–510.
Strange Situation. New York, NY: Routledge. Cassidy, J., Parke, R. D., Butkovsky, L., & Braungart, J. M.
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). (1992). Family-peer connections: The roles of emotional
Emotion-regulation strategies across psychopathology: A expressiveness within the family and children’s understanding
meta-analytic review. Clinical Psychology Review, 30, 217–237. of emotions. Child Development, 63, 603–618.
Allen, J. P., Hauser, S. T., Bell, K. L., & O’Connor, T. G. (1994). Chow, S.-M., Ram, N., Boker, S. M., Fujita, F., & Clore, G.
Longitudinal assessment of autonomy and relatedness in (2005). Emotion as a thermostat: Representing emotion
adolescent-family interactions as predictors of adolescent regulation using a damped oscillator model. Emotion, 5,
ego development and self-esteem. Child development, 65(1), 208–225.
179–194. Coan, J. A., & Allen, J. J. B. (2007). Handbook of emotion
Barrett, K. C., & Campos, J. J. (1987). Perspectives on emotional elicitation and assessment. New York, NY: Oxford University
development II: A functionalist approach to emotions. In Press.
J. D. Osofsky (Ed.), Handbook of infant development (2nd Cohn, J. F., & Tronick, E. Z. (1983). Three-month-old infants’
ed., pp. 555–578). Oxford, UK: John Wiley & Sons. reaction to simulated maternal depression. Child
Bayley, N. (1993). Bayley scales of infant development (2nd ed.). Development, 54, 185–193.
San Antonio, TX: Psychological Corporation. Cole, P. M. (1986). Children’s spontaneous control of facial
Bayley, N. (2006). Bayley scales of infant and toddler development. expression. Child Development, 57, 1309–1321.
San Antonio, TX: Pearson. Cole, P. M., Dennis, T. A., Smith-Simon, K. E., & Cohen, L. H.
Beauchaine, T. P. (2015). Future directions in emotion (2009). Preschoolers’ emotion regulation strategy
dysregulation and youth psychopathology. Journal of Clinical understanding: Relations with emotion socialization and
Child and Adolescent Psychology, 44, 875–896. child self-regulation. Social Development, 18, 324–352.
Beijersbergen, M. D., Bakermans-Kranenburg, M. J., Van Cole, P. M., Hall, S. E., & Hajal, N. J. (2017). Emotion
IJzendoorn, M. H., & Juffer, F. (2008). Stress regulation dysregulation as a vulnerability to psychopathology. In
in adolescents: Physiological reactivity during the Adult T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent
Attachment Interview and conflict interaction. Child psychopathology (3rd ed., pp. 346–386). Hoboken, NJ:
Development, 79, 1707–1720. Wiley.
Belsky, J. & Cassidy, J. (1994). Attachment theory and evidence. Cole, P. M., Jordan, P. R., & Zahn-Waxler, C. (1990). Mood
In M. Rutter & D. Hay (Eds.), Development through life: A induction stimulus for children. Bethesda, MD: National
handbook for clinicians (pp. 373–402). Oxford: Blackwell Institute of Mental Health.
Scientific Publications. Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion
Block, J., & Block, J. (1980). California Child Q-set. Palo Alto, regulation as a scientific construct: Methodological challenges
CA: Consulting Psychologists Press. and directions for child development research. Child
Braungart-Rieker, J. M., & Stifter, C. A. (1996). Infants’ Development, 75, 317–333.
responses to frustrating situations: Continuity and change in Cole, P. M., Zahn-Waxler, C., & Danielle, K. (1994). Expressive
reactivity and regulation. Child Development, 67, 1767–1779. control during a disappointment: Variations related to
Brazelton, T. B. (1973). The Neonatal Behavioral Assessment Scale. preschoolers’ behavior problems. Developmental Psychology,
Philadelphia, PA: Lippincott Williams & Wilkins. 30, 835–846.
Brazelton, T. B., & Nugent, J. K. (1995). Neonatal Behavioral Crowell, J. A., & Feldman, S. S. (1988). Mothers’ internal
Assessment Scale. Cambridge, UK: Cambridge University models of relationships and children’s behavioral and
Press. developmental status: A study of mother-child interaction.
Brenner, E. (2000). Mood induction in children: Methodological Child Development, 59, 1273–1285.
issues and clinical implications. Review of General Psychology, Crowell, S. E., Baucom, B. R., McCauley, E., Potapova, N. V.,
4, 264–283. Fitelson, M., Barth, H., . . . Beauchaine, T. P. (2013).
Brown, R. A., Kahler, C. W., & Strong, D. R. (2002). Distress Mechanisms of contextual risk for adolescent self-injury:
tolerance and duration of past smoking cessation attempts. Invalidation and conflict escalation in mother–child
Journal of Abnormal Psychology, 111, 180–185. interactions. Journal of Clinical Child and Adolescent
Buss, K. A., & Goldsmith, H. H. (1998). Fear and anger Psychology, 42, 467–480.
regulation in infancy: Effects on the temporal dynamics of Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C. J.,
affective expression. Child Development, 69, 359–374. Vasilev, C. A., & Stevens, A. L. (2008). Parent-child
Calkins, S. D., Dedmon, S. E., Gill, K. L., Lomax, L. E., & interactions, peripheral serotonin, and self-inflicted injury in
Johnson, L. M. (2002). Frustration in infancy: Implications adolescents. Journal of Consulting and Clinical Psychology, 76,
for emotion regulation, physiological processes, and 15–21.
temperament. Infancy, 3, 175–197. Cummings, E. M. (1987). Coping with background anger in
Cameron-Ponitz, C. E., McClelland, M. M., Jewkes, A. M., early childhood. Child Development, 58, 976–984.
Connor, C. M., Farris, C. L., & Morrison, F. J. (2008). Darwin, C. (1872). The expression of the emotions in man and
Touch your toes! Developing a direct measure of behavioral animals. London, UK: Murray.
regulation in early childhood. Early Childhood Research Daughters, S. B., Gorka, S. M., Magidson, J. F., MacPherson, L.,
Quarterly, 23, 141–158. & Seitz-Brown, C. J. (2013). The role of gender and race in

the relation between adolescent distress tolerance and development of symbolic competence. Infant Mental Health
externalizing and internalizing psychopathology. Journal of Journal, 18, 4–23.
Adolescence, 36, 1053–1065. Fosco, G. M., & Grych, J. H. (2013). Capturing the family
Denham, S., Mason, T., Caverly, S., Schmidt, M., Hackney, R., context of emotion regulation: A family systems model
Caswell, C., & DeMulder, E. (2001). Preschoolers at play: comparison approach. Journal of Family Issues, 34, 557–578.
Co-socialisers of emotional and social competence. International Frick, J. E., & Adamson, L. B. (2003). One still face, many
Journal of Behavioral Development, 25, 290–301. visions. Infancy, 4, 499–501.
Denham, S. A., Blair, K. A., DeMulder, E., Levitas, J., Sawyer, Garcia-Coll, C. T., Emmons, L., Vohr, B. R., Ward, A. M.,
K., Auerbach–Major, S., & Queenan, P. (2003). Preschool Brann, B. S., Shaul, P. W., . . . Oh, W. (1988). Behavioral
emotional competence: Pathway to social competence? Child responsiveness in preterm infants with intraventricular
Development, 74, 238–256. hemorrhage. Pediatrics, 81, 412–418.
Diamond, A., & Taylor, C. (1996). Development of an aspect of Goldsmith, H. (1993). Temperament: Variability in developing
executive control: Development of the abilities to remember emotion systems. In M. Lewis & J. M. Haviland (Eds.),
what I said and to “Do as I say, not as I do.” Developmental Handbook of emotions (pp. 353–364). New York, NY: Guilford.
Psychobiology, 29, 315–334. Goldsmith, H., & Rothbart, M. K. (1996). Prelocomotor and
Dishion, T. J., Nelson, S. E., Winter, C. E., & Bullock, B. M. locomotor laboratory temperament assessment battery (Lab-TAB;
(2004). Adolescent friendship as a dynamic system: Entropy version 3.0, technical manual). Madison, WI: University of
and deviance in the etiology and course of male antisocial Wisconsin Department of Psychology.
behavior. Journal of Abnormal Child Psychology, 32, 651–663. Goldsmith, H. H., & Rothbart, M. K. (1999). The laboratory
Drevets, W., & Raichle, M. (1998). Reciprocal suppression of temperament assessment battery. Locomotor Version, 3. Madison,
regional cerebral blood flow during emotional versus higher WI: University of Wisconsin Department of Psychology.
cognitive processes: Implications for interactions between Gottman, J. M., & Levenson, R. W. (1999). What predicts
emotion and cognition. In R. J. Davidson (Ed.), change in marital interaction over time? A study of alternative
Neuropsychological perspectives on affective and anxiety disorders models. Family Process, 38, 143–158.
(pp. 353–385). New York, NY: Psychology Press. Grant, D. A., & Berg, E. (1948). A behavioral analysis of degree
Durbin, E. C. (2010). Validity of young children’s self-reports of of reinforcement and ease of shifting to new responses in a
their emotion in response to structured laboratory tasks. Weigl-type card-sorting problem. Journal of Experimental
Emotion, 10, 519–535. Psychology, 38, 404–411.
Ehrmantrout, N., Allen, N. B., Leve, C., Davis, B., & Sheeber, Graziano, P. A., Keane, S. P., & Calkins, S. D. (2010). Maternal
L. (2011). Adolescent recognition of parental affect: Influence behaviour and children’s early emotion regulation skills
of depressive symptoms. Journal of Abnormal Psychology, 120, differentially predict development of children’s reactive control
628–634. and later effortful control. Infant and Child Development, 19,
Eisenberg, N., Fabes, R. A., Murphy, B., Maszk, P., Smith, M., & 333–353.
Karbon, M. (1995). The role of emotionality and regulation Grolnick, W. S., Bridges, L. J., & Connell, J. P. (1996). Emotion
in children’s social functioning: A longitudinal study. Child regulation in two-year-olds: Strategies and emotional
Development, 66, 1360–1384. expression in four contexts. Child Development, 67, 928–941.
Eisenberg, N., & Spinrad, T. L. (2004). Emotion-related Gronwall, D. M. A. (1977). Paced Auditory Serial-Addition
regulation: Sharpening the definition. Child Development, Task: A measure of recovery from concussion. Perceptual and
75, 334–339. Motor Skills, 44, 367–373.
Eisenberg, N., Zhou, Q., Spinrad, T. L., Valiente, C., Fabes, Gross, J. J. (2015). Emotion regulation: Current status and future
R. A., & Liew, J. (2005). Relations among positive parenting, prospects. Psychological Inquiry, 26, 1–26.
children’s effortful control, and externalizing problems: A Gross, J. J., & Thompson, R. A. (2007). Emotion regulation:
three-wave longitudinal study. Child Development, 76, Conceptual foundations. In J. J. Gross (Ed.), Handbook of
1055–1071. emotion regulation (pp. 3–24). New York, NY: Guilford.
Ekman, P., Friesen, W. V., & Tomkins, S. S. (1971). Facial affect Gross, J. J., & Jazaieri, H. (2014). Emotion, emotion regulation,
scoring technique: A first validity study. Semiotica, 3, 37–58. and psychopathology: An affective science perspective.
Ekman, P., & Rosenberg, E. L. (1997). What the face reveals: Basic Clinical Psychological Science, 2(4), 387–401.
and applied studies of spontaneous expression using the Facial Guo, Y., Leu, S. Y., Barnard, K. E., Thompson, E. A., & Spieker,
Action Coding System (FACS). New York, NY: Oxford S. J. (2015). An examination of changes in emotion co-
University Press. regulation among mother and child dyads during the strange
Fabes, R. A., & Eisenberg, N. (1992). Young children’s coping situation. Infant and Child Development, 24, 256–273.
with interpersonal anger. Child Development, 63, 116–128. Guttentag, R., & Ferrell, J. (2008). Children’s understanding of
Fabes, R. A., Eisenberg, N., Karbon, M., Troyer, D., & Switzer, G. anticipatory regret and disappointment. Cognition and
(1994). The relations of children’s emotion regulation to their Emotion, 22, 815–832.
vicarious emotional responses and comforting behaviors. Hare, T. A., Tottenham, N., Galvan, A., Voss, H. U., Glover,
Child Development, 65, 1678–1693. G. H., & Casey, B. J. (2008). Biological substrates of
Feldman, R., Eidelman, A. I., & Rotenberg, N. (2004). Parenting emotional reactivity and regulation in adolescence during an
stress, infant emotion regulation, maternal sensitivity, and the emotional go-nogo task. Biological Psychiatry, 63, 927–934.
cognitive development of triplets: A model for parent and Hauser, S. T., Powers, S. I., Noam, G. G., Jacobson, A. M., Weiss,
child influences in a unique ecology. Child Development, 75, B., & Follansbee, D. J. (1984). Familial contexts of adolescent
1774–1791. ego development. Child development, 55, 195–213.
Feldman, R., & Greenbaum, C. W. (1997). Affect regulation Hawes, D. J., Dadds, M. R., & Pasalich, D. S. (2013).
and synchrony in mother-infant play as precursors to the Observational coding strategies. In J. Comer & P. C. Kendall
Adrian and Berk 391

(Eds.), The Oxford handbook of research strategies for clinical Lindahl, K. M., Clements, M., & Markman, H. J. (1993).
psychology (pp. 120–141). New York, NY: Oxford University The development of marriage: A nine-year perspective. In
Press. T. Bradbury (Ed.), The developmental course of marital
Haynes, S. N., & O’Brien, W. H. (2003). Principles and practice dysfunction (pp. 205–236). New York, NY: Cambridge
of behavioral assessment. Berlin, Germany: Springer Science University Press.
and Business Media. Lorber, M. F., O'Leary, S. G., & Kendziora, K. T. (2003).
Heaton, R. K., & PAR Staff. (1993). Wisconsin Card Sorting Test: Mothers’ overreactive discipline and their encoding and
Computer version 2. Odessa, FL: Psychological Assessment appraisals of toddler behavior. Journal of Abnormal Child
Resources. Psychology, 31, 485–494.
Hinshaw, S. P., & Melnick, S. M. (1995). Peer relationships in Lütkenhaus, P., Grossmann, K. E., & Grossmann, K. (1985).
boys with attention-deficit/hyperactivity disorder with and Infant-mother attachment at twelve months and style of
without comorbid aggression. Development and Psychopathology, interaction with a stranger at the age of three years. Child
7, 627–647. Development, 56, 1538–1542.
Hubbard, J. A. (2001). Emotion expression processes in children’s Malone, S. M., Gunnar, M. R., & Fisch, R. O. (1985).
peer interaction: The role of peer rejection, aggression, and Adrenocortical and behavioral responses to limb restraint in
gender. Child Development, 72, 1426–1438. human neonates. Developmental Psychobiology, 18, 435–446.
Izard, C. E., & Dougherty, L. M. (1982). Two complementary Mangelsdorf, S. C., Shapiro, J. R., & Marzolf, D. (1995).
systems for measuring facial expressions in infants and Developmental and temperamental differences in emotion
children. Measuring Emotions in Infants and Children, 1, regulation in infancy. Child Development, 66, 1817–1828.
97–126. Marvin, R. S. (1977). An ethological-cognitive model for the
Izard, C. E., & Malatesta, C. Z. (1987). Perspectives on emotional attenuation of mother-child attachment behavior. In
development I: Differential emotions theory of early T. Alloway, L. Krames, & P. Pliner (Eds.), Advances in the
emotional development. In J. D. Osofsky (Ed.), Handbook of study of communication and affect (Vol. 3, pp. 25–60). New
infant development (2nd ed., pp. 494–554). Oxford, UK: York, NY: Plenum.
John Wiley & Sons. Maughan, A., & Cicchetti, D. (2002). Impact of child
Jahromi, L. B., Putnam, S. P., & Stifter, C. A. (2004). Maternal maltreatment and interadult violence on children’s emotion
regulation of infant reactivity from 2 to 6 months. regulation abilities and socioemotional adjustment. Child
Developmental Psychology, 40, 477–487. Development, 73, 1525–1542.
Jones, S., Carrere, S., & Gottman, J. M. (2005). Specific affect Melby, J. N., & Conger, R. D. (2001). The Iowa Family
coding system. In V. Manusov (Ed.), The sourcebook of Interaction Rating Scales: Instrument summary. In P. K. Kerig
nonverbal measures: Going beyond words (pp. 163–171). New & K. M. Lindahl (Eds.), Family observational coding
York, NY: Routledge. systems: Resources for systemic research (pp. 33–58). Mahwah,
Kaye, K. (1978). Discriminating among normal infants by NJ: Erlbaum.
multivariate analysis of Brazelton scores: Lumping and Melnick, S. M., & Hinshaw, S. P. (2000). Emotion regulation
smoothing. Monographs of the Society for Research in Child and parenting in ADHD and comparison boys: Linkages
Development, 43, 60–80. with social behaviors and peer preference. Journal of
Klimes-Dougan, B., & Zeman, J. (2007). Introduction to the Abnormal Child Psychology, 28, 73–86.
special issue of social development: Emotion socialization in Miller, A. L., McDonough, S. C., Rosenblum, K. L., & Sameroff,
childhood and adolescence. Social Development, 16, 203–209. A. J. (2002). Emotion regulation in context: Situational
Klinnert, M. D., McQuaid, E. L., McCormick, D., Adinoff, effects on infant and caregiver behavior. Infancy, 3, 403–433.
A. D., & Bryant, N. E. (2000). A multimethod assessment of Morris, A. S., Robinson, L. R., & Eisenberg, N. (2006). Applying
behavioral and emotional adjustment in children with a multimethod perspective to the study of developmental
asthma. Journal of Pediatric Psychology, 25, 35–46. psychology. In M. Eid & E. Diener (Eds.), Handbook of
Kobak, R. R., Cole, H. E., Ferenz-Gillies, R., Fleming, W. S., & multimethod measurement in psychology (pp. 371–384).
Gamble, W. (1993). Attachment and emotion regulation Washington, DC: American Psychological Association.
during mother-teen problem solving: A control theory analysis. Morris, A. S., Silk, J. S., Steinberg, L., Terranova, A. M., &
Child Development, 64, 231–245. Kithakye, M. (2010). Concurrent and longitudinal links
Kochanska, G., Murray, K. T., & Harlan, E. T. (2000). Effortful between children’s externalizing behavior in school and
control in early childhood: Continuity and change, observed anger regulation in the mother-child dyad. Journal
antecedents, and implications for social development. of Psychopathology and Behavioral Assessment, 32, 48–56.
Developmental Psychology, 36, 220–232. Murphy, F. C., Sahakian, B. J., Rubinsztein, J. S., Michael, A.,
Leary, A., & Katz, L. F. (2005). Observations of aggressive Rogers, R. D., Robbins, T. W., & Paykel, E. S. (1999).
children during peer provocation and with a best friend. Emotional bias and inhibitory control processes in mania
Developmental Psychology, 41, 124–134. and depression. Psychological Medicine, 29, 1307–1321.
Lejuez, C., Kahler, C. W., & Brown, R. A. (2003). A modified Nock, M. K., & Mendes, W. B. (2008). Physiological arousal,
computer version of the Paced Auditory Serial Addition Task distress tolerance, and social problem-solving deficits among
(PASAT) as a laboratory-based stressor. Behavior Therapist, adolescent self-injurers. Journal of Consulting and Clinical
26, 290–293. Psychology, 76, 28–38.
Lewis, M. D., & Granic, I. (2000). A new approach to the study Ponitz, C. C., McClelland, M. M., Jewkes, A. M., Connor,
of emotional development. In M. D. Lewis & I. Granic C. M., Farris, C. L., & Morrison, F. J. (2008). Touch your
(Eds.), Emotion, development, and self-organization: Dynamic toes! Developing a direct measure of behavioral regulation in
systems approaches to emotional development (pp. 1–12). early childhood. Early Childhood Research Quarterly, 23,
New York, NY: Cambridge University Press. 141–158.

Porges, S. W. (2011). The polyvagal theory: Neurophysiological coping assessed by ecological momentary assessment and
foundations of emotions, attachment, communication, and self- retrospective recall. Journal of Personality and Social
regulation. New York, NY: Norton & Company. Psychology, 74, 1670–1680.
Putallaz, M. (1983). Predicting children’s sociometric status from Strodtbeck, F. L. (1951). Husband-wife interaction over revealed
their behavior. Child Development, 54, 1417–1426. differences. American Sociological Review, 16, 468–473.
Reijntjes, A., Stegge, H., Terwogt, M. M., Kamphuis, J. H., & Suveg, C., Morelen, D., Brewer, G. A., & Thomassin, K. (2010).
Telch, M. J. (2006). Emotion regulation and its effects on The emotion dysregulation model of anxiety: A preliminary
mood improvement in response to in vivo peer rejection path analytic examination. Journal of Anxiety Disorders, 24,
challenge. Emotion, 6, 543–552. 924–930.
Renna, M. E., Chin, S., Seeley, S. H., Fresco, D. M., Heimberg, Suveg, C., Sood, E., Barmish, A., Tiwari, S., Hudson, J. L., &
R. G., & Mennin, D. S. (2017). The use of the mirror tracing Kendall, P. C. (2008). “I’d rather not talk about it”: Emotion
persistence task as a measure of distress tolerance in parenting in families of children with an anxiety disorder.
generalized anxiety disorder. Journal of Rational-Emotive and Journal of Family Psychology, 22, 875–884.
Cognitive-Behavior Therapy, 1–9. Tobin, R. M., & Graziano, W. G. (2011). The disappointing gift:
Reynolds, W. M. (1993). Self-report methodology. In Dispositional and situational moderators of emotional
T. H. Ollendick & M. Hersen (Eds.), Handbook of child and expressions. Journal of Experimental Child Psychology, 110,
adolescent assessment (pp. 98–123). Boston, MA: Allyn & 227–240.
Bacon. Tonyan, H. A. (2005). Coregulating distress: Mother-child
Rice, J. A., Levine, L. J., & Pizarro, D. A. (2007). “Just stop interactions around children’s distress from 14-24 months.
thinking about it”: Effects of emotional disengagement on International Journal of Behavioral Development, 29, 433–444.
children’s memory for educational material. Emotion, 7, Tronick, E. Z. (1989). Emotions and emotional communication
812–823. in infants. American Psychologist, 44, 112–119.
Robin, A. L., & Foster, S. L. (1984). Problem-solving Underwood, M. K. (2003). Social aggression among girls. New
communication training: A behavioral-family systems York, NY: Guilford Press.
approach to parent–adolescent conflict. Advances in Child Underwood, M. K., & Hurley, J. C. (1999). Emotion regulation
Behavioral Analysis and Therapy, 3, 195–240. and peer relationships during the middle childhood years. In
Rothbart, M. K., & Ahadi, S. A. (1994). Temperament and the C. Tamis-LeMonda & L. Balter (Eds.), Child psychology: A
development of personality. Journal of Abnormal Psychology, handbook of contemporary issues (pp. 237–258). Philadelphia,
103, 55–66. PA: Psychology Press.
Rothbart, M. K., & Bates, J. E. (2007). Temperament. In Volling, B. L., McElwain, N. L., & Miller, A. L. (2002). Emotion
W. Damon & N. Eisenberg (Eds.), Handbook of child regulation in context: The jealousy complex between young
psychology. Vol. 3: Social emotional and personality development siblings and its relations with child and family characteristics.
(pp. 105–176). New York, NY: Wiley. Child Development, 73, 581–600.
Rothbart, M. K., Posner, M. I., & Kieras, J. (2006). Weinberg, M. K., & Tronick, E. Z. (1998). Infant and caregiver
Temperament, attention, and the development of self- engagement phases system. Boston, MA: Harvard Medical
regulation. In K. McCartney & D. Phillips (Eds.), Blackwell School.
handbook of early childhood development (pp. 338–357). Weiss, J. A., Thomson, K., & Chan, L. (2014). A systematic
Hoboken, NJ: Blackwell Publishing. literature review of emotion regulation measurement in
Russell, J. A. (1980). A circumplex model of affect. Journal of individuals with autism spectrum disorder. Autism Research,
Personality and Social Psychology, 39, 1161–1178. 7, 629–648.
Saarni, C. (1979). Children’s understanding of display rules Whalen, D. J., Scott, L. N., Jakubowski, K. P., McMakin, D. L.,
for expressive behavior. Developmental Psychology, 15, Hipwell, A. E., Silk, J. S., & Stepp, S. D. (2014). Affective
424–429. behavior during mother–daughter conflict and borderline
Saarni, C. (1984). An observational study of children’s attempts personality disorder severity across adolescence. Personality
to monitor their expressive behavior. Child Development, 55, Disorders: Theory, Research, and Treatment, 5, 88–96.
1504–1513. Yap, M. B. H., Allen, N. B., & Ladouceur, C. D. (2008).
Schulz, K. P., Fan, J., Magidina, O., Marks, D. J., Hahn, B., & Maternal socialization of positive affect: The impact of
Halperin, J. M. (2007). Does the emotional go/no-go task invalidation on adolescent emotion regulation and depressive
really measure behavioral inhibition? Archives of Clinical symptomatology. Child Development, 79, 1415–1431.
Neuropsychology, 22, 151–160. Zahn-Waxler, C., Ridgeway, D., Denham, S., Usher, B., & Cole,
Shipman, K. L., & Zeman, J. (1999). Emotional understanding: P. M. (1993). Pictures of infants’ emotions: A task for assessing
A comparison of physically maltreating and nonmaltreating mothers’ and young children’s verbal communications about
mother-child dyads. Journal of Clinical Child Psychology, 28, affect. In R. N. Emde, J. D. Osofsky, & P. M. Butterfield
407–417. (Eds.), The IFEEL pictures: A new instrument for interpreting
Smith, R. E., Leffingwell, T. R., & Ptacek, T. J. (1999). Can emotions (pp. 217–236). Madison, CT: International
people remember how they coped? Factors associated with Universities Press.
discordance between same-day and retrospective reports. Zeanah, C. H., Boris, N. W., Heller, S. S., Hinshaw-Fuselier, S.,
Journal of Personality and Social Psychology, 76, 1050–1061. Larrieu, J. A., Lewis, M., . . . Valliere, J. (1997). Relationship
Stifter, C. A., & Braungart, J. M. (1995). The regulation of assessment in infant mental health. Infant Mental Health
negative reactivity in infancy: Function and development. Journal, 18, 182–197.
Developmental Psychology, 31, 448–455. Zeman, J., Cassano, M., Perry-Parrish, C., & Stegall, S. (2006).
Stone, A. A., Schwartz, J. E., Neale, J. M., Shiffman, S., Marco, Emotion regulation in children and adolescents. Journal of
C. A., Hickcox, M., . . . Cruise, L. J. (1998). A comparison of Developmental and Behavioral Pediatrics, 27, 155–168.
Adrian and Berk 393

Zeman, J., Klimes-Dougan, B., Cassano, M., & Adrian, M. Zinbarg, R. E., Suzuki, S., Uliaszek, A. A., & Lewis, A. R.
(2007). Measurement issues in emotion research with children (2010). Biased parameter estimates and inflated type I
and adolescents. Clinical Psychology: Science and Practice, 14, error rates in analysis of covariance (and analysis of partial
377–401. variance) arising from unreliability: Alternatives and
Zeman, J., Penza, S., Shipman, K., & Young, G. (1997). remedial strategies. Journal of Abnormal Psychology, 119,
Preschoolers as functionalists: The impact of social context 307–319.
on emotion regulation. Child Study Journal, 27, 41–67. Zisner, A., & Beauchaine, T. P. (2016). Psychophysiological
Zimmermann, P., Mohr, C., & Spangler, G. (2009). Genetic and methods and developmental psychopathology. In
attachment influences on adolescents’ regulation of autonomy D. Cicchetti (Ed.), Developmental psychopathology. Vol. 2:
and aggressiveness. Journal of Child Psychology and Psychiatry, Developmental neuroscience (3rd ed., pp. 832–884). Hoboken,
50, 1339–1347. NJ: Wiley.

CH A PT E R
Self-Report Assessment of Emotion
27 Dysregulation
Kim L. Gratz, Courtney N. Forbes, Linnie E. Wheeless, Julia R. Richmond, and Matthew T. Tull
Abstract
Self-report assessments remain among the most widely used measures for most psychological
constructs, due to their feasibility, ease of administration, low cost, and wide availability. Self-report
measures of emotion dysregulation are no exception. This chapter reviews two predominant
conceptualizations of emotion dysregulation (one of which focuses on dysregulated emotional
responses per se and another that focuses on maladaptive ways of responding to emotions), as well
as the empirical support for extant self-report measures of emotion dysregulation consistent with
both conceptualizations. Based on this review, the chapter concludes that both emotional responses
themselves and an individual’s responses to those emotions may evidence dysregulation and inform
our understanding of normal and abnormal development. Finally, future directions for research in this
area are discussed, including the need for studies examining the clinical utility of targeting responses to
emotions versus emotional experience per se in psychological interventions.
Keywords: emotion dysregulation, emotion regulation, emotional reactivity, self-report, assessment
Introduction down-regulate emotions, this limitation is arguably

Self-report assessments remain among the most less relevant to measures of emotion dysregulation
widely used measures for most psychological con- that assess a subjective sense of struggling with or
structs, and emotion dysregulation is no exception. being overwhelmed by emotions.
Indeed, despite the well-documented and widely Indeed, the very individuals who struggle to
acknowledged limitations of self-report measures identify how they are feeling or why they feel a cer-
(see Tull, Bornovalova, Patterson, Hopko, & Lejuez, tain way are likely well aware that their emotions
2008), their feasibility, ease of administration, low feel unclear, intense, out of control, and/or over-
cost, and wide availability make them by far the whelming (Gratz, 2007; Wolff, Stiglmayr, Bretz,
most common form of assessment (Stone, Bachrach, Lammers, & Auckenthaler, 2007). Even the most
Jobe, Kurtzman, & Cain, 2000). With regard to emotionally dysregulated individuals tend to be able
their noted limitations, one of the most common to identify that they dislike, judge, avoid, or other-
(particularly when it comes to measures of internal wise struggle with their emotions (Chapman, Gratz,
states, such as emotions) is that they rely on an indi- & Brown, 2006). For example, following an un-
vidual’s ability to recognize and accurately report on pleasant interpersonal interaction, an individual
these internal states—an ability that some individu- with borderline personality disorder (BPD) may not
als may not possess. Notably, however, although this be able to identify the specific emotions that are
limitation may negatively affect measures that ask present, but would likely be aware of the presence of
individuals to recognize and label emotions, iden- a state of arousal, discomfort, or general distress that
tify the function of and/or information provided by is unbearable, unacceptable, or overwhelming. Thus,
emotions, or report on specific strategies used to in addition to the fact that self-report measures of
395
emotion dysregulation are likely to remain the most modulation of emotions. Grounded in theory and
common, widely used, and feasible assessments in research on the functionality of emotions (Cole,
both clinical and research settings, the limitations Michel, & Teti, 1994; Ekman & Davidson, 1994;
associated with self-report measures of other R. A. Thompson, 1994) and paradoxical conse-
emotion-related constructs may be less applicable to quences of efforts to avoid or control emotions
measures of emotion dysregulation by virtue of the (e.g., Hayes, Luoma, Bond, Masuda, & Lillis,
nature of the construct itself. 2006), this conceptualization proposes that even
In this chapter, we review two predominant con- intense, reactive, or labile emotions are not inher-
ceptualizations of emotion dysregulation and their ently dysregulated and that responses to emotions
relative clinical utility, as well as the empirical sup- are more important than the quality of those
port for extant self-report measures of emotion dys- emotions.
regulation consistent with both conceptualizations. Although these conceptualizations of emotion
Finally, we discuss future directions for research in dysregulation represent two primary theoretical ap-
this area. proaches to this construct, one additional definition
of emotion dysregulation—often cited in person-
Conceptualizations of Emotion ality disorders literature—warrants discussion.
Dysregulation Specifically, some researchers refer to Livesley and
There are numerous (and often discrepant) concep- colleagues’ research on the factor structure of the
tual definitions of emotion regulation in the litera- Dimensional Assessment of Personality Pathology—
ture, with the relative utility and merits of each de- Basic Questionnaire (DAPP-BQ; Livesley & Jackson,
pendent on the research or clinical question of 2002) when defining emotion dysregulation.
interest (Gratz, Weiss, & Tull, 2015). Thus, it is not However, rather than being grounded in theory on
surprising that there is also not a single agreed-upon emotion dysregulation, the definition stemming
conceptualization of emotion dysregulation, al- from this work reflects simply a label given to an
though the relative lack of attention given to this empirically derived set of intercorrelated lower
construct (vs. emotion regulation) has resulted in order maladaptive personality traits. Namely, in
far fewer conceptualizations of emotion dysregula- their research examining the interrelations and hier-
tion than emotion regulation. In fact, most of the archical structure of 18 specific lower order traits
literature on emotion dysregulation relies on one of underlying personality disorders, a higher order
two primary conceptualizations of this construct. factor emerged that closely resembles borderline
The first conceptualization focuses on putatively personality pathology and is composed of traits cap-
dysregulated emotional responses per se, equating turing emotional, cognitive, interpersonal, and self/
emotion dysregulation with the temperamental identity dysfunction, including anxiousness, affec-
characteristics of emotional sensitivity, intensity, re- tive lability, insecure attachment, submissiveness,
activity, and slow return to baseline (e.g., Newhill, social avoidance, identity problems, and cognitive
Mulvey, & Pilkonis, 2004). According to this defi- dysregulation (Livesley, 2002; Livesley, Jang, &
nition, emotional responses that are particularly Vernon, 1998). As such, this higher order factor
intense, reactive, and long-lasting are inherently captures far more than emotional dysfunction and
dysregulated and may increase risk for maladaptive is instead similar to conceptualizations of BPD
behaviors aimed at regulating these emotions, such (Livesley et al., 1998; Hernandez et al., 2009).
as self-injury or substance misuse (Newhill, Bell, Nonetheless, because of the prominence and saliency
Eack, & Mulvey, 2010). of the emotion-related traits loading on this factor
In contrast, other researchers conceptualize (i.e., anxiousness and affective lability), Livesley and
emotion dysregulation as separate from the quality colleagues labeled this dimension “emotion dysreg-
of the emotional responses themselves (Gratz & ulation” (Livesley et al., 1998). Although labeling
Roemer, 2004; R. A. Thompson & Calkins, 1996), these emotion-related traits as emotion dysregula-
implying that there is a difference between one’s tion is consistent with the first conceptualization of
emotional temperament and emotion dysregula- emotion dysregulation described previously, the
tion. Specifically, Gratz and Roemer’s (2004) con- factor to which this label applies is not specific to
ceptualization focuses on maladaptive ways of emotional dysfunction and is better conceptualized
responding to emotions (regardless of their valence, as BPD-related pathology. Further, an additional
intensity, or reactivity), including deficits in the problem with using this research as the basis of a
understanding, acceptance, and effective use and/or conceptual definition of emotion dysregulation is
396 Self-Report Assessment of Emotion Dysregul ation

that this was never its intended purpose and the limited. Conversely, a conceptualization of emotion
definition stemming from this work is atheoretical. dysregulation that focuses on responses to emotions
may offer more direct and concrete clinical implica-
Unresolved Controversies tions, as responses to emotions are learned behaviors
As can be seen from the previous discussion, a pri- and thus can more readily be changed or relearned
mary controversy within this body of literature is (Gratz, 2007; Livesley, 2002).
how best to conceptualize the temperamental char-
acteristics of emotional sensitivity, reactivity, inten- Self-Report Measures of Emotion
sity, and lability. Although evidence suggests that Dysregulation
individuals who are more emotionally intense and Despite a growing interest in emotion dysregulation
reactive may be at greater risk for emotion dysregu- and the relevance of this construct to both normal
lation (Flett, Blankstein, & Obertynski, 1996), this development and psychopathology, there are sur-
relationship is not direct, and considerable research prisingly few measures grounded in either concep-
indicates that emotional intensity/reactivity in and tualization of emotion dysregulation that assess this
of itself is not associated with negative psychological construct comprehensively. Self-report measures of
outcomes (Gratz, 2006; Larsen & Diener, 1987; both overall emotion dysregulation and its various
Larsen, Diener, & Emmons, 1986; Tull, Jakupcak, dimensions are described next, organized according
McFadden, & Roemer, 2007; see also Gratz, Dixon- to the conceptualization of emotion dysregulation
Gordon, & Whalen, 2016). Further, evidence sug- to which they correspond.
gests that not only are these temperamental charac-
teristics not inherently maladaptive, they may Measures of Emotion Dysregulation as a
actually be adaptive in some circumstances. For ex- Temperamental Emotional Vulnerability
ample, emotional lability has a positive association Comprehensive
with creativity (Frantom & Sherman, 1999), and To date, there are few comprehensive measures that
has been linked to greater attention to emotional capture the conceptualization of emotion dysregula-
experiences within undergraduate and community tion as a temperamental emotional vulnerability
samples (R. J. Thompson, Dizén, & Berenbaum, among adults, and only one that was developed spe-
2009). Moreover, preliminary research suggests that cifically to assess this construct. Specifically, the
extremely low emotional lability increases risk for General Emotion Dysregulation Measure (GEDM;
psychopathology and related dysfunction (e.g., Newhill et al., 2004) was developed to assess the
Koval, Pe, Meers, & Kuppens, 2013; Rottenberg, conceptualization of emotion dysregulation as
Kasch, Gross, & Gotlib, 2002). Finally, the extent (1) high sensitivity to emotional stimuli, (2) high
to which these temperamental characteristics are amplitude of emotional response, and (3) slow
amenable to treatment is unclear, as evidence sug- return to baseline. Originally developed to consist
gests that these emotion-related traits are relatively of three subscales reflecting these three dimensions,
stable (Carstensen et al., 2011; de Clercq, van a principal components analysis of the original 18-
Leeuwen, van den Noortgate, de Bolle, & de Fruyt, item version of this measure within a sample of pa-
2009; Gunnar, Mangelsdorf, Larson, & Hertsgaard, tients with cluster B personality disorders produced
1989; McGlashan et al., 2005; Zanarini, Frankenburg, a 13-item measure consisting of a single factor.
Hennen, & Silk, 2003). Subsequently, confirmatory factor analysis of this
Given this literature, one downside of the first 13-item version within a nonclinical sample pro-
conceptualization of emotion dysregulation is that duced an 11-item version that was best represented
labeling certain temperamental emotional charac- by two factors reflecting (1) emotional intensity/
teristics as dysregulated may be inaccurate and a sensitivity (e.g., “I see myself as more sensitive to
misnomer. Such an approach fails to acknowledge emotions than other people” and “Feeling sad can
the more nuanced relations of these traits to risk overwhelm me”) and (2) slow return to baseline
and resilience or the moderating factors that may (e.g., “When I get emotional about something,
attenuate or potentiate their impact on functioning I have a hard time settling down”; Newhill et al.,
(e.g., Gratz, Dixon-Gordon, & Whalen, 2016). 2010). Participants are asked to rate each item using
Further, to the extent that temperamental charac- a 5-point Likert-type scale ranging from 1 (strongly
teristics are indeed less likely to change and, thus, disagree) to 5 (strongly agree).
less amenable to treatment, the clinical relevance Although there are few studies examining the
of such an approach to emotion dysregulation is GEDM, the 13-item version demonstrates significant
Gratz, Forbes, Wheeless, Richmond, and Tull 397

correlations with negative affect, affect intensity, 2008; Snorrason, Smári, & Ólafsson, 2010). The
and interpersonal problems (Newhill et al., 2004). ERS has also been found to be associated with inter-
Further, scores on this measure were associated with nalizing problems, reactive aggression, and suicidal
better recognition of emotion microexpressions ideation among girls in an urban middle school
(particularly those reflecting anger) within a non- sample (Evans et al., 2016). Finally, the ERS dem-
clinical sample (Svetieva & Frank, 2016). Notably, onstrates significant associations with emotion dys-
however, there is no evidence that this measure is regulation and related constructs, including poor
sensitive to change following psychological treat- emotional coping, negative and positive urgency,
ment. We identified only one study examining thought suppression, and maladaptive cognitive
changes in GEDM scores in response to a psycho- emotion regulation strategies (e.g., Evans et al., 2016;
logical intervention (i.e., an eight-week mindfulness Lannoy et al., 2014; Najmi, Wegner, & Nock, 2007).
meditation skills course), which found only small, To our knowledge, only one study has examined
nonsignificant pre- to postintervention changes whether the ERS is sensitive to change as a result of
(Turner, 2010). treatment. Specifically, Deckersbach et al. (2012)
Potentially complicating research in this area, examined changes in ERS scores from pretreatment
two widely used comprehensive measures consistent through three-month follow-up within a small trial
with the conceptualization of emotion dysregula- of a group-based mindfulness-based cognitive ther-
tion as a temperamental emotional vulnerability apy for adults with bipolar disorder (N = 12). Results
were not designed to measure emotion dysregulation. revealed significant reductions in ERS scores across
Instead, they were developed to assess emotional re- time, although when the changes occurred and
activity as distinct from emotion dysregulation. Yet, whether improvements were found from pre- to
despite assessing a putatively different construct, posttreatment remain unclear.
they map onto this particular conceptualization of A second measure of emotional reactivity that
emotion dysregulation and measure it compre- provides a comprehensive assessment of this con-
hensively. The first of these measures, the Emotion ceptualization of emotion dysregulation is the 30-
Reactivity Scale (ERS; Nock, Wedig, Holmberg, & item Perth Emotional Reactivity Scale (PERS; Becerra
Hooley, 2008), is a 21-item measure developed to & Campitelli, 2013; Becerra, Preece, Campitelli, &
assess emotional reactivity in adolescents and young Scott-Pillow, 2017). Drawing upon theoretical and
adults ages 12 to 19. The ERS consists of three sub- empirical work on the components and characteristics
scales: emotion sensitivity (e.g., “I tend to get emo- of emotional reactivity (Davidson, 1998; Linehan,
tional very easily”), emotion intensity (e.g., “When 1993), Becerra and Campitelli (2013) developed the
I experience emotions, I experience them very PERS to advance research on emotional reactivity
strongly/intensely”), and emotion persistence (e.g., by assessing emotional valence (i.e., positive or
“When I am angry/upset, it takes me longer than negative) in addition to the three dimensions of
most people to calm down”). Each item is rated on emotional reactivity (i.e., sensitivity, intensity, and
a 5-point Likert-type scale ranging from 0 (not at all persistence/duration) assessed by other extant meas-
like me) to 4 (completely like me), with total scores ures, such as the ERS. To this end, the PERS includes
ranging from 0 to 84. Notably, despite including six subscales: positive activation (e.g., “I tend to get
three subscales measuring emotional sensitivity, in- enthusiastic about things very quickly”), positive in-
tensity, and persistence, research suggests that the tensity (e.g., “I experience positive mood very
total score may best capture this construct (Nock strongly”), positive duration (e.g., “When I’m happy,
et al., 2008). the feeling stays with me for quite a while”), negative
The ERS is associated with negative affect and activation (e.g., “I tend to get upset very easily”), neg-
other temperamental vulnerabilities, including be- ative intensity (e.g., “My negative feelings feel very
havioral inhibition, effortful control (inversely re- intense”), and negative duration (e.g., “Once in a
lated), fear and shyness intensity, and perceptual negative mood, it’s hard to snap out of it”). The three
sensitivity (Nock et al., 2008). In addition, the ERS subscales within each valence domain can be com-
has been found to distinguish between adolescents bined into general positive and negative reactivity
and young adults with (vs. without) mood disor- scale scores. Items are rated on a 5-point Likert-type
ders, anxiety disorders, eating disorders, pathologi- scale ranging from 1 (very unlike me) to 5 (very like
cal skin picking, nonsuicidal self-injury, suicidal me), with higher scores indicating higher reactivity.
ideation, and past-year suicide attempts (Glenn, Preliminary evidence provides support for the
Blumenthal, Klonsky, & Hajcak, 2011; Nock et al., construct, convergent, and divergent validity of the

PERS and its subscales (Becerra et al., 2017). Flanagan, 2009), and social anxiety disorder
Specifically, scores on the subscales evidenced sig- (Mennin et al., 2009). AIM scores are also positively
nificant associations in expected directions with associated with BPD symptoms (Flett & Hewitt,
measures of psychopathology and emotion dysregu- 1995; Marshall-Berenz, Morrison, Schumacher, &
lation, including negative associations between the Coffey, 2011; Yen, Zlotnick, & Costello, 2002), bu-
general positive reactivity scale and measures of de- limia symptoms (Markey & Vander Wal, 2007),
pression, anxiety, and stress symptoms, and positive posttraumatic stress disorder symptoms (Marshall-
associations between the general negative reactivity Berenz et al., 2011; Tull et al., 2007), and depression
scale and both depression, anxiety, and stress symp- (Flett et al., 1996). Finally, AIM scores among un-
toms and multiple dimensions of emotion dysregu- dergraduate students are correlated with self-reported
lation conceptualized as maladaptive responses to intensity of daily emotions in a semester-long daily
emotions (e.g., difficulties controlling behaviors in diary study (Larsen & Diener, 1985).
the context of negative emotions and lack of access Use of the AIM in treatment outcome research is
to effective emotion regulation strategies; Becerra limited. One exception is a recent open trial of emo-
et al., 2017). tion regulation therapy for individuals with general-
ized anxiety disorder and co-occurring depressive
Dimension Specific symptoms (Mennin, Fresco, Ritter, & Heimberg,
Although the three measures described previously 2015). Although patients reported significant reduc-
provide a comprehensive assessment of emotion tions in negative affect intensity from pre- to post-
dysregulation as a temperamental emotional vulner- treatment, these gains were not maintained at the
ability, there are other measures of one or more of three-month follow-up.
the specific dimensions of emotion dysregulation Second, the Affective Lability Scale (ALS; Harvey,
described in this conceptualization that have more Greenberg, & Serper, 1989) is a 54-item self-report
widespread use and empirical support than these measure of affective lability, or intense and reactive
comprehensive measures. We review the two most shifts in emotions (American Psychiatric Association
well researched of these measures next. [APA], 2013; Gunderson, Zanarini, & Kisiel, 1996).
First, the Affect Intensity Measure (AIM; Larsen, As such, the construct of affective lability encom-
Diener, & Emmons, 1986) is a 40-item self-report passes both emotional intensity and emotional reac-
measure of trait emotional intensity and reactivity. tivity (Gratz et al., 2016). The ALS includes six
Although originally developed as a unidimensional subscales assessing shifts in depression, elation,
measure of affective intensity, research suggests that anger, and anxiety from one’s normal mood, as well
the AIM is multidimensional, measuring both posi- as shifts between the emotions of anxiety and de-
tive (e.g., “When I’m happy, I feel like I’m bursting pression and hypomania and depression. A total
with joy”) and negative (e.g., “When I do feel anxi- score reflecting overall affective lability can also be
ety, it is normally very strong”) emotional intensity obtained. Participants rate the extent to which each
and emotional reactivity (Weinfurt, Bryant, & item (e.g., “One minute I can be feeling OK and
Yarnold, 1994). Items on the AIM are rated on a then I feel tense, jittery, and nervous” and “There
6-point Likert-type scale ranging from 1 (never) to 6 are times when I’m so mad that my heart is pound-
(always), with higher scores on the measure corre- ing and then shortly afterwards I feel quite relaxed”)
sponding to greater emotional intensity and reactivity. is descriptive of themselves using a 4-point Likert-
There is extensive support for the construct and type scale ranging from 0 (very undescriptive) to 3
convergent validity of the AIM (Larsen & Diener, (very descriptive).
1985, 1987). For example, scores on the AIM are Research findings support the construct and
associated with maladaptive coping strategies and convergent validity of the ALS. For example, ALS
negative expectancies about mood regulation (Flett, scores are positively associated with aggression
Blankstein, & Obertynski, 1996), thought suppres- (Dvorak, Pearson, & Kuvaas, 2013), problematic
sion (Cheavens et al., 2005), and anxious/fearful alcohol use (Kuvaas, Dvorak, Pearson, Lamis, &
responding to bodily sensations (Vujanovic et al., Sargent, 2014; Simons, Oliver, Gaher, Ebel, &
2006). Further, scores on this measure and its sub- Brummels, 2005), and the use of hard exercise as a
scales are higher among individuals with bipolar compensatory behavior among individuals with bu-
disorder (Henry et al., 2008), BPD (Gratz, limia nervosa (Brownstone et al., 2013). Furthermore,
Rosenthal, Tull, Lejuez, & Gunderson, 2010), gen- scores on this measure are higher among individuals
eralized anxiety disorder (Mennin, McLaughlin, & with psychiatric disorders characterized by emotional

instability, including bipolar disorder (Henry et al., when distressed (e.g., When I’m upset, I lose con-
2008) and BPD (Koenigsberg et al., 2002; Solhan, trol over my behaviors”); (4) lack of emotional
Trull, Jahng, & Wood, 2009). awareness (e.g., “I pay attention to how I feel”
There is also an 18-item short form of the [reverse scored]); (5) limited access to emotion reg-
Affective Lability Scale (ALS-SF; Oliver & Simmons, ulation strategies perceived as effective (e.g., “When
2004). The ALS-SF includes three subscales assess- I’m upset, I know that I can find a way to eventually
ing shifts between anxiety and depression, depres- feel better” [reverse scored]); and (6) lack of emo-
sion and elation, and anger and normal mood. In an tional clarity (e.g., “I have difficulty making sense
undergraduate sample, the ALS-SF correlated sig- out of my feelings”). The DERS is scored so that the
nificantly with the original 54-item ALS and dem- overall score, as well as all subscale scores, reflect
onstrated similar relations to related constructs, in- greater emotion dysregulation.
cluding affect intensity, emotional control, and In support of the construct validity of this meas
depressive symptoms, as the original ALS (Oliver & ure, scores on the DERS have been found to be sig-
Simmons, 2004). Further, scores on this measure nificantly associated with a variety of behaviors
are positively associated with the number of both thought to serve an emotion-regulating function,
overall instances of deliberate self-harm and specific including deliberate self-harm (Gratz & Chapman,
self-harm behaviors (Dir, Karyadi, & Cyders, 2013), 2007; Gratz & Roemer, 2008; Gratz & Tull, 2010),
and are higher among individuals with cluster B (vs. chronic worry (Salters-Pedneault, Roemer, Tull,
cluster A or C) personality disorders (Look, Flory, Rucker, & Mennin, 2006; Vujanovic, Zvolensky, &
Harvey, & Siever, 2010). Finally, scores on the Bernstein, 2008), intimate partner abuse perpetra-
ALS-SF demonstrate significant positive associations tion among men (Gratz, Paulson, Jakupcak, & Tull,
with emotional intensity/reactivity on the AIM, ur- 2009), binge-eating (Whiteside et al., 2007), and
gency, and marijuana use, as well as negative associa- substance use (Fox, Axelrod, Paliwal, Sleeper, &
tions with self-control (Dvorak & Day, 2014). Sinha, 2007; Tull, Bardeen, DiLillo, Messman-
Moore, & Gratz, 2015). Further, scores on the
Measures of Emotion Dysregulation as DERS have been found to be heightened among
Maladaptive Responses to Emotions individuals with psychiatric disorders thought to be
Comprehensive characterized by emotion dysregulation, including
We are aware of only one comprehensive measure of BPD (Bornovalova et al., 2008; Gratz, Rosenthal,
emotion dysregulation based on Gratz and Roemer’s Tull, Lejuez, & Gunderson, 2006; Gratz, Tull,
(2004) conceptualization of this construct as Matusiewicz, Breetz, & Lejuez, 2013; Kuo &
maladaptive responses to emotions, the Difficulties Linehan, 2009), co-occurring BPD and substance
in Emotion Regulation Scale (DERS; Gratz & dependence (Gratz, Tull, Baruch, Bornovalova, &
Roemer, 2004). Notably, however, this measure is Lejuez, 2008), posttraumatic stress disorder (Tull,
widely used and has extensive empirical support. Barrett, McMillan, & Roemer, 2007), co-occurring
Specifically, the DERS is a comprehensive, 36-item, posttraumatic stress disorder and substance depend
self-report measure that assesses individuals’ typical ence (Weiss, Tull, Anestis, & Gratz, 2013), eating
levels of emotion dysregulation overall, as well as disorders (Harrison, Sullivan, Tchanturia, &
across a number of specific dimensions. Individuals Treasure, 2010), and social anxiety disorder (Blalock,
are asked to indicate how often the items apply to Kashdan, & Farmer, 2016). Finally, the DERS
themselves, with responses ranging from 1 to 5, demonstrates significant associations with a number
where 1 is “almost never (0%–10%),” 2 is “sometimes of constructs thought to be related to emotion dys-
(11%–35%),” 3 is “about half the time (36%–65%),” regulation, including positive associations with neg-
4 is “most of the time (66%–90%),” and 5 is “almost ative affect (Cisler, Olatunji, & Lohr, 2009; Johnson
always (91%–100%).” The DERS provides a total et al., 2008; Vujanovic et al., 2008), BPD pathology
score (ranging from 36 to 180) that represents over- (Fossati, Gratz, Somma, Maffei, & Borroni, 2016;
all emotion dysregulation, as well as six subscale Iverson, Follette, Pistorello, & Fruzzetti, 2012; Kuo,
scores: (1) nonacceptance of emotional responses Khoury, Metcalfe, Fitzpatrick, & Goodwill, 2015),
(e.g., “When I’m upset, I feel ashamed with myself anorexia nervosa symptom severity (Racine &
for feeling that way”); (2) difficulties engaging in Wildes, 2015), depression and anxiety symptom se-
goal-directed behaviors when distressed (e.g., “When verity (Abravanel & Sinha, 2015; Roemer et al.,
I’m upset, I have difficulty getting work done”); 2009; Tull, Stipelman, Salters-Pedneault, & Gratz,
(3) difficulties controlling impulsive behaviors 2009; Vujanovic et al., 2008), substance use coping

motives (Bonn-Miller, Vujanovic, Boden, & Gross, Sinha, 2011), and a group-based ACT for BPD
2011; Vujanovic, Marshall-Berenz, & Zvolensky, (Morton, Snowdon, Gopold, & Guymer, 2012),
2011), distress tolerance (Iverson et al., 2012), youth have found significant improvements in DERS
problem behaviors (Vasilev, Crowell, Beauchaine, scores from pre- to posttreatment. Further, studies
Mead, & Gatzke-Kopp, 2009), risky behaviors have also revealed significant improvements in
(Tull, Weiss, Adams, & Gratz, 2012; Weiss, Tull, DERS scores following inpatient, partial hospital-
Viana, Anestis, & Gratz, 2012), and experiential ization, and intensive outpatient treatments for sub-
avoidance (Gratz & Roemer, 2004; Iverson et al., stance use disorders and BPD (Fox et al., 2007;
2012; Tull & Gratz, 2008; Tull & Roemer, 2007), Gratz, Lacroce, & Gunderson, 2006).
and negative associations with emotional expression Notably, recent extensions of research on the
and processing (Johnson et al., 2008), mindfulness DERS have increased the clinical and research util-
(see Baer, Smith, Hopkins, Krietemeyer, & Toney, ity of this measure and its derivatives, resulting in
2006; Roemer et al., 2009), and self-compassion the development of state-based (S-DERS; Lavender,
(Roemer et al., 2009). Tull, DiLillo, Messman-Moore, & Gratz, 2017),
The DERS and its subscales are also associated positive emotion-specific (DERS-Positive; Weiss,
with objective measures of emotion dysregulation, Gratz, & Lavender, 2015), and brief (DERS-16;
including behavioral (Eichen, Chen, Boutelle, & Bjureberg et al., 2016) versions of this measure and
McCloskey, 2017; Gratz, Bornovalova, Delany- extending research on the psychometrics of the
Brumsey, Nick, & Lejuez, 2007; Gratz, Rosenthal, DERS to youth aged 10 and older (Neumann, van
et al., 2006; Gratz et al., 2013), neurological (Li, Lier, Gratz, & Koot, 2010; Perez, Venta, Garnaat, &
Huang, Yan, Bhagwagar, Milivojevic, & Sinha, Sharp, 2012; Sharp et al., 2011; Vasilev et al., 2009;
2008), and physiological (Vasilev et al., 2009; Weinberg & Klonsky, 2009). The availability of
Visted et al., 2017) measures. For example, the measures of both state emotion dysregulation and
DERS subscale of difficulties controlling impulsive positive emotion dysregulation increase the poten-
behaviors when distressed has been found to be tial scope of research on this construct. Likewise,
negatively associated with activation of the rostral the development of empirically supported brief ver-
anterior cingulate cortex (an area of the brain sions of the DERS is expected to increase the clini-
thought to be associated with inhibitory control) cal ease and feasibility of this measure, as well as the
among cocaine-dependent patients (Li et al., 2008). extent to which it is likely to be utilized in standard
Moreover, improvements in DERS scores following clinical and primary care settings. Indeed, a recent
12 months of dialectical behavior therapy (DBT) study found that three brief versions of the DERS
were significantly correlated with improved amyg- showed acceptable internal consistency and strong
dala habituation to repeated unpleasant pictures concordance with the original version, although the
(Goodman et al., 2014). original did account for additional variance in sev-
Finally, and speaking to the clinical relevance of eral clinical variables above and beyond the brief
both the DERS and the conceptualization of emo- versions of the measure (Hallion, Steinman, Tolin,
tion dysregulation on which it is based, extensive & Diefenbach, 2018). The authors conclude that
research demonstrates that the DERS is sensitive to the brief versions may be acceptable alternatives
change following psychological treatments. For to the original when participant or patient burden is
example, numerous studies have found significant a concern.
improvements in DERS scores following a brief
acceptance-based emotion regulation group therapy Dimension Specific
for women with self-injury and BPD (Gratz & Although there are certain subscales of other meas
Gunderson, 2006; Gratz, Tull, & Levy, 2014; Gratz ures that assess the converse of some of the dimen-
& Tull, 2011; Sahlin et al., 2017). Likewise, studies sions of emotion dysregulation as defined earlier
of DBT, cognitive-behavioral therapy (CBT), and (most notably, the private emotional attention sub-
acceptance and commitment therapy (ACT), in- scale of the Multidimensional Emotional Awareness
cluding CBT for bulimia nervosa and purging Questionnaire [Snell, 1999] and the attention to
disorder (MacDonald, McFarlane, Dionne, David, and clarity of feelings subscales of the Trait Meta-
& Olmsted, 2017), standard outpatient DBT Mood Scale [Salovey, Mayer, Goldman, Turvey, &
(Goodman et al., 2014), an adaptation of DBT for Palfai, 1995]), the Affective Control Scale (ACS;
the treatment of co-occurring BPD and substance Williams, Chambless, & Ahrens, 1997) is the only
use disorders (Axelrod, Perepletchikova, Holtzman, & measure of which we are aware that specifically

assesses one of these dimensions of emotion score and all subscale scores predicted greater
dysregulation. Specifically, developed to measure interference of film-related emotional material on a
fear of emotions (Williams et al., 1997), the 42-item modified emotional Stroop task (Salters-Pedneault
ACS assesses one aspect of the nonacceptance of et al., 2007). ACS scores have also been found to pre-
emotions in the form of a particular secondary emo- dict fear of laboratory-induced panic attack–related
tional response to emotions. The ACS consists of bodily sensations (Berg, Shapiro, Chambless, &
four subscales assessing fear of anxiety (e.g., “It Ahrens, 1998).
scares me when I am nervous”), anger (e.g., “I am Finally, and consistent with research on the
afraid that I will hurt someone if I get really DERS, there is considerable evidence that the ACS
furious”), depression (e.g., “Depression is scary to is sensitive to change following psychological inter-
me—I am afraid that I could get depressed and ventions. For example, individuals receiving an
never recover”), and positive emotion (e.g., “Being eight-week mindfulness-based stress reduction
filled with joy sounds great, but I am concerned that course demonstrated greater decreases in fears of de-
I could lose control over my actions if I get too expression and positive emotions from pre- to post-
cited”). A total score reflecting overall fear of emo- treatment compared to wait-list controls (Robins,
tions can also be obtained by summing the subscale Keng, Ekblad, & Brantley, 2012). Furthermore, these
scores. Participants rate each item based on the gains were maintained at two months posttreatment
extent to which the statement applies to them using (Robins et al., 2012). Significant improvements
a 7-point Likert-type scale ranging from 1 (very in ACS scores have also been found following
strongly disagree) to 7 (very strongly agree). transdiagnostic cognitive-behavioral treatment for
The ACS has been found to demonstrate signifi- emotional disorders (Sauer-Zavala et al., 2012),
cant associations with a variety of clinically relevant acceptance-based behavioral therapy for generalized
constructs. For example, ACS scores are positively anxiety disorder (Roemer & Orsillo, 2007), and a
associated with various forms of anxiety pathology 12-week DBT psychoeducation group among pa-
and related constructs, including generalized anxiety tients with bipolar disorder (Van Dijk, Jeffrey, &
disorder (Mennin, Heimberg, Turk, & Fresco, 2005; Katz, 2013).
Roemer, Salters, Raffa, & Orsillo, 2005), social anx-
iety disorder (Spokas, Luterek, & Heimberg, 2009), Conclusions and Future Directions
distress about obsessive-compulsive disorder symp- This review describes a variety of self-report meas
toms (Stern, Nota, Heimberg, Holaway, & Coles, ures of emotion dysregulation based on two distinct
2014), posttraumatic stress disorder symptom conceptualizations of this construct as involving (1)
severity (Tull et al., 2007), anxious arousal
dysregulated emotional responses (in the form of
(Werner-Seidler, Banks, Dunn, & Moulds, 2013), emotional sensitivity, reactivity, and/or intensity) or
worry (Roemer et al., 2005), and intolerance of un- (2) maladaptive responses to emotions regardless of
certainty (Lee, Orsillo, Roemer, & Allen, 2010). the quality of those emotions. An evaluation of
Likewise, higher ACS scores have been observed prominent measures consistent with both of these
among individuals with (vs. without) a history of conceptualizations of emotion dysregulation and
depression (Werner-Seidler et al., 2013) and are their dimensions suggests that both conceptualiza-
associated with greater anhedonia (Werner-Seidler tions are relevant to the presence and severity of
et al., 2013) and rumination (Giorgio et al., 2010). psychopathology, as all of the reviewed measures
ACS scores are also positively associated with BPD evidenced significant relations to a number of dif-
traits (even when controlling for emotional inten- ferent psychiatric difficulties. Together, this research
sity/reactivity; Yen et al., 2002). suggests that both emotional responses themselves
The ACS has also been found to predict re- and an individual’s responses to those emotions may
sponses to emotionally evocative stimuli within a evidence dysregulation and inform our understand-
laboratory setting. For example, overall fear of emo- ing of normal and abnormal development.
tion, as well as the fear of positive emotions, depres- Notably, however, the relevance of each of these
sion, and anxiety, predicted greater increases in conceptualizations of emotion dysregulation to the
negative affect and distress after watching a film pathogenesis and treatment of psychopathology is
clip depicting a sexual assault (Salters-Pedneault, less clear. In particular, despite evidence of signifi-
Gentes, & Roemer, 2007). Further, fear of positive cant relations of emotional intensity, reactivity,
emotions predicted increases in skin conductance in sensitivity, and lability to psychopathology, there is
response to the film clip, and both the overall ACS limited research suggesting that these emotion-related

traits are directly relevant to the development of to determine the way in which specific dimensions
psychopathology in the absence of other risk or vul- of the quality of emotions may affect specific re-
nerability factors, such as maladaptive responses to sponses to emotions and their subsequent influence
emotions. Indeed, studies show that relations be- on both the experience of those emotions and the
tween emotional intensity/reactivity and psychopa- occurrence of psychological symptoms. In addition,
thology weaken or become nonsignificant when treatment outcome research would benefit from in-
maladaptive responses to emotions are accounted corporating measures of both the quality of emo-
for (Gratz et al., 2008; Tull et al., 2007). Likewise, tions and maladaptive responses to emotions to
Dvorak et al. (2013) found that the association be- clarify the extent to which each of these is indeed
tween emotional lability and aggressive behaviors amenable to treatment, as well as the utility of tar-
was only significant in the context of high (vs. low) geting responses to emotions versus emotional expe-
levels of maladaptive responses to emotions (in the rience per se in psychological interventions.
form of difficulties controlling impulsive behaviors In addition, although there is considerable sup-
when distressed), and Gratz (2006) found that port for many of the self-report measures reviewed
emotional intensity/reactivity reliably distinguished here, much of this support comes from studies rely-
women with frequent self-harm from those without ing solely on self-report methods. Further research
self-harm only in the context of heightened levels of is needed to examine relations of self-report meas
both childhood maltreatment and emotional inex- ures of emotion dysregulation and its dimensions to
pressivity. Of course, the relative relevance of mal- objective measures of both emotional responses and
adaptive responses to emotions versus dysregulated maladaptive responses to emotions, such as psycho-
emotions per se to proximal psychological outcomes physiological measures (e.g., heart rate variability,
and functioning likely varies across development, skin conductance response, startle response), bio-
with the latter being more relevant in infancy and logical measures (e.g., cortisol reactivity), and be-
toddlerhood (prior to the development of metacog- havioral measures of emotion dysregulation and its
nitive awareness) and the former gaining relevance dimensions (e.g., Gratz et al., 2013). Although there
as children age. are some studies examining this question (particu-
Furthermore, there is almost no evidence that larly with regard to the associations of the DERS
traits of emotional intensity, reactivity, sensitivity, with behavioral measures; see Gratz, Rosenthal,
and/or lability change following treatment or are et al., 2006; Gratz et al., 2007, 2013), additional re-
amenable to psychological interventions (for excep- search is needed. Nonetheless, it is worth noting
tions, see Mennin et al., 2015, and Deckersbach et al., that studies utilizing behavioral measures of mal-
2012). As such, the clinical utility of this particu- adaptive responses to emotions have found differ-
lar conceptualization of emotion dysregulation ences in specific dimensions of emotion dysregula-
remains unclear. Conversely, there is extensive evi- tion as a function of the presence of psychopathology
dence that maladaptive responses to emotions, as (e.g., BPD, co-occurring posttraumatic stress disor-
assessed via the DERS and ACS, are sensitive to der) despite an absence of differences in emotional
change following psychological treatments, includ- reactivity to the tasks (e.g., Gratz, Rosenthal, et al.,
ing brief interventions designed specifically to target 2006; Tull, Gratz, Coffey, Weiss, & McDermott,
how individuals respond to their emotions (regard- 2013), suggesting that responses to emotions may
less of the nature or quality of those emotions; see, be more relevant to psychopathology than the emo-
e.g., Gratz & Gunderson, 2006; Gratz et al., 2014; tional response itself.
Roemer & Orsillo, 2007). Finally, as a field, we need to recognize that there
Nonetheless, additional research is needed to is likely variability in how individuals perceive
elucidate the relative contributions of each of these and respond to different emotions. Many of the
conceptualizations of emotion dysregulation to the measures described here (with the exception of the
development, maintenance, and treatment of psy- PERS, AIM, ACS, and DERS-Positive) focus on
chopathology. Specifically, future studies would the experience of negative (vs. positive) emotions,
benefit from examining the interplay between the and even fewer focus on discrete emotional states.
quality of one’s emotions and responses to those Nonetheless, researchers are beginning to recognize
emotions in the risk for specific forms of psychopa- that dysregulation of positive emotions may also in-
thology. For example, studies are needed that utilize crease risk for specific forms of psychopathology and
methodology (e.g., ecological momentary assessment, maladaptive behaviors (Gilbert, Nolen-Hoeksema,
experimental designs) that would allow researchers & Gruber, 2013; Weiss et al., 2015). In addition,

depending on an individual’s learning history, there Bornovalova, M. A., Gratz, K. L., Daughters, S. B., Nick, B.,
may be increased risk for dysregulated responding Delany-Brumsey, A., Lynch, T. R., . . . Lejuez, C. W. (2008).
A multimodal assessment of the relationship between
to some emotions versus others. For example, due emotion dysregulation and borderline personality disorder
to a history of invalidation, individuals with BPD among inner-city substance users in residential treatment.
may be more likely to experience dysregulated anger, Journal of Psychiatric Research, 42, 717–726.
shame, or guilt. Likewise, whereas individuals with Brownstone, L. M., Fitzsimmons-Craft, E. E., Wonderlich,
anxiety disorders may be more likely to experience S. A., Joiner, T. E., Le Grange, D., Mitchell, J. E., . . . Bardone-
Cone, A. M. (2013). Hard exercise, affect lability, and
dysregulation of fear and anxiety, those with de- personality among individuals with bulimia nervosa. Eating
pressive disorders may be more likely to experience Behaviors, 14, 413–419.
dysregulation of positive emotions and sadness. Carstensen, L. L., Turan, B., Scheibe, S., Ram, N., Ersner-
Unfortunately, there are currently very few meas- Hershfield, H., Samanez-Larkin, G. R., . . . Nesselroade, J. R.
ures (with the exception of the ALS and ACS) that (2011). Emotional experience improves with age: Evidence
based on over 10 years of experience sampling. Psychology
examine the dysregulation of specific emotional and Aging, 26, 21–33.
states. Thus, there may be utility in adapting extant Chapman, A. L., Gratz, K. L., & Brown, M. Z. (2006).
empirically supported measures of emotion dysreg- Solving the puzzle of deliberate self-harm: The experiential
ulation and its dimensions to assess the dysregula- avoidance model. Behaviour Research and Therapy, 44,
tion of specific emotional states, as was done with 371–394.
Cheavens, J. S., Rosenthal, M. Z., Daughters, S. B., Nowak, J.,
the DERS-Positive (a modification of the DERS; Kosson, D., Lynch, T. R., & Lejuez, C. W. (2005). An
Weiss et al., 2015). analogue investigation of the relationships among perceived
parental criticism, negative affect, and borderline personality
References disorder features: The role of thought suppression. Behaviour
Abravanel, B. T., & Sinha, R. (2015). Emotion dysregulation Research and Therapy, 43, 257–268.
mediates the relationship between lifetime cumulative adversity Cisler, J. M., Olatunji, B. O., & Lohr, J. M. (2009). Disgust
and depressive symptomatology. Journal of Psychiatric Research, sensitivity and emotion regulation potentiate the effect of
61, 89–96. disgust propensity on spider fear, blood-injection-injury
American Psychiatric Association. (2013). Diagnostic and fear, and contamination fear. Journal of Behavior Therapy and
statistical manual of mental disorders: DSM-5. Washington, Experimental Psychiatry, 40, 219–229.
DC: Author. Cole, P. M., Michel, M. K., & Teti, L. O. (1994). The
Axelrod, S. R., Perepletchikova, F., Holtzman, K., & Sinha, R. development of emotion regulation and dysregulation: A
(2011). Emotion regulation and substance use frequency in clinical perspective. Monographs of the Society for Research in
women with substance dependence and borderline personality Child Development, 59, 73–100.
disorder receiving dialectical behavior therapy. American Davidson, R. J. (1998). Affective style and affective disorders:
Journal of Drug and Alcohol Abuse, 37, 37–42. Perspectives from affective neuroscience. Cognition and
Baer, R. A., Smith, G. T., Hopkins, J., Krietemeyer, J., & Toney, Emotion, 12, 307–330.
L. (2006). Using self-report assessment methods to explore de Clercq, B., Van Leeuwen, K., Van Den Noortgate, W., De
facets of mindfulness. Assessment, 13, 27–45. Bolle, M., & De Fruyt, F. (2009). Childhood personality
Becerra, R., & Campitelli, G. (2013). Emotional reactivity: pathology: Dimensional stability and change. Development
Critical analysis and proposal of a new scale. International and Psychopathology, 21, 853–869.
Journal of Applied Psychology, 3, 161–168. Deckersbach, T., Hölzel, B. K., Eisner, L. R., Stange, J. P.,
Becerra, R., Preece, D., Campitelli, G., & Scott-Pillow, G. Peckham, A. D., Dougherty, D. D., . . . Nierenberg, A. A.
(2017). The assessment of emotional reactivity across negative (2012). Mindfulness-based cognitive therapy for nonremitted
and positive emotions: Development and validation of the patients with bipolar disorder. CNS Neuroscience and
Perth Emotional Reactivity Scale (PERS). Assessment, 1–13. Therapeutics, 18, 133–141.
Berg, C. Z., Shapiro, N., Chambless, D. L., & Ahrens, A. H. Dir, A. L., Karyadi, K., & Cyders, M. A. (2013). The uniqueness
(1998). Are emotions frightening? II: An analogue study of of negative urgency as a common risk factor for self-harm
fear of emotion, interpersonal conflict, and panic onset. behaviors, alcohol consumption, and eating problems.
Behaviour Research and Therapy, 36, 3–15. Addictive Behaviors, 38, 2158–2162.
Bjureberg, J., Ljótsson, B., Tull, M. T., Hedman, E., Sahlin, H., Dvorak, R. D., & Day, A. M. (2014). Marijuana and self-
Lundh, L., & . . . Gratz, K. L. (2016). Development and regulation: Examining likelihood and intensity of use and
validation of a brief version of the Difficulties in Emotion problems. Addictive Behaviors, 39, 709–712.
Regulation Scale: The DERS-16. Journal of Psychopathology Dvorak, R. D., Pearson, M. R., & Kuvaas, N. J. (2013). The five-
and Behavioral Assessment, 38, 284–296. factor model of impulsivity-like traits and emotional lability
Blalock, D. V., Kashdan, T. B., & Farmer, A. S. (2016). Trait and in aggressive behavior. Aggressive Behavior, 39, 222–228.
daily emotion regulation in social anxiety disorder. Cognitive Eichen, D. M., Chen, E., Boutelle, K. N., & McCloskey, M. S.
Therapy and Research, 40, 416–425. (2017). Behavioral evidence of emotion dysregulation in
Bonn-Miller, M. O., Vujanovic, A. A., Boden, M. T., & Gross, binge eaters. Appetite, 111, 1–6.
J. J. (2011). Posttraumatic stress, difficulties in emotion Ekman, P., & Davidson, R. J. (1994). The nature of emotion:
regulation, and coping-oriented marijuana use. Cognitive Fundamental questions. New York, NY: Oxford University
Behaviour Therapy, 40, 34–44. Press.

Evans, S. C., Blossom, J. B., Canter, K. S., Poppert-Cordts, K., Gratz, K. L., Dixon-Gordon, K. L., & Whalen, D. (2016). Dark
Kanine, R., Garcia, A., & Roberts, M. C. (2016). Self- side of the mood or sweet emotion? Toward a more nuanced
reported emotion reactivity among early-adolescent girls: understanding of emotional lability. In V. Zeigler-Hill &
Evidence for convergent and discriminant validity in an D. K. Marcus (Eds.), The dark side of personality. New York,
urban community sample. Behavior Therapy, 47, 299–311. NY: American Psychological Association.
Flett, G. L., Blankstein, K. R., & Obertynski, M. (1996). Affect Gratz, K. L., & Gunderson, J. G. (2006). Preliminary data on
intensity, coping styles, mood regulation expectancies, and acceptance-based emotion regulation group intervention
depressive symptoms. Personality and Individual Differences, for deliberate self-harm among women with borderline
20, 221–228. personality disorder. Behavior Therapy, 37, 25–35.
Flett, G. L., & Hewitt, P. L. (1995). Criterion validity and Gratz, K. L., Lacroce, D. M., & Gunderson, J. G. (2006).
psychometric properties of the affect intensity measure in a Measuring changes in symptoms relevant to borderline
psychiatric sample. Personality and Individual Differences, 19, personality disorder following short-term treatment across
585–591. partial hospital and intensive outpatient levels of care. Journal
Fossati, A., Gratz, K. L., Somma, A., Maffei, C., & Borroni, S. of Psychiatric Practice, 12, 153–159.
(2016). The mediating role of emotion dysregulation in Gratz, K. L., Paulson, A., Jakupcak, M., & Tull, M. T. (2009).
the relations between childhood trauma history and adult Exploring gender differences in the relationship between
attachment and borderline personality disorder features: A childhood maltreatment and intimate partner abuse: The
study of Italian nonclinical participants. Journal of Personality mediating role of emotion dysregulation. Violence and
Disorders, 30, 653–676. Victims, 24, 68–82.
Fox, H., Axelrod, S., Paliwal, P., Sleeper, J., & Sinha, R. (2007). Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment
Difficulties in emotion regulation and impulse control of emotion regulation and dysregulation: Development,
during cocaine abstinence. Drug and Alcohol Dependence, 89, factor structure, and initial validation of the Difficulties in
298–301. Emotion Regulation Scale. Journal of Psychopathology and
Frantom, C., & Sherman, M. F. (1999). At what price art? Behavioral Assessment, 26, 41–54.
Affective instability within a visual art population. Creativity Gratz, K. L., & Roemer, L. (2008). The relationship between
Research Journal, 12, 15–23. emotion dysregulation and deliberate self-harm among female
Gilbert, K. E., Nolen-Hoeksema, S., & Gruber, J. (2013). undergraduate students at an urban commuter university.
Positive emotion dysregulation across mood disorders: How Cognitive Behaviour Therapy, 37, 14–25.
amplifying versus dampening predicts emotional reactivity Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., &
and illness course. Behaviour Research and Therapy, 51, Gunderson, J. G. (2006). An experimental investigation of
736–741. emotion dysregulation in borderline personality disorder.
Giorgio, J. M., Sanflippo, J., Kleiman, E., Reilly, D., Bender, Journal of Abnormal Psychology, 115, 850–855.
R. E., Wagner, C. A., . . . Alloy, L. B. (2010). An experiential Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., &
avoidance conceptualization of depressive rumination: Three Gunderson, J. G. (2010). An experimental investigation of
tests of the model. Behaviour Research and Therapy, 48, emotional reactivity and delayed emotional recovery in
1021–1031. borderline personality disorder: The role of shame.
Glenn, C. R., Blumenthal, T. D., Klonsky, E. D., & Hajcak, G. Comprehensive Psychiatry, 51, 275–285.
(2011). Emotional reactivity in nonsuicidal self-injury: Gratz, K. L., & Tull, M. T. (2010). The relationship between
Divergence between self-report and startle measures. emotion dysregulation and deliberate self-harm among
International Journal of Psychophysiology, 80, 166–170. inpatient substance users. Cognitive Therapy and Research,
Goodman, M., Carpenter, D., Tang, C. Y., Goldstein, K. E., 34, 544–553.
Avedon, J., Fernandez, N., .
.
.
Hazlett, E. A. (2014). Gratz, K. L., & Tull, M. T. (2011). Extending research on the
Dialectical behavior therapy alters emotion regulation and utility of an adjunctive emotion regulation group therapy
amygdala activity in patients with borderline personality for deliberate self-harm among women with borderline
disorder. Journal of Psychiatric Research, 57, 108–116. personality pathology. Personality Disorders: Theory, Research,
Gratz, K. L. (2006). Risk factors for deliberate self-harm and Treatment, 2, 316–326.
among female college students: The role and interaction of Gratz, K. L., Tull, M. T., Baruch, D. E., Bornovalova, M. A., &
childhood maltreatment, emotional inexpressivity, and Lejuez, C. W. (2008). Factors associated with co-occurring
affect intensity/reactivity. American Journal of Orthopsychiatry, borderline personality disorder among inner-city substance
76, 238–250. users: The roles of childhood maltreatment, negative affect
Gratz, K. L. (2007). Targeting emotion dysregulation in the intensity/reactivity, and emotion dysregulation. Comprehensive
treatment of self-injury. Journal of Clinical Psychology, 63, Psychiatry, 49, 603–615.
1091–1103. Gratz, K. L., Tull, M. T., & Levy, R. (2014). Randomized
Gratz, K. L., Bornovalova, M. A., Delany-Brumsey, A., Nick, B., controlled trial and uncontrolled 9-month follow-up of an
& Lejuez, C. W. (2007). A laboratory-based study of the adjunctive emotion regulation group therapy for deliberate
relationship between childhood abuse and experiential self-harm among women with borderline personality disorder.
avoidance among inner-city substance users: The role of Psychological Medicine, 44, 2099–2112.
emotional nonacceptance. Behavior Therapy, 38, 256–268. Gratz, K. L., Tull, M. T., Matusiewicz, A. M., Breetz, A. A., &
Gratz, K. L., & Chapman, A. L. (2007). The role of emotional Lejuez, C. W. (2013). Multimodal examination of emotion
responding and childhood maltreatment in the development regulation difficulties as a function of co-occurring avoidant
and maintenance of deliberate self-harm among male personality disorder among women with borderline
undergraduates. Psychology of Men and Masculinity, personality disorder. Personality Disorders: Theory, Research,
8, 1–14. and Treatment, 4, 304–314.

Gratz, K. L., Weiss, N. H., & Tull, M. T. (2015). Examining Kuvaas, N. J., Dvorak, R. D., Pearson, M. R., Lamis, D. A., &
emotion regulation as an outcome, mechanism, or target Sargent, E. M. (2014). Self-regulation and alcohol use
of psychological treatment. Current Opinion in Psychology, involvement: A latent class analysis. Addictive Behaviors, 39,
3, 85–90. 146–152.
Gunderson, J. G., Zanarini, M. C., & Kisiel, C. L. (1996). Lannoy, S., Heeren, A., Rochat, L., Rossignol, M., Van der Linden,
Borderline personality disorder. In W. J. Livesley (Eds.), The M., & Billieux, J. (2014). Is there an all-embracing construct
DSM-IV personality disorders (pp. 141–157). New York, NY: of emotion reactivity? Adaptation and validation of the
Guilford Press. emotion reactivity scale among a French-speaking community
Gunnar, M. R., Mangelsdorf, S., Larson, M., & Hertsgaard, L. sample. Comprehensive Psychiatry, 55, 1960–1967.
(1989). Attachment, temperament, and adrenocortical Larsen, R. J., & Diener, E. (1985). A multitrait–multimethod
activity in infancy: A study of psychoendocrine regulation. examination of affect structure: Hedonic level and
Developmental Psychology, 25, 355–363. emotional intensity. Personality and Individual Differences,
Hallion, L. S., Steinman, S. A., Tolin, D. F., & Diefenbach, 6, 631–636.
G. J. (2018). Psychometric properties of the Difficulties Larsen, R. J., & Diener, E. (1987). Affect intensity as an
in Emotion Regulation Scale (DERS) and its short forms individual difference characteristic: A review. Journal of
in adults with emotional disorders. Frontiers in Psychology, Research in Personality, 21, 1–39.
9, 539. Larsen, R. J., Diener, E., & Emmons, R. A. (1986). Affect
Harrison, A., Sullivan, S., Tchanturia, K., & Treasure, J. (2010). intensity and reactions to daily life events. Journal of
Emotional functioning in eating disorders: Attentional bias, Personality and Social Psychology, 51, 803–814.
emotion recognition and emotion regulation. Psychological Lavender, J. M., Tull, M. T., DiLillo, D., Messman-Moore, T., &
Medicine, 40, 1887–1897. Gratz, K. L. (2017). Development and validation of a state-
Harvey, P. D., Greenberg, B. R., & Serper, M. R. (1989). The based measure of emotion dysregulation: The State Difficulties
Affective Lability Scales: Development, reliability and validity. in Emotion Regulation Scale (S-DERS). Assessment, 24,
Journal of Clinical Psychology, 45, 786–793. 197–209.
Hayes, S. C., Luoma, J. B., Bond, F. W., Masuda, A., & Lillis, J. Lee, J. K., Orsillo, S. M., Roemer, L., & Allen, L. B. (2010).
(2006). Acceptance and commitment therapy: Model, Distress and avoidance in generalized anxiety disorder:
processes and outcomes. Behaviour Research and Therapy, Exploring the relationships with intolerance of uncertainty
44, 1–25. and worry. Cognitive Behaviour Therapy, 39, 126–136.
Henry, C., Van den Bulke, D., Bellivier, F., Roy, I., Swendsen, J., Li, C. R., Huang, C., Yan, P., Bhagwagar, Z., Milivojevic, V., &
Bailara, K. M., . . . Leboyer, M. (2008). Affective lability and Sinha, R. (2008). Neural correlates of impulse control
affect intensity as core dimensions of bipolar disorders during during stop signal inhibition in cocaine-dependent men.
euthymic period. Psychiatry Research, 159, 1–6. Neuropsychopharmacology, 33, 1798–1806.
Hernandez, A., Gutiérrez, F., Valero, J., Gárriz, M., Labad, A., & Linehan, M. M. (1993). Cognitive-behavioral treatment of
Gutiérrez-Zotes, J. A. (2009). A genetic-behavioral alternative borderline personality disorder. New York, NY: Guilford Press.
to the personality disorders: The Livesley dimensional model. Livesley, W. J. (2002). Treating the emotional dysregulation
Actas Españolas de Psiquiatría, 37, 174–182. cluster of traits. Psychiatric Annals, 32, 601–607.
Iverson, K. M., Follette, V. M., Pistorello, J., & Fruzzetti, A. E. Livesley, W. J., & Jackson, D. N. (2002). Manual for the
(2012). An investigation of experiential avoidance, emotion dimensional assessment of personality problems-Basic
dysregulation, and distress tolerance in young adult questionnaire. London, UK: Research Psychologists’ Press.
outpatients with borderline personality disorder symptoms. Livesley, W. J., Jang, K. L., & Vernon, P. A. (1998). Phenotypic
Personality Disorders: Theory, Research, and Treatment, 3, and genetic structure of traits delineating personality
415–422. disorder. Archives of General Psychiatry, 55, 941–948.
Johnson, K. A., Zvolensky, M., Marshall, E. C., Gonzalez, A., Look, A. E., Flory, J. D., Harvey, P. D., & Siever, L. J. (2010).
Abrams, K., & Vujanovicv, A. A. (2008). Linkages between Psychometric properties of short form of the Affect Lability
cigarette smoking outcome expectancies and negative Scale (ALS-18). Personality and Individual Differences, 49,
emotional vulnerability. Addictive Behaviors, 33, 1416–1424. 187–191.
Koenigsberg, H. W., Harvey, P. D., Mitropoulou, V., Schmeidler, MacDonald, D. E., McFarlane, T. L., Dionne, M. M., David,
J., New, A. S., Goodman, M., . . . Siever, L. J. (2002). L., & Olmsted, M. P. (2017). Rapid response to intensive
Characterizing affective instability in borderline personality treatment for bulimia nervosa and purging disorder: A
disorder. American Journal of Psychiatry, 159, 784–788. randomized controlled trial of a CBT intervention to
Koval, P., Pe, M. L., Meers, K., & Kuppens, P. (2013). Affect facilitate early behavior change. Journal of Consulting and
dynamics in relation to depressive symptoms: Variable, Clinical Psychology, 85, 896–908.
unstable or inert? Emotion, 13, 1132–1141. Markey, M. A., & Vander Wal, J. S. (2007). The role of emotional
Kuo, J. R., Khoury, J. E., Metcalfe, R., Fitzpatrick, S., & intelligence and negative affect in bulimic symptomatology.
Goodwill, A. (2015). An examination of the relationship Comprehensive Psychiatry, 48, 458–464.
between childhood emotional abuse and borderline Marshall-Berenz, E. C., Morrison, J. A., Schumacher, J. A., &
personality disorder features: The role of difficulties with Coffey, S. F. (2011). Affect intensity and lability: The role of
emotion regulation. Child Abuse and Neglect, 39, 147–155. posttraumatic stress disorder symptoms in borderline
Kuo, J. R., & Linehan, M. M. (2009). Disentangling emotion personality disorder. Depression and Anxiety, 28, 393–399.
processes in borderline personality disorder: Physiological McGlashan, T. H., Grilo, C. M., Sanislow, C. A., Ralevski, E.,
and self-reported assessment of biological vulnerability, Morey, L. C., Gunderson, J. G., . . . Pagano, M. (2005). Two-
baseline intensity, and reactivity to emotionally evocative year prevalence and stability of individual DSM-IV criteria
stimuli. Journal of Abnormal Psychology, 118, 531–544. for schizotypal, borderline, avoidant, and obsessive-compulsive

personality disorders: Toward a hybrid model of axis II Roemer, L., Salters, K., Raffa, S. D., & Orsillo, S. M. (2005).
disorders. American Journal of Psychiatry, 162, 883–889. Fear and avoidance of internal experiences in GAD:
Mennin, D. S., Fresco, D. M., Ritter, M., & Heimberg, R. G. Preliminary tests of a conceptual model. Cognitive Therapy
(2015). An open trial of emotion regulation therapy for and Research, 29, 71–88.
generalized anxiety disorder and cooccurring depression. Rottenberg, J., Kasch, K. L., Gross, J. J., & Gotlib, I. H. (2002).
Depression and Anxiety, 32, 539–634. Sadness and amusement reactivity differentially predict
Mennin, D. S., Heimberg, R. G., Turk, C. L., & Fresco, D. M. concurrent and prospective functioning in major depressive
(2005). Preliminary evidence for an emotion dysregulation disorder. Emotion, 2, 135–146.
model of generalized anxiety disorder. Behaviour Research Sahlin, H., Bjureberg, J., Gratz, K. L., Tull, M. T., Hedman, E.,
and Therapy, 43, 1281–1310. Bjärehed, J., . . ., Hellner, C. (2017). Emotion regulation
Mennin, D. S., McLaughlin, K. A., & Flanagan, T. J. (2009). group therapy for deliberate self-harm: A multi-site evaluation
Emotion regulation deficits in generalized anxiety disorder, in routine care using an uncontrolled open trial design. BMJ
social anxiety disorder, and their co-occurrence. Journal of Open, 7(10):e016220.
Anxiety Disorders, 23, 866–871. Salovey, P., Mayer, J. D., Goldman, S. L., Turvey, C., & Palfai,
Morton, J., Snowdon, S., Gopold, M., & Guymer, E. (2012). T. P. (1995). Emotional attention, clarity, and repair:
Acceptance and commitment therapy group treatment for Exploring emotional intelligence using the Trait Meta-Mood
symptoms of borderline personality disorder: A public Scale. In J. W. Pennebaker (Ed.), Emotion, disclosure, and
sector pilot study. Cognitive and Behavioral Practice, 19, health (pp. 125–154). Washington, DC: American Psychological
527–544. Association.
Najmi, S., Wegner, D. M., & Nock, M. K. (2007). Thought Salters-Pedneault, K., Gentes, E., & Roemer, L. (2007). The role
suppression and self-injurious thoughts and behaviors. of fear of emotion in distress, arousal, and cognitive
Behaviour Research and Therapy, 45, 1957–1965. interference following an emotional stimulus. Cognitive
Neumann, A., van Lier, P. C., Gratz, K. L., & Koot, H. M. Behaviour Therapy, 36, 12–22.
(2010). Multidimensional assessment of emotion regulation Salters-Pedneault, K., Roemer, L., Tull, M. T., Rucker, L., &
difficulties in adolescents using the Difficulties in Emotion Mennin, D. S. (2006). Evidence of broad deficits in
Regulation Scale. Assessment, 17, 138–149. emotion regulation associated with chronic worry and
Newhill, C. E., Bell, M. M., Eack, S. M., & Mulvey, E. P. (2010). generalized anxiety disorder. Cognitive Therapy and Research,
Confirmatory factor analysis of the Emotion Dysregulation 30, 4 69–480.
Measure. Journal of the Society for Social Work and Research, 1, Sauer-Zavala, S., Boswell, J. F., Gallagher, M. W., Bentley, K. H.,
159–168. Ametaj, A., & Barlow, D. H. (2012). The role of negative
Newhill, C. E., Mulvey, E. P., & Pilkonis, P. A. (2004). Initial affectivity and negative reactivity to emotions in predicting
development of a measure of emotion dysregulation for outcomes in the unified protocol for the transdiagnostic
individuals with Cluster B personality disorders. Research on treatment of emotional disorders. Behaviour Research and
Social Work Practice, 14, 443–449. Therapy, 50, 551–557.
Nock, M. K., Wedig, M. M., Holmberg, E. B., & Hooley, J. M. Sharp, C., Pane, H., Ha, C., Venta, A., Patel, A. B., Sturek, J., &
(2008). The emotion reactivity scale: Development, evaluation, Fonagy, P. (2011). Theory of mind and emotion regulation
and relation to self-injurious thoughts and behaviors. Behavior difficulties in adolescents with borderline traits. Journal of the
Therapy, 39, 107–116. American Academy of Child and Adolescent Psychiatry, 50,
Oliver, M. N. I., & Simmons, J. A. (2004). The Affective Lability 563–573.
Scales: Development of a short-form measure. Personality Simons, J. S., Oliver, M. N. I., Gaher, R. M., Ebel, G., &
and Individual Differences, 37, 1279–1288. Brummels, P. (2005). Methamphetamine and alcohol abuse
Perez, J., Venta, A., Garnaat, S., & Sharp, C. (2012). The and dependence symptoms: Associations with affect lability
Difficulties in Emotion Regulation Scale: Factor structure and impulsivity in a rural treatment population. Addictive
and association with nonsuicidal self-injury in adolescent Behaviors, 30, 1370–1381.
inpatients. Journal of Psychopathology and Behavioral Assessment, Snell, W. E., Jr. (1999). The multidimensional emotional awareness
34, 393–404. questionnaire. Unpublished measure. Cape Girardeau, MO:
Racine, S. E., & Wildes, J. E. (2015). Dynamic longitudinal Southeast Missouri State University.
relations between emotion regulation difficulties and Snorrason, Í., Smári, J., & Ólafsson, R. P. (2010). Emotion
anorexia nervosa symptoms over the year following intensive regulation in pathological skin picking: Findings from a non-
treatment. Journal of Consulting and Clinical Psychology, 83, treatment seeking sample. Journal of Behavior Therapy and
785–795. Experimental Psychiatry, 41, 238–245.
Robins, C. J., Keng, S., Ekblad, A. G., & Brantley, J. G. (2012). Solhan, M. B., Trull, T. J., Jahng, S., & Wood, P. K. (2009).
Effects of mindfulness-based stress reduction on emotional Clinical assessment of affective instability: Comparing
experience and expression: A randomized controlled trial. EMA indices, questionnaire reports, and retrospective recall.
Journal of Clinical Psychology, 68, 117–131. Psychological Assessment, 21, 425–436.
Roemer, L., Lee, J. K., Salters-Pedneault, K., Erisman, S. M., Spokas, M., Luterek, J. A., & Heimberg, R. G. (2009). Social
Orsillo, S. M., & Mennin, D. S. (2009). Mindfulness and anxiety and emotional suppression: The mediating role of
emotion regulation difficulties in generalized anxiety disorder: beliefs. Journal of Behavior Therapy and Experimental
Preliminary evidence for independent and overlapping Psychiatry, 40, 283–291.
contributions. Behavior Therapy, 40, 142–154. Stern, M. R., Nota, J. A., Heimberg, R. G., Holaway, R. M., &
Roemer, L., & Orsillo, S. M. (2007). An open trial of an Coles, M. E. (2014). An initial examination of emotion
acceptance-based behavior therapy for generalized anxiety regulation and obsessive compulsive symptoms. Journal of
disorder. Behavior Therapy, 38, 72–85. Obsessive-Compulsive and Related Disorders, 3, 109–114.

Stone, A. A., Bachrach, C. A., Jobe, J. B., Kurtzman, H. S., & Turner, K. (2010). The promotion of successful aging through
Cain, V. S. (2000). The science of self-report: Implications mindfulness skills training (Doctoral dissertation). Retrieved
for research and practice. Mahwah, NJ: Lawrence Erlbaum from http://repository.upenn.edu/edissertations_sp2/1.
Associates. Van Dijk, S., Jeffrey, J., & Katz, M. R. (2013). A randomized,
Svetieva, E., & Frank, M. G. (2016). Empathy, emotion controlled, pilot study of dialectical behavior therapy skills in
dysregulation, and enhanced microexpression recognition a psychoeducational group for individuals with bipolar
ability. Motivation and Emotion, 40, 309–320. disorder. Journal of Affective Disorders, 145, 386–393.
Thompson, R. A. (1994). Emotion regulation: A theme in search Vasilev, C. A., Crowell, S. E., Beauchaine, T. P., Mead, H. K.,
of definition. Monographs of the Society for Research in Child & Gatzke-Kopp, L. M. (2009). Correspondence between
Development, 59, 25–52. physiological and self-report measures of emotion
Thompson, R. A., & Calkins, S. D. (1996). The double-edged dysregulation: A longitudinal investigation of youth with
sword: Emotional regulation for children at risk. Development and without psychopathology. Journal of Child Psychology
and Psychopathology, 8, 163–182. and Psychiatry, 50, 1357–1364.
Thompson, R. J., Dizén, M., & Berenbaum, H. (2009). The Visted, E., Sørensen, L., Osnes, B., Svendsen, J. L., Binder, P., &
unique relations between emotional awareness and facets of Schanche, E. (2017). The association between self-reported
affective instability. Journal of Research in Personality, 43, difficulties in emotion regulation and heart rate variability:
875–879. The salient role of not accepting negative emotions. Frontiers
Tull, M. T., Bardeen, J. R., DiLillo, D., Messman-Moore, T., & in Psychology, 8, 328.
Gratz, K. L. (2015). A prospective investigation of emotion Vujanovic, A. A., Marshall-Berenz, E. C., & Zvolensky, M. J.
dysregulation as a moderator of the relation between (2011). Posttraumatic stress and alcohol use motives: A test of
posttraumatic stress symptoms and substance use severity. the incremental and mediating role of distress tolerance.
Journal of Anxiety Disorders, 29, 52–60. Journal of Cognitive Psychotherapy, 25, 130–141.
Tull, M. T., Barrett, H. M., McMillan, E. S., & Roemer, L. Vujanovic, A. A., Zvolensky, M. J., & Bernstein, A. (2008).
(2007). A preliminary investigation of the relationship The interactive effects of anxiety sensitivity and emotion
between emotion regulation difficulties and posttraumatic dysregulation in predicting anxiety-related cognitive and
stress symptoms. Behavior Therapy, 38, 303–313. affective symptoms. Cognitive Therapy and Research, 32,
Tull, M. T., Bornovalova, M. A., Patterson, R., Hopko, D. R., & 803–817.
Lejuez, C. W. (2008). Analogue research. In D. McKay Vujanovic, A. A., Zlovensky, M. J., Gibson, L. E., Lynch, T. R.,
(Ed.), Handbook of research methods in abnormal and Leen-Feldner, E. W., Feldner, M. T., & Bernstein, A.
clinical psychology (pp. 61–78). Thousand Oaks, CA: Sage (2006). Affect intensity: Association with anxious and
Publications. fearful responding to bodily sensations. Anxiety Disorders, 20,
Tull, M. T., & Gratz, K. L. (2008). Further examination of the 192–206.
relationship between anxiety sensitivity and depression: The Weinberg, A., & Klonsky, E. D. (2009). Measurement of
mediating role of experiential avoidance and difficulties emotion dysregulation in adolescents. Psychological Assessment,
engaging in goal-directed behavior when distressed. Journal 21, 616–621.
of Anxiety Disorders, 22, 199–210. Weinfurt, K. P., Bryant, F. B., & Yarnold, P. R. (1994). The factor
Tull, M. T., Gratz, K. L., Coffey, S. F., Weiss, N. H., & structure of the Affect Intensity Measure: In search of a
McDermott, M. J. (2013). Examining the interactive effect measurement model. Journal of Research in Personality, 28,
of posttraumatic stress disorder, distress tolerance, and 314–331.
gender on residential substance use disorder treatment Weiss, N. H., Gratz, K. L., & Lavender, J. M. (2015). Factor
retention. Psychology of Addictive Behaviors, 27, 763–773. structure and initial validation of a multidimensional
Tull, M. T., Jakupcak, M., McFadden, M. E., & Roemer, L. measure of difficulties in the regulation of positive emotions:
(2007). The role of negative affect intensity and the fear of The DERS-Positive. Behavior Modification, 39, 431–453.
emotions in posttraumatic stress symptom severity among Weiss, N. H., Tull, M. T., Anestis, M. D., & Gratz, K. L. (2013).
victims of childhood interpersonal violence. Journal of The relative and unique contributions of emotion dysregulation
Nervous and Mental Disease, 195, 580–587. and impulsivity to post-traumatic stress disorder among
Tull, M. T., & Roemer, L. (2007). Emotion regulation difficulties substance dependent patients. Drug and Alcohol Dependence,
associated with the experience of uncued panic attacks: 128, 45–51.
Evidence of experiential avoidance, emotional nonacceptance, Weiss, N. H., Tull, M. T., Viana, A. G., Anestis, M. D., & Gratz,
and decreased emotional clarity. Behavior Therapy, 38, K. L. (2012). Impulsive behaviors as an emotion regulation
378–391. strategy: Examining associations between PTSD, emotion
Tull, M. T., Stipelman, B. A., Salters-Pedneault, K., & Gratz, dysregulation, and impulsive behaviors among substance
K. L. (2009). An examination of recent non-clinical panic dependent inpatients. Journal of Anxiety Disorders, 26,
attacks, panic disorder, anxiety sensitivity, and emotion 453–458.
regulation difficulties in the prediction of generalized anxiety Werner-Seidler, A., Banks, R., Dunn, B. D., & Moulds, M. L.
disorder in an analogue sample. Journal of Anxiety Disorders, (2013). An investigation of the relationship between positive
23, 275–282. affect regulation and depression. Behaviour Research and
Tull, M. T., Weiss, N. H., Adams, C. E., & Gratz, K. L. Therapy, 51, 46–56.
(2012). The contribution of emotion regulation difficulties Whiteside, U., Chen, E., Neighbors, C., Hunter, D., Lo, T., &
to risky sexual behavior within a sample of patients in Larimer, M. (2007). Difficulties regulating emotions: Do
residential substance abuse treatment. Addictive Behaviors, binge eaters have fewer strategies to modulate and tolerate
37, 1084–1092. negative affect? Eating Behaviors, 8, 162–169.

Williams, K. E., Chambless, D. L., & Ahrens, A. (1997). Are Yen, S., Zlotnick, C., & Costello, E. (2002). Affect regulation in
emotions frightening? An extension of the fear of fear women with borderline personality disorder traits. Journal of
construct. Behaviour Research and Therapy, 35, 239–248. Nervous and Mental Disease, 190, 693–696.
Wolff, S., Stiglmayr, C., Bretz, H. J., Lammers, C. H., & Zanarini, M. C., Frankenburg, F. R., Hennen, J., & Silk, K. R.
Auckenthaler, A. (2007). Emotion identification and (2003). The longitudinal course of borderline
tension in female patients with borderline personality psychopathology: 6-year prospective follow-up of the
disorder. British Journal of Clinica Psychology, 46, phenomenology of borderline personality disorder. American
347–360. Journal of Psychiatry, 160, 274–283.

CH A PT E R
Assessment of Emotion
28 Dysregulation Using Ecological
Momentary Assessment
Heather T. Schatten, Kenneth J. D. Allen, and Michael F. Armey
Abstract
As emotion is a dynamic construct, ecological momentary assessment (EMA) methods, which gather
data at multiple time points in individuals’ real-world environments, in the moment, are particularly
well suited to measure emotion dysregulation and related constructs. EMA methods can identify
contextual events that prompt or follow an emotional response. This chapter provides an overview of
traditional methods of studying emotion dysregulation and how EMA can be used to capture emotion
dysregulation in daily life, both within and independent of psychiatric diagnoses. It reviews the literature
on emotion dysregulation and related constructs within specific diagnoses (e.g., depression, bipolar
disorder, borderline personality disorder, and eating disorders) and behaviors (e.g., suicide, nonsuicidal
self-injury, and alcohol use). Finally, it discusses future directions in EMA research, as well as its
implications for psychological treatment.
Keywords: ecological momentary assessment (EMA), emotion, emotion dysregulation, experience

sampling, mobile devices
Introduction and review findings from EMA studies across a

In its simplest form, emotion regulation has been variety of diagnoses and problem behaviors.
defined as the “processes by which individuals influ-
ence which emotions they have, when they have Traditional Measures of Emotion
them, and how they experience and express these Dysregulation
emotions” (Gross, 1998, p. 275). Elaborating on Traditionally, emotion dysregulation has been meas-
this definition, Gratz and Roemer (2004) note that ured as a static construct using self-report measures
emotion regulation involves “(a) awareness and un- or observed behavior. For example, the Difficulties
derstanding of emotions, (b) acceptance of emotions, in Emotion Regulation Scale (DERS; Gratz &
(c) ability to control impulsive behaviors and behave Roemer, 2004) is a widely-used self-report measure
in accordance with desired goals when experiencing that asks respondents to rate emotion regulation
negative emotions, and (d) ability to use situation- difficulties when distressed; shorter versions have
ally appropriate emotion regulation strategies flexi- been recently introduced (Hallion, Steinman, Tolin,
bly to modulate emotional responses as desired in & Diefenbach, 2018). Behavioral paradigms have
order to meet individual goals and situational de- been developed to capture different aspects of emo-
mands” (pp. 42–43). For our purposes, we adopt a tion reactivity and regulation, such as emotional
definition of emotion dysregulation that encapsulates versions of the Attention Network Task (Tully,
difficulties in any of these areas. We briefly review Lincoln, & Hooker, 2012) and Stroop tests, which
traditional approaches to assessment of emotion dys- examine interference control over emotional in-
regulation, introduce the utility of ecological momen- formation (see Mathews & MacLeod, 2005, for a
tary assessment (EMA) of emotion dysregulation, review); emotional go/no-go (Hare et al., 2008) and
411
emotional stop-signal tasks (Allen & Hooley, 2015; an emotional response. In this chapter, we review
Allen & Hooley, 2018), which assess emotional re- ways in which EMA is well suited to capture emo-
sponse inhibition; and the Trier Social Stress Test tion dysregulation in daily life, both within and in-
(Kirschbaum, Pirke, & Hellhammer, 1993), a stress dependent of psychiatric problems.
induction used to evaluate physiological stress, in-
cluding adrenocorticotropin (ACTH) and cortisol Ecological Momentary Assessment
responses. EMA encapsulates a set of methods employed to
Psychophysiological assessments can also capture better understand the phenomenology of a particu-
emotion dysregulation, if stimulus conditions are lar emotion, behavior, or cognition within the con-
carefully controlled. For example, respiratory sinus text of participants’ real-world experiences (Bolger,
arrhythmia (RSA; also known as heart rate variabil- Davis, & Rafaeli, 2003). These methods are partic-
ity, cardiac vagal control, or vagal tone) appears to ularly useful when researchers are interested in un-
mark emotion regulation capacity in healthy adults derstanding (1) group differences and (2) the natural
(see Balzarotti, Biassoni, Colombo, & Ciceri, 2017, history of individuals through repeated, within-
for review), whereas low resting RSA and RSA with- subject assessments; real-world contexts and influ-
drawal to stressors index emotion dysregulation (see ences on affect, behavior, and cognition; and the
Beauchaine, 2015, for review). Emotional responses temporal sequencing of events to explore causality.
are also evident in the noncontent features of speech, We briefly review the characteristics, benefits, and
such as fundamental frequency (see Giddens, Barron, limitations of EMA next; however, a more thorough
Byrd-Craven, Clark, & Winter, 2013, for review). review can be found elsewhere (Shiffman, Stone, &
Brain-based indices using electroencephalogram Hufford, 2008).
(see Coan & Allen, 2004, for review), event-related In EMA, brief questionnaires and assessments are
potentials (see Hajcak, MacNamara, & Olvet, 2010, presented to participants through a handheld com-
for a review), and magnetic resonance imaging puting device on preselected schedules, optimized
(e.g., Hare et al., 2008; Morawetz, Bode, Derntl, & to capture relevant information about phenomena
Heekeren, 2017) have also been used to explore of interest. EMA descends from paper-and-pencil
emotion regulation. “daily diary” studies (Korotitsch & Nelson-Gray,
As with all measures, traditional methodologies 1999) and other “experience sampling” (Hektner,
have many strengths but are limited in several key Schmidt, & Csikszentmihalyi, 2007), “self-report
ways. First, many rely on aggregate ratings of emo- EMA” (Stone & Shiffman, 1994), or “real time data
tion (e.g., DERS items beginning with “When capture” methods (Stone & Broderick, 2007).
I’m upset…”) and are subject to autobiographical These methods have been in use, in some form,
memory effects, such as random error and systematic since the beginning of structured psychological as-
bias due to heuristics and retrieval (Bradburn, Rips, sessment; however, technological innovations over
& Shevell, 1987). Self-reports also tend to reflect the past two decades have revolutionized our under-
self-conceptualizations, and it is not uncommon for standing of daily experience of affect, behavior, and
respondents to organize or modify responses to reflect cognition. For assessments to be truly “ecological,”
self-perception or worldviews, rather than actual they should occur in real-world environments (i.e.,
events (Ross, 1989). Likewise, responses to behav- participants’ homes), rather than through repeated
ioral tasks are often collected cross-sectionally; these measures in a research context (e.g., a lab). Likewise,
narrow slices of behavior, under specific conditions, the “momentary” component of these methods refers
reduces the generalizability of findings. to the assessment of state, rather than trait, constructs.
When considering how to most accurately meas- For example, an EMA measure of anger would ask
ure emotional experiences, we must recognize that participants to rate how angry they feel right now,
emotions are dynamic. Thinking about emotion as a rather than how they feel in general. Most modern
static construct, in which participants report overall EMA software programs allow for both random and
levels of positive affect (PA) or negative affect (NA), event-cued assessments, where participants choose to
neglects information that could be gained from a complete an EMA when a certain event happens in
moment-to-moment assessment of emotional expe- their lives (e.g., a fight with a partner).
rience (Trull, Lane, Koval, & Ebner-Priemer, 2015).
In contrast, EMA methods allow researchers to Ecological Momentary Assessment Strengths
measure experiences in the moment. These methods EMA has a number of benefits when compared to
can identify contextual events that prompt or follow cross-sectional methods. These methods significantly
412 Assessing Emotion Dysregul ation in Daily Life

reduce self-report biases and effects of social desira- Ecological Momentary Assessment of
bility on responding (Ebner-Priemer & Trull, 2009; Emotion Dysregulation
Shiffman et al., 2008). This emphasis on experien- Here, we provide an overview of EMA research on
tial states is often implemented by limiting the re- emotion dysregulation as it applies to individual
sponse window for assessments (e.g., within 10 min- differences, contextual factors, and physiological
utes of a prompt). To further reduce biases, most correlates. In addition, we discuss the use of EMA
EMAs are delivered randomly throughout the day, to examine emotion dysregulation within specific
to limit the impact of participant expectancies on disorders (e.g., depressive disorders) or behaviors
responding. The use of EMA in combination with (e.g., NSSI).
cross-sectional, self-report measures assessing simi-
lar constructs permits the comparison of state and Individual Differences in Emotional
trait measures to better elucidate patterns of discrep- Trajectory and in Response to Stressors
ancy or concordance, and can provide incremental Ecological methods can elucidate associations be-
construct validity above and beyond self-report, tween emotion dysregulation and individual differ-
permitting improved prediction of low base rate be- ences, including demographics, personality factors,
haviors such as nonsuicidal self-injury (NSSI; Armey, and responses to stressful life events. For example,
2012). One particular strength of these methods is one study collected emotion-related data five times
the identification of antecedents—which are often daily for 1 week from individuals ranging in age
affective in nature—to problematic behaviors. EMA from 18 to 94 (Carstensen, Pasupathi, Mayr, &
facilitates the examination of cyclical and nonlinear Nesselroade, 2000). Results suggested that the fre-
processes over time (Trull et al., 2008) or changes in quency of NA decreased over the lifespan, declining
affective state before, during, and after behavior until age 60, but the frequency of PA or the intensity
(e.g., self-harm; Armey, Crowther, & Miller, 2011). of both NA and PA did not. Older people had more
Finally, using branching questions in EMA can differentiated emotional experiences and were able
significantly reduce participant burden by limiting to better regulate emotions. In addition, individuals
the length of assessments. with lower momentary PA ratings over 1 day had
greater odds of death relative to those with higher
Ecological Momentary Assessment momentary PA ratings (Steptoe & Wardle, 2011).
Limitations Demographic factors are also associated with specific
Despite these strengths, there are several practical emotions, such as happiness over time collected via
and methodological limitations associated with experience sampling methods. Csikszentmihalyi and
EMA. Although handheld computing devices are Hunter (2003) reported that the highest levels of
nearly ubiquitous, access may be limited for some happiness over a week’s time were experienced by
populations, and it can be expensive for researchers teens in working-class communities, and happiness
to provide devices to participants. Open-source and decreased over the teenage years.
free EMA software packages have increasingly been Beyond demographics, EMA can shed light on
replaced by paid or subscription services, which can how personality variables influence response to
increase costs of research. Further, storage and anal- stressful life events. Using a daily diary approach,
ysis of EMA data is a growing problem for the field. Bolger and Schilling (1991) examined same-day and
Even a relatively small EMA study can have hun- later-day responses to stressors and found that those
dreds of thousands of data points, which may neces- who were high in neuroticism experienced more
sitate a dedicated data manager or statistician. distress in response to specific stressors (e.g., argu-
While these data sets can be analyzed with conven- ments with spouse). D. J. Miller, Vachon, and
tional within-subject regression models (Schwartz Lynam (2009) reported that NA instability and trait
& Stone, 1998, 2007), the true potential of these neuroticism were related but independent con-
data can only be unlocked through techniques such structs, with neuroticism more strongly related to
as intensive longitudinal modeling (Walls & Schafer, overall NA. In another study, adolescent romantic
2006), growth curve modeling (Armey et al., 2011), relationship dyads were assessed twice weekly for
dynamic systems models (e.g., Butner, Amazeen, & 12 weeks (Rogers, Ha, Updegraff, & Iida, 2018).
Mulvey, 2005; Chow, Ram, Boker, Fujita, & Clore, Daily conflict predicted greater same-day NA, and
2005), and time-varying effects models (Shiyko, NA was transmitted between partners. Among
Burkhalter, Li, & Park, 2014), which are not com- adult males, stressful events were associated with
monly a part of the social scientist skill set. increases in NA, but perceived controllability
Schat ten, Allen, and Armey 413

a ttenuated these negative effects (van Eck, Nicolson, Ecological Momentary Assessment and
& Berkhof, 1998). Psychophysiological Measures
Gray’s (1987) model of emotion describes two EMA affect ratings can be combined with other
motivational systems—the behavioral activation sources of data (e.g., psychophysiology) for a more
system (BAS), which drives appetitive behavior, and comprehensive picture of processes associated with
the behavioral inhibition system (BIS), which drives emotion dysregulation. In one study of global life
avoidance behavior. In accordance with this model, satisfaction, participants completed a salivary cortisol
Gable, Reis, and Elliot (2000) examined BIS/BAS sample at each EMA assessment (Smyth, Zawadzki,
associations with daily diary NA and PA. Here, BIS Juth, & Sciamanna, 2017), with life satisfaction
sensitivity predicted daily average NA, while BAS predicting lower momentary cortisol levels, greater
and BIS sensitivity predicted daily PA. Another arousal, and more positively valenced affect. Similarly,
study of male community residents signaled to re- over two separate days, Steptoe, Gibson, Hamer,
spond to surveys eight times daily found that par- and Wardle (2007) examined PA measured by EMA
ticipants high in trait NA reported more distress and salivary cortisol collected throughout the day.
to current-day problems, with slower recovery the Results suggested that rising cortisol output meas-
following day (Marco & Suls, 1993). These results ured in the first hour after waking was negatively
point to consistent relationships between personal- associated with EMA-reported PA. EMA methods
ity traits and affective responses; however, one EMA can also be collected simultaneously with methods
study found that fluctuations in affect accounted for such as actigraphy, defined as the measurement of
most, but not all, of the variance in personality movement and rest cycles. M. A. Miller and col-
states (Wilson, Thompson, & Vazire, 2017). Overall, leagues (2015) collected both EMA and actigraphy
these studies demonstrate that within- and between- data to elucidate the relationship between chrono-
person traits influence experiences of affect in re- type and PA and NA rhythms, measured hourly,
sponse to stressful life events. and found that individuals with an evening chrono-
type had delayed and blunted PA rhythms. Using
Analysis of Specific Emotions over Time multiple sources of data yoked to EMA allows for a
EMA methods allow for a more nuanced under- more complete understanding of objective and sub-
standing of specific emotional experiences through- jective experiences of emotion dysregulation.
out the day and over time. Csikszentmihalyi and
Hunter (2003) found that among teens, happiness Ecological Momentary Assessment of
is lowest on Sundays, that it increases slightly each Emotion Dysregulation in Psychological
day, and that the first part of the day—structured by Disorders and Behaviors
work or school—is less happy. In a sample of work- Emotion dysregulation is a transdiagnostic risk
ing women, happiness was also lower in the first factor for psychopathology (Beauchaine, 2015; Cole,
part of the day (Dockray et al., 2010). Hall, & Hajal, 2008). There is a burgeoning litera-
EMA data can also be used to develop latent ture using EMA to examine emotion dysregulation
affect intensity profiles (Cushing, Marker, Bejarano, in psychological disorders (e.g., Armey, Schatten,
Crick, & Huffhines, 2017), suggesting that overall Haradhvala, & Miller, 2015; Ebner-Priemer &
patterns of mood can be determined by more than Trull, 2009; Myin-Germeys et al., 2009; Santangelo,
one emotional state. Examining emotions over time Bohus, & Ebner-Priemer, 2014). To follow, we focus
can also provide information about the duration of on key and recent findings regarding ecologically
emotional responses. In a sample of college students measured emotion dysregulation in mood disorders,
completing daily assessments, joy episodes were self-injurious thoughts and behaviors, substance
longer lasting than episodes of anger, which were use, eating disorders, and borderline personality
longer lasting than fear episodes, suggesting that the disorder (BPD).
duration of an emotional experience varies across
emotions (Verduyn, Delvaux, Van Coillie, Tuerlinckx, Unipolar Depression
& Van Mechelen, 2009). In a follow-up study, the EMA measures of daily affect generally show poor
authors found that the greater the importance of concordance with retrospective self-report measures,
the emotion-eliciting situation and the higher the which tend to exaggerate symptoms (Ebner-Priemer
initial intensity of the emotion, the longer the epi- & Trull, 2009); evidence suggests that this may be
sodes lasted. especially true in depression. Specifically, depressed

patients demonstrate less accurate recall of daily NA In sum, EMA studies assessing the temporal
but not PA compared to nonclinical controls, who dynamics of affect in depression reveal that daily
show an intensification bias in retrospective reports emotion dysregulation primarily involves elevated
of PA (Ben-Zeev, Young, & Madsen, 2009). EMA NA variability and enhanced reactivity to stressful
studies also find that depressed participants have events. Furthermore, momentary NA instability and
higher daily average NA and lower PA (Bowen, Peters, negative emotional reactivity are positively correlated
Marwaha, Baetz, & Balbuena, 2017; Myin-Germeys in depressed individuals (R. J. Thompson et al.,
et al., 2003; Peeters, Berkhof, Delespaul, Rottenberg, 2012). There is also evidence for persistently blunted
& Nicolson, 2006), and more frequent days charac- PA, but this finding is not universal (e.g., Bowen
terized by elevated NA, even though depressed and et al., 2017).
nondepressed participants report a similar number of
negative events (Chepenik et al., 2006). Such studies Bipolar Disorder
also reveal nuance in these patterns that further reflect The mood shifts inherent to bipolar disorder occur
emotion dysregulation, such as greater NA variability on the scale of days to weeks (American Psychiatric
from day to day (Bowen et al., 2017; Chepenik et al., Association, 2013); however, EMA data provide val-
2006) and moment to moment (Peeters et al., 2006; uable insight into the daily emotion dysregulation
R. J. Thompson et al., 2012). This instability has occurring during and between manic episodes.
been prospectively linked to depressive symptoms Relative to healthy controls, patients with remitted
in women with a history of major depression (Wichers bipolar disorder report higher daily NA and lower
et al., 2010). In contrast, PA gradually increases PA (Havermans, Nicolson, Berkhof, & deVries,
throughout the day, with a later peak in depressed 2010), comparable to the pattern observed in de-
patients compared to healthy controls (Peeters et al., pression. Further, this interepisode pattern of daily
2006), but exhibits comparable momentary varia- affect predicts future depressive, but not manic,
bility (R. J. Thompson et al., 2012). symptoms 1 month later (Gershon & Eidelman,
EMA research also supports the idea that emo- 2015). Bipolar spectrum pathology is associated
tion dysregulation increases the risk for depression. with elevated daily NA, affective variability (Kwapil
For example, Wichers and colleagues (2007) sug- et al., 2012), and increasing levels of certain types
gested that negative emotional reactivity to daily of PA (i.e., “exuberance”) from noon to midnight
stress may be a depression endophenotype (i.e., a (Kwapil et al., 2012; Walsh, Royal, Brown, Barrantes-
behavioral response pattern with heritable biologi- Vidal, & Kwapil, 2012).
cal underpinnings; Gottesman & Gould, 2003). Some EMA evidence suggests a distinct pattern
Specifically, twins diagnosed with depression re- of emotion dysregulation between manic episodes.
ported increased NA following stressful life events, Compared to healthy individuals and those with re-
with more pronounced elevations in monozygotic mitted depression, patients with bipolar disorder
than dizygotic twins. This finding is consistent with report increased daily PA plus life satisfaction, as well
enhanced NA reactivity to life stressors observed as increased NA with functional impairment, rela-
in depressed patients (Myin-Germeys et al., 2003), tive to healthy controls (Gruber, Kogan, Mennin, &
which persists even following remission (O’Hara, Murray, 2013). They also experience decreasing PA
Armeli, Boynton, & Tennen, 2014). over the course of the day (Myin-Germeys et al.,
PA may serve as a buffer between stressful life 2003). Longer term studies of daily affect in patients
events and NA in depression; for example, experi- with bipolar disorder reveal that euphoric mood fre-
encing PA during stressful moments attenuates the quently occurs outside of hypomanic or manic epi-
association between event-related stress and subse- sodes (Bauer et al., 2006). The temporal course of
quent NA among depressed individuals (Wichers emotion dysregulation in bipolar illness may involve
et al., 2007). Daily PA similarly reduces the associa- elevated NA that precedes momentary impulsivity,
tion between perceived stress and NA in adults with which in turn predicts reduced PA (Depp et al.,
a history of depression (O’Hara et al., 2014). In con- 2016). Finally, EMA findings do not indicate a
trast, people with major depression report no PA strong relation between bipolar disorder and emo-
change following daily stressors (Myin-Germeys et al., tion reactivity to daily stressors (Havermans et al.,
2003; R. J. Thompson et al., 2012), distinct from 2010; Havermans, Nicolson, Berkhof, & deVries,
patterns observed in bipolar disorder and nonaffec- 2011). These data implicate both positive and nega-
tive psychosis (Myin-Germeys et al., 2003). tive emotion dysregulation in bipolar disorder.

Self-Injurious Thoughts and Behaviors with SI, past suicidal behavior, and future SA likeli-
Suicide hood among individuals with BPD (Links et al.,
Despite the emphasis on emotion dysregulation 2007; Links, Eynan, Heisel, & Nisenbaum, 2008).
in theoretical models of suicide (Law et al., 2015; In an inmate sample, momentary feelings of anger
Linehan, 1993), EMA remains an underutilized ap- were associated with concurrent, but not subse-
proach in the study of self-injurious thoughts and quent, SI (Humber, Emsley, Pratt, & Tarrier, 2013).
behaviors (SITBs; Davidson, Anestis, & Gutierrez, Similarly, recent EMA work from our research
2017; Kleiman & Nock, 2018). This may be due to group using time-varying effect models (TVEMs)
practical challenges of working with institutional suggests that individual-level increases in NA over
review boards to approve potentially high-risk re- time are strongly associated with increases in SI
search and concerns about iatrogenic effects of re- (Armey, Brick, Schatten, Nugent, & Miller, 2019)
peated evaluation of emotions and self-harm, which in a sample of psychiatric patients recently discharged
are unfounded (Cha et al., 2016; Gould et al., 2005). from the hospital. Despite substantial evidence
Indeed, research supports the feasibility and accept- linking elevated NA to suicidal thinking, a recent
ability of EMA in recent suicide attempters (Husky study suggests that SI may persist due to its rein-
et al., 2014; Law et al., 2015). Empirical work in this forcing effects on mood: Kleiman and colleagues
area is essential; unlike affect and psychological (2018) examined changes in affect surrounding SI
symptoms, which tend to be exaggerated in retro- in adults with a recent SA. They found that PA in-
spective reports (Ebner-Priemer & Trull, 2009; creased and sadness decreased from pre- to post-SI
Shiffman et al., 2008), global recall may promote assessments, and SI predicted subsequent increased
underreporting of suicidal ideation (SI; e.g., Torous PA and decreased NA.
et al., 2015). Furthermore, daily life emotion dys- As in depression, EMA implicates daily mood
regulation is highly predictive of SITBs across di- instability in the prediction of suicidality. NA vari-
agnoses. Trajectories of daily NA and PA in a pilot ability, but not average levels of affect, predicted the
study of patients with bipolar disorder predicted frequency and severity of SI in a sample of individu-
SI with 88% sensitivity and 95% specificity, strongly als at high risk for psychosis (Palmier-Claus, Taylor,
outperforming in-person clinical assessments (W. K. Gooding, Dunn, & Lewis, 2012). Additionally,
Thompson, Gershon, O’Hara, Bernert, & Depp, Links et al. (2007) found an association between
2014). A recent study in patients with bipolar type II emotion reactivity to environmental stressors and
similarly found that daily ratings of depressed mood daily SI in BPD. These authors identified a sub-
predicted increased SI 2 weeks later with excellent group of patients with BPD reporting the most sui-
accuracy [area under the curve (AUC) = .78–.91; cidal behavior, based on high levels of daily NA
Depp, Thompson, Frank, & Swartz, 2017]. intensity and mood amplitude. Overall, the EMA
EMA studies also elucidate the types of emotion literature indicates that negative affective intensity
dysregulation most relevant to SITBs, which may and instability predict SI (Spangenberg, Forkmann,
be population specific. For example, a study in adult & Glaesmer, 2015), although research examining
inpatients with depression indicated that sadness, these phenomena in larger samples is needed to de-
tension, and boredom preceded SI within a time termine the long-term predictive utility of momen-
span of hours, whereas other forms of NA (e.g., tary emotion dysregulation.
hopelessness, anhedonia, worthlessness) did not
(Ben-Zeev, Young, & Depp, 2012). Another recent Nonsuicidal Self-Injury
study in adults discharged from the hospital follow- Recent research suggests that NSSI may be one of
ing a serious suicide attempt (SA) confirmed daily the strongest predictors of future SITBs (Ribeiro
sadness as a short-term predictor of SI (Husky et al., et al., 2016), and these behaviors are associated with
2017). Other research by this group suggests that mood and anxiety disorders transdiagnostically (e.g.,
hopelessness and loneliness correlate with momen- Andover, Pepper, Ryabchenko, Orrico, & Gibb,
tary SI but do not predict SI changes beyond several 2005). Consistent with findings in depression,
hours (Kleiman et al., 2017). In contrast, among NSSI history is associated with daily life emotion
adolescents with a history of NSSI, a range of NA dysregulation in the form of higher NA and lower
states (particularly sadness, worthlessness, self-hatred, PA (Bresin, 2014; Santanagelo, Koenig, et al., 2017;
and anger) were observed prior to SI (Nock, Prinstein, Victor & Klonsky, 2014), as well as instability in
& Sterba, 2009). Daily emotion dysregulation in NA (Bresin, 2014) and overall affect (Santangelo,
the form of negative mood intensity is associated Koenig, et al., 2017). EMA and daily diary research

tend to support an automatic negative reinforcement that emotion dysregulation in NSSI may primarily
function of NSSI, suggesting that these behaviors involve affective variability at the state and trait
serve to reduce NA (Armey, Crowther, & Miller, level, in addition to high daily NA/low daily PA.
2011; Nock et al., 2009; Shingleton et al., 2013). Daily life emotion dysregulation may promote
Specifically, undergraduates engaging in NSSI re- NSSI urges in certain affective and cognitive con-
ported increased NA in the hours preceding an ep- texts, specifically when feeling sad/worthless, over-
isode, followed by reduced NA post-NSSI (Armey whelmed, scared/anxious, rejected/hurt, or criticized/
et al., 2011). A recent study in a large sample of insulted (Nock et al., 2009; Shingleton et al., 2013).
youth with BPD similarly observed increases in NA, Despite the association between various NA states
as well as decreased PA, 15 and 10 hours (respec- and NSSI thoughts, Nock and colleagues (2009)
tively) prior to NSSI, and this affective pattern found that feelings of rejection, anger, and numb-
was reversed after the episode (Andrewes, Hulbert, ness were associated with increased odds of actually
Cotton, Betts, & Channen, 2017a). Further, the engaging in NSSI, whereas sadness and worthless-
number of co-occurring negative emotions similarly ness were not. Elevated anger, guilt, and self-loathing
preceded NSSI episodes, peaked during episodes, were found to precede NSSI (Armey et al., 2011),
and decreased afterward, a pattern mirrored by self- peaking during the episode, and decreasing in in-
reported distress (Andrewes et al., 2017b). Although tensity after. Results from a daily diary study suggest
elevated NA prospectively predicted NSSI likeli- that trait negative urgency moderates the relation
hood in another recent study of inpatients with between emotion dysregulation and NSSI engage-
BPD features, NSSI engagement was concurrently ment, indicating that daily sadness predicts NSSI
associated with elevated NA and reduced PA and only among undergraduates who tend to react im-
predicted continued increases in NA hours later pulsively to negative emotions (Bresin, Carter, &
(Houben et al., 2017). A sample of women with bu- Gordon, 2013). Moreover, variability in NA and ru-
limia nervosa also reported momentary increased mination independently and interactively predict
NA and decreased PA prior to NSSI; however, NA NSSI episodes (Selby, Franklin, Carson-Wong, &
remained unchanged following the episode, while Rizvi, 2013). The effect of momentary rumination
PA increased (Muehlenkamp et al., 2009). Similarly, on NSSI urges and behaviors was replicated in a
EMA studies of NSSI also provide evidence for au- study of patients with BPD (Zaki, Coifman, Rafaeli,
tomatic positive reinforcement (Nock et al., 2009; Berenson, & Downety, 2013). The relationship
Selby, Nock, & Kranzler, 2014), suggesting that between rumination and NSSI was attenuated, how-
some individuals engage in these behaviors in order ever, among participants in this group, who demon-
to generate affective states. Support for multiple re- strated better emotion differentiation. In another
inforcement functions using EMA methods corrob- EMA study in individuals with BPD and anxiety
orate the assertion that emotion dysregulation is a disorders, momentary NA was found to predict sub-
core characteristic of NSSI (Andover & Morris, sequent NSSI urges only when self-concept clarity
2014; Hooley & Franklin, 2018; Nock, 2009). was low (Scala et al., 2018). Taken together, these
In addition to affective valence, EMA research findings suggest that it may be useful to examine
suggests that variability in affective responding may affective states as they interact with trait characteris-
be associated with NSSI episodes. In a sample of tics and cognitive factors.
women with eating disorders, Vansteelandt and col-
leagues (2013) found that variability in affective ac- Borderline Personality Disorder
tivation (regardless of valence) predicted NSSI acts. Affective instability is considered a central feature
A follow-up study among individuals with BPD of BPD. EMA research generally finds that BPD
suggests that beyond simply reducing NA, NSSI is characterized by affective instability in natural
may serve an affect stabilization function, as more contexts (Santangelo, Reinhard, et al., 2017; see
frequent NSSI in this sample was associated with Santangelo, Bohus, et al., 2014, for a review), includ-
reduced variance in affective valence and activation ing variability in NA (Jahng, Wood, & Trull, 2008;
(Vansteelandt et al., 2017). Even controlling for av- Trull et al., 2008) and PA (Russell, Moskowitz,
erage levels of NA and momentary variability in Zuroff, Sookman, & Paris, 2007), as well as rapid
affect, the interaction between past suicide attempts fluctuations from positive to negative mood (Ebner-
and trait affective lability was found to predict NSSI Priemer, Kuo, et al., 2007; Houben, Vansteelandt,
episodes in women diagnosed with bulimia nervosa et al., 2016). In general, affective instability measured
(Anestis et al., 2012). Overall, this literature suggests using retrospective self-report concords poorly with

ecological assessments in patients with BPD (Solhan patients with psychosis and healthy controls (Glaser,
et al., 2009), especially compared to global recall of Os, Mengelers, & Myin-Germeys, 2008). BPD
stable phenomena (e.g., elevated NA; Ebner-Primer, traits predict perceived stressfulness of daily life
Bohus, & Kuo, 2007; Links, Heisel, & Garland, events in women with bulimia nervosa (Pearson
2003). Findings have indicated the superiority of et al., 2017). This sensitivity may be particularly
EMA methods for determining psychophysiological salient in the sensitivity of interpersonal stressors.
hyperarousal associated with emotion dysregulation Within patients with BPD, a variety of stressors
in BPD compared to laboratory studies (Ebner- (particularly being involved in a disagreement) pre-
Priemer, Welch, et al., 2007; Ebner-Priemer et al., dict elevated NA, feeling emotionally overwhelmed,
2008; Lieb et al., 2004). and feeling out of control (Chaudhury et al., 2017).
Again, EMA minimizes recall bias inherent to These patients report associations between rejection
global self-report or interview measures, which tend and sadness at the momentary, daily, and person
to exaggerate the intensity of NA and underestimate level, whereas depressed patients report this associa-
PA in patients with BPD compared to healthy con- tion only at the momentary level (Hepp et al., 2017).
trols, who show the opposite effect (Ebner-Priemer Patients with BPD also reported a stronger link
et al., 2006; see also Ben-Zeev et al., 2009). Despite between momentary/daily interpersonal problems
these biases, EMA findings suggest that patients and feelings of hostility. BPD traits similarly predict
with BPD experience a greater variety of negative daily aggression via increased NA (particularly anger)
emotions, more intense NA, and fewer positive following perceived rejection (Scott et al., 2017).
emotions compared to clinical and healthy control In accordance with prevailing theoretical models,
groups (Ebner-Priemer, Welch, et al., 2007; Tomko daily life emotion dysregulation in BPD is character-
et al., 2015; Wolff, Stiglmayr, Bretz, Lammers, & ized by affective instability. Specifically, EMA data
Auckenthaler, 2007). Examinations of the temporal indicate variability in NA at the momentary and
sequence of momentary emotions in BPD indicate daily level, as well as rapid swings between negative
less activation (or initiation) of positive mood states and positive emotional states. BPD may also involve
(specifically joy and interest), greater persistence higher NA/lower PA on average, with a greater
of negative mood, and more frequent switching number of co-occurring negative emotions, and
between different types of NA, such as anxiety, sad- more switching between them. However, there is
ness, and anger (Reisch, Ebner-Priemer, Tschacher, also evidence that affective instability (Santangelo,
Bohus, & Linehan, 2008). Reinhard, et al., 2014) and emotional switching
Ecological research on emotion dysregulation in (Houben, Bohus, et al., 2016) are not specific to
BPD often focuses on risky or self-destructive behav- BPD, and may represent transdiagnostic forms of
iors thought to serve an emotion regulation function, emotion dysregulation. Finally, EMA also provides
including self-harm (Andrewes et al., 2017a, 2017b; support for the conceptualization of impulsive or
Links et al., 2007, 2008; Nisenbaum, Links, Eynan, risky behavior as attempts to regulate emotions in
& Heisel, 2010), substance use (Jahng et al., 2011), patients with BPD.
and disordered eating (Selby et al., 2012). A three-
way interaction between momentary rumination, Eating Disorders
NA, and BPD symptom severity predicts engagement Affect regulation has also been conceptualized as a
in these types of impulsive behaviors 2 to 3 hours primary motivation underlying eating disorder be-
later (Selby & Joiner, 2013). As another example, a havior (Bydlowski et al., 2005; Haynos & Fruzzetti,
recent study examined the relationship between 2011; Lavender et al., 2015; Polivy & Herman,
alcohol consumption rate, subjective stimulation 2002). The majority of EMA studies support this
(a measure of alcohol’s rewarding pharmacological notion, particularly highlighting the role of negative
effects), and mood in patients with BPD and con- reinforcement in these behaviors. For example, in
trols (Carpenter et al., 2017). Stimulation was asso- obese adults, NA predicts binge eating at the daily
ciated with enhanced PA in both groups, but also level (Berg et al., 2014), and discrete episodes are pre-
with reduced NA in the BPD group, suggesting that ceded by increased NA, particularly in the form of
patients consume alcohol more quickly to regulate guilt, which are, in turn, followed by decreased NA
emotion (Carpenter et al., 2017). at the momentary level (Berg et al., 2015). Guilt is
There is also evidence for heightened stress sensi- also especially associated with episodes of behavior
tivity in BPD (i.e., larger increases in NA and de- associated with bulimia nervosa, such as binge eating,
creases in PA after a stressful event) compared to purging, and binge-purge episodes (Berg et al., 2013).

A large naturalistic study of affect in anorexia nervosa suggests that PA increases and NA decreases in
(AN) by Engel and colleagues (2013) found that the hours preceding a drinking episode, and these
NA also increases prior to AN-related behaviors trends continue after the first drink (Treloar, Piasecki,
(e.g., loss-of-control eating and purging) and de- McCarthy, Sher, & Heath, 2015). Daily dysregula-
creases subsequently. EMA data also reveal that AN- tion in specific types of NA (e.g., irritability, loneli-
related behaviors are most likely to occur during ness) increases the risk for subsequent alcohol-related
periods of heightened anxiety (Lavender et al., problems in the evening regardless of consumption
2013). Mood instability seems particularly relevant level (Simons et al., 2005). An EMA study in under-
to weight loss activities in AN. According to find- age social drinkers found that the ability to differen-
ings by Selby and colleagues (2015), such activities tiate discrete types of momentary NA reduced the
are associated with variability in both NA and PA, effect of elevated NA on later consumption, sug-
which also interact to predict attempted weight loss. gesting a protective role for emotion differentiation
In sum, studies of daily life emotion dysregulation in (Kashdan, Ferssizidis, Collins, & Muraven, 2010).
eating disorders largely support the role of associated Affective variability may have greater implications
behaviors in reducing NA and further implicate for alcohol use in clinical populations beyond mo-
affective variability in the maintenance of AN. mentary or daily NA/PA. For example, affective
variability is associated with concurrent alcohol use
Alcohol Use and Substance Use Craving among patients with BPD, in contrast to predicting
EMA is particularly suited for use in substance use next-day drinking among patients with depression
research, as substance use is discrete and episodic (Jahng et al., 2011).
(Shiffman, 2009). In this section, we focus on alco- Another focus of EMA in substance use is crav-
hol use, an area of substance use research where ing. A review of this literature indicates that real-
EMA methods have often been applied. In addition, world emotion dysregulation increases subsequent
we discuss craving across a variety of substances, craving across a variety of substances (Serre, Fatseas,
another important focus of EMA research. Swendsen, & Auriacombe, 2015). Craving may also
Models of substance use have emphasized emo- involve an interaction between daily-level affect and
tional reinforcement processes, proposing that sub- person-level mood. Among patients with opioid
stances provide intrinsic reward or pleasure that independence, those with high average NA reported
itially facilitates enhanced PA, and use is maintained increased craving on days they experienced height-
and progresses to addiction through negative rein- ened NA, whereas patients with low average PA
forcement (i.e., to escape, alleviate, or avoid NA reported more craving on days they experienced
or withdrawal; Baker et al., 2004; Wise & Koob, particularly low PA (Huhn et al., 2016). Studies
2014). EMA data are generally consistent with these further suggest that aspects of real-world emotion
models, corroborating findings from self-report dysregulation might interact with craving to predict
(e.g., Cooper, Frone, Russell, & Mudar, 1995; Sher, use or relapse. Buckner and colleagues have found
Grekin, & Williams, 2005) and experimental stud- that momentary anxiety sensitivity (2011) and social
ies (e.g., Allen & Gabbay, 2013; Greeley & Oei, anxiety (2012) interact with craving to predict sub-
1999) of alcohol use. Some research indicates that sequent cannabis use.
anxiety experienced during the day increases drink- To summarize, real-world emotion dysregulation
ing levels that night (Simons, Dvorak, Batien, & influences substance use in multiple ways. Among
Wray, 2010; Swendsen et al., 2000; but see also people who drink alcohol, heightened PA increases
Dvorak & Simons, 2014), as well as dependence the amount consumed, whereas heightened NA
symptoms (Dvorak, Pearson, & Day, 2014). This predicts subsequent alcohol-related problems. EMA
effect is particularly evident among individuals who data also support both positive and negative rein-
report trait impulsivity in response to negative emo- forcement models of alcohol use, as individuals
tions (i.e., negative urgency; Simons et al., 2010). report elevated PA and reduced NA once they begin
Even more consistently, ecological studies have found drinking. There is only equivocal evidence for the
an association between daily PA and likelihood of relationship between daily life emotion dysregula-
drinking, consumption levels, and intoxication at tion and subsequent use of substances other than
night (Dvorak & Simons, 2014; Simons et al., 2010; alcohol; however, both increased NA and PA pre-
Trull, Wycoff, Lane, Carpenter, & Brown, 2016). dict craving across substances. Certain types of NA
A large ecological investigation of the temporal (particularly anxiety) may also lead to use in mo-
dynamics of affect in relation to alcohol consumption ments of increased craving, perhaps especially for

individuals who are high in negative urgency. life, permits researchers to examine the incremental
Finally, daily affective variability might have specific utility of these measurements in predicting out-
associations with substance use across different comes of interest. Research identifying and compar-
forms of psychopathology. atively evaluating predictors of behavioral and psy-
chopathology outcomes at multiple levels of analysis
Conclusions is essential to elucidate the emotion dysregulation
The literature reviewed in this chapter supports the construct.
use of EMA methods to measure emotion dysregu- Clearly, EMA is an indispensable tool for captur-
lation both in the context of psychological disorders ing the phenomenology of emotion dysregulation,
and as a distinct construct. Since emotions are dy- and it also has clinical utility. Data gleaned from
namic, EMA permits research on emotion dysregu- EMA can provide information about response to
lation by gathering data multiple times daily. These psychological treatment. For example, in depres-
methods allow for the identification of contextual sion, lower levels of negative emotional reactivity to
factors that influence emotional responding, as life stress were associated with positive early re-
well as interactions between trait characteristics and sponse to cognitive therapy (Cohen, Gunthert,
momentary emotion states. Although a strength of Butler, O’Neill, & Tolpin, 2005); conversely, per-
EMA is the ability to reduce the impact of autobio- sistently elevated NA on the day following a stressor
graphic memory effects and similar sources of error predicts a slower therapeutic response (Cohen et al.,
on responding, the momentary capture of emotion 2008). Similarly, daily variability in NA, but not
using EMA methods is still reliant on individuals’ PA, is related to slower treatment response, whereas
self-report of their current affect state, which may a high daily PA-to-NA ratio predicts earlier symp-
still be subject to some degree of bias. tom reduction (Husen, Rafaeli, Rubel, Bar-Kalifa,
To collect objective data without relying on self- & Lutz, 2016). Longitudinal research indicates that
report measures, researchers have begun to leverage baseline instability of momentary affect predicts
information gathered by hardware and software depressive relapse (Timm et al., 2017). Thus, changes
sensors already on mobile phones, which Asselbergs in affect, rather than presence of specific emotional
and colleagues (2016) refer to as “unobtrusive EMA.” states, may be more useful in determining treatment
This is related to the popularized concept of “digital response.
phenotyping,” in which sensor data are used to pre- Finally, if used to deliver interventions to people
dict behavior and psychopathology (Insel, 2017). during their daily life, EMA technologies can be
Although unobtrusive EMA or digital phenotyping termed ecological momentary interventions (EMIs).
cannot directly access an individual’s affective expe- EMIs are ecologically valid because they occur in
rience, it can provide clues based on psychophysio- individuals’ natural environments and intervention
logical responding, contextual factors, and behavior components are provided at specific moments or
(Asselbergs et al., 2016). LiKamWa, Liu, Lane, and in specific contexts (see Heron & Smyth, 2010, for
Zhong (2013) predicted fluctuations of self-reported review). Given the association between emotion
mood with 93% accuracy using variables including dysregulation and psychopathology, EMIs devel-
mobile phone use, physical activity, and social activ- oped to specifically target emotion-related “events”
ity, while Asselbergs and colleagues (2016) accurately (e.g., emotional variability, experiencing particular
predicted 55% to 76% of EMA mood scores. Future emotions simultaneously) by providing interven-
research leveraging advanced statistical techniques tion in response to these events are worthy of fur-
for large datasets will provide researchers with the ther study. In sum, EMA is a particularly well-
ability to take advantage of unobtrusive data col- suited research method for the assessment of
lected automatically on smartphones. dynamic processes such as emotion dysregulation,
At this stage, however, gathering EMA data in with the potential to use the information gained
conjunction with data collected via digital pheno- from these assessments to deliver timely and tar-
typing methods is fundamental for multiple reasons. geted interventions.
EMA data can serve as a ground truth for sensor
data; in fact, analyzing data on self-reported affective Acknowledgments
Dr. Armey’s effort is supported by R01 MH095786, R01
states in conjunction with objective measures allows MH097741, and R01 MH112674. Dr. Schatten’s effort is sup-
for an examination of convergent validity. Collecting ported by R01 MH112674, and R01 MH108610. Dr. Allen’s
subjective and objective data simultaneously, in daily effort is supported by R01 MH108610 and R01 MH112674.

References affective processing model of negative reinforcement.
Allen, K. J. D., & Gabbay, F. H. (2013). The amphetamine Psychological Review, 111, 33–51.
response moderates the relationship between negative Balzarotti, S., Biassoni, F., Colombo, B., & Ciceri, M. (2017).
emotionality and alcohol use. Alcoholism: Clinical and Cardiac vagal control as a marker of emotion regulation in
Experimental Research, 37, 348–360. healthy adults: A review. Biological Psychology, 130, 54–66.
Allen, K. J. D., & Hooley, J. M. (2015). Inhibitory control in Bauer, M., Grof, P., Rasgon, N. L., Marsh, W., Munoz, R. A.,
people who self-injure: Evidence for impairment and Sagduyu, K., . . . Whybrow, P. C. (2006). Self-reported data
enhancement. Psychiatry Research, 225, 631–637. from patients with bipolar disorder: Impact on minimum
Allen, K. J. D., & Hooley, J. M. (2018). Negative emotional episode length for hypomania. Journal of Affective Disorders,
response inhibition: Support for a cognitive mechanism 96, 101–105.
underlying negative urgency in nonsuicidal self-injury. Beauchaine, T. P. (2015). Respiratory sinus arrhythmia: A
Manuscript submitted for publication. transdiagnostic biomarker of emotion dysregulation and
American Psychiatric Association. (2013). Diagnostic and psychopathology. Current Opinion in Psychology, 3, 43–47.
statistical manual of mental disorders (5th ed.). Arlington, VA: Ben-Zeev, D., Young, M. A., & Depp, C. A. (2012). Real-time
American Psychiatric Publishing. predictors of suicidal ideation: Mobile assessment of
Andover, M. S., & Morris, B. W. (2014). Expanding and hospitalized depressed patients. Psychiatry Research, 197, 55–59.
clarifying the role of emotion regulation in nonsuicidal self- Ben-Zeev, D., Young, M. A., & Madsen, J. W. (2009).
injury. Canadian Journal of Psychiatry, 59, 569–575. Retrospective recall of affect in clinically depressed individuals
Andover, M. S., Pepper, C. M., Ryabchenko, K. A., Orrico, and controls. Cognition and Emotion, 23, 1021–1040.
E. G., & Gibb, B. E. (2005). Self-mutilation and symptoms Berg, K. C., Crosby, R. D., Cao, L., Crow, S. J., Engel, S. G.,
of depression, anxiety, and borderline personality disorder. Wonderlich, S. A., & Peterson, C. B. (2015). Negative affect
Suicide and Life-Threatening Behavior, 35, 581–591. prior to and following overeating-only, loss of control eating-
Andrewes, H. E., Hulbert, C., Cotton, S. M., Betts, J., & only, and binge eating episodes in obese adults. International
Chanen, A. M. (2017a). Ecological momentary assessment of Journal of Eating Disorders, 48, 641–653.
nonsuicidal self-injury in youth with borderline personality Berg, K. C., Crosby, R. D., Cao, L., Peterson, C. B., Engel,
disorder. Personality Disorders: Theory, Research, and Treatment, S. G., Mitchell, J. E., & Wonderlich, S. A. (2013). Facets of
8, 357–365. negative affect prior to and following binge-only, purge-only,
Andrewes, H. E., Hulbert, C., Cotton, S. M., Betts, J., & and binge/purge events in women with bulimia nervosa.
Chanen, A. M. (2017b). An ecological momentary assessment Journal of Abnormal Psychology, 122, 111–118.
investigation of complex and conflicting emotions in youth Berg, K. C., Peterson, C. B., Crosby, R. D., Cao, L., Crow, S. J.,
with borderline personality disorder. Psychiatry Research, 252, Engel, S. G., & Wonderlich, S. A. (2014). Relationship
102–110. between daily affect and overeating-only, loss of control
Anestis, M. D., Silva, C., Lavender, J. M., Crosby, R. D., eating-only, and binge eating episodes in obese adults.
Wonderlich, S. A., Engel, S. G., & Joiner, T. E. (2012). Psychiatry Research, 215, 185–191.
Predicting nonsuicidal self-injury episodes over a discrete Bolger, N., Davis, A., & Rafaeli, E. (2003). Diary methods:
period of time in a sample of women diagnosed with bulimia Capturing life as it is lived. Annual Review of Psychology, 54,
nervosa: An analysis of self-reported trait and ecological 579–616.
momentary assessment based affective lability and previous Bolger, N., & Schilling, E. A. (1991). Personality and the problems
suicide attempts. International Journal of Eating Disorders, of everyday life: The role of neuroticism in exposure and
45, 808–811. reactivity to daily stressors. Journal of Personality, 59, 355–386.
Armey, M. F. (2012). Ecological momentary assessment and Bowen, R., Peters, E., Marwaha, S., Baetz, M., & Balbuena, L.
intervention in nonsuicidal self-injury: A novel approach to (2017). Moods in clinical depression are more unstable than
treatment. Journal of Cognitive Psychotherapy, 26, 299–317. severe normal sadness. Frontiers in Psychiatry, 8, 1–6.
Armey, M. F., Brick, L. A., Schatten, H. T., Nugent, N. R., & Bradburn, N. M., Rips, L. J., & Shevell, S. K. (1987). Answering
Miller, I. W. (under review). Ecologically assessed affect and autobiographical questions: The impact of memory and
suicidal ideation follow psychiatric inpatient admission. inference on surveys. Science, 236, 157–161.
Manuscript submitted for publication. Bresin, K. (2014). Five indices of emotion regulation in
Armey, M. F., Crowther, J. H., & Miller, I. W. (2011). Changes in participants with a history of nonsuicidal self-injury: A daily
ecological momentary assessment reported affect associated diary study. Behavior Therapy, 45, 56–66.
with episodes of non-suicidal self-injury. Behavior Therapy, Bresin, K., Carter, D. L., & Gordon, K. H. (2013). The
42, 579–588. relationship between trait impulsivity, negative affective
Armey, M. F., Schatten, H. T., Haradhvala, N., & Miller, I. W. states, and urge for nonsuicidal self-injury: A daily diary
(2015). Ecological momentary assessment (EMA) of study. Psychiatry Research, 205, 227–231.
depression-related phenomena. Current Opinion in Buckner, J. D., Crosby, R. D., Silgado, J., Wonderlich, S. A., &
Psychology, 4, 21–25. Schmidt, N. B. (2012). Immediate antecedents of marijuana
Asselbergs, J., Ruwaard, J., Ejdys, M., Schrader, N., Sijbrandij, use: An analysis from ecological momentary assessment. Journal
M., & Riper, H. (2016). Mobile phone-based unobtrusive of Behavior Therapy and Experimental Psychiatry, 43, 647–655.
ecological momentary assessment of day-to-day mood: Buckner, J. D., Zvolensky, M. J., Smits, J. A. J., Norton, P. J.,
An explorative study. Journal of Medical Internet Research, Crosby, R. D., Wonderlich, S. A., & Schmidt, N. B. (2011).
18, e72. Anxiety sensitivity and marijuana use: An analysis from
Baker, T. B., Piper, M. E., McCarthy, D. E., Majeskie, M. R., & ecological momentary assessment. Depression and Anxiety,
Fiore, M. C. (2004). Addiction motivation reformulated: An 28, 420–426.

Butner, J., Amazeen, P. G., & Mulvey, G. M. (2005). Multilevel Depp, C. A., Moore, R. C., Dev, S. I., Mausbach, B. T., Eyler,
modeling of two cyclical processes: Extending differential L. T., & Granholm, E. L. (2016). The temporal course and
structural equation modeling to nonlinear coupled systems. clinical correlates of subjective impulsivity in bipolar disorder
Psychological Methods, 10, 159–177. as revealed through ecological momentary assessment.
Bydlowski, S., Corcos, M., Jeammet, P., Paterniti, S., Berthoz, S., Journal of Affective Disorders, 193, 145–150.
Laurier, C., . . . Consoli, S. M. (2005). Emotion-processing Depp, C. A., Thompson, W. K., Frank, E., & Swartz, H. A.
deficits in eating disorders. International Journal of Eating (2017). Prediction of near-term increases in suicidal ideation
Disorders, 37, 321–329. in recently depressed patients with bipolar II disorder using
Carpenter, R. W., Trela, C. J., Lane, S. P., Wood, P. K., Piasecki, intensive longitudinal data. Journal of Affective Disorders,
T. M., & Trull, T. J. (2017). Elevated rate of alcohol 208, 363–368.
consumption in borderline personality disorder patients in Dockray, S., Grant, N., Stone, A. A., Kahneman, D., Wardle, J.,
daily life. Psychopharmacology, 234, 3395–3406. & Steptoe, A. (2010). A comparison of affect ratings
Carstensen, L. L., Pasupathi, M., Mayr, U., & Nesselroade, J. R. obtained with ecological momentary assessment and the
(2000). Emotional experience in everyday life across the day reconstruction method. Social Indicators Research, 99,
adult life span. Journal of Personality and Social Psychology, 269–283.
79, 644–655. Dvorak, R. D., Pearson, M. R., & Day, A. M. (2014). Ecological
Cha, C. B., Glenn, J. J., Deming, C. A., D’Angelo, E. J., Hooley, momentary assessment of acute alcohol use disorder symptoms:
J. M., Teachman, B. A., & Nock, M. K. (2016). Examining Associations with mood, motives, and use on planned drinking
potential iatrogenic effects of viewing suicide and self-injury days. Experimental and Clinical Psychopharmacology, 22,
stimuli. Psychological Assessment, 28, 1510–1515. 285–297.
Chaudhury, S. R., Galfalvy, H., Biggs, E., Choo, T.-H., Mann, Dvorak, R. D., & Simons, J. S. (2014). Daily associations
J. J., & Stanley, B. (2017). Affect in response to stressors and between anxiety and alcohol use: Variation by sustained
coping strategies: An ecological momentary assessment study attention, set shifting, and gender. Psychology of Addictive
of borderline personality disorder. Borderline Personality Behaviors, 28, 969–979.
Disorder and Emotion Dysregulation, 4, 8. Ebner-Priemer, U. W., Bohus, M., & Kuo, J. (2007). Can
Chepenik, L. G., Thomas, T. H., Oslin, D., Datto, C., retrospective interviews assess instability? A comparison of
Zubritsky, C., & Katz, I. R. (2006). A daily diary study of ambulatory assessment and expert interviews regarding
late-life depression. American Journal of Geriatric Psychiatry, DSM-IV criteria for borderline personality disorder. In
14, 270–279. M. Sorbi, H. Rüddel, & M. Bühring (Eds.), Frontiers in
Chow, S. M., Ram, N., Boker, S. M., Fujita, F., & Clore, G. stepped eCare (pp. 25–37). Utrecht, Netherlands: University
(2005). Emotion as a thermostat: Representing emotion Utrecht.
regulation using a damped oscillator model. Emotion, 5, Ebner-Priemer, U. W., Kuo, J., Kleindienst, N., Welch, S. S.,
208–225. Reisch, T., Reinhard, I., . . . Bohus, M. (2007). State affective
Coan, J. A., & Allen, J. J. (2004). Frontal EEG asymmetry as a instability in borderline personality disorder assessed by
moderator and mediator of emotion. Biological Psychology, ambulatory monitoring. Psychological Medicine, 37, 961–970.
67, 7–50. Ebner-Priemer, U. W., Kuo, J., Schlotz, W., Kleindienst, N.,
Cohen, L. H., Gunthert, K. C., Butler, A. C., O’Neill, S. C., & Rosenthal, M. Z., Detterer, L., . . . Bohus, M. (2008). Distress
Tolpin, L. H. (2005). Daily affective reactivity as a and affective dysregulation in patients with borderline
prospective predictor of depressive symptoms. Journal of personality disorder: A psychophysiological ambulatory
Personality, 73, 1687–1714. monitoring study. Journal of Nervous and Mental Disease,
Cohen, L. H., Gunthert, K. C., Butler, A. C., Parrish, B. P., 196, 314–320.
Wenze, S. J., & Beck, J. S. (2008). Negative affective spillover Ebner-Priemer, U. W., Kuo, J., Welch, S. S., Thielgen, T., Witte,
from daily events predicts early response to cognitive therapy S., Bohus, M., & Linehan, M. M. (2006). A valence-
for depression. Journal of Consulting and Clinical Psychology, dependent group-specific recall bias of retrospective self-
76, 955–965. reports: A study of borderline personality disorder in
Cole, P. M., Hall, S. E., & Hajal, N. (2008). Emotion everyday life. Journal of Nervous and Mental Disease, 194,
dysregulation as a risk factor for psychopathology. Child and 774–779.
Adolescent Psychopathology, 2, 341–373. Ebner-Priemer, U. W., & Trull, T. J. (2009). Ambulatory
Cooper, M. L., Frone, M. R., Russell, M., & Mudar, P. (1995). assessment: An innovative and promising approach for
Drinking to regulate positive and negative emotions: A clinical psychology. European Psychologist, 14, 109–119.
motivational model of alcohol use. Journal of Personality and Ebner-Priemer, U. W., Welch, S. S., Grossman, P., Reisch, T.,
Social Psychology, 69, 990–1005. Linehan, M. M., & Bohus, M. (2007). Psychophysiological
Csikszentmihalyi, M., & Hunter, J. (2003). Happiness in ambulatory assessment of affective dysregulation in
everyday life: The uses of experience sampling. Journal of borderline personality disorder. Psychiatry Research, 150,
Happiness Studies, 4, 185–199. 265–275.
Cushing, C. C., Marker, A. M., Bejarano, C. M., Crick, C. J., & Engel, S. G., Wonderlich, S. A., Crosby, R. D., Mitchell, J. E.,
Huffhines, L. P. (2017). Latent variable mixture modeling of Crow, S., Peterson, C. B., . . . Gordon, K. H. (2013). The role
ecological momentary assessment data: Implications for of affect in the maintenance of anorexia nervosa: Evidence
screening and adolescent mood profiles. Journal of Child and from a naturalistic assessment of momentary behaviors and
Family Studies, 26, 1565–1572. emotion. Journal of Abnormal Psychology, 122, 709–719.
Davidson, C. L., Anestis, M. D., & Gutierrez, P. M. (2017). Gable, S. L., Reis, H. T., & Elliot, A. J. (2000). Behavioral
Ecological momentary assessment is a neglected methodology activation and inhibition in everyday life. Journal of
in suicidology. Archives of Suicide Research, 21, 1–11. Personality and Social Psychology, 78, 1135–1149.

Gershon, A., & Eidelman, P. (2015). Inter-episode affective Hepp, J., Lane, S. P., Carpenter, R. W., Niedtfeld, I., Brown, W. C.,
intensity and instability: Predictors of depression and & Trull, T. J. (2017). Interpersonal problems and negative affect
functional impairment in bipolar disorder. Journal of Behavior in borderline personality and depressive disorders in daily
Therapy and Experimental Psychiatry, 46, 14–18. life. Clinical Psychological Science, 5, 470–484.
Giddens, C. L., Barron, K. W., Byrd-Craven, J., Clark, K. F., & Heron, K. E., & Smyth, J. M. (2010). Ecological momentary
Winter, A. S. (2013). Vocal indices of stress: A review. Journal interventions: Incorporating mobile technology into
of Voice, 27, 390.e21–390.e29. psychosocial and health behaviour treatments. British Journal
Glaser, J.-P., Os, J. V., Mengelers, R., & Myin-Germeys, I. of Health Psychology, 15, 1–39.
(2008). A momentary assessment study of the reputed Hooley, J. M., & Franklin, J. C. (2018). Why do people hurt
emotional phenotype associated with borderline personality themselves? A new conceptual model of nonsuicidal self-
disorder. Psychological Medicine, 38, 1231–1239. injury. Clinical Psychological Science, 6, 428–451.
Gottesman, I. I., & Gould, T. D. (2003). The endophenotype Houben, M., Bohus, M., Santangelo, P. S., Ebner-Priemer, U.,
concept in psychiatry: Etymology and strategic intentions. Trull, T. J., & Kuppens, P. (2016). The specificity of emotional
American Journal of Psychiatry, 160, 636–645. switching in borderline personality disorder in comparison
Gould, M. S., Marrocco, F. A., Kleinman, M., Thomas, J. G., to other clinical groups. Personality Disorders: Theory, Research,
Mostkoff, K., Cote, J., & Davies, M. (2005). Evaluating and Treatment, 7, 198–204.
iatrogenic risk of youth suicide screening programs: A Houben, M., Claes, L., Vansteelandt, K., Berens, A., Sleuwaegen,
randomized controlled trial. Journal of the American Medical E., & Kuppens, P. (2017). The emotion regulation function
Association, 293, 1635–1643. of nonsuicidal self-injury: A momentary assessment study
Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment in inpatients with borderline personality disorder features.
of emotion regulation and dysregulation: Development, Journal of Abnormal Psychology, 126, 89–95.
factor structure, and initial validation of the difficulties in Houben, M., Vansteelandt, K., Claes, L., Sienaert, P., Berens, A.,
emotion regulation scale. Journal of Psychopathology and Sleuwaegen, E., & Kuppens, P. (2016). Emotional switching in
Behavioral Assessment, 26, 41–54. borderline personality disorder: A daily life study. Personality
Gray, J. A. (1987). The psychology of fear and stress (2nd ed.). Disorders: Theory, Research, and Treatment, 7, 50–60.
Cambridge, UK: Cambridge University Press. Huhn, A. S., Harris, J., Cleveland, H. H., Lydon, D. M.,
Greeley, J., & Oei, T. (1999). Alcohol and tension reduction. In Stankoski, D., Cleveland, M. J., . . . Bunce, S. C. (2016).
H. T. Blane & K. E. Leonard (Eds.), Psychological theories of Ecological momentary assessment of affect and craving in
drinking and alcoholism (pp. 14–53). New York, NY: patients in treatment for prescription opioid dependence.
Guilford Press. Brain Research Bulletin, 123, 94–101.
Gross, J. J. (1998). Sharpening the focus: Emotion regulation, Humber, N., Emsley, R., Pratt, D., & Tarrier, N. (2013). Anger
arousal, and social competence. Psychological Inquiry, 9, as a predictor of psychological distress and self-harm ideation
287–290. in inmates: A structured self-assessment diary study.
Gruber, J., Kogan, A., Mennin, D., & Murray, G. (2013). Real- Psychiatry Research, 210, 166–173.
world emotion? An experience-sampling approach to Husen, K., Rafaeli, E., Rubel, J. A., Bar-Kalifa, E., & Lutz, W.
emotion experience and regulation in bipolar I disorder. (2016). Daily affect dynamics predict early response in CBT:
Journal of Abnormal Psychology, 122, 971–983. Feasibility and predictive validity of EMA for outpatient
Hajcak, G., MacNamara, A., & Olvet, D. M. (2010). Event- psychotherapy. Journal of Affective Disorders, 206, 305–314.
related potentials, emotion, and emotion regulation: An Husky, M., Olié, E., Guillaume, S., Genty, C., Swendsen, J., &
integrative review. Developmental Neuropsychology, 35, Courtet, P. (2014). Feasibility and validity of ecological
129–155. momentary assessment in the investigation of suicide risk.
Hallion, L. S., Steinman, S. A., Tolin, D. F., & Diefenbach, G. J. Psychiatry Research, 220, 564–570.
(2018). Psychometric properties of the Difficulties in Emotion Husky, M., Swendsen, J., Ionita, A., Jaussent, I., Genty, C., &
Regulation Scale (DERS) and its short forms in adults with Courtet, P. (2017). Predictors of daily life suicidal ideation in
emotional disorders. Frontiers in Psychology, 9, 539. adults recently discharged after a serious suicide attempt: A
Hare, T. A., Tottenham, N., Galvan, A., Voss, H. U., Glover, pilot study. Psychiatry Research, 256, 79–84.
G. H., & Casey, B. (2008). Biological substrates of emotional Insel, T. R. (2017). Digital phenotyping: Technology for a new
reactivity and regulation in adolescence during an emotional science of behavior. JAMA, 318, 1215–1216.
go-nogo task. Biological Psychiatry, 63, 927–934. Jahng, S., Solhan, M. B., Tomko, R. L., Wood, P. K., Piasecki,
Havermans, R., Nicolson, N. A., Berkhof, J., & deVries, M. W. T. M., & Trull, T. J. (2011). Affect and alcohol use: An
(2010). Mood reactivity to daily events in patients with ecological momentary assessment study of outpatients with
remitted bipolar disorder. Psychiatry Research, 179, 47–52. borderline personality disorder. Journal of Abnormal Psychology,
Havermans, R., Nicolson, N. A., Berkhof, J., & deVries, M. W. 120, 572–584.
(2011). Patterns of salivary cortisol secretion and responses to Jahng, S., Wood, P. K., & Trull, T. J. (2008). Analysis of affective
daily events in patients with remitted bipolar disorder. instability in ecological momentary assessment: Indices using
Psychoneuroendocrinology, 36, 258–265. successive difference and group comparison via multilevel
Haynos, A. F., & Fruzzetti, A. E. (2011). Anorexia nervosa as a modeling. Psychological Methods, 13, 354–375.
disorder of emotion dysregulation: Evidence and treatment Kashdan, T. B., Ferssizidis, P., Collins, R. L., & Muraven, M.
implications. Clinical Psychology: Science and Practice, 18, (2010). Emotion differentiation as resilience against excessive
183–202. alcohol use: An ecological momentary assessment in
Hektner, J. M., Schmidt, J. A., & Csikszentmihalyi, M. (2007). underage social drinkers. Psychological Science, 21, 1341–1347.
Experience sampling method: Measuring the quality of everyday Kirschbaum, C., Pirke, K.-M., & Hellhammer, D. H. (1993).
life. Thousand Oaks, CA: Sage. The “Trier Social Stress Test”—a tool for investigating

psychobiological stress responses in a laboratory setting. Mathews, A., & MacLeod, C. (2005). Cognitive vulnerability to
Neuropsychobiology, 28, 76–81. emotional disorders. Annual Review of Clinical Psychology, 1,
Kleiman, E. M., Coppersmith, D. D., Millner, A. J., Franz, P. J., 167–195.
Fox, K. R., & Nock, M. K. (2018). Are suicidal thoughts Miller, D. J., Vachon, D. D., & Lynam, D. R. (2009).
reinforcing? A preliminary real-time monitoring study on the Neuroticism, negative affect, and negative affect instability:
potential affect regulation function of suicidal thinking. Establishing convergent and discriminant validity using
Journal of Affective Disorders, 232, 122–126. ecological momentary assessment. Personality and Individual
Kleiman, E. M., & Nock, M. K. (2018). Real-time assessment of Differences, 47, 873–877.
suicidal thoughts and behaviors. Current Opinion in Miller, M. A., Rothenberger, S. D., Hasler, B. P., Donofry, S. D.,
Psychology, 22, 33–37. Wong, P. M., Manuck, S. B., . . . Roecklein, K. A. (2015).
Kleiman, E. M., Turner, B. J., Fedor, S., Beale, E. E., Huffman, Chronotype predicts positive affect rhythms measured by
J. C., & Nock, M. K. (2017). Examination of real-time ecological momentary assessment. Chronobiology International,
fluctuations in suicidal ideation and its risk factors: Results 32, 376–384.
from two ecological momentary assessment studies. Journal Morawetz, C., Bode, S., Derntl, B., & Heekeren, H. R. (2017).
of Abnormal Psychology, 126, 726–738. The effect of strategies, goals and stimulus material on the
Korotitsch, W. J., & Nelson-Gray, R. O. (1999). An overview of neural mechanisms of emotion regulation: A meta-analysis of
self-monitoring research in assessment and treatment. fMRI studies. Neuroscience and Biobehavioral Reviews, 72,
Psychological Assessment, 11, 415–425. 111–128.
Kwapil, T. R., Barrantes-Vidal, N., Armistead, M. S., Hope, Muehlenkamp, J. J., Engel, S. G., Wadeson, A., Crosby, R. D.,
G. A., Brown, L. H., Silvia, P. J., & Myin-Germeys, I. (2012). Wonderlich, S. A., Simonich, H., & Mitchell, J. E. (2009).
The expression of bipolar spectrum psychopathology in daily Emotional states preceding and following acts of non-
life. Journal of Affective Disorders, 130, 166–170. suicidal self-injury in bulimia nervosa patients. Behaviour
Lavender, J. M., De Young, K. P., Anestis, M. D., Wonderlich, Research and Therapy, 47, 83–87.
S. A., Crosby, R. D., Engel, S. G., . . . Le Grange, D. (2013). Myin-Germeys, I., Oorschot, M., Collip, D., Lataster, J.,
Associations between retrospective versus ecological Delespaul, P., & Van Os, J. (2009). Experience sampling
momentary assessment measures of emotion and eating research in psychopathology: Opening the black box of daily
disorder symptoms in anorexia nervosa. Journal of Psychiatric life. Psychological Medicine, 39, 1533–1547.
Research, 47, 1514–1520. Myin-Germeys, I., Peeters, F., Havermans, R., Nicolson, N. A.,
Lavender, J. M., Wonderlich, S. A., Engel, S. G., Gordon, K. H., DeVries, M. W., Delespaul, P., & Van Os, J. (2003).
Kaye, W. H., & Mitchell, J. E. (2015). Dimensions of Emotional reactivity to daily life stress in psychosis and
emotion dysregulation in anorexia nervosa and bulimia affective disorder: An experience sampling study. Acta
nervosa: A conceptual review of the empirical literature. Psychiatrica Scandinavica, 107, 124–131.
Clinical Psychology Review, 40, 111–122. Nisenbaum, R., Links, P. S., Eynan, R., & Heisel, M. J. (2010).
Law, K. C., Khazem, L. R., & Anestis, M. D. (2015). The role of Variability and predictors of negative mood intensity in
emotion dysregulation in suicide as considered through the patients with borderline personality disorder and recurrent
ideation to action framework. Current Opinion in Psychology, suicidal behavior: Multilevel analyses applied to experience
3, 30–35. sampling methodology. Journal of Abnormal Psychology, 119,
Lieb, K., Rexhausen, J. E., Kahl, K. G., Schweiger, U., Philipsen, 433–439.
A., Hellhammer, D. H., & Bohus, M. (2004). Increased Nock, M. K. (2009). Why do people hurt themselves? New
diurnal salivary cortisol in women with borderline personality insights into the nature and functions of self-injury. Current
disorder. Journal of Psychiatric Research, 38, 559–565. Directions in Psychological Science, 18, 78–83.
LiKamWa, R., Liu, Y., Lane, N. D., & Zhong, L. (2013). Nock, M. K., Prinstein, M. J., & Sterba, S. K. (2009). Revealing
Moodscope: Building a mood sensor from smartphone usage the form and function of self-injurious thoughts and
patterns. Paper presented at the Proceedings of the 11th Annual behaviors: A real-time ecological assessment study among
International Conference on Mobile Systems, Applications, adolescents and young adults. Journal of Abnormal Psychology,
and Services. Taipei, Taiwan. 118, 816–827.
Linehan, M. M. (1993). Cognitive-behavioral treatment of O’Hara, R. E., Armeli, S., Boynton, M. H., & Tennen, H.
borderline personality disorder. New York, NY: Guilford Press. (2014). Emotional stress-reactivity and positive affect among
Links, P. S., Eynan, R., Heisel, M. J., Barr, A., Korzekwa, M., college students: The role of depression history. Emotion, 14,
McMain, S., & Ball, J. S. (2007). Affective instability and 193–202.
suicidal ideation and behavior in patients with borderline Palmier-Claus, J. E., Taylor, P. J., Gooding, P., Dunn, G., &
personality disorder. Journal of Personality Disorders, 21, 72–86. Lewis, S. W. (2012). Affective variability predicts suicidal
Links, P. S., Eynan, R., Heisel, M. J., & Nisenbaum, R. (2008). ideation in individuals at ultra-high risk of developing
Elements of affective instability associated with suicidal psychosis: An experience sampling study. British Journal of
behaviour in patients with borderline personality disorder. Clinical Psychology, 51, 72–83.
Canadian Journal of Psychiatry, 53, 112–116. Pearson, C. M., Lavender, J. M., Cao, L., Wonderlich, S. A.,
Links, P. S., Heisel, M., & Garland, A. (2003). Affective Crosby, R. D., Engel, S. G., . . . Crow, S. J. (2017). Associations
instability in personality disorders. American Journal of of borderline personality disorder traits with stressful events
Psychiatry, 160, 394–395. and emotional reactivity in women with bulimia nervosa.
Marco, C. A., & Suls, J. (1993). Daily stress and the trajectory of Journal of Abnormal Psychology, 126, 531–539.
mood: Spillover, response assimilation, contrast, and chronic Peeters, F., Berkhof, J., Delespaul, P., Rottenberg, J., & Nicolson,
negative affectivity. Journal of Personality and Social Psychology, N. A. (2006). Diurnal mood variation in major depressive
64, 1053–1063. disorder. Emotion, 6, 383–391.

Polivy, J., & Herman, C. P. (2002). Causes of eating disorders. positive emotional instability on promoting weight loss
Annual Review of Psychology, 53, 187–213. activities in anorexia nervosa. Frontiers in Psychology, 6, 1260.
Reisch, T., Ebner-Priemer, U. W., Tschacher, W., Bohus, M., & Selby, E. A., Doyle, P., Crosby, R. D., Wonderlich, S. A., Engel,
Linehan, M. M. (2008). Sequences of emotions in patients S. G., Mitchell, J. D., & Le Grange, D. (2012). Momentary
with borderline personality disorder. Acta Psychiatrica emotion surrounding bulimic behaviors in women with
Scandinavica, 118, 42–48. bulimia nervosa and borderline personality disorder. Journal
Ribeiro, J. D., Franklin, J. C., Fox, K. R., Bentley, K. H., of Psychiatric Research, 46, 1492–1500.
Kleiman, E. M., Chang, B. P., & Nock, M. K. (2016). Self- Selby, E. A., Franklin, J. C., Carson-Wong, A., & Rizvi, S. L.
injurious thoughts and behaviors as risk factors for future (2013). Emotional cascades and self-injury: Investigating
suicide ideation, attempts, and death: A meta-analysis of instability of rumination and negative emotion. Journal of
longitudinal studies. Psychological Medicine, 46, 225–236. Clinical Psychology, 69, 1213–1227.
Rogers, A. A., Ha, T., Updegraff, K. A., & Iida, M. (2018). Selby, E. A., & Joiner, T. E. (2013). Emotional cascades as
Adolescents’ daily romantic experiences and negative mood: prospective predictors of dysregulated behaviors in borderline
A dyadic, intensive longitudinal study. Journal of Youth and personality disorder. Personality Disorders: Theory, Research,
Adolescence, 47, 1517–1530. and Treatment, 4, 168–174.
Ross, M. (1989). Relation of implicit theories to the construction Selby, E. A., Nock, M. K., & Kranzler, A. (2014). How does self-
of personal histories. Psychological Review, 96, 341–357. injury feel? Examining automatic positive reinforcement in
Russell, J. J., Moskowitz, D. S., Zuroff, D. C., Sookman, D., & adolescent self-injurers with experience sampling. Psychiatry
Paris, J. (2007). Stability and variability of affective experience Research, 215, 417–423.
and interpersonal behavior in borderline personality disorder. Serre, F., Fatseas, M., Swendsen, J., & Auriacombe, M. (2015).
Journal of Abnormal Psychology, 116, 578–588. Ecological momentary assessment in the investigation of
Santangelo, P. S., Bohus, M., & Ebner-Priemer, U. W. (2014). craving and substance use in daily life: A systematic review.
Ecological momentary assessment in borderline personality Drug and Alcohol Dependence, 148, 1–20.
disorder: A review of recent findings and methodological Sher, K. J., Grekin, E. R., & Williams, N. A. (2005). The
challenges. Journal of Personality Disorders, 28, 555–576. development of alcohol use disorders. Annual Review of
Santangelo, P. S., Koenig, J., Funke, V., Parzer, P., Resch, F., Ebner- Clinical Psychology, 1, 493–523.
Priemer, U. W., & Kaess, M. (2017). Ecological momentary Shiffman, S. (2009). Ecological momentary assessment (EMA)
assessment of affective and interpersonal instability in in studies of substance use. Psychological Assessment, 21,
adolescent non-suicidal self-injury. Journal of Abnormal Child 486–497.
Psychology, 45, 1429–1438. Shiffman, S., Stone, A. A., & Hufford, M. R. (2008). Ecological
Santangelo, P. S., Reinhard, I., Koudela-Hamila, S., Bohus, M., momentary assessment. Annual Review of Clinical Psychology,
Holtmann, J., Eid, M., & Ebner-Priemer, U. W. (2017). 4, 1–32.
The temporal interplay of self-esteem instability and Shingleton, R. M., Eddy, K. T., Keshaviah, A., Franko, D. L.,
affective instability in borderline personality disorder Swanson, S. A., Yu, J. S., . . . Herzog, D. B. (2013). Binge/
patients’ everyday lives. Journal of Abnormal Psychology, 126, purge thoughts in nonsuicidal self-injurious adolescents: An
1057–1065. ecological momentary analysis. International Journal of
Santangelo, P. S., Reinhard, I., Mussgay, L., Steil, R., Sawitzki, Eating Disorders, 46, 684–689.
G., Klein, C., . . . Ebner-Priemer, U. W. (2014). Specificity of Shiyko, M. P., Burkhalter, J., Li, R., & Park, B. J. (2014).
affective instability in patients with borderline personality Modeling nonlinear time-dependent treatment effects: An
disorder compared to posttraumatic stress disorder, bulimia application of the generalized time-varying effect model
nervosa, and healthy controls. Journal of Abnormal Psychology, (TVEM). Journal of Consulting and Clinical Psychology, 82,
123, 258–272. 760–772.
Scala, J. W., Levy, K. N., Johnson, B. N., Kivity, Y., Ellison, Simons, J. S., Dvorak, R. D., Batien, B. D., & Wray, T. B. (2010).
W. D., Pincus, A. L., . . . Newman, M. G. (2018). The role of Event-level associations between affect, alcohol intoxication,
negative affect and self-concept clarity in predicting self- and acute dependence symptoms: Effects of urgency, self-
injurious urges in borderline personality disorder using control, and drinking experience. Addictive Behaviors, 35,
ecological momentary assessment. Journal of Personality 1045–1053.
Disorders, 32(Supplement), 36–57. Simons, J. S., Gaher, R. M., Oliver, M. N., Bush, J. A., &
Schwartz, J. E., & Stone, A. A. (1998). Strategies for analyzing Palmer, M. A. (2005). An experience sampling study of
ecological momentary assessment data. Health Psychology, 17, associations between affect and alcohol use and problems
6–16. among college students. Journal of Studies on Alcohol, 66,
Schwartz, J. E., & Stone, A. A. (2007). The analysis of real-time 459–469.
momentary data: A practical guide. In A. Stone, S. Shiffman, Smyth, J. M., Zawadzki, M. J., Juth, V., & Sciamanna, C. N.
A. Arienza, & L. Nebeling (Eds.), The science of real-time data (2017). Global life satisfaction predicts ambulatory affect,
capture: Self-reports in health research (pp. 76–113). New York, stress, and cortisol in daily life in working adults. Journal of
NY: Oxford University Press. Behavioral Medicine, 40, 320–331.
Scott, L. N., Wright, A. G. C., Beeney, J. E., Lazarus, S. A., Solhan, M. B., Trull, T. J., Jahng, S., & Wood, P. K. (2009).
Pilkonis, P. A., & Stepp, S. D. (2017). Borderline personality Clinical assessment of affective instability: Comparing EMA
disorder symptoms and aggression: A within-person process indices, questionnaire reports, and retrospective recall.
model. Journal of Abnormal Psychology, 126, 429–440. Psychological Assessment, 21, 425–436.
Selby, E. A., Cornelius, T., Fehling, K. B., Kranzler, A., Panza, Spangenberg, L., Forkmann, T., & Glaesmer, H. (2015).
E. A., Lavender, J. M., . . . Grange, D. L. (2015). A perfect Investigating dynamics and predictors of suicidal behaviors
storm: Examining the synergistic effects of negative and using ambulatory assessment. Neuropsychiatrie, 29, 139–143.

Steptoe, A., Gibson, E. L., Hamer, M., & Wardle, J. (2007). impulsivity in psychiatric out-patients’ daily lives. Addiction,
Neuroendocrine and cardiovascular correlates of positive 111, 2052–2059.
affect measured by ecological momentary assessment and by Tully, L. M., Lincoln, S. H., & Hooker, C. I. (2012). Impaired
questionnaire. Psychoneuroendocrinology, 32, 56–64. executive control of emotional information in social
Steptoe, A., & Wardle, J. (2011). Positive affect measured using anhedonia. Psychiatry Research, 197, 29–35.
ecological momentary assessment and survival in older men van Eck, M., Nicolson, N. A., & Berkhof, J. (1998). Effects of
and women. Proceedings of the National Academy of Sciences, stressful daily events on mood states: Relationship to global
108, 18244–18248. perceived stress. Journal of Personality and Social Psychology,
Stone, A. A., & Broderick, J. E. (2007). Real-time data 75, 1572–1585.
collection for pain: Appraisal and current status. Pain Vansteelandt, K., Claes, L., Muehlenkamp, J., De Cuyper, K.,
Medicine, 8, S85–S93. Lemmens, J., Probst, M., . . . Pieters, G. (2013). Variability
Stone, A. A., & Shiffman, S. (1994). Ecological momentary in affective activation predicts non-suicidal self-injury in
assessment (EMA) in behavioral medicine. Annals of eating disorders. European Eating Disorders Review, 21,
Behavioral Medicine, 16, 199–202. 143–147.
Swendsen, J. D., Tennen, H., Carney, M. A., Affleck, G., Willard, Vansteelandt, K., Houben, M., Claes, L., Berens, A., Sleuwaegen,
A., & Hromi, A. (2000). Mood and alcohol consumption: E., Sienaert, P., & Kuppens, P. (2017). The affect stabilization
An experience sampling test of the self-medication hypothesis. function of nonsuicidal self injury in borderline personality
Journal of Abnormal Psychology, 109, 198–204. disorder: An ecological momentary assessment study.
Thompson, R. J., Mata, J., Jaeggi, S. M., Buschkuehl, M., Jonides, Behaviour Research and Therapy, 92, 41–50.
J., & Gotlib, I. H. (2012). The everyday emotional experience Verduyn, P., Delvaux, E., Van Coillie, H., Tuerlinckx, F., & Van
of adults with major depressive disorder: Examining Mechelen, I. (2009). Predicting the duration of emotional
emotional instability, inertia, and reactivity. Journal of experience: Two experience sampling studies. Emotion, 9,
Abnormal Psychology, 121, 819–829. 83–91.
Thompson, W. K., Gershon, A., O’Hara, R., Bernert, R. A., & Victor, S. E., & Klonsky, E. D. (2014). Daily emotion in non-
Depp, C. A. (2014). The prediction of study-emergent suicidal suicidal self-injury. Journal of Clinical Psychology, 70,
ideation in bipolar disorder: A pilot study using ecological 364–375.
momentary assessment data. Bipolar Disorders, 16, 669–677. Walls, T. A., & Schafer, J. L. (2006). Models for intensive
Timm, C., Ubl, B., Zamoscik, V., Ebner-Priemer, U., Reinhard, longitudinal data. London, UK: Oxford University Press.
I., Huffziger, S., .
.
.
Kuehner, C. (2017). Cognitive and Walsh, M. A., Royal, A., Brown, L. H., Barrantes-Vidal, N., &
affective trait and state factors influencing the long-term Kwapil, T. R. (2012). Looking for bipolar spectrum
symptom course in remitted depressed patients. PloS One, psychopathology: Identification and expression in daily life.
12, e0178759. Comprehensive Psychiatry, 53, 409–421.
Tomko, R. L., Lane, S. P., Pronove, L. M., Treloar, H. R., Brown, Wichers, M. C., Myin-Germeys, I., Jacobs, N., Peeters, F., Kenis,
W. C., Solhan, M. B., . . . Trull, T. J. (2015). Undifferentiated G., Derom, C., . . . van Os, J. (2007). Evidence that moment-
negative affect and impulsivity in borderline personality and to-moment variation in positive emotions buffer genetic risk
depressive disorders: A momentary perspective. Journal of for depression: A momentary assessment twin study. Acta
Abnormal Psychology, 124, 740–753. Psychiatrica Scandinavica, 115, 451–457.
Torous, J., Staples, P., Shanahan, M., Lin, C., Peck, P., Keshavan, Wichers, M., Peeters, F., Geschwind, N., Jacobs, N., Simons, C.,
M., & Onnela, J.-P. (2015). Utilizing a personal smartphone Derom, C., . . . Van Os, J. (2010). Unveiling patterns of
custom app to assess the Patient Health Questionnaire-9 affective responses in daily life may improve outcome
(PHQ-9) depressive symptoms in patients with major prediction in depression: A momentary assessment study.
depressive disorder. JMIR Mental Health, 2, e8. Journal of Affective Disorders, 124, 191–195.
Treloar, H., Piasecki, T. M., McCarthy, D. M., Sher, K. J., & Wilson, R. E., Thompson, R. J., & Vazire, S. (2017). Are
Heath, A. C. (2015). Ecological evidence that affect and fluctuations in personality states more than fluctuations in
perceptions of drink effects depend on alcohol expectancies. affect? Journal of Research in Personality, 69, 110–123.
Addiction, 110, 1432–1442. Wise, R. A., & Koob, G. F. (2014). The development and
Trull, T. J., Lane, S. P., Koval, P., & Ebner-Priemer, U. W. (2015). maintenance of drug addiction. Neuropsychopharmacology,
Affective dynamics in psychopathology. Emotion Review, 7, 39, 254–262.
355–361. Wolff, S., Stiglmayr, C., Bretz, H. J., Lammers, C. H., &
Trull, T. J., Solhan, M. B., Tragesser, S. L., Jahng, S., Wood, Auckenthaler, A. (2007). Emotion identification and tension
P. K., Piasecki, T. M., & Watson, D. (2008). Affective in female patients with borderline personality disorder.
instability: Measuring a core feature of borderline personality British Journal of Clinical Psychology, 46, 347–360.
disorder with ecological momentary assessment. Journal of Zaki, L. F., Coifman, K. G., Rafaeli, E., Berenson, K. R., &
Abnormal Psychology, 117, 647–661. Downey, G. (2013). Emotion differentiation as a protective
Trull, T. J., Wycoff, A. M., Lane, S. P., Carpenter, R. W., & factor against nonsuicidal self-injury in borderline personality
Brown, W. C. (2016). Cannabis and alcohol use, affect and disorder. Behavior Therapy, 44, 529–540.

CH A PT E R
Treating Emotion Dysregulation
29 in Externalizing Disorders
Dominika A. Winiarski, April L. Brown, Niranjan S. Karnik, and Patricia A. Brennan
Abstract
Externalizing behaviors are characterized by outward displays of aggression, impulsivity, and

deceitfulness, and are often taken out on an individual’s environment or on another person in that
environment. One of the proposed underlying risk factors for externalizing behavior is emotion
dysregulation. This chapter summarizes several empirically supported treatments for emotion
dysregulation among children, adolescents, and adults with externalizing behavior problems.
Cognitive-behavioral, mindfulness-based, and dialectical behavioral therapy approaches are reviewed,
with particular emphasis on the importance of matching the aforementioned empirically based
treatments to the developmental level of the patient. Furthermore, this chapter summarizes notable
work that has been done to identify children at risk for externalizing behavior problems earlier in
development, and to then subsequently teach emotion regulatory strategies in a preventative manner.
Clinical implications and future directions for research are also discussed.
Keywords: externalizing, emotion dysregulation, intervention, prevention, developmental
Introduction that are most efficacious for preventing the emer-

In this chapter, we discuss emotion-focused treat- gence of clinically significant behavioral problems
ments of externalizing behavior problems in youth. among at-risk youth. We end with a discussion of
Our aims are to review this literature and to high- remaining questions and suggestions for future di-
light research that demonstrates utility in managing rections for this rapidly expanding area of inquiry.
the symptoms of externalizing behavior by targeting
emotion dysregulation specifically. We begin with a Brief Overview of Externalizing Behavior
brief descriptive overview of disruptive and impul- Externalizing psychopathology is characterized by
sive behaviors, and highlight the role that emotion undercontrolled, hyperactive, aggressive, defiant,
dysregulation plays in the development and mainte- and/or deceitful behaviors, and includes disruptive,
nance of externalizing disorders in youth, to illus- impulse control, and conduct disorders (Gartstein,
trate why treatments targeting emotion dysregula- Putnam, & Rothbart, 2012). Disorders that fall
tion in these populations yield so much promise. under the externalizing domain of psychopathology
We then review theoretical bases of emotion dys- involve maladaptive behaviors directed toward one’s
regulation and discuss how this research can inform external environment that result in functional im-
our knowledge of externalizing behavior, as well as pairment in at least one domain (e.g., school, work,
how mental health care providers working with social relationships, or family functioning; Hasin
these populations should measure emotion dysregu- et al., 2013). Externalizing behaviors can also manifest
lation. We then discuss specific treatments that as substance- and alcohol-related disorders during
target emotion dysregulation among children, ado- adolescence and adulthood (Farmer et al., 2016;
lescents, and adults, with emphasis on treatments Hasin et al., 2013). Although a certain degree of
427
e xternalizing behavior during early childhood (i.e., Hoeksema, 2012). Volitional emotion regulation is
ages 2 to 3) is normal (e.g., Tremblay, 2000), chil- driven by explicit goals, requires conscious effort,
dren who display high levels of externalizing behav- and demands attentional resources. Following from
iors later in childhood are at risk of developing path- this definition, emotion dysregulation refers to inap-
ological outcomes, including delinquency during propriate experience or expression of emotion that
adolescence and an increased likelihood of criminal- interferes with goal-directed behavior (Gratz &
ity in adulthood (Armistead, Wierson, Forehand, & Roemer, 2004; Gross & Thompson, 2007).
Frame, 1992; Broidy et al., 2003). Contemporary models of psychopathology view
Children who consistently engage in externaliz- emotion dysregulation as a core feature of both in-
ing behavior may be diagnosed with syndromes ternalizing and externalizing problems (e.g.,
including oppositional defiant disorder (ODD)
Beauchaine, 2015).
and conduct disorder (CD; American Psychiatric
Association [APA], 2013). ODD consists of a pat- Emotion Dysregulation in Externalizing
tern of emotional and behavioral symptoms that Behaviors
involve angry and irritable mood, vindictiveness, Externalizing disorders have traditionally been con-
argumentativeness, and defiant behavior. Children ceptualized as problems of behavior and cognition,
with ODD refuse to comply with authority and but behaviors that fall under this domain are inex-
often deliberately provoke others (APA, 2013). CD tricably linked with emotional processes.
consists of a pattern of behavior in which social Disorganization, explosiveness, and defiance are
norms and rights of others are violated. Many, hallmarks of externalizing psychopathology, and
though not all, children and adolescents with CD there is clear evidence that emotion dysregulation is
are aggressive and deceitful. Both ODD and CD associated with aggressive behavior, impulsivity, and
often co-occur with, and are developmental se- substance use (e.g., Beauchaine, 2012; Roberton,
quelae of, attention deficit hyperactivity disorder Daffern, & Bucks, 2012). In fact, undercontrolled
(ADHD; APA, 2013)—a behavioral syndrome behaviors including anger, frustration, and hostility
characterized by hyperactivity, impulsivity, and in- are common among children, adolescents, and
attention. It is not surprising that problems with adults with externalizing disorders, and manifest as
impulsivity, emotional volatility, and self-regulation a difficulty in regulating emotional responses in
are shared features among children with these exter- various situations (e.g., Robins, John, Caspi,
nalizing behavior diagnoses (see Beauchaine, Zisner, Moffitt, & Stouthamer-Loeber, 1996; Roeser &
& Sauder, 2017). Eccles, 2014). There is also a growing body of litera-
ture that identifies associations between externaliz-
Externalizing Disorders and Emotion ing behavior and inadequate self-regulation, includ-
Dysregulation ing problems inhibiting behavior and controlling
Defining Emotion Regulation attentional and cognitive processing (Roberton
Over the past 20 or so years, clinical researchers et al., 2012). Children diagnosed with externalizing
have specified how emotion regulation is associated disorders score significantly lower on measures of
with psychopathology. Current diagnostic manuals attention regulation, inhibition, and effortful con-
in psychiatry reveal that many, if not most, diagnos- trol. They also score higher on impulsivity and dis-
tic criteria contain emotion-related problems (APA, play more negative reactions to disappointment
2013; Mullin & Hinshaw, 2007), and that intense (Eisenberg et al., 2001; Roberton et al., 2012).
and/or prolonged experience of one or more nega- Historically, externalizing syndromes have been
tive emotions is maladaptive. Emotion dysregula- classified as disruptive behavior disorders in the
tion has therefore been cited as a broad, rather than DSM, but evidence suggests that emotion dysregu-
specific, risk factor for psychopathology (e.g., lation is also a core deficit (e.g., Cavanagh, Quinn,
Beauchaine, 2012). Duncan, Graham, & Balbuena, 2017). For example,
A comprehensive discussion of emotion regula- Cavanagh et al. (2017) noted that ODD and emo-
tion is beyond the scope of this chapter but can be tion dysregulation load onto a single factor and sug-
found in other chapters of this volume. Briefly, gested that ODD may be better conceptualized as
however, emotion regulation often refers to the an emotion dysregulation disorder rather than a
adaptiveness with which individuals monitor, evalu- disruptive disorder per se. Others have noted that
ate, and modify the nature and course of their emo- emotion dysregulation becomes more entrenched
tional responses to environmental demands (Nolen- and pervasive among children who progress past
428 Treating Emotion Dysregul ation

ADHD and into ODD, CD, and delinquency as poverty are all childhood vulnerabilities/risk factors
they mature (Beauchaine et al., 2017). for aggression. Equifinality suggests that a given
Similar patterns have emerged in research with outcome may come about as a result of any one or a
adults. For example, Cohn and colleagues (2010) combination of these risk factors. When studying
cited emotion dysregulation as a mediator between how emotion dysregulation relates to externalizing
restrictive emotionality and aggression—a link driven disorders, it is important to consider these perspec-
largely by lack of acceptance and inability to tolerate tives because contexts shape behavior. Although
emotional experiences. Other researchers cite emo- longitudinal studies demonstrate that preschool
tion dysregulation as a predictor of partner abuse emotion dysregulation (e.g., low frustration toler-
among men. Tager, Good, and Brammer (2010), for ance and irritability) predicts subsequent psychopa-
example, found that men who had difficulty man- thology (e.g., Maire, Galera, Meyer, Salla, & Michel,
aging negative affect were more likely to engage in 2017), the specific manner in which emotion dys-
intimate partner violence. Collectively, these studies regulation is expressed may depend on environmen-
demonstrate that poor emotion regulation is asso- tal factors.
ciated with externalizing behaviors at all ages—
consistent with the notion that effective emotion Measuring Externalizing Behavior and
regulation is critical for mental health (e.g., Nolen- Emotion Dysregulation
Hoeksema, 2012). Before discussing treatment, it is important to sum-
The concept of emotion dysregulation originated marize assessment methods for measuring emotion
in the borderline personality disorder (BPD) litera- dysregulation among externalizing samples. Given
ture (see Linehan, 1993). BPD is a pervasive pattern space constraints, this section is brief. Interested
of instability in emotion, impulse control, and inter- readers are referred elsewhere for more comprehen-
personal relationships (see Lieb, Zanarini, Schmahl, sive coverage (e.g., Beauchaine, 2015; Part V of this
Linehan, & Bohus, 2004). From Linehan’s (1993) volume). Many of these assessment tools are used in
perspective, the inability to regulate intense emo- both clinical and research settings, including evalu-
tional responses underlies many behaviors associated ations of evidence-based interventions.
with BPD, including self-harm, which by many ac-
counts serves emotion regulation functions (e.g., Externalizing Behavior Measures
Bentley, Nock, & Barlow, 2014; Klonsky, 2009). This In addition to using DSM-5 criteria to assess the
conceptualization of harmful behaviors as an emo- presence of externalizing syndromes such as ODD,
tion regulation strategy has been supported empiri- CD, or ADHD during clinical interviewing, mental
cally by the research literature (e.g., Briere & Gil, health professionals often utilize a range of ob-
1998; Klonsky, 2011), and therefore has utility when server- and self-report measures to quantify exter-
discussing emotion regulation in relation to external- nalizing behaviors. A variety of assessment tools
izing psychopathology. exist for measuring externalizing behavior problems
among children, but only the most frequently used
Developmental Considerations are discussed here. The Conners’ Rating Scales (CRS-
Two important concepts may serve as guides for R; Conners, 2001) use a multi-informant approach
understanding developmental pathways through
to capture a range of internalizing and externalizing
which emotion dysregulation disrupts develop- problem behaviors among youth ages 3 to 17 years.
mental processes: multifinality and equifinality. The Behavioral Assessment System for Children
Multifinality refers to the possibility of multiple de- (BASC; Reynolds & Kamphaus, 1992; Reynolds &
velopmental outcomes from the same risk factor Kamphaus, 1998) is another well-established assess-
(e.g., Mullin & Hinshaw, 2007). This concept may ment and takes a multi-informant approach for chil-
be applied when discussing differential outcomes dren and adolescents ages 2½ to 18 years.
among youth with emotion dysregulation who later However, the most popular assessment tool is
develop either predominant internalizing or exter- the Achenbach System of Empirically Based
nalizing disorders, depending on a host of environ- Assessment for School-Age Children (ASEBA;
mental factors. Conversely, equifinality refers to Achenbach & Rescorla, 2001), which includes three
the same developmental outcome that comes about instruments for measuring emotional and behav-
as the result of numerous risk factors (Mullin & ioral problems: the parent-report Child Behavior
Hinshaw, 2007). For example, poor emotion regu- Checklist (CBCL), the adolescent Youth Self-
lation, exposure to violence, and neighborhood Report (YSR) form, and the Teacher Report Form
Winiarski, Brown, Karnik, and Brennan 429

(TRF). The ASEBA school-age instruments are 1996). The Children’s Emotion Management Scales
standardized to national norms that assess adaptive (Zeman, Shipman, & Penza-Clyve, 2001) were de-
and maladaptive functioning in children and ado- signed to assess two skills involved in acquiring
lescents. ASEBA components are widely used in emotional competence: (1) management of sadness
research studies and across mental health facilities, through inhibition of expression and dysregulated
schools, and medical settings (Bordin et al., 2013). expression and (2) methods of effective coping with
The Externalizing Problems subscale is one of sadness experience among individuals ages 7 to 17.
the most common measures cited in the literature Similarly, the Emotion Expression Scale for Children
on disruptive behavior in youth (Cheong & assesses reluctance to express negative emotions to
Raudenbush, 2000). others and awareness of emotions (Penza-Clyve &
Zeman, 2002).
Emotion Dysregulation Measures One of the most well-established self-report
Emotion dysregulation is also quantified using a va- tools, however, is the Difficulties with Emotion
riety of measures and methods, including behav- Regulation Scale (DERS; Gratz & Roemer, 2004),
ioral observation, informant report, self-report, which has been validated on adults but is being
and physiological function (see Beauchaine, 2015). used increasingly with adolescents. DERS evaluates
Behavioral observational methods are often consid- (1) awareness and understanding of emotions,
ered the gold standard in developmental research. (2) acceptance of emotions, (3) the ability to engage
These include direct indices such as aggressive out- in goal-directed behavior and inhibit impulsive
bursts, and more subtle markers such as tone of behavior when experiencing negative emotions, and
voice, nonverbal cues, and body language. Notably, (4) access to emotion regulation strategies perceived
however, observational approaches do not capture as effective. The most commonly used parent- and
internal processes related to emotions (Adrian, teacher-report measure is the Emotion Regulation
Zeman, & Veits, 2011). Checklist (ER Checklist; Shields & Cicchetti,
In their 35-year review of emotion regulation 1997), which assesses core aspects of emotion regu-
assessment across four developmental stages (i.e., in- lation, such as negative affect and mood lability, as
fancy, toddler/preschool, middle childhood, and ad- well as processes central to adaptive regulation. The
olescence), Adrian and colleagues (2011) indicated perspective that emotion dysregulation and exter-
that the most rigorous studies use multimethod as- nalizing behaviors arise from the complex interplay
sessment, including at least one physiological meas- of numerous biopsychosocial factors is reflected in
ure. Among the most common physiological indices multimethod assessment methods used to capture
of emotion regulation/dysregulation is respiratory these constructs in both research and clinical
sinus arrhythmia (RSA), which, given appropriate settings.
stimulus conditions, marks parasympathetic-linked
cardiac activity (e.g., Thayer, Hansen, Saus-Rose, & Treating Emotion Dysregulation in
Johnsen, 2009). Some studies also use functional Externalizing Behavior Problems
magnetic resonance imaging (fMRI; particularly The utility of targeting emotion dysregulation in the
frontal function during emotion evocation) and treatment of externalizing behavior problems has
event-related potentials (e.g., Hare et al., 2008). been well established in the literature. For example,
Cortisol reactivity remains a commonly used physi- in a recent study of Multisystemic Therapy, changes
ological index of dysregulation in studies of aggres- in emotion dysregulation distinguished treatment
sive and delinquent behaviors across the lifespan responders from nonresponders (Winiarski et al.,
(e.g., Allwood, Handwerger, Kivlighan, Granger, & 2017). Specifically, females who demonstrated re-
Stroud, 2011; Alink et al., 2008; Popma et al., 2007; ductions in emotion dysregulation as measured by
Sondeijker et al., 2007). caregiver reports over the course of the intervention
A number of self- and other-report measures have were more likely to evidence successful treatment
also been validated to measure emotion dysregula- responses. Emotion regulation also mediates rela-
tion among children, adolescents, and adults. The tions between (1) peer victimization and stressful
Emotion-Affect Regulation Interview, for example, life events and (2) future aggression (Herts,
is a semistructured interview that uses vignettes to McLaughlin, & Hatzenbuehler, 2012). Although
assess emotion regulation decisions, reasons and researchers have clearly shown that emotion dys-
methods of regulation, and emotion self-efficacy regulation is one mechanism through which exter-
among children and adolescents (Zeman & Garber, nalizing behaviors develop, further work is needed

to better apply our understanding of treatment executive functioning capabilities. The executive
mechanisms to the next iteration of targeted inter- functioning processes are generally thought to
ventions for these populations. mature gradually across development and coincide
Initially, there was some skepticism about the with the development of the frontal lobes.
methodological soundness of the existing literature Developmental scientists often discuss the discon-
on this topic, particularly among child populations. nect that occurs between the development of the
For example, Zwi and colleagues (2011) evaluated amygdala (the emotional control center of the
the effectiveness of parent training programs (dis- brain), which occurs early in childhood, and the
cussed in greater detail in Treating Emotion frontal lobes (the inhibitory center of the brain),
Dysregulation in Children in treating ADHD in chil- which occurs throughout childhood and into ado-
dren and adolescents and found that, although these lescence and early adulthood. This disconnect is
programs appear to have positive impacts on child cited as a reason that children and especially adoles-
behavior, the poor methodological quality of many cents experience higher rates of emotional volatility
existing studies made it difficult for the authors to than adults (Silvers et al., 2016). Effective emotion
form substantive clinical practice guidelines. Studies regulation is critical for appropriate socioemotional
since then have made a more concerted effort to ad- development (e.g., Southam-Gerow & Kendall,
dress these limitations by specifically evaluating me- 2002), and studies have shown that impairments
diators of treatment. For example, a recent study in the ability to regulate negative emotional states
demonstrated that measuring cardiac activity and as early as childhood place individuals at risk for
reactivity among children being treated for ADHD externalizing psychopathology (e.g., Kochanska &
proved to be a reliable biomarker for identifying the Knaack, 2003).
most neurobiologically at-risk children requiring Given that the development of the executive
further treatment (Beauchaine et al., 2013). functioning system is dependent on age and that
Despite some early criticism, the literature on most existing treatments work on explicitly target-
treatments for emotion dysregulation among ex- ing self-regulation, it makes sense to examine treat-
ternalizing populations has overall greatly ex- ment of emotion dysregulation in externalizing be-
panded in the last several years to include inter- havior from a developmental perspective, beginning
ventions across all stages of development. In in childhood and into adolescence and adulthood.
addition, many treatments for externalizing be- Not surprisingly, some of these treatments are more
havior problems have been developed to include efficacious at certain ages than others, and the reader
both parent and child intervention components will see that this chapter is more heavily weighted
in an effort to directly target a child’s developing toward interventions for children and adolescents.
emotion regulatory system. For example, Carolyn Young children, for example, are more likely to ben-
Webster-Stratton’s Incredible Years Program (de- efit from behavioral-based interventions that heav-
scribed in detail in Treating Emotion Dysregulation ily involve parents, rather than cognitively mediated
in Children includes both a parent and a child interventions, given their less advanced cognitive
focus on emotion regulation, and has shown effi- reasoning abilities. Equally important to note, how-
cacy in reducing externalizing behavior problems, ever, is the idea that interventions should not be
including ODD (e.g., Webster-Stratton & Reid, selected exclusively based on age, but rather based
2010) and ADHD (Webster-Stratton, Reid, & on a child’s developmental level. That is, if a child’s
Beauchaine, 2011). developmental age and chronological age are not
In addition to the cardiac biomarkers discussed commensurate with one another, the clinician
previously, specific cognitive and behavioral features would be advised to select a treatment course that is
of emotion dysregulation among youth with exter- most appropriate to the individual’s developmental
nalizing behavior include difficulties decreasing level to increase receptivity and compliance. This
their own negative affect, weak emotional under- important clinical observation has been made by
standing and expression, poor attention control, many others in the field as well (e.g., Webster-
difficulty inhibiting inappropriate behaviors, and Stratton, 2008d). Likewise, it is important to keep
acting out aggressively in response to negative emo- in mind that although certain interventions are
tions (e.g., Barkley, 1997; Keenan, 2000; Macklem, more effective at younger ages (e.g., parent manage-
2008; Sjöwall, Roth, Lindqvist, & Thorell, 2013; ment training), the tools that parents can glean
Shaw, Stringaris, Nigg, & Leibenluft, 2014). In from these interventions can be critical in supple-
sum, these individuals experience deficits in their menting more individually tailored interventions

for older youth as well (i.e., adolescent-focused in- Roberton, Daffern, & Bucks, 2012). This premise
terventions also benefit from parental involvement). was central to the development of DBT (Linehan,
Before presenting specific treatments for each 1993), which combines principles of changing be-
age group, we will briefly discuss three primary, em- havior with principles of acceptance and mindful-
pirically validated treatment models for the treat- ness (Macpherson, Cheavens, & Fristad, 2013).
ment of emotion dysregulation among individuals The last intervention we will discuss in this review
with externalizing behavior problems: Cognitive is mindfulness. Although mindfulness is an impor-
Behavioral Therapy, Dialectical Behavior Therapy, tant component of DBT, it can also be used as a
and Mindfulness-based interventions. standalone treatment. Broadly speaking, mindful-
ness teaches nonreactive perspectives on thoughts,
Overview of Existing Treatments for emotional states, and body sensations (Kabat-Zinn,
Emotion Dysregulation 2013). It is used for stress reduction (Sharma &
Cognitive-Behavioral therapy (CBT) relies heavily Rush, 2014), coping with pain (Garmon et al., 2014;
on constructs borrowed from learning and informa- Hilton et al., 2017; Kabat-Zinn, 1982), and treat-
tion processing theories (Beck & Fernandez, 1998). ment of a variety of psychiatric conditions including
Individuals are taught to evaluate and challenge spe- depression (Greeson et al., 2015) and anxiety (Arch
cific perceptions that cause maladaptive behavior et al., 2013). Recent research indicates that mindful-
and/or emotional reactions. CBT operates under ness meditation practices alter attentional networks
the assumption that thoughts, feelings, and behav- in the brain (Jha, Krompinger, & Baime, 2007) and
iors are all interconnected. Thus, “cognitive distor- reduce amygdala reactivity. Notably, the amygdala is
tions” can result in strong emotional responses that implicated in emotional processing of virtually all
can affect behavior, including impulsivity, aggres- stimuli (Desbordes et al., 2012). By teaching indi-
sion, and/or substance abuse, which together are viduals to be more aware of their thought processes,
hallmark characteristics of delinquent youth. mindfulness may slow emotional and behavioral re-
Likewise, dialectical behavior therapy (DBT) sponses to events. Unlike traditional CBT, mindful-
similarly proposes that dysregulation stems from ness does not attempt to change thoughts in any
distorted cognitive appraisals of situations and way, but rather teaches individuals nonreactive alter-
emotional cues. More specifically, DBT posits that native strategies for managing mood and negative
challenges with emotion regulation are the result of cognitions (Chambers, Gullone, & Allen, 2009;
biosocial transactions in which biological sensitivity Kabat-Zinn et al., 1992; Nolen-Hoeksema, 2012).
to emotions interact with aversive experiences, which
leads to neurobiological dysfunction and inefficient Treating Emotion Dysregulation in Children
emotion management (e.g., Crowell, Beauchaine, Consistent with the tradition of manualized treat-
& Linehan, 2009). The primary goal of DBT is to ment for CBT, parent management training (PMT)
teach clients to actively regulate emotion, using six was developed as a strategy to teach parents behav-
“transacting subsystems” (Neacsiu, Bohus, & Linehan, ioral strategies for managing disruptive behaviors
2014). DBT emphasizes attending to cues within (e.g., Forgatch & Kjobl, 2016; Kazdin, 1997; McCart
relevant contexts and acknowledging how appraisals & Sheidow, 2017), particularly among younger chil-
influence the course of an emotional response, dren. Various PMT models have been developed,
thereby emphasizing regulation after cue appraisal including the Oregon Model (PMTO), which, like
(Neacsiu et al., 2014). most models, teaches parents to use praise and in-
Linehan’s (1993) biosocial theory is applicable to centives, set consistent limits, monitor children’s
a wide range of disorders for which emotion dysreg- behavior, use effective family problem-solving tools,
ulation is a feature. Emotions arise in response to and increase care and involvement (Forgatch &
environmental cues. Cues are appraised, which trig- Patterson, 2010). Although PMT was not initially
gers an emotional response consisting of biological developed to address emotion dysregulation, it has
changes, response tendencies, and actions. These are been modified to directly teach parents ways to
affected by proximal and distal emotion vulnerabil- model and to reinforce appropriate regulatory strate-
ity factors. It is therefore hypothesized that emotion gies for their children, as demonstrated by the em-
dysregulation is a transdiagnostic phenomenon, as pirically supported Incredible Years Program, which
reactivity to emotional cues coupled with insuffi- has been modified to include parent, teacher, and
cient regulation strategies may result in psychopa- child training components (e.g., Webster-Stratton, 1
thology (e.g., Beauchaine, 2012; Neacsiu et al., 2014; 984, 2000, 2008a, 2008b, 2008c).

Together with a therapist, parents identify spe- aging their children’s behaviors, PMT also focuses
cific disruptive, impulsive, and/or inattentive be- on teaching a child’s caregivers new ways to reduce
haviors that they would like to target with their negative parenting behaviors and increase positive
child, and then parents learn to monitor the behav- parenting.
ior (e.g., count and graph the number of times a Emotion regulation capacities measured as early
child hits a sibling each day). Once specific behav- as 1 year of age have predicted subsequent external-
iors are identified, parents are taught ways to attend izing symptoms (Halligan et al., 2013), which sup-
to positive behaviors, ignore negative behaviors, ports the proposal that emotion dysregulation plays
and develop contingency management programs in a role in atypical child development. Therefore, in-
which desired activities are contingent on specific terventions like DBT and mindfulness, which were
positive behaviors. Parents are taught to reward specifically designed to teach individuals to regulate
children for desired behaviors, such as following their emotions, can be applied to younger popula-
rules, remaining attentive to tasks, and responding tions as well. Although perhaps not a first-line
in more appropriate ways to frustration (i.e., learn- treatment, it is important to appreciate that DBT
ing to walk away and take a “reset” vs. throwing a (with modifications) can be successfully imple-
tantrum). Over time, one marker of treatment suc- mented among preadolescent populations. DBT for
cess is a child’s improved self-regulation. Simply Children (DBT-C; Perepletchikova & Goodman,
put, when children learn that disruptive and unde- 2014) was developed using core DBT principles,
sirable behaviors will be ignored or, in more ex- but simplifies and reorganizes the skills-training
treme cases, punished (i.e., through removal of manual, incorporates psychoeducation compo-
privileges), whereas self-regulation will be praised, nents, utilizes child-friendly materials and activities,
be rewarded, and lead to privileges, children and involves caregivers. A key mechanism of change
become more likely to use adaptive strategies for DBT is helping individuals with emotion dys-
moving forward (Kazdin, 1997). regulation to engage in functional, life-enhancing
When intervening with young children with ex- behavior despite intense negative emotional states
ternalizing behavior problems, it is essential that (Lynch, Chapman, Rosenthal, Kuo, & Linehan,
parenting be leveraged to improve emotion dysreg- 2006). DBT presumes that maladaptive behaviors
ulation because of its critical role in shaping and stem from a skills deficit, problematic expectations,
maintaining self-regulation. In infancy, children’s and emotion inhibition. DBT-C targets these fac-
emotions are regulated in dyadic interactions with tors via direct skills training and practice, teaching
their caregivers, which gradually changes across de- the child to modulate behavioral responses and
velopment (Sroufe, 1995; Cole, Martin, & Dennis, increase self-regulatory capacity (Perepletchikova
2004). This mutual regulation of emotion is equally & Goodman, 2014). DBT-C has yielded promising
important among toddlers and preschoolers (Cole, results, as indicated by a recent randomized con-
Teti, & Zahn-Waxler, 2003). Furthermore, effective trolled trial conducted in an outpatient setting
emotion regulation arises from complex interac- for children with disruptive mood dysregulation
tions between neurobiological predispositions (e.g., disorder (characterized by temper tantrums and ag-
genetic, neural) and environmental factors (e.g., gression). Children treated with DBT-C had signif-
parenting, peer affiliations). Thus, the family envi- icantly fewer behavioral outbursts and less anger/
ronment itself shapes and reinforces the develop- irritable mood than controls (Perepletchikova, 2016).
ment of dysregulated emotional processing and In recent years, mindfulness has also gained con-
later disruptive behavior (Snyder, Schrepferman, & siderable support among young populations with
St. Peter, 1997; Snyder, Stoolmiller, Wilson, & behavior problems or at increased risk for developing
Yamamoto, 2003). behavior problems. In a sample of second- and third-
In fact, research indicates positive associations grade students, an 8-week mindfulness intervention
between maternal sensitivity to children’s emotional was effective in improving behavior regulation and
cues and their use of effective emotion regulation executive functioning, according to parent and
strategies. Not surprisingly, negative parenting, teacher report (Flook et al., 2010). Raters endorsed
which is characterized by hostility and low sensitiv- improvements in children’s abilities to shift, initiate,
ity to children’s emotional cues, is often associated and monitor. Although not a clinical sample, the re-
with children’s emotion dysregulation (Sheffield sults of this study suggest that mindfulness interven-
Morris, Silk, Steinberg, Myers, & Robinson, 2007). tions may be effective in helping young children
In addition to teaching different strategies for man- better manage their attention and behavior.

Despite promising findings reported by some re- terventions with a stronger cognitive component
searchers on the effects of mindfulness in reducing would be better suited for this population than for
externalizing symptomatology in younger samples, their younger counterparts.
other studies have produced mixed results. For ex- One program that seeks to improve youth exter-
ample, van der Oord and colleagues (2012) evalu- nalizing behavior problems by modifying hostile at-
ated a joint mindfulness/mindful parent training tributional biases and behavioral responses to those
intervention for a group of 8- to 12-year-old children biases is the Chicago Becoming a Man (BAM) pro-
diagnosed with ADHD and their parents. Parents gram, which was created by two nonprofit organiza-
and teachers were asked to report on ADHD and tions, Youth Guidance and World Sport Chicago
ODD symptoms at the beginning and end of treat- (Ludwig & Shah, 2014). This program uses CBT to
ment. In addition, parents were also asked to rate teach youth to “cognitively slow down” and verbally
their own ADHD symptoms along with parenting mediate their decision making, thereby reducing
stress and overreactivity. Reduction in parent-reported emotionally reactive and poorly thought out impul-
ADHD behaviors of themselves and their children sive behavior. It is estimated that this type of inter-
were found, as were reductions in parental stress and vention would yield a $30 gain for society for every
overreactivity. However, there were no effects on $1 invested in its development and implementation
teacher ratings of externalizing behavior. (Ludwig & Shah, 2014). Effectiveness studies com-
Overall, the evidence suggests that PMT-based pleted to date show that BAM reduces recidivism
interventions are the most effective at treating exter- among adjudicated youth, improves school attend
nalizing behavior and dysregulation in young chil- ance and graduation rates, and reduces involvement
dren. DBT-based interventions have demonstrated in violent crime (Ludwig & Shah, 2014).
success, but additional long-term studies are needed. Similarly, DBT has been used to treat opposi-
Likewise, mindfulness-based approaches are in- tional behaviors, difficulties with interpersonal rela-
creasingly gaining traction and acceptance at the tionships, and poor responses to stress among ado-
elementary school–aged level, but additional work lescent samples. Nelson-Gray and colleagues (2006)
is necessary to fully support the enthusiasm and specifically map DBT treatment targets onto ODD
long-term benefits for this intervention among this criteria within a sample of adolescents, including
age group. emotion dysregulation (e.g. “often loses temper”),
interpersonal effectiveness (e.g., “often argues with
Treating Emotion Dysregulation adults”), and distress tolerance (e.g., “is often touchy
in Adolescents or easily annoyed by others”). They implemented a
Adolescence is stereotypically seen as a developmen- modified skills training component of DBT into
tal period plagued by impulsivity and poor decision group therapy for 32 adolescents with ODD and
making. In fact, some researchers have even postu- observed reductions in caregiver reports of ODD
lated that “adolescence limited” delinquent behav- symptoms and CBCL externalizing symptoms, as
ior is developmentally normative (see classic review well as improvements in interpersonal strength on
in Moffitt, 1993), further highlighting the accept the Behavioral and Emotional Rating Scale, which
ance of some degree of “bad behavior” during this captures the ability to interact with others in social
period of “storm and stress.” Of course, some ado- situations. Nevertheless, without a control group,
lescents engage in clinically significant levels of im- the researchers could not examine the effectiveness
pulsive and disruptive behaviors well beyond what of this treatment over other existing treatments for
is written off as “typical adolescence” and character- externalizing behavior.
istic of clinical diagnoses of ODD, CD, and Others have found success in implementing
ADHD. One promising avenue of research with DBT among incarcerated youth. DBT is especially
this population relies on the principles of CBT to well suited for the treatment of problems typically
address hostile attributional biases (Dodge, Bates, seen in prison samples, such as violent aggression
& Peitit, 1990). This topic has been studied exten- and poor impulse control, and sometimes self-harm
sively among youth with CD and ODD, as well as (Berzins & Trestman, 2004). Because DBT is highly
among youth who have grown up in adverse envi- structured, it can be especially helpful at the onset
ronments (and are thus at risk of developing disrup- of treatment of a youth offender, when he or she is
tive behavior problems). Given the significantly most behaviorally dysregulated and possibly engag-
improved cognitive reasoning abilities that teens ing in suicidal behavior or nonsuicidal self-injury.
have over younger children, it makes sense that in- For example, Eric Trupin applied a modified DBT

intervention among female juvenile offenders DBT, which was initially developed to treat
(Trupin, Stewart, Beach, & Boesky, 2002). The re- borderline personality in adults, has proven effective
sults of the intervention were mixed; there was a in treating a variety of externalizing problems in
reduction in problem behaviors in one unit but not adult prisoner samples. For example, Moore and
in another. Another research group evaluated dia- colleagues (2016) demonstrated the effectiveness of
lectical behavior therapy-corrections modified a brief 8-week DBT skills group among a sample of
(DBT-CM) among a sample of 38 male adolescents male jail inmates. The researchers found that par-
with difficult-to-manage aggression and found sig- ticipation in this group improved coping skills and
nificant changes in physically aggressive behaviors led to decreases in externalization of blame. The au-
(Shelton, Kesten, Zhang, & Trestman, 2011). Of thors call for additional controlled trials of short-
course, more work is needed to understand the spe- term DBT groups among various samples of prison
cific mechanisms of change in these populations, populations. A larger 16-week DBT-CM effective-
but for now, DBT has shown preliminary evidence ness study among male and female adolescent and
of its effectiveness among adolescent populations adult inmates similarly found this treatment to be
with externalizing problems. effective in decreasing aggression, both at the con-
clusion of the intervention and at a 12-month inter-
Treating Emotion Dysregulation in Adults vention follow-up (Shelton, Sampl, Kesten, Zhang,
The section on treating emotion dysregulation in & Trestman, 2009).
adults is considerably shorter given that many of
the interventions summarized previously for ado- A Comment on Early Intervention and
lescents are also effective for adults. Also, given Prevention
greater prevention efforts, an increasing number of An important question is whether youth who are at
children and adolescents are identified and treated risk of developing externalizing disorders should be
earlier in development, thereby reducing the risk of identified and treated earlier, thereby reducing the
prolonged externalizing behavior problems into personal, familial, and societal burdens of future be-
adulthood (see more detailed discussion of this havior problems. Findings reviewed in this chapter
point in the section on early intervention and pre- suggest that emotion regulation might be a fruitful
vention later). target for such prevention efforts. A larger body of
In adults with ADHD, a mindfulness interven- empirical research also suggests that emotion regu-
tion yielded reductions in self-reported symptoms lation deficits may be an important mediator be-
from pre- to postintervention (Zylowska et al., 2008). tween environmental risk factors and the develop-
The 8-week mindfulness program improved conflict ment of later psychopathology. For example, in a
attention and set shifting—executive function skills longitudinal study of 317 children at high risk for
that are often compromised among individuals with conduct disorder, researchers found that elevated
ADHD. In addition, “novice meditators” who com- emotion dysregulation at school entry predicted
pleted an intensive 10-day mindfulness retreat re- mood disturbance (i.e., anger, suicidality, dysphoric
ported improvements in depressive symptoms, rumi- mood) in late adolescence. In addition, West and
nation, and performance measures of working colleagues (2001) demonstrated that, among a na-
memory and sustained attention (Chambers, Chuen tionally representative sample of 22,782 children
Yee Lo, & Allen, 2008). enrolled in kindergarten programs from 1998 to
Integrative body–mind training, which draws on 1999, risk factors associated with poverty predicted
meditation and mindfulness, encourages individuals development of poorer emotion regulation. Physical
not to exert effort in controlling their thoughts, but maltreatment has also been found to relate to poor
rather to focus on body sensations, including breath- regulation of affect and behavior, thereby predispos-
ing, and relaxation cues from the instructor. A brief ing children to higher rates of externalizing behav-
5-day practice among undergraduate Chinese stu- ior problems (Shackman & Pollak, 2014). Others
dents demonstrated increased self- regulation as have found that early emotion regulation abilities
measured by improved performance on a computer- partially mediate the relationship between maternal
ized test of attention (Tang et al., 2007). Collectively, psychopathology and youth behavioral difficulties,
these studies suggest that mindfulness plays an im- including both internalizing and externalizing
portant role in the mediation of executive function symptomatology (Kaufman et al., 2017). These
processes that underlie emotion regulation/dysregu- studies all illustrate that it is imperative to not only
lation (Flook et al., 2010). identify risk factors for emotion dysregulation but

also design interventions that can be applied as early terventions for at-risk youth should consider the im-
in development as possible to mitigate negative con- portant role of key executive functioning strategies
sequences of early adverse experiences on children’s in emotion regulation, particularly during critical
mental health. windows of development across childhood.
Of relevance to prevention of externalizing dis- Another early intervention program, Fast Track,
orders, researchers modified a mindfulness-based employed a multicomponent approach to treat chil-
curriculum for children in early elementary school dren who are at risk for future antisocial behavior
and found considerable improvements across sev- (Conduct Problems Prevention Research Group
eral domains of executive function (Flook et al., [CPPRG], 1999). Modules included a classroom-
2010). Furthermore, Mendelson and colleagues based training, social skills training, academic tutor-
(2010) developed a 12-week mindfulness program ing, parent training, and home visits. By the end of
for a sample of 97 fourth- and fifth-grade students. first grade, children who participated in Fast Track
Intervention components included yoga-based performed better on emotion recognition and
physical activity, breathing strategies, and guided improved their coping with social difficulties.

mindfulness practices. Researchers used parent-, Moreover, children in the intervention were less
teacher-, and self-report scales to evaluate children’s likely to suggest aggressive responses to hypothetical
responses to stress, relations with peers and school, social provocation situations (CPPRG, 1999). By
positive and negative emotions, and depressive the end of third grade, 37% of the intervention
symptoms. The intervention was feasible among group was classified as “free of serious conduct
urban youth and reduced problematic patterns of problem dysfunction” relative to 27% of controls
stressful responding among children. The authors (CPPRG, 2002).
concluded that the intervention was useful in en- Fast Track also produces significant but modest
hancing self-regulation and reducing behavioral and improvements in emotion regulation among fourth-
cognitive activation (Mendelson et al., 2010). As and fifth-grade students. Specifically, the program
reduced behavioral activation is often implicated in reduced the likelihood of problem behaviors by
explosive and impulsive outbursts characteristic of 6% to 7% in the domains of social competence,
many externalizing behavior disorders (Mendelson peer deviance, and conduct problems at home and
et al., 2010), this intervention likely reduces these in the community (CPPRG, 2004). A recent study
disorders as well. (Sorensen, Dodge, & CPPRG, 2016) shed light on
Longitudinal research also demonstrates long- the specific mechanisms by which Fast Track was
term benefits of teaching emotion management effective and concluded that increasing children’s
strategies among children at younger ages. For exam- intrapersonal skills in emotion regulation made
ple, the PATHS (Promoting Alternative THinking them less prone to impulsive outbursts commonly
Strategies) prevention program is based on an seen among individuals with ODD and CD.
affective-behavioral-cognitive-dynamic model of

child development and draws on several develop- Special Considerations for Intervention
mental principles to teach children self-regulation Although the empirically supported treatments dis-
strategies (Kam, Greenberg, & Kusche, 2004). cussed previously are useful for individuals with ex-
When applied in a preschool Head Start program, ternalizing behavior problems, it is also important
PATHS improved emotional knowledge and re- to recognize that certain subgroups may be espe-
duced social withdrawal (Domitrovich, Cortes, & cially likely (or unlikely) to benefit from these inter-
Greenberg, 2007) among children. Another study ventions. For example, Winiarski and colleagues
examined the mediating role of neurocognitive fac- (2017) found that improvements in emotion regula-
tors in the relationship between PATHS involve- tion over the course of multisystemic family therapy
ment and behavioral outcomes among 318 second- predicted successful treatment response only among
and third-grade students (Riggs, Greenberg, Kusche, adolescent females. It is well known that females
& Pentz, 2006). Participants were administered a use certain emotion regulation strategies more
brief IQ task, a Stroop Test (a well-validated measure effectively than males (Nolen-Hoeksema, 2012).
of inhibitory control), and a verbal fluency task. Importantly, Nolen-Hoeksema suggested that fur-
Engagement in PATHS resulted in improvements in ther information is needed to understand how men
inhibitory control, which in turn predicted decreases regulate their emotions. Because externalizing be-
in externalizing behavior as measured by the CBCL. havior problems are more common among males,
The authors concluded that future iterations of in- such information could inform future iterations of

behavioral treatments aimed at targeting emotion plinary, multimethod research is needed to translate
dysregulation in this population. scientific knowledge concerning the mechanisms
In addition to sex effects, other factors may influ- underlying emotion dysregulation and externalizing
ence the effectiveness of interventions for emotion behavior problems into a greater range of develop-
dysregulation—and/or the effects of other interven- mentally appropriate, effective treatment strategies.
tions on emotion dysregulation—among those with For example, despite the success of CBT-based
externalizing disorders. As discussed previously, models in treating externalizing behavior, they are
many interventions teach participants to “slow” their not a panacea, and, again, many questions remain
cognitive processes and emotional reactions. Such about mechanisms of treatment response. In one
interventions would likely be most effective for those study, children and their parents participated in a
with more reactive forms of externalizing behavior combined PMT/CBT program. The CBT portion
(e.g., aggression). Reactive aggression is character- of treatment taught children strategies for reapprais-
ized by responsiveness to social provocation, whereas ing social situations and learning to inhibit respond-
proactive aggression is more instrumental and not ing until those reappraisals took hold. The PMT
characterized by emotional responses to others’ dis- portion taught parents strategies for reducing hos-
tress (Crick et al., 1996; Dodge et al., 1990; Dodge tile interactions with their children. Results indi-
& Coie, 1987; Raine et al., 2006). In fact, it is often cated reductions in ventral prefrontal activation
conceptualized as “cold-blooded” and characteristic from pretreatment to posttreatment. This pattern of
of psychopaths (Raine et al., 2006). In theory, reac- findings suggests changes in prefrontal cortical reg-
tively aggressive individuals can be taught “cool ulatory processes, which the authors conclude may
down” strategies (like those taught in BAM or explain why treatment responders showed increased
DBT). In contrast, proactively aggressive individuals cognitive flexibility and “openness” in social situa-
are believed to have greater control over their be- tions (Lewis et al., 2008). This finding is notewor-
haviors, which could indicate that the interventions thy given the important role that the prefrontal
outlined previously would not be as effective for this cortex plays in the regulation of emotion, and re-
subgroup. sults of this nature have clear applicability to the
Those who are exposed to stress early in devel- development and refinement of intervention strate-
opment may also be good candidates for interven- gies for youth with externalizing behavior problems.
tions targeting emotion dysregulation, particularly A continued focus is also needed on rigorous
early intervention (e.g., PATHS and Fast Track). methodology and replication in intervention re-
Data from the animal and human literature indi- search with children, particularly in regard to new
cate that exposure to early life stress greatly in- strategies that might be effective in improving emo-
creases the likelihood of aggression and violence tion regulation and behavior. Mindfulness-based
later in life (Dodge et al., 1990; Ethier, Lemelin, & interventions have received considerable attention
Lacharité, 2004; Hildyard & Wolfe, 2002; Loeber in previous years, especially in terms of implemen-
& Stouthamer-Loeber, 1998). Thus, if providers tation into school-based curricula for younger chil-
begin intervening at earlier ages among those who dren. Despite what is known about the utility of
are exposed to chronic early life stress or trauma, mindfulness in treating a variety of emotional and
existing treatments may prove to be more effica- physical conditions, less is known about the mech-
cious in reducing the development of externalizing anisms through which mindfulness mitigates core
behavior problems. characteristics of different externalizing behaviors.
Moreover, given the lack of randomized controlled
Future Directions trials and longitudinal effectiveness studies in this
Emotion dysregulation is a core feature of external- relatively new field of inquiry, it is too early to tell
izing behavior. Perhaps not surprisingly, several whether mindfulness-based approaches are as effec-
studies now demonstrate that (1) improvements in tive as some of the more well-supported and empir-
emotion regulation following treatment are associ- ically verified CBT/PMT-based interventions. In
ated with positive long-term therapeutic outcomes fact, some researchers have called for more carefully
for children with externalizing disorders, and (2) designed studies that are grounded in developmen-
improved emotion regulation differentiates re- tal theory and use multiple indices of therapeutic
sponders from nonresponders (Herts et al., 2012; change to justify the recent rise in enthusiasm for
Sorensen et al., 2016; Winiarski et al., 2017). Yet mindfulness practices in schools (Greenberg &
despite such promising results, ongoing interdisci- Harris, 2012). Others argue that it is difficult to

generalize positive effects of mindfulness to younger Armistead, L., Wierson, M., Forehand, R., & Frame, C. (1992).
populations given weak methodological designs (e.g., Psychopathology in incarcerated juvenile delinquents: Does
it extend beyond externalizing problems? Adolescence, 106,
small samples, lack of randomization and control 309–314.
groups) and overreliance on self-report or report by Barkley, R. A. (1997). Behavioral inhibition, sustained attention,
“nonblind” raters (Burke, 2010). Because mindful- and executive functions: Constructing a unifying theory of
ness has shown potential among other populations, it ADHD. Psychological Bulletin, 121, 65–94.
at least deserves more attention among younger chil- Beauchaine, T. P. (2012). Physiological markers of emotional and
behavioral dysregulation in externalizing psychopathology.
dren to understand how (and if) it can be tailored to Monographs for the Society for Research in Child Development,
this age group. Moving forward, it is essential for re- 77, 79–86.
searchers to standardize intervention and assessment Beauchaine, T. P. (2015). Future directions in emotion
tools before attempting to draw meaningful conclu- dysregulation and youth psychopathology. Journal of Clinical
sions about the utility of these mindfulness-based Child and Adolescent Psychology, 44, 875–896.
Beauchaine, T. P., Gatzke-Kopp, L. M., Neuhaus, E., Chipman,
interventions for preventing emotion dysregulation J., Reid, M. J., & Webster-Stratton, C. (2013). Sympathetic-
among youth at risk for externalizing behavior prob- and parasympathetic-linked cardiac function and prediction
lems and effective non-mindfulness-based alterna- of externalizing behavior, emotion regulation, and prosocial
tives for younger age groups. behavior among preschoolers treated for ADHD. Journal of
Considerable progress has been made in recent Consulting and Clinical Psychology, 81, 481–493.
Beauchaine, T. P., Zisner, A., & Sauder, C. L. (2017). Trait
years in linking emotion dysregulation to specific impulsivity and the externalizing spectrum. Annual Review of
externalizing behaviors. Even more exciting is that Clinical Psychology, 13, 343–368.
research findings are now illustrating that some Beck, R., & Fernandez, E. (1998). Cognitive-behavioral therapy
of the most successful interventions for reducing in the treatment of anger: A meta-analysis. Cognitive Therapy
externalizing behavior are those that integrate an and Research, 22, 63–74.
Bentley, K. H., Nock, M. K., & Barlow, D. H. (2014). The
emotion regulation component, whether directly or four-function model of nonsuicidal self-injury: Key
indirectly. As the literature in this field continues to directions for future research. Clinical Psychological Science,
grow, both science and practice will benefit from the 2, 638–656.
application of multimethod approaches to better Berzins, L. G., & Trestman, R. L. (2004). The development and
understand the moderating and mediating mecha- implementation of dialectical behavior therapy in forensic
settings. International Journal of Forensic Mental Health, 3,
nisms that link emotion dysregulation to external- 93–103.
izing behaviors. Bordin, I. A., Rocha, M. M., Paula, C. S., Teixeira, M. C. T.,
Achenbach, T. M., Rescorla, L. A., & Silvares, E. F. (2013).
References Child Behavior Checklist (CBCL), Youth Self-Report (YSR)
Achenbach, T. M., & Rescorla, L. A. (2001). Manual for the and Teacher’s Report Form (TRF): An overview of the
ASEBA school-age forms and profiles. Burlington, VT: development of the original and Brazilian versions. Cadernos
University of Vermont, Research Center for Children, Youth, de Saúde Pública, 29, 13–28.
and Families. Briere, J., & Gil, E. (1998). Self-mutilation in clinical and general
Adrian, M., Zeman, J., & Veits, G. (2011). Methodological population samples: Prevalence, correlates, and functions.
implications of the affect revolution: A 35-year review of American Journal of Orthopsychiatry, 68, 609–620.
emotion regulation assessment in children. Journal of Broidy, L. M., Tremblay, R. E., Brame, B., Fergusson, D., John, L.,
Experimental Child Psychology, 110, 171–197. Laird, R., . . . Vitaro, F. (2003). Developmental trajectories of
Alink, L. R., van Ijzendoorn, M. H., Bakermans-Kranenburg, childhood disruptive behaviors and adolescent delinquency:
M. J., Mesman, J., Juffer, F., & Koot, H. M. (2008). Cortisol A six-site, cross-national study. Developmental Psychology, 39,
and externalizing behavior in children and adolescents: 222–245.
Mixed meta-analytic evidence for the inverse relation of basal Burke, C. A. (2010). Mindfulness-based approaches with
cortisol and cortisol reactivity with externalizing behavior. children and adolescents: A preliminary review of current
Developmental Psychobiology, 50, 427–450. research in an emergent field. Journal of Child and Family
Allwood, M., Handwerger, K., Kivlighan, K. T., Granger, D., & Studies, 19, 133–144.
Stroud, L. R. (2011). Direct and moderating links of salivary Cavanagh, M., Quinn, D., Duncan, D., Graham, T., &
alpha-amylase and cortisol stress-reactivity to youth behavioral Balbuena, L. (2017). Oppositional defiant disorder is better
and emotional adjustment. Biological Psychology, 88, 57–64. conceptualized as a disorder of emotional regulation. Journal
American Psychiatric Association. (2013). Diagnostic and of Attention Disorders, 21, 381–389.
statistical manual of mental disorders (5th ed.). Arlington, VA: Chambers, R., Chuen Yee Lo, B., & Allen, N. B. (2008). The
American Psychiatric Association. impact of intensive mindfulness training on attentional
Arch, J. J., Ayers, C. R., Baker, A., Almklov, E., Dean, D. J., & control, cognitive style, and affect. Cognitive Therapy and
Craske, M. G. (2013). Randomized clinical trial of adapted Research, 32, 303–322.
mindfulness-based stress reduction versus group cognitive Chambers, R., Gullone, E., & Allen, N. B. (2009). Mindful
behavioral therapy for heterogeneous anxiety disorders. emotion regulation: An integrative review. Clinical Psychology
Behaviour Research and Therapy, 51, 185–196. Review, 29, 560–572.

Cheong, Y. F., & Raudenbush, S. W. (2000). Measurement disorders as predictors of alcohol use disorder onset during
and structural models for children’s problem behaviors. three developmental periods. Drug and Alcohol Dependence,
Psychological Methods, 5, 477–495. 164, 38–46.
Cohn, A. M., Jakupcak, M., Seibert, L. A., Hildebrandt, T. B., & Flook, L., Smalley, S. L., Kitil, M. J., Galla, B. M., Kaiser-
Zeichner, A. (2010). The role of emotion dysregulation in the Greenland, S., Locke, J., . . . Kasari, C. (2010). Effects of
association between men’s restrictive emotionality and use of mindful awareness practices on executive functions in
physical aggression. Psychology of Men and Masculinity, 11, elementary school children. Journal of Applied School
53–64. Psychology, 26, 70–95.
Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion Forgatch, M. S., & Kjobl, J. (2016). Parent Management
regulation as a scientific construct: Methodological challenges Training-Oregon Model: Adapting intervention with
and directions for child development research. Child rigorous research. Family Process, 55, 500–513.
Development, 75, 317–333. Forgatch, M. S., & Patterson, G. R. (2010). Parent Management
Cole, P. M., Teti, L. O., & Zahn-Waxler, C. (2003). Mutual Training-Oregon Model: An intervention for antisocial
emotion regulation and the stability of conduct problems behavior in children and adolescents. In J. R. Weisz &
between preschool and early school age. Development and A. E. Kazdin (Eds.), Evidence-based psychotherapies for
Psychopathology, 15, 1–18. children and adolescents (2nd ed., pp. 159–178). New York,
Conduct Problems Prevention Research Group. (1999). Initial NY: Guilford Press.
impact of the Fast Track Prevention Trial for conduct Garmon, B., Philbrick, J., Becker, D., Schorling, J., Padrick, M.,
problems: I. The high risk sample. Journal of Consulting and Goodman, M., & Owens, J. E. (2014). Mindfulness-based
Clinical Psychology, 67, 631–647. stress reduction for chronic pain: A systematic review. Journal
Conduct Problems Prevention Research Group. (2002). of Pain Management, 7, 23–36.
Evaluation of the first 3 years of the Fast Track Prevention Gartstein, M. A., Putnam, S. P., & Rothbart, M. K. (2012).
Trial with children at high risk for adolescent conduct Etiology of preschool behavior problems: Contributions of
problems. Journal of Abnormal Child Psychology, 30, 19–35. temperament attributes in early childhood. Etiology of
Conduct Problems Prevention Research Group. (2004). The Preschool Behavior Problems, 33, 197–211.
effects of the Fast Track Program on serious problem Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment
outcomes at the end of elementary school. Journal of Clinical of emotion regulation and dysregulation: Development,
Child and Adolescent Psychology, 33, 650–661. factor structure, and Initial validation of the difficulties in
Conners, C. K. (2001). Conners’ Rating Scales—Revised: Technical emotion regulation scale. Journal of Psychopathology and
manual. North Tonawanda, NY: Multi-Health System. Behavioral Assessment, 26, 41–54.
Crick, N. R., Dodge, K. A., & Url, S. (1996). Social information- Greenberg, M. T., & Harris, A. R. (2012). Nurturing mindfulness
processing mechanisms in reactive and proactive aggression. in children and youth: Current state of research. Child
Child Development, 67, 993–1002. Development Perspectives, 6, 161–166.
Crowell, S. E., Beauchaine, T. P., & Linehan, M. M. (2009). A Greeson, J. M., Smoski, M. J., Suarez, E. C., Brantley, J. G.,
biosocial developmental model of borderline personality: Ekbland, A. G., Lynch, T. R., & Wolever, R. Q. (2015).
Elaborating and extending Linehan’s theory. Psychological Decreased symptoms of depression after mindfulness-based
Bulletin, 135, 495–510. stress reduction: Potential moderating effects of religiosity,
Desbordes, G., Negi, L. T., Pace, T. W. W., Wallace, B. A., spirituality, trait mindfulness, sex and age. Journal of
Raison, C. L., & Schwartz, E. L. (2012). Effects of mindful- Alternative and Complementary Medicine, 21, 166–174.
attention and compassion meditation training on amygdala Gross, J. J., & Thompson, R. A. (2007). Emotion regulation:
response to emotional stimuli in an ordinary, non-meditative Conceptual foundations. In J. J. Gross (Ed.), Handbook of
state. Frontiers in Human Neuroscience, 6, 1–15. emotion regulation. New York, NY: Guilford Press.
Dodge, K. A., Bates, J. E., & Peitit, G. S. (1990). Mechanisms in Halligan, S. L., Cooper, P. J., Fearon, P., Wheeler, S. L., Crosby,
the cycle of violence. Science, 250, 1678–1683. M., & Murray, L. (2013). The longitudinal development
Dodge, K. A., & Coie, J. D. (1987). Social information- of emotion regulation capacities in children at risk for
processing factors in reactive and proactive aggression in externalizing disorders. Development and Psychopathology,
children’s peer groups. Journal of Personality and Social 25, 391–406.
Psychology, 53, 1146–1158. Hare, T. A., Tottenham, N., Galvan, A., Voss, H. U., Glover,
Domitrovich, C. E., Cortes, R. C., & Greenberg, M. T. (2007). G. H., & Casey, B. J. (2008). Biological substrates of
Improving young children’s social and emotional competence: emotional reactivity and regulation in adolescence
A randomized trial of the preschool “PATHS” curriculum. during an emotional go-nogo task. Biological Psychiatry,
Journal of Primary Prevention, 28, 67–91. 63, 927–934.
Eisenberg, N., Cumberland, A., Spinrad, T. L., Fabes, R. A., Hasin, D. S., O’Brien, C. P., Auriacombe, M., Borges, G.,
Shepard, S. A., Reiser, M., . . . Guthrie, I. K. (2001). The Bucholz, K., Budney, A., . . . Schuckit, M. (2013). DSM-5
relations of regulation and emotionality to children’s criteria for substance use disorders: Recommendations and
externalizing and internalizing problem behavior. Child rationale. American Journal of Psychiatry, 170, 834–851.
Development, 72, 1112–1134. Herts, K. L., McLaughlin, K. A., & Hatzenbuehler, M. L.
Ethier, L. S., Lemelin, J. P., & Lacharité, C. (2004). A (2012). Emotion dysregulation as a mechanism linking stress
longitudinal study of the effects of chronic maltreatment on exposure to adolescent aggressive behavior. Journal of
children’s behavioral and emotional problems. Child Abuse Abnormal Child Psychology, 40, 1111–1122.
and Neglect, 28, 1265–1278. Hildyard, K. L., & Wolfe, D. A. (2002). Child neglect:
Farmer, R. F., Gau, J. M., Seeley, J. R., Kosty, D. B., Sher, K. J., Developmental issues and outcomes. Child Abuse and Neglect,
& Lewinsohn, P. M. (2016). Internalizing and externalizing 26, 679–695.

Hilton, L., Hempel, S., Ewing, B. A., Apaydin, E., Xenakis, L., Lynch, T. R., Chapman, A. L., Rosenthal, M. Z., Kuo, J. R., &
Newberry, S., . . . Maglione, M. A. (2017). Mindfulness Linehan, M. M. (2006). Mechanisms of change in dialectical
meditation for chronic pain: Systematic review and meta- behavior therapy: Theoretical and empirical observations.
analysis. Annals of Behavioral Medicine, 51, 199–213. Journal of Clinical Psychology, 62, 459–480.
Jha, A. P., Krompinger, J., & Baime, M. J. (2007). Mindfulness Macklem, G. L. (2008). Practitioner’s guide to emotion regulation
training modifies subsystems of attention. Cognitive, Affective, in school-aged children. New York, NY: Springer.
and Behavioral Neuroscience, 7, 109–119. Macpherson, H. A., Cheavens, J. S., & Fristad, M. A. (2013).
Kabat-Zinn, J. (1982). An outpatient program in behavioral Dialectical behavior therapy for adolescents: Theory, treatment
medicine for chronic pain patients based on the practice adaptations, and empirical outcomes. Clinical Child and Family
of mindfulness meditation: Theoretical considerations and Psychology Review, 16, 59–80.
preliminary results. General Hospital Psychiatry, 4, 33–47. Maire, J., Galera, C., Meyer, E., Salla, J., & Michel, G. (2017). Is
Kabat-Zinn, J. (2013). Full catastrophe living: Using the wisdom of emotional lability a marker for attention deficit hyperactivity
your body and mind to face stress, pain, and illness. New York, disorder, anxiety and aggression symptoms in preschoolers?
NY: Bantam Books. Child and Adolescent Mental Health, 22, 77–83.
Kabat-Zinn, J. D., Massion, A. O., Kristeller, J., Peterson, L. G., McCart, M. R., & Sheidow, A. J. (2017). Evidence-based
Fletcher, K. E., Pbert, L., . .
.
Santorelli, S. F. (1992). psychosocial treatments for adolescents with disruptive
Effectiveness of a meditation-based stress reduction program behavior. Journal of Clinical Child and Adolescent Psychology,
in the treatment of anxiety disorders. American Journal of 45, 529–563.
Psychiatry, 149, 936–943. Mendelson, T., Greenberg, M. T., Dariotis, J. K., Feagans
Kam, C. M., Greenberg, M. T., & Kusche, C. A. (2004). Gould, L., Rhoades, B. L., & Leaf, P. J. (2010). Feasibility
Sustained effects of the PATHS curriculum on the social and and preliminary outcomes of a school-based mindfulness
psychological adjustment of children in special education. intervention for urban youth. Journal of Abnormal Psychology,
Journal of Emotional and Behavioral Disorders, 12, 66–78. 38, 985–994.
Kaufman, E. A., Puzia, M. E., Mead, H. K., Crowell, S. E., Moffitt, T. E. (1993). Adolescence-limited and life-course-
McEachern, A., & Beauchaine, T. P. (2017). Children’s persistent antisocial behavior: A developmental taxonomy.
emotion regulation difficulties mediate the association between Psychological Review, 100, 674.
maternal borderline and antisocial symptoms and youth Moore, K. E., Folk, J. B., Boren, E. A., Tangney, J. P., Fischer, S.,
behavior problems over 1 year. Journal of Personality Disorders, & Schrader, S. W. (2016). Pilot study of a brief dialectical
31, 170–192. behavior therapy skills group for jail inmates. Psychological
Kazdin, A. E. (1997). Parent management training: Evidence, Services. Advance online publication. http://psycnet.apa.org/
outcomes, and issues. Journal of the American Academy of record/2016-43612-001.
Child and Adolescent Psychiatry, 36, 1349–1356. Mullin, B. C., & Hinshaw, S. P. (2007). Emotion regulation and
Keenan, K. (2000). Emotion dysregulation as a risk factor for externalizing disorders in children and adolescents. In
child psychopathology. Clinical Psychology: Science and J. J. Gross (Ed.), Handbook of emotion regulation (pp. 523–541).
Practice, 7, 418–434. New York, NY: Guilford.
Klonsky, E. D. (2009). The functions of self-injury in young Neacsiu, A. D., Bohus, M., & Linehan, M. M. (2014). Dialectical
adults who cut themselves: Clarifying the evidence for affect- behavior therapy: An intervention for emotion dysregulation.
regulation. Psychiatry Research, 166, 260–268. In J. J. Gross (Ed.), Handbook of emotion regulation (2nd. ed.,
Klonsky, E. D. (2011). Non-suicidal self-injury in United States pp. 491–507). New York, NY: Guilford.
adults: Prevalence, sociodemographics, topography and Nelson-Gray, R. O., Keane, S. P., Hurst, R. M., Mitchell, J. T.,
functions. Psychological Medicine, 41, 1981–1986. Warburton, J. B., Chok, J. T., & Cobb, A. R. (2006).
Kochanska, G., & Knaack, A. (2003). Effortful control as a A modified DBT skills training program for oppositional
personality characteristic of young children: Antecedents, defiant adolescents: Promising preliminary findings. Behaviour
correlates, and consequences. Journal of Personality, 71, Research and Therapy, 44, 1811–1820.
1087–1112. Nolen-Hoeksema, S. (2012). Emotion regulation and
Lewis, M. D., Granic, I., Lamm, C., Zelazo, P. D., Stieben, psychopathology: The role of gender. Annual Review of
J. I. M., Todd, R. M., . . . Pepler, D. (2008). Changes in the Clinical Psychology, 8, 161–187.
neural bases of emotion regulation associated with clinical Penza-Clyve, S., & Zeman, J. (2002). Initial validation of the
improvement in children with behavior problems. emotion expression scale for children (EESC). Journal of
Development and Psychopathology, 20, 913–939. Clinical Child and Adolescent Psychology, 31, 540–547.
Lieb, K., Zanarini, M. C., Schmahl, C., Linehan, M. M., & Perepletchikova, F. (2016). Dialectical behavior therapy for
Bohus, M. (2004). Borderline personality disorder. Lancet, preadolescent children in outpatient care settings: Strategies,
364, 453–461. procedures, and techniques. Journal of the American Academy
Linehan, M. M. (1993). Cognitive-behavioral treatment of of Child and Adolescent Psychiatry, 55, S18.
borderline personality disorder. New York, NY: Guilford. Perepletchikova, F., & Goodman, G. (2014). Two approaches to
Loeber, R., & Stouthamer-Loeber, M. (1998). Development of treating preadolescent children with severe emotional and
juvenile aggression and violence. American Psychologist, 53, behavioral problems: Dialectical behavior therapy adapted
242–259. for children and mentalization-based child therapy. Journal
Ludwig, J., & Shah, A. (2014). Think before you act: A new of Psychotherapy Integration, 24, 298.
approach to preventing youth violence and dropout. Retrieved Popma, A., Doreleijers, T. A. H., Jansen, L. M. C., Van Goozen,
July 24, 2017, from http://www.hamiltonproject.org/assets/ S. H. M., Van Engeland, H., & Vermeiren, R. (2007). The
legacy/files/downloads_and_links/v10_THP_LudwigDisc diurnal cortisol cycle in delinquent male adolescents and
Paper.pdf. normal controls. Neuropsychopharmacology, 32, 1622–1628.

Raine, A., Dodge, K., Loeber, R., Gatzke-Kopp, L., Lynam, D., Snyder, J., Schrepferman, L., & St. Peter, C. (1997). Origins
Reynolds, C., . . . Liu, J. (2006). The reactive-proactive of antisocial behavior: Negative reinforcement and affect
aggression questionnaire: Differential correlates of reactive dysregulation of behavior as socialization mechanisms in
and proactive aggression in adolescent boys. Aggressive family interaction. Behavior Modification, 21, 187–215.
Behavior, 32, 159–171. Snyder, J., Stoolmiller, M., Wilson, M., & Yamamoto, M.
Reynolds, C. R., & Kamphaus, R. W. (1992). Behavioral assessment (2003). Child anger regulation, parental responses to
system for children manual. Circle Pines, MN: American children’s anger displays, and early child antisocial behavior.
Guidance Service. Social Development, 12, 335–360.
Reynolds, C. R., & Kamphaus, R. W. (1998). Behavioral Sondeijker, F. E. P. L., Ferdinand, R. F., Oldehinkel, A. J.,
assessment system for children manual (2nd ed.). Circle Pines, Veenstra, R., Tiemeier, H., Ormel, J., & Verhulst, F. C.
MN: American Guidance Service. (2007). Disruptive behaviors and HPA-axis activity in young
Riggs, N. R., Greenberg, M. T., Kusche, C. A., & Pentz, M. A. adolescent boys and girls from the general population.
(2006). The mediational role of neurocognition in the Journal of Psychiatric Research, 41, 570–578.
behavioral outcomes of a social-emotional prevention Sorensen, L. C., Dodge, K. A., & the Conduct Problems
program in elementary school students: Effects of the Prevention Research Group. (2016). How does the Fast Track
PATHS curriculum. Prevention Science, 7, 91–102. Intervention prevent adverse outcomes in young adulthood?
Roberton, T., Daffern, M., & Bucks, R. S. (2012). Emotion Child Development, 87, 429–445.
regulation and aggression. Aggression and Violent Behavior, Southam-Gerow, M. A., & Kendall, P. C. (2002). Emotion
17, 72–82. regulation and understanding: Implications for child
Robins, R. W., John, O. P., Caspi, A., Moffitt, T. E., & psychopathology and therapy. Clinical Psychology Review,
Stouthamer-Loeber, M. (1996). Resilient, overcontrolled, 22, 189–222.
and undercontrolled boys: Three replicable personality types. Sroufe, L. A. (1995). Emotional development: The organization of
Journal of Personality and Social Psychology, 70, 157–171. emotional life in the early years. New York, NY: Cambridge
Roeser, R. W., & Eccles, J. S. (2014). Schooling and the mental University Press.
health of children and adolescents in the United States. In Tager, D., Good, G. E., & Brammer, S. (2010). “Walking
M. Lewis & K. D. Rudolph (Eds.), Handbook of developmental over ’em ”: An exploration of relations between emotion
psychopathology (pp. 163–184). New York, NY: Springer dysregulation, masculine norms, and intimate partner abuse
Science and Business Media. in a clinical sample of men. Psychology of Men and Masculinity,
Shackman, J. E., & Pollak, S. D. (2014). Impact of physical 11, 233–239.
maltreatment on the regulation of negative affect and Tang, Y-Y., Ma, Y., Wang, J., Fan, Y., Feng, S., Lu, Q., Yu,
aggression. Development and Psychopathology, 26, 1021–1033. Q., . . . Posner, M. I. (2007). Short-term meditation training
Sharma, M., & Rush, S. E. (2014). Mindfulness-based stress improves attention and self-regulation. PNAS, 104,
reductions as a stress management intervention for health 17152–17156.
individuals: A systematic review. Journal of Evidence-Based Thayer, J. F., Hansen, A. L., Saus-Rose, E., & Johnsen, B. H.
Complementary and Alternative Medicine, 19, 271–286. (2009). Heart rate variability, prefrontal neural function,
Shaw, P., Stringaris, A., Nigg, J., & Leibenluft, E. (2014). and cognitive performance: The neurovisceral integration
Emotion dysregulation in attention deficit hyperactivity perspective on self-regulation, adaptation, and health. Annals
disorder. American Journal of Psychiatry, 171, 276–293. of Behavioral Medicine, 37, 141–153.
Sheffield Morris, A., Silk, J. S., Steinberg, L., Myers, S. S., & Tremblay, R. E. (2000). The development of aggressive
Robinson, L. R. (2007). The role of the family context in the behavior during childhood: What have we learned in the
development of emotion regulation. Social Development, 16, past century? International Journal of Behavioral Development,
361–388. 24, 129–141.
Shelton, D., Kesten, K., Zhang, W., & Trestman, R. (2011). Trupin, E. W., Stewart, D. G., Beach, B., & Boesky, L. (2002).
Impact of a dialectic behavior therapy—Corrections Modified Effectiveness of a dialectical behaviour therapy program for
(DBT-CM) upon behaviorally challenged incarcerated male incarcerated female juvenile offenders. Child and Adolescent
adolescents. Journal of Child and Adolescent Psychiatric Nursing, Mental Health, 7, 121–127.
24, 105–113. van der Oord, S., Bogels, S. M., & Peijnenburg, D. (2012).
Shelton, D., Sampl, S., Kesten, K. L., Zhang, W., & Trestman, The effectiveness of mindfulness training for children with
R. L. (2009). Treatment of impulsive aggression in ADHD and mindful parenting for their parents. Journal of
correctional settings. Behavioral Sciences and the Law, 27, Child and Family Studies, 21, 139–147.
787–800. Webster-Stratton, C. (1984). A randomized trial of two parent-
Shields, A., & Cicchetti, D. (1997). Emotion regulation among training programs for families with conduct-disordered children.
school-age children: The development and validation of a Journal of Consulting and Clinical Psychology, 52, 666–678.
new Criterion Q-Sort Scale. Developmental Psychology, 33, Webster-Stratton, C. (2000). The Incredible Years Training
906–916. Series. OJJDP Juvenile Justice Bulletin. 1–23. http://www.
Silvers, J. A., Insel, C., Powers, A., Franz, P., Helion, C., Martin, incredibleyears.com/article/the-incredible-years-training-series/.
R. E., . . . Ochsner, K. N. (2016). vlPFC–vmPFC–amygdala Webster-Stratton, C. (2008a). Incredible Years Parents and
interactions underlie age-related differences in cognitive Children Series: BASIC Preschool/Early Childhood Program
regulation of emotion. Cerebral Cortex, 27, 1–13. Curriculum. Seattle, WA.
Sjöwall, D., Roth, L., Lindqvist, S., & Thorell, L. B. (2013). Webster-Stratton C. (2008b). Basic Preschool Home Visiting-
Multiple deficits in ADHD: Executive dysfunction, delay Coaches and Parents Manual. Seattle, WA.
aversion, reaction time variability, and emotional deficits. Webster-Stratton, C. (2008c). Incredible Years Parents and Children
Journal of Child Psychology and Psychiatry, 54, 619–627. Series: Baby and Toddlers Program Curriculum. Seattle, WA.

Webster-Stratton, C. (2008d). Tailoring the Incredible Years Winiarski, D. A., Schechter, J. C., Brennan, P. A., Foster, S. L.,
parenting program according to children’s developmental needs Cunningham, P. B., & Whitmore, E. A. (2017). Adolescent
and family risk factors. In J. M. Briesmeister & C. E. Schaefer physiological and behavioral patterns of emotion dysregulation
(Eds.), Handbook of parent training (pp. 305–344). NJ: John predict multisystemic therapy response. Journal of Emotional
Wiley & SonsHoboken. and Behavioral Disorders, 25, 131–142.
Webster-Stratton, C., & Reid, M. J. (2010). The Incredible Zeman, J., & Garber, J. (1996). Display rules for anger, sadness,
Years Parents, Teachers and Children Training Series: A and pain: It depends on who is watching. Child Development,
multifaceted treatment approach for young children with 67, 957–973.
conduct problems. In J. Weisz & A. Kazdin (Eds.), Evidence- Zeman, J., Shipman, K., & Penza-Clyve, S. (2001). Development
based psychotherapies for children and adolescents (2nd ed.). and initial validation of the Children’s Sadness Management
New York, NY: Guilford. Scale. Journal of Nonverbal Behavior, 25, 187–205.
Webster-Stratton, C. H., Reid, M. J., & Beauchaine, T. (2011). Zwi, M., Jones, H., Thorgaard, C., York, A., Dennis, J. A. (2011).
Combining parent and child training for young children Parent training interventions for attention deficit hyperactivity
with ADHD. Journal of Clinical Child and Adolescent disorder (ADHD) in children aged 5 to 18 years. Cochrane
Psychology, 40(2), 191–203. Database of Systematic Reviews, 12, CD003018.
West, J., Denton, K., & Reaney, L. M. (2001). The kindergarten Zylowska, L., Ackerman, D. L., Yang, M. H., Futrell, J. L.,
year: Findings from the Early Childhood Longitudinal Horton, N. L., Hale, T. S., . . . Smalley, S. L. (2008).
Study, kindergarten class of 1998–1999 (Publication Mindfulness meditation training in adults and adolescents
No. NCES2001-023). Washington, DC: National Center with ADHD: A feasibility study. Journal of Attention Disorders,
for Education Statistics. 11, 737–746.

CH A PTE R
Treating Emotion Dysregulation
30 in Internalizing Disorders
Christiane Kehoe and Sophie Havighurst
Abstract
Dysregulation of emotions is a core feature of virtually all internalizing disorders. This chapter reviews
the literature on relations between emotion dysregulation and internalizing disorders, with specific
attention to the treatment of emotion dysregulation as a transdiagnostic focus. It describes several
commonly used therapy approaches, considering how each targets emotion dysregulation. It also
reviews the efficacy of programs with regard to reducing maladaptive emotion regulation strategies.
Finally, it outlines how parent emotion dysregulation is targeted in emotion socialization parenting
programs (the Tuning into Kids suite of programs). These programs provide parents with skills to
manage their and their children’s emotions effectively. The chapter finishes with summarizing how
treatments for emotion dysregulation may be strengthened.
Keywords: intervention, emotion regulation, emotion socialization, internalizing disorders, parenting
Introduction portend a range of other problems including

The last three decades have seen noteworthy substance abuse (Hussong, Jones, Stein, Baucom, &
advances in psychosocial conceptualizations and
Boeding, 2011), poor work productivity (Birnbaum
treatments of internalizing disorders. Internalizing et al., 2010), and suicide (Eaton et al., 2013). In ad-
disorders, which are sometimes referred to as emo- dition, the economic burden of internalizing disor-
tional disorders, include various anxiety disorders ders on societal and personal levels is substantial.
(e.g., separation anxiety), mood disorders (e.g., In the United States, for example, 31.5% of annual
depression), and somatoform disorders (e.g., com- total expenditures for mental health are spent on
plaints about physiological pain or problems with- people with anxiety disorders (DuPont et al., 1996).
out an organic cause). They are among the most Despite increased understanding of the etiology of
common mental health problems experienced by internalizing disorders and many novel treatments,
children, adolescents, and adults, and often result the prevalence of mood and anxiety disorders re-
in significant impairment even when symptoms do mains high, and a substantial number (30%–50%)
not meet criteria for a clinical diagnosis (Angold, of children, adolescents, and adults do not improve
Costello, Farmer, Burns, & Erkanli, 1999; Bongers, (Baghai, Moller, & Rupprecht, 2006; March et al.,
Koot, van der Ende, & Verhulst, 2003). 2004; Weisz, McCarty, & Valeri, 2006). This
According to the World Health Organization highlights the importance of striving to improve
(WHO; 2017), 4.4% of the global population suffer approaches to treatment.
from a depressive disorder, and 3.6% suffer from an Internalizing disorders are defined in large part
anxiety disorder. Both are more prevalent among by dysregulated mood and/or emotion (Kovács &
females than males. Furthermore, lifetime preva- Devlin, 1998). Given this, it is unsurprising that
lences of depressive and anxiety disorders are 19% collectively, internalizing disorders show consider-
and 29%, respectively (Kessler et al., 2005), and able overlap in phenomenology, vulnerability, and
443
risk factors. It is well established that individuals & Mead, 2007). For example, early attachment
with depression and/or anxiety experience diffi- relationships provide bases for adaptive (and mala-
culties with emotion dysregulation, including ex- daptive) emotion regulation and shape the way the
periencing negative emotions more frequently, at central nervous system processes emotions (Schore
heightened intensity, and for longer durations than & Schore, 2008). In responsive relationships, chil-
typically developing individuals (Beauchaine, 2015; dren develop skills in identifying, understanding,
Trosper, Whitton, Brown, & Pincus, 2012; Zahn- and regulating emotions, which in turn provides
Waxler, Klimes-Dougan, & Slattery, 2000). At least foundations for healthy emotional functioning
some of these difficulties are underpinned by prob- (Morris, Silk, Steinberg, Myers, & Robinson, 2007).
lems with identifying, understanding, and regulat- Therefore, revisiting family-of-origin messages
ing emotional arousal, all of which can be targeted about emotions may be important to consider when
in interventions (Barlow et al., 2010; Dozois, Seeds, teaching emotion regulation skills to reduce inter-
& Collins, 2009; Weersing, Rozenman, Maher- nalizing disorders.
Bridge, & Campo, 2012). Given shared vulnerabili- In developing our parenting program that tar-
ties to and symptoms of emotional disturbance gets emotional competencies (the Tuning into Kids
across disorders, “transdiagnostic” approaches to [TIK] suite of programs; Havighurst & Harley,
prevention and intervention that target common 2007; Havighurst, Harley, Kehoe, & Pizarro, 2012;
factors have gained traction in the literature (e.g., Havighurst, Harley, Kehoe, & Wilson, 2011;
Aldao, Nolen-Hoeksema, & Schweizer, 2010; Barlow Havighurst, Harley, & Wilson, 2010), we focus on
et al., 2010; Zahn-Waxler et al., 2000). Nevertheless, teaching parents how to respond to their children’s
there remains considerable variation in how skill emotions in ways that help develop emotional com-
deficits are addressed across treatments. Depending petencies. TIK teaches parents emotion coaching,
on underpinning theories, some interventions ad- where parents scaffold children’s learning about
dress different emotional deficits and use different emotions within a supportive, emotionally accept-
methods to target these deficits. ing relationship. By improving emotional commu-
The dominant approach used to address emotion nication in families, we have found that parents,
dysregulation among those with internalizing prob- partners, adolescents, and young children all show
lems is cognitive-behavioral therapy (CBT), which decreases in internalizing difficulties (Havighurst &
focuses on changing disordered patterns of thinking Kehoe, 2017; Havighurst, Wilson, Harley, Prior, &
and behaving by teaching reappraisal and accept Kehoe, 2010; Kehoe, Havighurst, & Harley,
ance regulation skills. However, adaptive cognitive 2014a, 2014b; Wilson, Havighurst, Kehoe, & Harley,
strategies can be difficult to use when an individual 2016). Our approach to treating emotion dysregula-
is emotionally activated, a time when maladaptive tion targets intraindividual aspects of emotion regu-
strategies are most likely to be triggered (Aldao & lation (e.g., recognition, awareness, understanding,
Mennin, 2012; Aldao & Nolen-Hoeksema, 2012; and dampening of one’s own emotions) and aims to
Aldao et al., 2010; Suchy, 2011). Furthermore, CBT improve coregulation of emotions (e.g., interper-
requires cognitive abilities that are not developed sonal emotion regulation; see Havighurst & Kehoe,
fully among very young children (Weiner, Freedheim, 2017 for a detailed review). In addition, we recog-
Stricker, & Widiger, 2003). nize the importance of culture and family of origin
Up to 50% of adult psychiatric disorders first in shaping both nonconscious and conscious emo-
emerge in childhood or adolescence (e.g., Belfer, tion regulation processes, including beliefs and at-
2008), which highlights the importance of developing titudes about emotions and “self-talk” we use during
evidence-based prevention programs. Internalizing emotional moments. Targeting these aspects of
disorders are highly familial, so children with de- emotional competence and recognizing familial and
pression and/or anxiety often have a parent with a cultural factors that shape learning about emotions
similar condition. Familial transmission results is an approach with particular promise for preven-
from biological factors, which create vulnerability tion (Kring, 2010; Trosper, Buzzella, Bennett, &
toward developing disorders (e.g., high sensitivity to Ehrenreich, 2009). By teaching parents how to
emotional stimuli, high reactivity and emotion in- optimally respond to their children’s emotional

tensity, slow return to baseline), environmental risk experiences and expression, parents learn self-talk
factors (e.g., modeling, social learning experiences, strategies that they can use to address their own
instrumental conditioning), and their interactions emotional struggles. Our studies show that a brief
(see Beauchaine, 2015; Beauchaine, Gatzke-Kopp, group parenting intervention can reduce internalizing

difficulties in parents, partners, adolescents, and Mental Disorders, fifth edition (DSM-5; American
young children (Havighurst & Kehoe, 2017; Psychiatric Association, 2013), these disorders share
Havighurst, Wilson, et al., 2010; Kehoe et al., 2014a, significant phenotypic overlap and indicate anxious,
2014b; Wilson et al., 2016). sad, empty, and irritable mood, often accompanied
In this chapter we first provide more elaborated by somatic and cognitive symptoms that adversely
definitions of key concepts, including definitions of affect functioning. Many individuals with internal-
internalizing disorders, emotion, emotional regula- izing disorders experience heightened emotional
tion, and emotion dysregulation. We then provide a reactivity, experience hypersensitivity to threat, have
brief summary of the key emotion processing–related a tendency to experiencing negative emotions as
deficits among individuals with internalizing aversive, and engage in cognitive and behavioral
problems and disorders, and draw from the neuro- avoidance (Campbell-Sills, Ellard, & Barlow, 2015;
science literature for explanations of some of these Zahn-Waxler et al., 2000). Thus, ineffective strate-
deficits. Next, we describe a model of emotion reg- gies for regulating acute and/or enduring negative
ulation that is informed by current therapeutic emotions are part of the phenomenology of inter-
approaches to treating internalizing disorders. We nalizing disorders (Campbell-Sills et al., 2015), and
describe how some frequently used interventions teaching adaptive ways of processing and managing
target emotion dysregulation and review their effi- emotions is important.
cacy in treating internalizing disorders, including
moderating and mediating effects. Finally, we em- Emotion, Emotion Regulation, and
phasize the importance of prevention and early in- Emotion Dysregulation
tervention, and describe how we target emotion Historically, there has been considerable debate
dysregulation in the Tuning into Kids, Tuning into about definitions of emotions and emotion process-
Teens, and Tuning into Toddlers parenting programs ing. For the purpose of this chapter we define emo-
(hereafter referred to as TIK). To teach parents ef- tions as “episodic, relatively short-term, biologically
fective emotion coaching, we dedicate significant based patterns of perception, experience, physiol-
effort toward helping parents regulate their own ogy, action and communication that occur in re-
emotions that occur in response to their own life sponse to specific physical and social challenges and
stressors and challenges of parenting. We also pro- opportunities” (Keltner & Gross, 1999, p. 467). We
pose theoretical mechanisms through which learn- distinguish emotions from “mood,” which consists
ing and change might occur among both parents of more prolonged emotional states. Consistent with
and children/adolescents. We finish by summariz- other chapters in this volume, we endorse a func-
ing shortcomings of current theoretical models and tionalist perspective in which emotions promote
interventions. survival, including social affiliative purposes. For ex-
ample, sadness may indicate loss and can elicit care
Internalizing Disorders: Definition responses; fear may alert us to danger and elicit
and Key Features avoidance responses; anger may help us to stand
As outlined previously, “internalizing” is a broad up for our rights and elicit distance to ensure
term used to describe anxiety, mood, and somato- self-protection. Emotions are expressed across
form disorders. These disorders are often combined multiple response systems (neural, physiological,
based on factor analyses of symptoms, which yield cognitive, behavioral), which ideally coordinate to
high correlations in almost every study in which facilitate appraisals of and reactions to situations
they are assessed—regardless of age (Achenbach, (Cole, Martin, & Dennis, 2004; Frijda, 1986).
1991; Trosper et al., 2012). Internalizing disorders Emotions include both conscious and unconscious
are characterized by internal distress involving components.
“intro-punitive” emotions (e.g., feelings of guilt, The ability to manage emotions and their expres-
shame, fear, anxiety, sadness, and/or sorrow; see sions adaptively is sometimes referred to as “emo-
Zahn-Waxler et al., 2000). Anxiety disorders in- tional competence” (Campos, Mumme, Kermoian,
clude social anxiety, generalized anxiety disorder, & Campos, 1994; Saarni, 1999), “affective social
panic disorder, and separation anxiety disorder. competence” (Halberstadt, Denham, & Dunsmore,
Mood disorders include major depressive disorder, 2001), or “emotional intelligence” (Salovey & Sluyter,
persistent depressive disorder (formerly dysthymic 1997; Zeidner, Roberts, & Matthews, 2008). The
disorder), and premenstrual dysphoric disorder. As definition of emotional competence adopted in this
outlined in the Diagnostic and Statistical Manual of chapter is based on the functionalist perspective
Kehoe and Havighurst 445

outlined previously, which views effective emotional 2015). Menin and Fresco (2010) define emotion
experience and expression as “flexible, contextually dysregulation broadly as involving “maladaptive
bound, and goal-directed” (Campos et al., 1994, emotional responsiveness reflected in dysfunctional
p. 284). Emotional competence is composed of understanding, reactivity and management” (Menin
several interrelated skills, including the ability to & Fresco, 2010, p. 361). Similarly, Gratz and Roemer
recognize, understand, and regulate emotional experi- (2004) assert that emotion dysregulation encom-
ence and expression in interpersonal and intraper- passes multiple dimensions, including (1) difficul-
sonal situations (Halberstadt et al., 2001; Saarni, ties in awareness and understanding of emotions,
1999). Adaptive function requires competence in each (2) difficulties in accepting emotions, (3) difficulties
of these domains (Pons, Harris, & de Rosnay, 2004). in the ability to control impulsive behaviors and
Although there is general agreement that emotional behave in accordance with desired goals when expe-
competence involves the ability to recognize, under- riencing negative emotions, and (4) difficulties in
stand, express, and regulate emotions effectively the ability to use situationally appropriate emotion
in accordance with cultural expectations, there are regulation strategies flexibly to modulate emotional
slight differences in conceptualizations of compo- responses as desired to meet individual goals and
nents of emotional competence. For example, situational demands. Difficulties in these various
Saarni’s (1999) definition also includes empathic aspects of emotional competencies are thought to
responding to others and the capacity for emotional underlie many disorders, including internalizing
self-efficacy, including “accepting one’s emotional disorders, and are thus important targets.
experience, whether eccentric or culturally conven-
tional” and “living in accordance with one’s per- Emotion Dysregulation and
sonal theory of emotions” (p. 5). Halberstadt et al. Internalizing Disorders
(2001) include the ability to send and receive affec- Adults with internalizing difficulties and disorders
tive messages, highlighting social aspects of emo- report deficits in emotional competence compared
tional competence. to those without internalizing difficulties: This in-
Emotion regulation is an aspect of emotional cludes lower emotion awareness, decreased emo-
competence and involves all aspects of emotional tional clarity, lower emotion acceptance, and mal-
competence. Development of emotional competence adaptive emotion regulation strategies, such as use
is sequential, beginning with emotion awareness and of cognitive and behavioral avoidance, social
understanding and advancing to more sophisticated withdrawal, expressive suppression, poor problem
cognitive skills in adolescence (Booker & Dunsmore, solving and cognitive reappraisal strategies, and ru-
2017; Pons et al., 2004). There are currently several mination (Campbell-Sills et al., 2015). Depressed
definitions and models of emotion regulation; the individuals also have a harder time thinking about
most commonly used is the process model. In this positive events as a strategy to recover from negative
model, Gross (1998) defines emotion regulation as affect (see Joormann & Siemer, 2015). Similarly, in-
processes individuals use to influence which emotions vestigations into relations between internalizing dis-
they have, when they have them, and how they ex- orders and emotional competencies in young people
perience and express emotions. Emotion regulation find that adolescents with internalizing problems
can involve generating, maintaining, increasing, or are worse than their peers at identifying facial
decreasing either positive or negative emotions expressions of happiness, sadness, and disgust

(p. 275). Others, including several authors in this (Simonian, Beidel, Turner, Berkes, & Long, 2001),
volume, note that aspects of emotion regulation have less emotion understanding (Fernández-
can also be automated (e.g., Thompson, 1990). Berrocal, Alcaide, Extremera, & Pizarro, 2006;
According to this perspective, “emotion regulation Southam-Gerow & Kendall, 2002), are less emo-
can be defined as the set of processes through which tionally aware (Rieffe & De Rooij, 2012; Zeman,
emotional experience and expression are shaped, Shipman, & Suveg, 2002), and have difficulties
whether volitionally or automatically, in the service down-regulating negative emotions and/or main-
of adaptive behavior” (Beauchaine, 2015, p. 876). taining positive emotions (Acremont & van der
Emotion dysregulation, on the other hand, refers Linden, 2007; Chaplin, 2006; Silk, Steinberg, &
to emotional experiences that are too extreme, too Sheffield Morris, 2003; Suveg & Zeman, 2004;
intense, or of too long duration to be functional. Fernández-Berrocal et al., 2006; Yap, Allen, &
Emotion dysregulation therefore interferes with Sheeber, 2007). Thus, individuals with internalizing
appropriate goal-directed behavior (Beauchaine,
disorders have a range of emotional competence

deficits, including difficulties down-regulating aladaptive attempts to regulate unwanted emotions
m
emotions and using more maladaptive emotion reg- at both antecedent-focused and response-focused
ulation strategies. stages. Notably, however, strategies may differ de-
pending on whether an emotional response is “acute”
Emotion Regulation Models That or an “enduring mood state.” When using maladap-
Undergird Therapeutic Approaches tive strategies to regulate emotion states, a situation
The most renowned model of emotion regula is created whereby emotions are intensified and pro-
tion is Gross’s (1998) process model (see also longed, or whereby the short-term goal of reducing
Gross & Thompson, 2007). Gross suggests a the unwanted emotion is outweighed by negative
“situation-attention-appraisal-response” sequence of consequences in the long term. For example, avoid-
emotion experience, whereby emotions may be ance of situations an individual is anxious about
generated and regulated at various stages along (maladaptive emotion regulation during situation
a timeline of unfolding emotional responding. selection) may maintain symptoms because emo-
The model distinguishes between antecedent-focused tions are not being processed and habituation is pre-
and response-focused emotion regulation. vented. Similarly, in the case of mood disorders,
Antecedent-focused emotion regulation occurs social withdrawal (a type of avoidance) may result
early, and refers to “things one does before the emo- in increased loneliness, exacerbating unwanted
tion response tendencies have become fully acti- emotions. Campbell-Sills and Barlow also suggested
vated and have changed one’s behavior and one’s that the use of safety signals/behaviors (e.g., needing
peripheral physiological responding.” Response- to have a partner/parent around all the time, use of
focused emotion regulation occurs later and refers talismans) is a maladaptive strategy used to modify
to “things one does once an emotion is already an emotion during situation modification, whereas
under way, after the response tendencies have al- use of thought suppression, distraction, worry, and
ready been generated” (Gross & Thompson, 2007, rumination are maladaptive strategies used during
p. 15). Antecedent-focused emotion regulation inattention deployment. All are thought to prevent
volves four categories, including (1) situation se- emotion processing and habituation and to increase
lection (approaching or avoiding certain people, emotion intensity. Furthermore, Campbell-Sills and
places, or activities to increase or avoid an emotion Barlow termed “rationalization” (i.e., dampening
in the first place, which therefore occurs prior to the down the importance of something one has avoided)
emotion-eliciting situation), (2) situation modifica- as a maladaptive cognitive change strategy with
tion (being in a situation that has induced emotion long-term costs when it interferes with important
and trying to change the emotion occurring during goals. Finally, suppression may be a maladaptive re-
the situation), (3) attentional deployment (being in sponse modulation strategy that involves cognitive
a situation that has induced emotion and trying to processes (e.g., actively trying not to think about,
change how you are responding to the emotion feel, or do something) and behavioral processes
during attention to emotional experience, such as (e.g., actively trying not to express an emotion)—
shifting attention), and (4) cognitive change (chang- each of which can be adaptive in certain situations,
ing how one thinks about the emotion-eliciting sit- but can maintain or heighten emotion intensity and
uation during the emotional experience). Response- prevent habituation if used excessively (Campbell-
focused regulation, on the other hand, involves Sills & Barlow, 2007).
response modulation (5) to modify the experience, Although Gross (1998) acknowledges that emo-
the behavior, or the physiology linked to the emotion regulation can be controlled and conscious as
tion response, for example, suppressing emotion well as uncontrolled and unconscious, he places
expression or telling oneself not to feel an emo- greater emphasis on cognitive processes as causal
tion. Thus, this model proposes five broad fami- mechanisms. Current opinion is that antecedent-
lies of emotion regulation strategies that can occur focused strategies are more adaptive and effective
during and after the process of emotion generation compared with response-focused strategies. This
(Gross, 2007). Among these options, each can be view may have come about because the majority of
adaptive or maladaptive depending on context research has focused on comparing cognitive emo-
(English, Lee, John, & Gross, 2017). tion regulation strategies, such as reappraisal (con-
Following from the process model, Campbell- sidered an adaptive antecedent-focused strategy),
Sills and Barlow (2007) proposed that many clini- with use of emotion suppression (considered a
cal features of anxiety and mood disorders are maladaptive response-focused strategy). However, it

may be easier to regulate emotions at the earliest reassuring). For example, when children seek
point of stress perception. In certain situations, comfort or express anger, parents may calm them or
emotion dysregulation (i.e., moments of high escalate them (both response-focused strategies), with
arousal) impairs cognitive function, making it diffi- long-term consequences for children’s emotion reg-
cult to access cognitive strategies (Farb et al., 2015; ulation capacity (see, e.g., Beauchaine & Zalewski,
LeDoux, 1998). Furthermore, not all adaptive 2016; Crowell et al., 2017). Coregulation can also
emotion regulation involves cognitive regulation, occur at various antecedent-focused stages. For ex-
and it is possible that response-focused strategies ample, parents, partners, or others may collude in
can be adaptive in moments of high emotion dys- avoidance, may help with reappraisal, may help
regulation (e.g., diaphragmatic breathing, progres- shift attention, may be happy to be a “safety signal”
sive muscle relaxation, using coping statements or (to help modify an emotion-eliciting situation), or
self-compassion, telling a supportive person how may encourage suppression. Recent work by English
you feel, etc.). Indeed, naming emotions reduces et al. (2017) also shows that the presence of others
emotional reactivity (Matthew et al., 2007). In ad- influences the regulation strategies used. For exam-
dition, recent research using experience sampling ple, individuals are less likely to use suppression
techniques to assess emotion regulation strategies when alone, but more likely to use suppression in
in “daily life” indicates that strategy use is context the presence of nonclose others or when they want
dependent and often follows from goals people to maintain positive appearances. Depending on
have (e.g., to self-soothe, help others, get on with social context, suppression is sometimes necessary.
work, keep up appearances) and who is present Nevertheless, if one uses “self-validating” or “self-
(e.g., a person close to the individual or a stranger; normalizing” internal dialogue (e.g., having self-
English et al., 2017). compassion), emotional arousal may not remain
Another important consideration comes from high. Research is needed to delineate how individu-
neuroscience research conducted by LeDoux in the als use multiple strategies in different “real world”
1990s, which indicates that a reflexive, fast response contexts. In summary, attempts to coregulate may
system sends information via sensory organs through be adaptive or maladaptive at each stage of Gross’s
the thalamus to the amygdala to allow for effortless, (1998) model.
automated responding (e.g., when touching a hot- Finally, studies indicate that individuals use a
plate or missing a step). A slower processing path- range of noncognitive strategies as well (Heiy &
way loops through the hippocampus and cortex Cheavens, 2014; Thayer, Newman, & McClain,
for further evaluation (Cozolino, 2010). At times, 1994). For example, engaging in activities to keep
therefore, emotions are triggered quickly and auto- busy (behavioral distraction), sleeping on it, and en-
matically, and at other times we engage higher cortical gaging in exercise are all strategies that individuals
regions to reappraise situations. Moreover, physiolog- use to regulate emotion (Heiy & Cheavens, 2014).
ical arousal can also be modulated by both top-down Research shows that increasing sleep and engaging
(mind–body) and bottom-up (body–mind) strate- in exercise improve emotion regulation and enhance
gies, with bidirectional influence (Damasio, 1999; treatment of internalizing disorders (Byrne &
Porges, 2009a,b). For example, changing facial ex- Byrne, 1993; Taylor & Pruiksma, 2014). These strat-
pression or body posture can influence mood states egies can also be used proactively to prevent dys-
(Stepper & Strack, 1993), and some mindfulness regulation of emotions by increasing one’s tolerance
activities (e.g., mindfully drinking a glass of water, levels (Linehan, 2015; Sunderland, 2006). Many
mindful slow walking) can reduce negative affect individuals with internalizing disorders suffer from
(Farb, Anderson, & Segal, 2012). Furthermore, sleep problems, which often precede the disorder
some emotion regulation processes are homeostatic and impair treatment response (see Taylor &
and therefore automated, such as when the para- Pruiksma, 2014). Considering these additional
sympathetic nervous system down-regulates arousal strategies in treatment may help to target emotion
following stressors (Campbell-Sills & Barlow, 2007; dysregulation. We now turn to various therapies
Porges, 1995). that target emotion dysregulation to treat internal-
In addition, Hofmann (2014) notes that Gross’s izing disorders and examine their efficacy to date.
(1998) model focuses primarily on intrapersonal
emotion regulation and dysregulation, with less at- Treating Internalizing Disorders
tention to interpersonal processes including coregu- A number of psychological therapies target emotion
lation by others (i.e., empathic listening, soothing, dysregulation in treating internalizing disorders.

Some do so directly whereas others do so less directly. mechanisms of change alongside efficacy results. In
These include cognitive-behavioral therapy (CBT), contrast, more information regarding mediators of
emotion-focused therapy (EFT), mindfulness-based program efficacy is available from trials conducted
interventions, dialectical behavior therapy (DBT), with children and adolescents. These show mixed
and acceptance and commitment therapy (ACT). results regarding support for underlying theory of
We describe each approach, focusing on how they CBT. One study examined positive and negative
target emotion dysregulation and summarizing effi- self-statements as mediators of change in anxiety
cacy in terms of treatment outcomes. and found that changes in anxious self-statements—
but not positive or depressive self-statements—me-
Cognitive-Behavioral Therapy diated changes in anxiety (Kendall & Treadwell,
The most commonly used psychological treatment 2007). In another evaluation of the efficacy of CBT
for internalizing disorders is CBT. CBT is based on among 145 children and adolescents with anxiety
social learning principles, focusing largely on cogni- disorders, increases in positive thoughts and coping
tive and behavioral correlates of mental health con- strategies postintervention preceded and contrib-
ditions. Dysfunctional patterns of thinking and uted to decreases in anxiety symptoms at 3-month
behaving are assumed to affect emotional states. follow-up, whereas changes in negative thoughts,
Thus, maladaptive thoughts, attitudes, and beliefs although reduced, did not precede symptom
are core targets of therapy. Faulty information proc- reduction (Hogendoorn et al., 2014). Interestingly,
essing biases and dysfunctional schemas are assumed Hogendoorn et al. also found that reduced anxiety
to underlie dysfunctional patterns of thinking and symptoms preceded reductions in avoidant coping
behaving, and are therefore additional foci of ther- (conceptualized as actions, repression, and wishful
apy. An additional important component of treat- thinking). Finally, a small study among adults with
ing anxiety disorders is exposure therapy, which panic disorder showed that changes in panic-related
allows for habituation of feared responses. In theory, thinking mediated changes in panic severity follow-
targeting these domains should lead to changes in ing CBT treatment (Hofmann et al., 2007). Studies
one’s emotions and symptoms (Clark & Beck, 2010). investigating mechanisms of change are still sparse,
Of note, these targets of CBT map well onto Gross’s yet they are important in identifying key targets for
(1998) process model, as outlined previously. intervention.
CBT components include teaching cognitive
strategies (e.g., self-monitoring, cognitive restruc- Emotion-Focused Therapy
turing, problem solving, coping skills), behavioral EFT (L. S. Greenberg & Paivio, 1997) emerged in
strategies (e.g., encouraging use of hierarchies to the 1980s at a time when CBT was already used
face feared situations and overcome avoidance, widely. EFT addresses aspects of emotional process-
scheduling pleasant events, teaching breathing and ing in therapy that are not targeted directly by CBT.
relaxation strategies), and social skills training. The This approach teaches participants to be aware of,
therapeutic relationship is viewed as important in accept, express, and regulate emotions, and to dif-
creating a collaborative process for individuals to ferentiate adaptive from maladaptive emotional re-
learn new skills in short-term therapy (6 to 12 actions within short-term therapy (8 to 20 sessions).
sessions). Changes in emotion regulation are an im- Therapists guide clients toward emotions and ex-
portant outcome of CBT but are typically not a ploring early experience, memories, and images that
specific target. Nevertheless, individuals learn skills shape memories of emotions, also called “emotional
to reduce aversive emotional states through activi- schemes.” Emotional schemes contribute to auto-
ties they engage in (i.e., exposure) or new cognitive matic responses in a similar way that core maladap-
strategies they can apply to reduce arousal. Few tive schemas determine dysfunctional patterns of
studies have examined emotion dysregulation as a thinking or behaving. In theory, emotional schemes
direct treatment outcome. Rather, the focus has are automated “neural programs” that are stored in
been on reducing negative cognitions to reduce limbic memory networks and activate emotional re-
depression or anxiety (Clark & Beck, 2010). sponses (L. S. Greenberg, 2002). Therapy helps cli-
Numerous studies support CBT for treating in- ents to make sense of emotional experiences in the
ternalizing disorders among children, adolescents, context of an empathic, attuned therapeutic rela-
and adults (e.g., Chu & Harrison, 2007; Hollon & tionship. EFT distinguishes between primary and
Beck, 2000; NICE, 2010). To date, however, relatively secondary emotional responses. Primary emotions
few studies conducted with adults have evaluated are the initial emotional reaction to a situation

(e.g., feeling powerless), whereas secondary emotions that assists individuals in focusing attention to
occur in response to having the primary emotion moment-to-moment experience (Dumas, 2005;
(e.g., feeling angry when feeling powerless, or feel- Goldstein, 2002). These skills are presumed to pro-
ing guilty about feeling angry). Thus, secondary vide insight and self-understanding, reduce reactiv-
emotions often involve thoughts and feelings about ity, and improve emotion regulation (see J. Kabat-
emotions (meta-emotion), or learned ways of ex- Zinn, 1982; Segal, Williams, & Teasdale, 2002). A
pressing emotions, and are easier to be aware of core assumption of mindfulness therapies is that
and express. psychological problems occur when people become
EFT recognizes two different paths for producing overly caught up in thinking about the past or fear
emotions, one fast and automated, involving brain- the future, both of which interfere with effective re-
stem and gut responses, and the other slow, involv- sponding in the present (Segal et al., 2002). By in-
ing the neocortex in appraisal (see also LeDoux, creasing awareness and attention, mindfulness helps
1998; Cozolino, 2010). Emotion scheme processing change ineffective, automated patterns of respond-
is the principal target of EFT, whereby clients are ing that are resistant to treatment with traditional
helped to understand and make meaning of emo- behavioral approaches (Bargh & Ferguson, 2000;
tional experiences and reactions. Change is thought Dumas, 2005).
to occur through targeting difficulties in emotion Mindfulness changes emotion regulation prima-
awareness, expression, regulation, and reflection of rily by targeting “attention deployment” (shifting
primary emotions and triggers. Therapists facilitate attention to the present and remaining nonjudg-
change in contexts of an empathically attuned, mental). In turn, this facilitates new situation per-
validating relationship that facilitates skills in un- ception and allows for new appraisals and responses
derstanding and managing emotions, in particular (Farb et al., 2015). Mindfulness improves meta-
“self-soothing” (L. Greenberg, 2010). cognitive insight, increases the ability to differenti-
Evidence for the efficacy of EFT with internal- ate emotions, and increases acceptance of emotional
izing difficulties in adults is considerable, especially experiences/nonreactive awareness. All of these
for depression but also for anxiety (L. Greenberg & skills facilitate engagement of adaptive emotion
Watson, 2006; L. Greenberg, 2017). Emotionally regulation (e.g., cognitive reappraisal, acceptance,
focused therapy for couples and families, developed problem solving) and reduce maladaptive emotion
by Johnson (who collaborated with Greenberg regulation (e.g., experiential avoidance, rumination,
on early instantiations of EFT), is also efficacious suppression; Chambers, Gullone, & Allen, 2009;
(Wiebe & Johnson, 2016). Both target emotion Farb et al., 2015).
dysregulation, with positive effects (L. Greenberg, Mindfulness interventions have been used suc-
2010). Studies that directly examine moderators cessfully to treat a variety of psychiatric and medical
of program effects and mechanisms of change are problems (J. Kabat-Zinn, 2003), including anxiety,
needed. depression, and pain among adults (Hofmann,
Sawyer, Witt, & Oh, 2010; Khoury et al., 2013). To
Mindfulness-Based Interventions date, however, few studies have investigated media-
Mindfulness-based interventions emerged in the tors or moderators of change. Nevertheless, a recent
1990s, and integrate Eastern Buddhist philosophy systematic review of 19 studies (including 8 target-
with Western psychological concepts to assist clients ing depression and 2 targeting anxiety) indicates
in managing emotions and stress that occur across that changes in mindfulness and repetitive negative
mental health conditions (for a review see Gu, thinking yield changes in mental health outcomes
Strauss, Bond, & Cavanagh, 2015). Mindfulness- (Gu et al., 2015). Further research is needed to in-
based interventions include mindfulness-based cog- vestigate if other aspects of function targeted by
nitive therapy, DBT, and ACT. All target emotion mindfulness therapy contribute to changes in anxi-
dysregulation and provide clients with skills to resist ety and depression.
patterns of maladaptive thinking and behavior.
Mindfulness has been defined as “awareness that Dialectic Behavior Therapy
emerges through paying attention on purpose, in DBT (Linehan, 1993) combines Western CBT with
the present moment, and non-judgmentally to Eastern Buddhist practice of mindfulness into a
the unfolding of experience moment by moment” therapy targeting emotion dysregulation directly
(J. Kabat-Zinn, 2003, p. 145). Mindfulness is among individuals with mood disorders or those
both a state of mind and a disciplined practice who engage in self-harm or suicidal ideation and/or

have borderline personality disorder (BPD). It is the avoidance, frequent impulsive behaviors; Crowell
most comprehensive therapy in terms of targeting et al., 2008).
emotion dysregulation. Developed in the late 1980s, As outlined in the DBT manual (Linehan, 2015),
DBT helps clients identify triggers for emotion four primary skill sets taught in DBT that assist in
dysregulation and helps them learn skills to cope reducing emotion dysregulation include mindful-
under emotionally arousing situations. Standard ness, interpersonal effectiveness, emotion regula-
DBT is an intensive treatment, consisting of individ- tion, and distress tolerance. Skills are taught to help
ual therapy, weekly group/individual skills training, individuals recognize, describe, and label emotions
telephone coaching, and a therapist consultation and their functions. Individuals learn skills in iden-
team (Linehan, 1993, 2015). DBT views dysregu- tifying beliefs about emotions and cognitive restruc-
lated emotional responses as driven by distorted turing techniques to shift maladaptive thoughts,
perception and dysfunctional thinking, and also by beliefs, and assumptions about events. DBT focuses
automatic unconscious responses, such as biochem- on proactive emotion regulation whereby clients
ical changes, physiological changes, and action learn skills in how to engage in self-care and actions
tendencies that can occur prior to distorted cogni- that are self-soothing (such as paying attention to
tions (see Neacsiu, Bohus, & Linehan, 2015). the senses). Finally, therapy assists individuals in de-
Dysfunctional behaviors (e.g., self-harm, suicidal veloping action plans for times when they experi-
behaviors, emotion suppression, overcontrol, sub- ence extreme emotions and identifies “breakdown
stance use disorders, overeating) are viewed as efforts points” when higher order cognitive skills are less
individual engage in to regulate or avoid painful effective. At these times, distress tolerance skills are
emotions. used to help individuals identify what to do at
DBT seeks a synthesis between opposing natural “crisis” times when emotions are extreme. Distress
tensions to facilitate change by helping clients ac- tolerance skills include sitting with emotions until
knowledge, understand, accept, and sit with emo- they lessen, using other mindfulness techniques,
tional experiences on the one hand, but also prevent using STOP skills (Stop, Take a step back, Observe
and halt negative emotions on the other. DBT fol- the situation, and Proceed effectively), and using
lows from the biosocial developmental model of the TIP skill (change body Temperature, engage
BPD (Crowell, Beauchaine, & Lenzenweger, 2008; in Intense physical exercise, and use Progressive
Crowell, Beauchaine, & Linehan, 2009; Linehan, muscle relaxation). Learning these skills occurs with
1993), which proposes that biological vulnerabilities therapists and DBT skills trainers who are validat-
(genetic influences, neural, temperamental) predis- ing to counteract current situations and histories of
pose children to high impulsivity, negative affectivity, invalidation. DBT is effective in treating a range of
and emotional sensitivity. Trait impulsivity interacts disorders. Although most DBT research addresses
with adverse caregiving experiences to magnify BPD (Kliem, Kröger, & Kossfelder, 2010), a number
emotional lability by invalidating children’s emo- of studies have shown efficacy in treating emotion
tions, failing to provide adequate guidance in man- dysregulation, treatment-resistant depression, and
aging emotions, and negatively reinforcing aversive anxiety disorders (see Linehan, 2015 for a review).
emotional expressions. Over time repeated transac- Although a variety of potential mechanisms of change
tions between children’s heritable vulnerabilities have been identified (Lynch, Chapman, Rosenthal,
and inconsistent/inadequate caregiving shape and Kuo, & Linehan, 2006), intervention research that
maintain emotion dysregulation (including high tests these putative mechanisms in relation to inter-
emotional sensitivity, intense response to emotional nalizing disorders is sparse.
stimuli, and slow calming from emotional arousal).
Specific deficits are foci of treatment, such as distorted Acceptance and Commitment Therapy
information processing, dysregulation of the sense of ACT is another approach that combines mindful-
self, inability to achieve non-mood-dependent goals, ness techniques with CBT skills to alter patterns of
inability to control mood-dependent behavior, and dysfunctional behavior as a way of treating psycho-
frequent shutting down/freezing, which results in pathology. Developed by Hayes in the 1980s, ACT
pervasive social (e.g., social isolation, dysregulated helps clients accept and tolerate negative emotions
relationships), cognitive (self-hatred, hopelessness, rather than avoid or extinguish them. Thus, in con-
disorganization, dissociation, low self-efficacy), trast to traditional CBT, ACT does not focus on
emotional (emotional vulnerability, sadness, shame, changing people’s unwanted thoughts. Instead,
anger), and behavioral difficulties (withdrawal, it aims to promote psychological flexibility and

ac ceptance of thoughts as thoughts rather than Yeomans, & Geller, 2007). ACT has also proved
truths. Psychological flexibility refers to “the ability superior in reducing self-reported depression com-
to contact the present moment and, based on what pared with CBT. For example, Zettle, Rains, and
the situation affords, to change or persist with be- Hayes (2011) reported that posttreatment levels of
havior in accordance with one’s person values” cognitive defusion mediated therapeutic effects
(Flaxman, Blackledge, & Bond, 2011, p. vii). By fo- at follow-up for participants who received ACT,
cusing on effective living rather than emotion reg- whereas depressogenic thoughts and dysfunctional
ulation, effects of emotions are dampened. ACT attitudes did not mediate change in depression for
employs six therapeutic processes: acceptance, either condition. Finally, in a small study of adults,
diffusion, contact with the present moment, self-as- reductions in anxiety sensitivity and cognitive
context, values, and committed action. Emotional defusion mediated effects of both CBT and ACT
acceptance and emotional diffusion are key strate- on posttreatment reductions in worrying, but not
gies used to bring about this shift. Experiential behavioral avoidance or depression (Arch, Wolitzky-
avoidance and emotion suppression are key dysreg- Taylor, Eifert, & Craske, 2012).
ulation strategies that are targeted by ACT. This concludes our review of interventions. In
Although initial reviews of research evidence summary, although several therapies are effective in
showed inconsistent findings for ACT for treating treating internalizing disorders, few target emotion
depression and anxiety (e.g., Powers, Zum Vorde dysregulation directly, and emotion dysregulation
Sive Vording, & Emmelkamp, 2009), a 2015 meta- has not been a primary outcome in most studies.
analysis found that ACT is more effective than pla- Long-term outcome data are also sparse, so to date
cebo or treatment as usual in treating anxiety, de- we know little about what individuals do to manage
pression, and substance use disorders (A-Tjak et al., their emotions in daily life after receiving therapy.
2015). Moreover, it is as effective as CBT (Öst, Future research should address mechanisms more
2014). There are now about 200 randomized con- directly so we learn more about specific techniques
trolled trials of ACT, yet most of have been con- that improve emotion regulation and specific tech-
ducted with adults. Thus, efficacy is unknown niques that are effective for individuals with sub-
among adolescents. types of emotion regulation problems; there may be
A few studies have investigated mechanisms of specific subgroups of individuals with internalizing
change in ACT for internalizing disorders. Pots, difficulties who respond better to one treatment
Trompetter, Schreurs, and Bohlmeijer (2016) ex- over another.
amined psychological flexibility and five aspects of We now describe our own emotion-focused
mindfulness (observing, describing, acting with parenting program, Tuning into Kids. This program
awareness, nonjudging of inner experience, nonre- targets parental emotion dysregulation and im-
acting to inner experience) as potential mediators of proves emotional communication in families to
depression using web-based ACT. They found im- prevent internalizing and externalizing disorders
provements in psychological flexibility and observ- among children and adolescents.
ing. Moreover, nonjudging of inner experience
mediated effects of the intervention on depression Targeting Emotion Dysregulation in
posttreatment, but by follow-up psychological Parenting Interventions
flexibility, describing, and nonjudging of inner ex- Most adolescents who struggle with internalizing
periences mediated effects of the intervention on (and other psychiatric) difficulties do not access
depression. Several other studies have compared treatment (Yap, Reavley, & Jorm, 2013). Universal
ACT and CBT and investigated mechanisms of parenting interventions may offer an opportunity to
change for each approach. In one example, reduc- better engage this population. Parents are in the best
tions in experiential avoidance and negative cogni- position to teach their children and adolescents ef-
tions mediated effects of ACT on social anxiety and fective emotion regulation strategies, both by mod-
anhedonic depression (Niles et al., 2014). For CBT, eling adaptive strategies themselves and by engaging
only negative cognitions mediated effects. In another in discussions about different ways of managing
study, changes in observing mediated outcomes for emotions. Parents’ abilities to deal effectively with
participants who received CBT, whereas changes in their children’s emotions affect parenting efficacy
experiential avoidance, acting with awareness, and and emotional communication in the family (Dix,
acceptance mediated outcomes for participants 1991; Hughes & Gullone, 2010; Morris et al., 2007;
who received ACT (Forman, Herbert, Moitra, Silk et al., 2011). When parents experience high

levels of negative affect and have ineffective emotion on several other theoretical perspectives including
regulation strategies, they are likely to either with- attachment theory (Ainsworth, Blehar, Waters, &
draw or express negative emotions in a dysregulated Wall, 1978; Laible & Thompson, 1998), mindful-
manner, resulting in neglectful, reactive, and/or ness theory (M. Kabat-Zinn & Kabat-Zinn, 1997),
hostile discipline practices (Bariola, Gullone, & and the humanistic approach, which values the
Hughes, 2011; Gottman, 1991; Mence et al., 2014). importance of empathy and emotions in human re-
Heightened emotional arousal makes it difficult for lationships (Faber & Mazlish, 1980; Ginott, 1965;
individuals to access strategies to constructively Gottman & DeClaire, 1997; Gottman, Katz, &
manage feelings when solving emotional problems Hooven, 1997; Rogers, 1961). TIK draws from simi-
(Maliken & Katz, 2013) and results in both parents’ lar concepts and strategies used in emotion-focused
and youths’ reciprocally escalating emotions (Burke, therapy and DBT, and provides theoretical explana-
Pardini, & Loeber, 2008; Sheeber et al., 2011). tions to parents about children’s emotion dysregula-
Historically, much of the work that examined these tion through use of neuroscience, similar to popular
aspects of family function was among families of parenting books by Sunderland and Siegel (e.g.,
children with externalizing behaviors, yet newer Siegel & Bryson, 2011; Siegel & Hartzell, 2004;
data show similar patterns of escalation among fam- Sunderland, 2006). Emotion coaching was initially
ilies of children with internalizing difficulties as well described by Gottman et al. (1997), who specified a
(e.g., Crowell et al., 2014, 2017). Targeting such five-step process of responding to emotions that—
parenting behaviors may help to prevent children according to Gottman and DeClaire (1997)—yields
from developing long-term emotional difficulties. optimal socioemotional developmental in children.
Currently, few programs focus on teaching When children experience emotions, parents are
parents skills in emotional competence to improve taught to (1) notice the emotion, (2) see it as an op-
parent–child emotional communication with the portunity for intimacy and teaching, (3) communi-
aim of fostering healthy affective development. cate understanding and acceptance of the emotion,
(4) assist children to use words to describe how they
Tuning into Kids feel, and (5) if necessary, assist with problem solving
The Tuning into Kids (TIK) suite of programs tar- and/or limit setting around behavior. The TIK
gets a number of aspects of parent and child/adoles- program focuses on increasing skills required to
cent emotion dysregulation. Designed as a group facilitate each of these steps. Although the program
parenting program delivered across either 6 sessions is aimed at improving parenting, parents are pro-
(in universal settings) or 8 to 10 sessions (in selected/ vided with many opportunities to increase their
indicated prevention/early intervention programs), own emotional literacy and understand their own
TIK targets ways in which parents respond to chil- patterns of emotion reaction, expression and regula-
dren’s emotional experiences and expression, creating tion. In teaching parents how to respond to others’
an emotionally validating context for promoting emotions in a way that is regulating, parents learn to
healthy development in young people. The pro- validate their own emotions as they arise. Thus, the
gram, first developed for parents of preschoolers, program is particularly helpful for parents who
has been adapted and extended for fathers and for struggle with emotion regulation or have children
parents of toddlers, primary-school-aged children, with these difficulties.
and adolescents, as well as for parents of children
who experience trauma or have difficulties with Components of TIK that target
anxiety and behavior problems. A multisystemic emotion dysregulation
version called “Whole School Approach: Tuning Emotions lie at the heart of parent–child communi-
into Teens” targets the young people directly (grade cation, and for most parents, parenting elicits intense
8 and 9 students), as well as their teachers and par- emotional reactions. Throughout TIK, we consider
ents, and is currently being trialed. parallel processes in which parents develop their
The TIK program is based on emotion socializa- emotion regulation and teach their children about
tion theory, which shows that children’s and adoles- emotions. We target emotion dysregulation in our
cents’ emotional functioning is enhanced when program by focusing on teaching both intraregula-
parents actively coach their children’s emotions (i.e., tion skills and interpersonal coregulation skills,
respond supportively to emotions), rather than dis- teaching strategies for use with both lower intensity
miss emotions (i.e., respond harshly or critically or and higher intensity emotions, and teaching strate-
minimize children’s emotions). The program draws gies to proactively calm oneself and strengthen

cognitive regulation. We provide parents with of their children’s anger, sadness, and fear declines
psychoeducation about anxiety, including informa- from preschool to early adolescence (Stettler &
tion regarding effects of temperament and parent- Katz, 2014). Many parents struggle to identify their
ing on anxiety. We teach parents to become better at children’s emotions and focus instead on misbehav-
recognizing anxiety and ways of responding that iors or their own overwhelmed feelings. As a result,
normalize and validate children’s emotional experi- children sometimes escalate their emotions before
ences. In addition, we explore how parents feel parents notice. TIK helps parents recognize emo-
toward emotions by examining family-of-origin tions by attending to facial expressions, body lan-
responses to feelings and functions of emotions. guage, and tone of voice, and by identifying a time
Finally, the emotion coaching style provides parents when their child is likely to want to talk about his or
with a model of responding that is regulating for her emotions (such as while driving in the car or at
themselves, yet simple to understand and follow. bedtime). Later in the program parents are taught
Throughout our six sessions, we focus on teaching about primary and secondary emotions and recog-
parents the emotional skills required to use emotion nizing feelings behind their child/adolescent’s anger
coaching. and irritability (e.g., disappointment, powerless-
We use four main approaches for improving par- ness, anxiety). In the adolescent version of the pro-
ents’ abilities to manage emotions: (1) teaching skills gram, parents also learn that feeling rejected by their
in emotion awareness; (2) teaching skills in emotion teen can trigger anger. Many parents report that
understanding (including family-of-origin effects these skills are mutually beneficial for them and
on emotion competence and meta-emotion phi- their child.
losophy—i.e., beliefs and reactions to emotions); Helping parents to become aware of and name
(3) teaching parents specific skills in emotion regu- emotions (steps 1 and 4 of emotion coaching) pro-
lation, including “proactive” and “in the moment” vides parents with an “anchor for present-moment
regulation strategies; and (4) teaching parents to awareness,” not unlike focusing the breath in mind-
emotion coach their child to reduce parent and fulness meditation (Hill & Updegraff, 2012). This
child reactivity. In running many parenting groups enables parents to modify dysfunctional processes
using TIK, we have found all four of these compo- of suppressing emotions or becoming emotionally
nents to be important for changing how parents reactive and increases awareness of how they and
regulate their emotions, which in turn affects their their child are feeling—effectively a “top down”
parenting around emotions. The aim of our program process of emotion regulation. Parents report being
is to teach parents skills so that they can respond to calmer when attempting to identify emotions. The
children’s emotion experience and expression in a focus on awareness of emotions also enables parents
way that facilitates intimacy and connection. When to be more “present” during interactions and en-
parents respond in an emotion coaching way, hances empathic responding, facilitating greater
children feel validated, accepted, and emotionally intimacy and connection (Block-Lerner, Adair,
secure. Next we describe our philosophy and differ- Plumb, Rhatigan, & Orsillo, 2007; Yap, Allen, &
ent exercises we use in TIK to build parental emo- Ladouceur, 2008), consistent with mindfulness in-
tion awareness and understanding. terventions (Duncan, Coatsworth, & Greenberg,
2009). By increasing awareness of emotions and at-
Teaching parents skills in emotion tending to children’s emotions, invalidating pat-
awareness terns of interactions that have become automatized
As noted earlier, emotion awareness includes the can be recognized and changed (Bargh & Ferguson,
capacity to notice and accurately identify one’s 2000; Dumas, 2005).
own and others’ emotions (Halberstadt et al., 2001;
Saarni, 1999). Skills in emotion awareness are scaf- Teaching parents skills in emotion
folded across the program, beginning with asking understanding
parents to pay attention to their own and their Responding to challenging behaviors and intense
children’s emotions and to consider emotions emotions in one’s children can lead to strong feel-
behind verbal statements, behaviors, and situations. ings in parents (e.g., powerlessness, guilt, helpless-
Considerable attention is paid to increasing parents’ ness, anger, rage, sadness, embarrassment, shame)
awareness of their children’s emotions (especially and may remind parents of family-of-origin and
lower intensity emotions) with reciprocal benefits for other past experiences. We learn about emotions
emotional learning. Ordinarily, parental awareness from those with whom we have close relationships

(such as parents, siblings, and peers)—experiences for change (see L. S. Greenberg & Pascual-Leone,
that shape our attitudes and reactions to emotions 2006; Lane, Ryan, Nadel, & Greenberg, 2015). To
(Dunn, Brown, & Beardsall, 1991). Identifying alter intergenerational patterns of emotionally re-
messages parents received about emotions during jecting parenting, it is necessary to develop con-
their childhood (e.g., anger must not be expressed; nected relationships, learn emotional and cognitive
crying and showing sadness is weak; it is silly to regulation skills, and work through past experiences
worry) influences their capacity to remain calm and (Leerkes & Crockenberg, 2006).
responsive when faced with the stress of parenting Asking parents to reflect on and consider family-
and strong emotions in themselves and their chil- of-origin issues surrounding emotional experiences
dren. Thus, it is critical to address parents’ capacity to is similar to schema-focused or emotion-focused
regulate emotions as they arise during parent–child psychotherapy, in which changes occur by accessing
interactions by exploring their experiences in their past experiences and evoking emotions consistent
own family of origin. As noted previously, this af- with these memories to work through and alter au-
fects one’s meta-emotion philosophy (MEP)—how tomatic dysfunctional patterns of thinking, feeling,
they feel about feelings (Gottman et al., 1997). behaving, and interacting (L. S. Greenberg & Safran,
MEPs develop by adolescence (Hunter et al., 2011) 1989). Intense automatic reactions are reduced be-
but continue to crystallize, ultimately affecting our cause emotions no longer activate (often uncon-
responses to our own and others’ emotions. sciously) remembered past emotional experiences.
In TIK, we try to shift parents’ attitudes about Reflection on past (emotional) familial experiences
emotions by noting that all emotions are acceptable; is also a core component of psychoanalytic psycho-
they are important for survival and serve social therapy and is seen as integral to reducing the influ-
functions. This is often a challenging idea for par- ence of defenses (Freud, 1896).
ents who may hold strong attitudes about emotions
and their expression (e.g., it is not okay to hate; jeal- Teaching parents skills in emotion
ousy is bad; anxiety is debilitating). Many parents regulation
report feeling annoyed with their child’s anxiety, Development of emotion regulation and stress
sadness, or anger. management skills is important for mental health
In session 4, parents learn that suppression of and effective parenting (Aldao et al., 2010). If par-
thoughts, feelings, and behaviors can lead to height- ents are overwhelmed by stress and regulate their
ening of their intensity and frequency. We then link emotions ineffectively, they also struggle to emotion
this understanding to responding to children’s fears coach. In TIK, we teach three ways of regulating
and worries, explaining that going straight to saying emotions: pausing, calming, and releasing. We also
“don’t worry” or “you’ll be okay” or to other reassur- teach strategies parents can use in advance (i.e., self-
ance responses can convey to children that their care) and “in the moment,” with a specific focus on
feelings are invalid. Although anxious children often regulating anger, anxiety, and stress.
find reassurance responses calming and tend to seek Toward regulating emotion in advance, we en-
them out, such responses are not easily internalized courage proactive “emotional refueling.” In contrast
and children may not learn to use self-accepting and to avoidance behaviors, proactive emotion regula-
self-soothing internal self-talk. It may also foster an tion in the form of self-care is adaptive antecedent-
attitude about emotions that is nonaccepting, a key focused emotion regulation—that is, “things one
attitudinal factor in promoting use of emotion sup- does before the emotion response tendencies have
pression or avoidance, which relates to internalizing become fully activated and have changed one’s be-
difficulties (Gottman et al., 1997; Lougheed & havior and one’s peripheral physiological respond-
Hollenstein, 2012). ing” (Gross, 2007, p. 15). In TIK, we encourage
We believe that exploring beliefs about emotions self-care behaviors that ideally occur daily to main-
and one’s history with emotions is critical to assist- tain and promote physical and emotional well-being,
ing parents to learn emotion coaching. Increasing including sleep, exercise, use of social support, emo-
emotion understanding and insight reduces parental tion regulation strategies, and mindfulness prac-
reactivity (both how they respond to general stress tices. For individuals with internalizing disorders,
and parenting stress), creating calm and focus that self-care is vital to calmness and increased positive
are necessary for parents to adopt a child-centered mood. Just as a professional sports team must pre-
approach when responding to children’s emotions. pare for “match day,” we need to prepare ourselves
Others have also found this process to be important to cope with “match day” moments—situations of

high emotional arousal. We need to be fit, have Self-care also includes adequate nutrition and
adequate sleep and nutrition, and practice skills for sleep, avoiding screen time prior to bed, and using
use on the day. Regularly tuning into lower inten- mindfulness techniques (e.g., guided relaxation,
sity emotion arousal, such as mild frustration or mindful eating, mindful walking, etc.). Mindfulness
stress, and viewing this as a prompt for self-care is taught in sessions 3 and 4 in facilitator-led medi-
allows us to regulate emotions when they are still at tation/relaxation activities. Parents are provided
low intensity. Self-care activities can also incorporate with Internet links and encouraged to continue
diaphragmatic breathing, which can later be used in practicing these skills to proactively down-regulate
moments of high-intensity arousal. Practicing in ad- emotional intensity and stress. These techniques
vance is important to avoid creating negative are important in other emotion regulation–focused
associations; if we use slow breathing only during interventions for adults (e.g., mindfulness; Duncan
moments of high anxiety, we come to associate trying et al., 2009; Linehan, Bohus, & Thomas, 2007)
to breathe calmly with danger. and for children (e.g., the PATHS program;
Sunderland (2006) writes about self-care as M. T. Greenberg, Kusche, Cook, & Quamma, 1995).
“emotional refueling,” highlighting two types: auto- Parents often do not recognize the importance of
regulation and interactive regulation. Autoregulation self-care and report feeling guilty and selfish about
includes self-care activities that we engage in on our taking this time. Others are impeded from using
own, whereas interactive regulation includes self- self-care because of limited resources. By exploring
care activities that we engage in with others. In our barriers to self-care, these beliefs can be addressed
programs we break these two categories down fur- and parents can learn that looking after one’s emo-
ther: autoregulation that is “calming,” allowing us tional well-being is an important proactive emotion
to “tune out” (e.g., having a bath, strolling, lying on regulation strategy to help manage the stress of par-
the bed listening to soft music, meditation, slow di- enting, thereby enabling parents to be emotionally
aphragmatic breathing, yin yoga, gentle de-stressing responsive. Many times, the self-care activities par-
massage, coloring or painting), and autoregulation ents choose may not allow them to return to a calm
that allows us to “let off steam” (e.g., exercise, state (e.g., when only using “letting off steam” ac-
stretching, progressive muscle relaxation, drum- tivities, or when watching TV or reading a book is
ming, movement meditation, singing, vinyasa yoga, the “calming” strategy of choice). We note that ide-
working with clay, juggling). Similarly, interactive ally parents should engage in 5 to 10 minutes per
regulation can also be “calming” (e.g., having a day of “tuning out” calming, such as using guided
cuddle, lying side by side, listening to gentle music relaxation, mindful coloring, lying down to rest, or
together) or allow us to “let off steam” together quietly sitting in a park. We also encourage parents
(e.g., exercise together, watch sports or TV together, to role-model self-care and encourage opportunities
sing together, make music together). Ideally, we for their children to engage in self-care.
engage in all four types of self-care and encourage Regarding emotion regulation in the moment,
parents, teens, and teachers to build opportunities we encourage use of “building in a pause,” and emo-
into the day. tional release (i.e., “letting off steam”) strategies and
Self-care behaviors are calming for our nervous calming strategies. Regulation in the moment is a
system and allow us to return closer to homeostatic bottom-up method of regulation that uses simple
baseline, thereby reducing reactivity. Regular prac- preplanned behaviors that signal safety. Much like
tice of self-care helps reduce stress by signaling the preplanning and practice used in fire drills, par-
safety. Self-care is vital to prevent reactive parenting. ents choose and try out building in a pause, letting
In our program we provide a clear rationale for why off steam, and using calming strategies by practicing
self-care is important, highlighting that these activi- them in advance and trying them in the moment.
ties allow us to strengthen the capacity to return to “Building in a pause” is one of the simplest “in
a calmer baseline faster. We also recognize that self- the moment” techniques parents learn and is
care is individualized; we need to find something critical for reducing emotional reactivity during
that works for us. Not everyone finds massage calm- high-intensity moments. Parents are taught that
ing, and for some of us “tuning out” while having a during moments of “flooding,” it is difficult to access
cup of tea can evoke anxiety-provoking thoughts. cognitive strategies and therefore pausing can be more
Finding something in each category that is doable effective. Breaking eye contact, closing your mouth,
often (ideally daily) is an important part of targeting walking a few steps, taking slower and deeper
emotion dysregulation. breaths through the nose, tapping fingers together,

having a sip of water, attending to one’s sensorium something to overcome or avoid. Rather, they are
(smell, colors, textures), or running hands under encouraged to view their child as struggling and to
cold water are some strategies that can help in mo- develop confidence as they work through each emo-
ments of high-intensity arousal. These allow parents tion coaching step. For example, “What is he/she
to engage in controlled activities at times when they feeling?,” “Can I teach him/her?,” “Can I label the
are feeling out of control, thereby “taking the edge” emotion?,” “Can I empathize?,” or “Can I breathe
off of high-intensity emotions. Building in a pause slowly and slow down my reactions until my child
allows parents to widen the gap between stimulus calms?,” and then, “What might we do to work
and response, and helps them avoid automatic reac- through this situation?” Helping parents dynami-
tions. This allows returning to more child-centered cally adjust their responses in emotional moments
parenting. Parents learn to wait a few moments until enhances their ability to regulate their own emo-
emotional intensity has lessened before using more tions and gives them tangible skills for responding
cognitive emotion regulation strategies or respond- to their child.
ing to their children using words. Emotion coaching is regulating for children.
Emotional release activities include going for a When they are emotionally reactive and their par-
run or a walk, having a good cry, twisting a towel, or ents respond in ways that validate, it is calming for
weeding the garden. These strategies are explored the child. With effective emotion coaching, parents
with parents to find those that fit with their pre- remain nonjudging, calm, and accepting. They are
ferred way of calming or releasing physical aspects taught to normalize and validate their children’s
of emotions. Calming strategies may include par- emotional experiences, and to label primary emotions
ents breathing slowly, having some quiet time in if applicable. If parents’ own emotion intensity is
their room, having a bath or a shower, or talking to too high to respond calmly, they are encouraged to
someone they find calming. These are consistent use emotion regulation strategies to role-model
with the anxiety management techniques used in adaptive ways of managing emotions. The aim is to
CBT (Beck, Rush, Shaw, & Emery, 1979; Hawton, avoid minimizing children’s emotional experiences,
Salkovskis, Kirk, & Clark, 1989). Stress-releasing allowing them to process emotions in their own
activities, such as tense and release, enable one to let time. In our data, reducing parents’ dismissive re-
go of strong emotions that occur during fight-or- sponses is key to reducing internalizing difficulties
flight responding, and are also an effective component (Kehoe et al., 2014a). Therefore, we focus on learn-
of CBT (Beck et al., 1979; Hawton et al., 1989). ing what emotion dismissing looks like, teaching
parents that (1) the word “why” communicates
Teaching parents emotion coaching judgment; (2) going straight to problem solving, re-
Emotion coaching is a way of responding that assurance, or advice is invalidating; (3) engaging in
allows parents to coregulate their child. Teaching defensive responding or moralizing is disconnect-
parents the five steps of emotion coaching outlined ing, guilt inducing, and shaming; and (4) the word
by Gottman and DeClaire (1997) helps them regu- “but” wipes out the good work of validating (e.g., “I
late their own emotions because they shift to a more know you are worried about going to school, but
child-centered approach in which they proceed you just have to go”). The way parents respond to
through five practical steps to handle emotions their children’s emotions eventually becomes children’s
children experience. First, as mentioned earlier, internal self-talk. If parents are dismissing of emo-
parents attend to their children’s emotions, which tions, children develop an emotion-dismissing
assists parents in being present in the moment. model of self-talk and more negative beliefs about
Second, parents are encouraged to “reappraise” their emotions (see also Hunter et al., 2011). The five
children’s emotional reactions as opportunities to steps of emotion coaching provide a useful model
connect and teach. For example, instead of thinking for teaching self-acceptance and compassion, where
“Oh, he is such a difficult child!,” “She is so out of individuals may “emotion coach” themselves.
control!,” “I can't stand this!,” or “Why does he In summary, the skills and techniques taught in
have to always get so anxious!” (which contributes TIK assist parents to regulate emotions and develop
to parents’ emotions escalating), we encourage par- skills to help their children learn to understand and
ents to slow down and think about how to connect. regulate their emotions. For many parents the goal
This is a form of cognitive reappraisal (Gross & of intervention is, at a minimum, to help them be
Thompson, 2007) whereby parents no longer see aware of and prevent automatic, emotionally dis-
their children’s emotions as overwhelming and missive parenting reactions that are a product of

their family-of-origin experiences. Insight and Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K. K.,
awareness that engage higher order cognitive regula- Boisseau, C. L., Allen, L. B., & Ehrenreich, J. T. M. (2010).
Unified protocol for transdiagnostic treatment of emotional
tion is important but not achieved by all. Thus, tangi- disorders: Therapist guide. New York, NY: Oxford University
ble skills that help parents and adolescents regulate Press.
emotions at times when they are emotionally over- Beauchaine, T. P. (2015). Future directions in emotion
whelmed and flooded are critical to program suc- dysregulation and youth psychology. Journal of Clinical Child
cess. Much of the content of TIK is consistent with and Adolescent Psychology, 44, 875–896.
other third-wave therapies that have targeted emo- Polyvagal theory and developmental psychopathology:
tion regulation as a key component of the interven- Emotion dysregulation and conduct problems from
tion and shows considerable promise for preventing preschool to adolescence. Biological Psychology, 74, 174–184.
and treating internalizing problems in children, Beauchaine, T. P., & Zalewski, M. (2016). Physiological and
adolescents, and adults. developmental mechanisms of emotional lability in coercive
relationships. In T. J. Dishion & J. J. Snyder (Eds.), The
Oxford handbook of coercive relationship dynamics (pp. 39–52).
References New York, NY: Oxford University Press.
A-Tjak, J. G., Davis, M. L., Morina, N., Powers, M. B., Smits, Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979).
J. A., & Emmelkamp, P. M. (2015). A meta-analysis of the Cognitive therapy of depression. New York, NY: Guilford Press.
efficacy of acceptance and commitment therapy for clinically Belfer, M. L. (2008). Child and adolescent mental disorders: The
relevant mental and physical health problems. Psychotherapy magnitude of the problem across the globe. Journal of Child
and Psychosomatics, 84, 30–36. Psychology and Psychiatry, 49, 226–236
Achenbach, T. M. (1991). Manual for the Child Behavior Checklist: Birnbaum, H. G., Kessler, R. C., Kelley, D., Ben-Hamadi, R.,
4-18 and 1991a profile. Burlington, VT: University of Vermont, Joish, V. N., & Greenberg, P. E. (2010). Employer burden of
Department of Psychiatry. mild, moderate, and severe major depressive disorder: Mental
Acremont, M., & van der Linden, M. (2007). How is impulsivity health services utilization and costs, and work performance.
related to depression in adolescence? Evidence from a French Depression and Anxiety, 27, 78–89.
validation of the cognitive emotion regulation questionnaire. Block-Lerner, J., Adair, C., Plumb, J. C., Rhatigan, D. L., &
Journal of Adolescence, 30, 271–282. Orsillo, S. M. (2007). The case for mindfulness-based
Ainsworth, M. D. S., Blehar, M. C., Waters, E., & Wall, S. approaches in the cultivation of empathy: Does nonjudgmental,
(1978). Patterns of attachment. Hillsdale, NJ: Erlbaum. present-moment awareness increase capacity for perspective-
Aldao, A., & Mennin, D. S. (2012). Paradoxical cardiovascular taking and empathic concern? Journal of Marital and Family
effects of implementing adaptive emotion regulation strategies Therapy, 33, 501–516.
in generalized anxiety disorder. Behaviour Research and Bongers, I. L., Koot, H. M., van der Ende, J., & Verhulst, F. C.
Therapy, 50, 122–130. (2003). The normative development of child and adolescent
Aldao, A., & Nolen-Hoeksema, S. (2012). When are adaptive problem behavior. Journal of Abnormal Psychology, 112,
strategies most predictive of psychopathology? Journal of 179–192.
Abnormal Psychology, 121, 276–281. Booker, J. A., & Dunsmore, J. C. (2017). Affective social
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion- competence in adolescence: Current findings and future
regulation strategies across psychopathology: A meta-analytic directions. Social Development, 26, 3–20.
review. Clinical Psychology Review, 30, 217–237. Burke, J. D., Pardini, D. A., & Loeber, R., (2008). “Reciprocal
American Psychiatric Association. (2013). Diagnostic and statistical relationships between parenting behavior and disruptive
manual of mental disorders (5th ed.). Arlington, VA: Author. psychopathology from childhood through adolescence.”
Angold, A., Costello, E. J., Farmer, E. M. Z., Burns, B. J., & Journal of Abnormal Child Psychology, 36(5), 679–692.
Erkanli, A. (1999). Impaired but undiagnosed. Journal of the Byrne, A., & Byrne, D. G. (1993). The effect of exercise on
American Academy of Child and Adolescent Psychiatry, 38, depression, anxiety and other mood states: A review. Journal
129–137. of Psychosomatic Research, 37, 565–574.
Arch, J. J., Wolitzky-Taylor, K. B., Eifert, G. H., & Craske, Campbell-Sills, L., & Barlow, D. H. (2007). Incorporating
M. G. (2012). Longitudinal treatment mediation of emotion regulation into conceptualizations and treatments
traditional cognitive behavioral therapy and acceptance of anxiety and mood disorders. In J. J. Gross (Ed.),
and commitment therapy for anxiety disorders. Behaviour Handbook of emotion regulation (pp. 542–559). New York,
Research and Therapy, 50, 469–478. NY: Guilford.
Baghai, T. C., Moller, H. J., & Rupprecht, R. (2006). Recent Campbell-Sills, L., Ellard, K. K., & Barlow, D. H. (2015).
progress in pharmacological and non-pharmacological Emotion regulation in anxiety disorders. In J. J. Gross (Ed.),
treatment options of major depression. Current Pharmaceutical Handbook of emotion regulation (2nd ed., pp. 393–412).
Design, 12, 503–515. New York, NY: Guilford.
Bargh, J. A., & Ferguson, M. J. (2000). Beyond behaviourism: Campos, J. J., Mumme, D. L., Kermoian, R., & Campos, R. G.
On the automaticity of higher mental processes. Psychological (1994). A functionalist perspective on the nature of emotion.
Bulletin, 126, 925–945. Monographs of the Society for Research in Child Development,
Bariola, E., Gullone, E., & Hughes, E. (2011). Child and 59, 284–303.
adolescent emotion regulation: The role of parental emotion Chambers, R., Gullone, E., & Allen, N. B. (2009). Mindful
regulation and expression. Clinical Child and Family Psychology emotion regulation: An integrative review. Clinical Psychology
Review, 14, 198–212. Review, 29, 560–572.

Chaplin, T. M. (2006). Anger, happiness, and sadness: English, T., Lee, I. A., John, O. P., & Gross, J. J. (2017).
Associations with depressive symptoms in late adolescence. Emotion regulation strategy selection in daily life: The role
Journal of Youth and Adolescence, 75, 317–333. of social context and goals. Motivation and Emotion, 41,
Chu, B. C., & Harrison, T. L. (2007). Disorder-specific effects of 230–242.
CBT for anxious and depressed youth: A meta-analysis of Faber, A., & Mazlish, E. (1980). How to talk so kids will listen and
candidate mediators of change. Clinical Child and Family listen so kids will talk. New York, NY: Avon Books.
Psychology Review, 10, 352–372. Farb, N. A. S., Anderson, A. K., Irving, J. A., & Segal, Z. V.
Clark, D. A., & Beck, A. T. (2010). Cognitive theory and therapy (2015). Mindfulness interventions and emotion regulation.
of anxiety and depression: Convergence with neurobiological In J. J. Gross (Ed.), Handbook of emotion regulation (2nd ed.,
findings. Trends in Cognitive Sciences, 14, 418–424. pp. 548–568). New York, NY: Guilford.
Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion Farb, N. A. S., Anderson, A. K., & Segal, Z. V. (2012). The
regulation as a scientific construct: Methodological challenges mindful brain and emotion regulation in mood disorders.
and directions for child development research. Child Canadian Journal of Psychiatry, 57, 70–77.
Development, 75, 317–333. Fernández-Berrocal, P., Alcaide, R., Extremera, N., & Pizarro, D.
Cozolino, L. (2010). The neuroscience of psychotherapy: Healing the (2006). The role of emotional intelligence in anxiety and
social brain. New York, NY: Norton. depression among adolescents. Individual Differences Research,
Crowell, S. E., Baucom, B. R., Yaptangco, M., Bride, D., Hsiao, 4, 16–27.
R., McCauley, E., & Beauchaine, T. P. (2014). Emotion Flaxman, P., Blackledge, J. T., & Bond, F. W. (2011). Acceptance
dysregulation and dyadic conflict in depressed and typical and commitment therapy: Distinctive features. Hove:
adolescents: Evaluating concordance across psycho Routledge.
physiological and observational measures. Biological Psychology, Forman, E. M., Herbert, J. D., Moitra, E., Yeomans, P. D., &
98, 50–58. Geller, P. A. (2007). A randomized controlled effectiveness
Crowell, S. E., Beauchaine, T. P., & Lenzenweger, M. F. (2008). trial of acceptance and commitment therapy and cognitive
The development of borderline personality disorder and therapy for anxiety and depression. Behavior Modification,
self-inflicted injury: A biosocial developmental model. In 31, 772–799.
T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent Freud, S. (1896). The aetiology of hysteria (standard ed., Vol. 7).
psychopathology (pp. 510–539). Hoboken, NJ: Wiley. London, UK: Hogarth Press.
Crowell, S. E., Beauchaine, T. P., & Linehan, M. (2009). A Frijda, N. H. (1986). The emotions. New York, NY: Cambridge
biosocial developmental model of borderline personality: University Press.
Elaborating and extending Linehan’s theory. Psychological Ginott, H. G. (1965). Between parent and child. New York, NY:
Bulletin, 135, 495–510. Macmillan.
Crowell, S. E., Butner, J., Wiltshire, T. J., Munion, A. K., Goldstein, J. (2002). One dharma: The emerging western Buddhism.
Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating San Francisco, CA: Harper.
emotional and biological sensitivity to maternal behavior Gottman, J. M. (1991). Chaos and regulated change in families:
among depressed and self-injuring adolescent girls using A metaphor for the study of transitions. In P. A. Cowan &
nonlinear dynamics. Clinical Psychological Science, 5, M. Hetherington (Eds.), Family transitions (pp. 247–272).
272–285. Hillsdale, NJ: Erlbaum.
Damasio, A. R. (1999). The feeling of what happens: Body and Gottman, J. M., & DeClaire, J. (1997). The heart of parenting:
emotion in the making of consciousness. New York, NY: How to raise an emotionally intelligent child. London, UK:
Harcourt Brace. Bloomsbury.
Dix, T. (1991). The affective organization of parenting: Adaptive Gottman, J. M., Katz, L. F., & Hooven, C. (1997). Meta-emotion:
and maladaptive processes. Psychological Bulletin, 110, 3–25. How families communicate emotionally. Mahway, NJ:
Dozois, D. J. A., Seeds, P. M., & Collins, K. A. (2009). Erlbaum.
Transdiagnostic approaches to the prevention of depression Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment
and anxiety. Journal of Cognitive Psychotherapy, 23, 44–59. of emotion regulation and dysregulation: Development,
Dumas, J. E. (2005). Mindfulness-based parent training: factor structure, and initial validation of the Difficulties in
Strategies to lessen the grip of automaticity in families with Emotion Regulation Scale. Journal of Psychopathology and
disruptive children. Journal of Clinical Child and Adolescent Behavioral Assessment, 26, 41–54.
Psychology, 34, 779–791. Greenberg, L. S. (2010). “Emotion-focused therapy: A clinical
Duncan, L. G., Coatsworth, J. D., & Greenberg, M. T. (2009). synthesis.” Focus, 8(1), 32–42.
A model of mindful parenting: Implications for parent-child Greenberg, L. (2017). Emotion-focused therapy of depression.
relationships and prevention research. Clinical Child and Person-Centred and Experiential Psychotherapies, 16, 106–117.
Family Psychology Review, 12, 255–270. Greenberg, L., & Watson, J. (2006). Emotion-focused therapy
Dunn, J., Brown, J., & Beardsall, L. (1991). Family talk about of depression. Washington, DC: American Psychological
feeling states and children’s later understanding of others’ Association.
emotions. Developmental Psychology, 27 448–455. Greenberg, L. S. (2002). Emotion-focused therapy: Coaching
DuPont, R. L., Rice, D. P., Miller, L. S., Shiraki, S. S., Rowland, clients to work through their feelings. Washington, DC:
C. R., & Harwood, H. J. (1996). Economic costs of anxiety American Psychological Association.
disorders. Anxiety, 2, 167–172. Greenberg, L. S., & Paivio, S. C. (1997). Working with emotions
Eaton, N. R., Krueger, R. F., Keyes, K. M., Wall, M., Hasin, in psychotherapy. New York, NY: Guilford Press.
D. S., Markon, K. E., . . . Grant, B. F. (2013). The structure Greenberg, L. S., & Pascual-Leone, A. (2006). Emotion in
and predictive validity of the internalizing disorders. Journal psychotherapy: A practice-friendly research review. Journal of
of Abnormal Psychology, 122, 86–92. Clinical Psychology, 62, 611–630.

Greenberg, L. S., & Safran, J. D. (1989). Emotion in Hogendoorn, S. M., Prins, P. J. M., Boer, F., Vervoort, L.,
psychotherapy. American Psychologist, 44, 19–29. Wolters, L. H., Moorlag, H., .
.
.
Haan, E. D. (2014).
Greenberg, M. T., Kusche, C. A., Cook, E. T., & Quamma, J. P. Mediators of cognitive behavioral therapy for anxiety-
(1995). Promoting emotional competence in school-aged disordered children and adolescents: Cognition, perceived
children: The effects of the PATHS curriculum. Development control, and coping. Journal of Clinical Child and Adolescent
and Psychopathology, 7, 117–136. Psychology, 43, 486–500.
Gross, J. J. (1998). The emerging field of emotion regulation: An Hollon, S. D., & Beck, A. T. (2000). Cognitive therapy.
integrative review. Journal of General Psychology, 2, 271–299. In A. E. Kazdin (Ed.), Encyclopedia of psychology (Vol. 2,
Gross, J. J., & Thompson, R. A. (2007). Emotion regulation: pp. 169–172). Washington, DC: American Psychological
Conceptual foundations. In J. J. Gross (Ed.), The handbook of Association.
emotion regulation (pp. 3–24). New York, NY: Guilford. Hughes, E. K., & Gullone, E. (2010). Parent emotion
Gu, J., Strauss, C., Bond, R., & Cavanagh, K. (2015). How do socialisation practices and their associations with personality
mindfulness-based cognitive therapy and mindfulness-based and emotion regulation. Personality and Individual Differences,
stress reduction improve mental health and wellbeing? A 49, 694–699.
systematic review and meta-analysis of mediation studies. Hunter, E., Katz, L., Shortt, J., Davis, B., Leve, C., Allen, N., &
Clinical Psychology Review, 37, 1–12. Sheeber, L. B. (2011). How do I feel about feelings? Emotion
Halberstadt, A. G., Denham, S. A., & Dunsmore, J. C. (2001). socialization in families of depressed and healthy adolescents.
Affective social competence. Social Development, 10, 79–119. Journal of Youth and Adolescence, 40, 428–441.
Havighurst, S. S., & Harley, A. (2007). Tuning into Kids: Hussong, A. M., Jones, D. J., Stein, G. L., Baucom, D. H., &
Emotionally intelligent parenting program manual. Melbourne, Boeding, S. (2011). An internalizing pathway to alcohol and
Australia: University of Melbourne. substance use disorders. Psychology of Addictive Behaviour,
Havighurst, S. S., Harley, A. H., Kehoe, C. E., & Pizarro, E. 25, 390–404.
(2012). Tuning in to teens: Emotionally intelligent parenting Joormann, J., & Siemer, M. (2015). Emotion regulation in mood
program manual. Melbourne, Australia: University of disorders. In J. J. Gross (Ed.), Handbook of emotion regulation
Melbourne. (2nd ed., pp. 413–427). New York, NY: Guilford.
Havighurst, S. S., Harley, A., Kehoe, C. E., & Wilson, K. R. Kabat-Zinn, J. (1982). An out-patient program in behavioral
(2011). Tuning into Toddlers: Emotionally intelligent parenting medicine for chronic pain patients based on the practice of
program manual. Melbourne, Australia: University of mindfulness meditation: Theoretical considerations and
Melbourne. preliminary results General Hospital Psychiatry, 4, 33–47.
Havighurst, S. S., Harley, A. E., & Wilson, K. R. (2010). Dads Kabat-Zinn, J. (2003). Mindfulness-based interventions in
tuning into kids: Program manual. Melbourne, Australia: context: Past, present, and future. Clinical Psychology: Science
University of Melbourne. and Practice, 10, 144–156.
Havighurst, S. S., & Kehoe, C. E. (2017). The role of parental Kabat-Zinn, M., & Kabat-Zinn, J. (1997). Everyday blessings:
emotion regulation in parent emotion socialization: The inner work of mindful parenting. New York, NY:
Implications for intervention. In K. Deater-Deckard & Hyperion.
R. Panneton (Eds.), Parental stress and early child development: Kehoe, C. E., Havighurst, S. S., & Harley, A. E. (2014a).
Adaptive and maladaptive outcomes (pp. 285–307). New Examining the efficacy of an emotion-focused parenting
York, NY: Springer. intervention in reducing pre-adolescents’ internalising and
Havighurst, S. S., Wilson, K. R., Harley, A. E., Prior, M. R., & externalising problems. Paper presented at the 28th
Kehoe, C. E. (2010). Tuning in to Kids: Improving emotion International Congress of Applied Psychology, Paris, France.
socialization practices in parents of preschool children— Kehoe, C. E., Havighurst, S. S., & Harley, A. E. (2014b). Tuning
findings from a community trial. Journal of Child Psychology in to teens: Improving parent emotion socialization to reduce
and Psychiatry, 51, 1342–1350. youth internalizing difficulties. Social Development, 23,
Hawton, K., Salkovskis, P. M., Kirk, J., & Clark, D. M. (1989). 413–431.
Cognitive behaviour therapy for psychiatric problems: A practical Keltner, D., & Gross, J. J. (1999). Functional accounts of
guide. Oxford, UK: Oxford University Press. emotions. Cognition and Emotion, 13, 467–480.
Heiy, J. E., & Cheavens, J. S. (2014). Back to basics: A naturalistic Kendall, P. C., & Treadwell, K. R. H. (2007). The role of self-
assessment of the experience and regulation of emotion. statements as a mediator in treatment for youth with anxiety
Emotion, 14, 878–891. disorders. Journal of Consulting and Clinical Psychology, 75,
Hill, C. L. M., & Updegraff, J. A. (2012). Mindfulness and its 380–389.
relationship to emotional regulation. Emotion, 12, 81–90. Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas,
Hofmann, S. G. (2014). Interpersonal emotion regulation model K. R., & Walters, E. E. (2005). Lifetime prevalence and
of mood and anxiety disorders. Cognitive Therapy Research, age-of-onset distributions of DSM-IV disorders in the
38, 483–492. National Comorbidity Survey replication. Archives of General
Hofmann, S. G., Sawyer, A. T., Witt, A. A., & Oh, D. (2010). Psychiatry, 62, 593–602.
The effect of mindfulness-based therapy on anxiety and Khoury, B., Lecomte, T., Fortin, G., Masse, M., Therien, P.,
depression: A meta-analytic review. Journal of Consulting and Bouchard, V., . . . Hofmann, S. G. (2013). Mindfulness-based
Clinical Psychology, 78, 169–183. therapy: A comprehensive meta-analysis. Clinical Psychology
Hofmann, S. G., Suvak, M. K., Barlow, D. H., Shear, M. K., Review, 33, 763–771.
Meuret, A. E., Rosenfield, D., . . . Woods, S. W. (2007). Kliem, S., Kröger, C., & Kossfelder, J. (2010). Dialectical
Preliminary evidence for cognitive mediation during behavior therapy for borderline personality disorder: A meta-
cognitive-behavioral therapy of panic disorder. Journal of analysis using mixed-effects modeling. Journal of Consulting
Consulting and Clinical Psychology, 75, 374–379. and Clinical Psychology, 78, 936–951.

Kovács, M., & Devlin, B. (1998). Internalizing disorders in In J. J. Gross (Ed.), Handbook of emotion regulation (2nd ed.,
childhood. Journal of Child Psychology and Psychiatry and pp. 491–507). New York, NY: Guilford.
Allied Disciplines, 39, 47–63. NICE. National Collaborating Centre for Mental Health (UK).
Kring, A. M. (2010). The future of emotion research in the study (2010). Depression. The treatment and management of
of psychopathology. Emotion Review, 2, 225–228. depression in adults (updated ed.). Leicester, UK: British
Laible, D. J., & Thompson, R. A. (1998). Attachment and Psychological Society.
emotional understanding in preschool children. Developmental Niles, A. N., Burklund, L. J., Arch, J. J., Lieberman, M. D.,
Psychology, 34, 1038–1045. Saxbe, D., & Craske, M. G. (2014). Cognitive mediators of
Lane, R. D., Ryan, L., Nadel, L., & Greenberg, L. (2015). treatment for social anxiety disorder: Comparing acceptance
Memory reconsolidation, emotional arousal, and the process and commitment therapy and cognitive-behavioral therapy.
of change in psychotherapy: New insights from brain science. Behavior Therapy, 45, 664–677.
Behavioral and Brain Sciences, 38, e1. Öst, L. G. (2014). The efficacy of acceptance and commitment
LeDoux, J. E. (1998). The emotional brain: The mysterious therapy: An updated systematic review and meta-analysis.
underpinnings of emotional life. New York, NY: Simon & Behaviour Research and Therapy, 61, 105–121.
Schuster. Pons, F., Harris, P. L., & de Rosnay, M. (2004). Emotion
Leerkes, E. M., & Crockenberg, S. C. (2006). Antecedents of comprehension between 3 and 11 years: Developmental
mothers’ emotional and cognitive responses to infant distress: periods and hierarchical organization. European Journal of
The role of family, mother, and infant characteristics. Infant Developmental Psychology, 1, 127–152.
Mental Health Journal, 27, 405–428. Porges, S. W. (1995). Orienting in a defensive world: Mammalian
Linehan, M. M. (1993). Skills training manual for treating modifications of our evolutionary heritage. A polyvagal
borderline personality disorder. New York, NY: Guilford. theory. Psychophysiology, 32, 301–318.
Linehan, M. M. (2015). DBT skills training manual (2nd ed.). Porges, S. W. (2009a). The polyvagal theory: New insights into
New York, NY: Guilford Press. adaptive reactions of the autonomic nervous system.
Linehan, M. M., Bohus, M., & Thomas, R. L. (Eds.). (2007). Cleveland Clinic Journal of Medicine, 76, S86–S90.
Dialectical behavior therapy for pervasive emotion dysregulation: Porges, S. W. (2009b). Reciprocal influences between body and
Theoretical and practical underpinnings. New York, NY: brain in the perception and expression of affect: A polyvagal
Guilford. perspective. In D. Fosha, D. J. Siegel, & M. Solomon
Lougheed, J. P., & Hollenstein, T. (2012). A limited repertoire of (Eds.), The healing power of emotion: Affective neuroscience,
emotion regulation strategies is associated with internalizing development, and clinical practice (pp. 27–54). New York,
problems in adolescence. Social Development, 21, 704–721. NY: Norton.
Lynch, T. R., Chapman, A. L., Rosenthal, M. Z., Kuo, J. R., & Pots, W. T. M., Trompetter, H. R., Schreurs, K. M. G., &
Linehan, M. M. (2006). Mechanisms of change in dialectic Bohlmeijer, E. T. (2016). How and for whom does web-
behavior therapy: Theoretical and empirical observations. based acceptance and commitment therapy work? Mediation
Journal of Clinical Psychology, 62, 459–480. and moderation analyses of web-based ACT for depressive
Maliken, A. C., & Katz, L. F. (2013). “Exploring the impact symptoms. BMC Psychiatry, 16, 158–171.
of parental psychopathology and emotion regulation on Powers, M. B., Zum Vorde Sive Vording, M. B., & Emmelkamp,
evidence-based parenting interventions: A transdiagnostic P. M. (2009). Acceptance and commitment therapy: A meta-
approach to improving treatment effectiveness.” Clinical analytic review. Psychotherapy and Psychosomatics, 78, 73–80.
Child and Family Psychology Review, 16(2), 173–186. Rieffe, C., & De Rooij, M. (2012). The longitudinal relationship
March, J., Silva, S., Petrycki, S., Curry, J., Wells, K., Fairbank, between emotion awareness and internalising symptoms
J., . . . Severe, J. (2004). Treatment for adolescents with during late childhood. European Child and Adolescent
depression study (TADS) team. JAMA, 292, 807–820. Psychiatry, 21, 349–356.
Matthew, D. L., Naomi, I. E., Molly, J. C., Sabrina, M. T., Rogers, C. (1961). On becoming a person: A therapist’s view of
Jennifer, H. P., & Baldwin, M. W. (2007). Putting feelings psychotherapy. London, UK: Constable.
into words: Affect labeling disrupts amygdala activity Saarni, C. (1999). The development of emotional competence. New
in response to affective stimuli. Psychological Science, 18, York, NY: Guilford.
421–428. Salovey, P., & Sluyter, D. J. (Eds.). (1997). Emotional development
Mence, M., Hawes, D. J., Wedgwood, L., Morgan, S., Barnett, and emotional intelligence: Educational implications. New
B., Kohlhoff, J., & Hunt, C. (2014). Emotional flooding and York, NY: Harper Collins.
hostile discipline in the families of toddlers with disruptive Schore, J. R., & Schore, A. N. (2008). Modern attachment
behavior problems. Journal of Family Psychology, 28, 12–21. theory: The central role of affect regulation in development
Menin, D. S., & Fresco, D. M. (2010). Emotion regulation as an and treatment. Clinical Social Work Journal, 36, 9–20.
integrative framework for understanding and treating Segal, Z. V., Williams, J. M. G., & Teasdale, T. D. (2002).
psychopathology. In A. M. Kring & D. M. Sloan (Eds.), Mindfulness-based cognitive therapy for depression: A new
Emotion regulation and psychopathology: A transdiagnostic approach to preventing relapse. New York, NY: Guilford.
approach to etiology and treatment (pp. 356–379). New York, Siegel, D. J., & Bryson, T. P. (2011). The whole-brain child: 12
NY: Guilford. revolutionary strategies to nurture your child’s developing mind,
Morris, A. S., Silk, J. S., Steinberg, L., Myers, S. S., & Robinson, survive everyday parenting struggles, and help your family
L. R. (2007). The role of the family context in the thrive. New York, NY: Delacorte Press.
development of emotion regulation. Social Development, 16, Siegel, D. J., & Hartzell, M. (2004). Parenting from the inside
361–388. out. New York, NY: Penguin.
Neacsiu, A. D., Bohus, M., & Linehan, M. M. (2015). Dialectic Silk, J. S., Shaw, D. S., Prout, J. T., O’Rourke, F., Lane, T. J., &
behavior therapy: An intervention for emotion dysregulation. Kovács, M. (2011). Socialization of emotion and offspring

internalizing symptoms in mothers with childhood-onset distress: Developing a transdiagnostic internalizing toolbox
depression. Journal of Applied Developmental Psychology, 32, for pediatric practice. Cognitive and Behavioral Practice,
127–136. 19, 68–82.
Silk, J. S., Steinberg, L., & Sheffield Morris, A. (2003). Adolescents’ Weiner, I. B., Freedheim, D. K., Stricker, G., & Widiger, T. A.
emotion regulation in daily life: Links to depressive symptoms (2003). Handbook of psychology: Clinical psychology. New
and problem behavior. Child Development, 74, 1869–1880. York, NY: Wiley.
Simonian, S. J., Beidel, D. C., Turner, S. M., Berkes, J. L., & Weisz, J. R., McCarty, C. A., & Valeri, S. M. (2006). Effects of
Long, J. H. (2001). Recognition of facial affect by children psychotherapy for depression in children and adolescents: A
and adolescents diagnosed with social phobia. Child meta-analysis. Psychological Bulletin, 132, 132–149.
Psychiatry and Social Development, 32, 137–145. Wiebe, S. A., & Johnson, S. M. (2016). A review of the research
Southam-Gerow, M. A., & Kendall, P. C. (2002). Emotion in emotionally focused therapy for couples. Family Process,
regulation and understanding: Implications for child psychopa 55, 390–407.
thology and therapy. Clinical Psychology Review, 22, 189–222. Wilson, K. R., Havighurst, S. S., Kehoe, C. E., & Harley,
Stepper, S., & Strack, F. (1993). Proprioceptive determinants of A. E. (2016). Dads tuning into Kids: Preliminary
emotional and nonemotional feelings. Journal of Personality evaluation of a fathers' parenting program. Family Relations,
and Social Psychology, 64, 211–220. 65, 535–549.
Stettler, N., & Katz, L. F. (2014). Changes in parents’ meta- World Health Organization. (2017). Depression and other
emotion philosophy from preschool to early adolescence. common mental disorders: Global health estimates. Retrieved
Parenting: Science & Practice, 14, 162–174. from http://apps.who.int/iris/bitstream/10665/254610/1/
Suchy, Y. (2011). Clinical neuropsychology of emotion. New York, WHO-MSD-MER-2017.2-eng.pdf on 8/10/2017.
NY: Guilford. Yap, M. B. H., Allen, N., & Sheeber, L. B. (2007). Using an
Sunderland, M. (2006). The science of parenting: A practical emotion regulation framework to understand the role of
guidance on sleep, crying, play and building emotional wellbeing temperament and family processes in risk for adolescent
for life. London, UK: Dorling Kindersley. depressive disorders. Clinical Child and Family Psychology
Suveg, C., & Zeman, J. (2004). Emotion regulation in children Review, 10, 180–196.
with anxiety disorders. Journal of Clinical Child and Adolescent Yap, M. B. H., Allen, N. B., & Ladouceur, C. D. (2008).
Psychology, 33, 750–759. Maternal socialization of positive affect: The impact of
Taylor, D. J., & Pruiksma, K. E. (2014). Cognitive and invalidation on adolescent emotion regulation and depressive
behavioural therapy for insomnia (CBT-I) in psychiatric symptomatology. Child Development, 79, 1415–1431.
populations: A systematic review. International Review of Yap, M. B., Reavley, N. J., & Jorm, A. F. (2013). Associations
Psychiatry, 26, 205–213. between stigma and help-seeking intentions and beliefs:
Thayer, R. E., Newman, J. R., & McClain, T. M. (1994). Self- Findings from an Australian national survey of young people.
regulation of mood: Strategies for changing a bad mood, Psychiatry Research, 210, 1154–1160.
raising energy, and reducing tension. Journal of Personality Zahn-Waxler, C., Klimes-Dougan, B., & Slattery, M. J. (2000).
and Social Psychology, 67, 910–925. Internalizing problems of childhood and adolescence:
Thompson, R. A. (1990). Emotion and self-regulation. In Prospects, pitfalls, and progress in understanding the
R. A. Thomspon (Ed.), Nebraska Symposium on Motivation: development of anxiety and depression. Development and
Vol. 36: Socioemotional development (pp. 383–483). Lincoln, Psychopathology, 12, 443–466.
NE: University of Nebraska Press. Zeidner, M., Roberts, R. D., & Matthews, G. (2008). The
Trosper, S., Buzzella, B., Bennett, S., & Ehrenreich, J. (2009). science of emotional intelligence: Current consensus and
Emotion regulation in youth with emotional disorders: controversies. European Psychologist, 13, 64–78.
Implications for a unified treatment approach. Clinical Child Zeman, J., Shipman, K., & Suveg, C. (2002). Anger and sadness
and Family Psychology Review, 12, 234–254. regulation: Predictions to internalizing and externalizing
Trosper, S., Whitton, S., Brown, T., & Pincus, D. (2012). symptoms in children. Journal of Clinical Child and
Understanding the latent structure of the emotional disorders Adolescent Psychology, 31, 393–398.
in children and adolescents. Journal of Abnormal Child Zettle, R. D., Rains, J. C., & Hayes, S. C. (2011). Processes of
Psychology, 40, 621–632. change in acceptance and commitment therapy and cognitive
Weersing, V. R., Rozenman, M. S., Maher-Bridge, M., & therapy for depression: A mediation reanalysis of Zettle and
Campo, J. V. (2012). Anxiety, depression, and somatic Rains. Behavior Modification, 35, 265–283.

CH A PTE R
Dialectical Behavior Therapy and
31 Treatment of Emotion Dysregulation
Alexander L. Chapman and Nora H. Hope
Abstract
Developed to treat highly suicidal patients and often associated with the treatment of borderline
personality disorder (BPD), dialectical behavior therapy (DBT) has evolved into a transdiagnostic
treatment addressing emotion dysregulation. DBT is an emotion-focused, comprehensive
cognitive-behavioral treatment including individual therapy, group skills training, between-session
skills coaching (phone coaching), and a therapist consultation team. Several elements of DBT address
emotion dysregulation directly or indirectly, including emotion regulation skills, distress tolerance
strategies to dampen physiological arousal and curb impulses to engage in problematic behaviors, and
individual therapy interventions to reduce emotion dysregulation. Growing evidence suggests that DBT
may address behavioral, cognitive, physiological, and neurobiological aspects of emotion dysregulation.
Future directions should include increasing multimethod research on the effects of DBT on emotion
dysregulation, streamlining treatment, making DBT more efficient and targeted, and conceptualizing
DBT’s place within the spectrum of other emotion-focused transdiagnostic treatments.
Keywords: dialectical behavior therapy, emotion dysregulation, emotion, borderline personality

disorder, transdiagnostic
Introduction Eberle, Kramer, Wiesmann, & Linehan, 2014; Ritschel,

In dialectical behavior therapy (DBT; Linehan, Lim, & Stewart, 2015).
1993a), emotion dysregulation is viewed as a core DBT targets emotion dysregulation in several
vulnerability underlying borderline personality dis- ways. The skills training component of DBT in-
order (BPD) and related behavioral and interper- cludes an emotion regulation module designed to
sonal problems. Many extreme behaviors observed decrease emotion dysregulation directly (Linehan,
in BPD (e.g., suicidal behaviors, substance use, in- 1993b, 2014), and other skills that target emotion
terpersonal conflict) are viewed as either natural con- dysregulation indirectly. For instance, distress toler-
sequences of emotion dysregulation or attempts to ance strategies can help reduce harmful impulsivity,
relieve distress associated with emotion dysregula- mindfulness skills can help a client step back from
tion. Although associated predominantly with the emotional storms, and interpersonal effectiveness
treatment of BPD, DBT includes skills and inter- skills can reduce maladaptive communication and
ventions designed to target emotion dysregulation conflict occurring in the context of emotion dys-
broadly, both within and outside of BPD. Given the regulation. DBT also emphasizes emotions and
relevance of emotion dysregulation across many emotion dysregulation as they emerge. For example,
clinical problem areas (e.g., anger management when a client is emotionally dysregulated during a
problems, mood and anxiety disorders), DBT is well session, this presents an opportunity to help him or
positioned as a potentially transdiagnostic treatment her learn to reduce emotion dysregulation. Some
approach (Neacsiu, Bohus, & Linehan, 2014; Neacsiu, strategies for this include mindfulness of emotions
463
(e.g., observing and labeling emotional states), in- (e.g., a reciprocal vs. irreverent style or demeanor),
formal exposure to build tolerance of emotions, dis- (2) treatment strategies (e.g., problem solving vs.
tress tolerance strategies to reduce physiological validation), (3) skills coaching, and (4) case man-
arousal, and contingency management strategies to agement (e.g., a balance between modifying the pa-
block problematic behavior (e.g., threats, yelling) tient’s environment and helping the patient solve
while simultaneously eliciting and reinforcing more problems independently). Additionally, in DBT,
adaptive behavior (e.g., effective communication, many existing CBT-oriented coping strategies and
skills use). In this chapter, we discuss a DBT-oriented interventions are packaged as skills, forming the
conceptualization of emotions and emotion dysregu- four core DBT skills modules of mindfulness, inter-
lation, describe how DBT targets emotion dysregu- personal effectiveness, emotion regulation, and dis-
lation, summarize evidence from cutting-edge re- tress tolerance (Linehan, 1993b, 2014). Consistent
search on neurobiological changes in response to with a dialectical framework, some DBT skills
DBT, and discuss future directions. emphasize acceptance (such as mindfulness and dis-
tress tolerance), whereas others emphasize change
Overview of Dialectical Behavior Therapy (such as emotion regulation and interpersonal
When Dr. Marsha Linehan sought to develop a effectiveness).
treatment for highly suicidal individuals with Instead of performing these interventions on cli-
complex mental health concerns, she began with ex- ents, DBT therapists help clients to learn, practice,
isting, evidence-based treatments. At the time, these strengthen, and generalize skills that are effective for
treatments largely included cognitive-behavioral a variety of clinical problems. Forming new habits
therapy (CBT) techniques, including cognitive and reversing entrenched patterns of emotion dys-
therapy, relaxation skills, and behavioral approaches regulation takes consistent practice (e.g., greater
such as skills training, exposure, and contingency client-reported skills use was found to mediate treat-
management. A common thread across CBT inter- ment outcomes; Neacsiu, Rizvi, & Linehan, 2010).
ventions was the notion that clients needed to Thus, among other approaches that help clients gen-
change their thinking patterns and behavior to over- eralize therapy to their everyday lives, DBT guides
come mental health problems. Although CBT clients to become their own therapists.
sometimes yielded good outcomes, many highly As a comprehensive treatment designed for com-
suicidal, complex clients experienced this approach plex, multiproblem clients, DBT addresses several
as invalidating (Linehan, 1993a). These clients had domains within a structured treatment framework.
been suffering from intense emotional turmoil, There are five primary functions of comprehensive
sometimes for many years, and the message that DBT treatment: (1) improving client motivation to
they just needed to change their thoughts and be- change, (2) increasing client capabilities, (3) facili-
haviors seemed overly simplistic and unrealistic. tating generalization of behavioral skills to the
To address the limitations of CBT, Dr. Linehan client’s natural environment, (4) structuring the

began to incorporate specific practices (mindful- client’s treatment and natural environments, and
ness, Zen practice, acceptance) designed to convey (5) maintaining and enhancing clinician motivation
acceptance of clients and help clients accept them- and skills. Structurally, four modes of treatment
selves. Of course, empathy, validation, and self- address these functions, including individual ther-
acceptance alone are inadequate for highly suicidal apy, group skills training, telephone coaching, and a
patients with BPD, who need effective tools for re- therapist consultation team (see Table 31.1 for the
ducing misery and building “a life worth living” structure and functions of comprehensive DBT).
(e.g., a values-driven life that helps the client see In the 27 years since publication of the first ran-
function or meaning in committing to staying alive; domized controlled trial (RCT) supporting efficacy
Linehan, 1993a). Recognizing the need to balance of DBT for reducing parasuicidal behavior (e.g., sui-
acceptance strategies with evidence-based change cide attempts and self-injury; Linehan, Armstrong,
strategies, Linehan cohered this emerging treatment Suarez, Allmon, & Heard, 1991), mounting evidence
with a dialectical philosophy, which emphasizes a has supported DBT as a treatment for BPD. To
balance and synthesis between acceptance and date, over 20 published RCTs have examined stand-
change. The DBT therapist seeks to incorporate ac- ard DBT (including individual therapy, telephone
ceptance and change dialectically in all aspects of consultation, group skills training, and the DBT
treatment delivery, including (1) therapeutic style consultation team), and over 15 published RCTs
464 Dialectical Behavior Therapy

Table 31.1. Dialectical Behavioral Therapy Modes that up- or downregulate emotion-related physiol-
and Functions ogy, and so on (Gross, 1998). Emotion regulation
tends to occur in motivationally relevant contexts,
Mode Function
or situations that bear relevance to the individual’s
Individual Improve motivation, generalize goals. For example, a frustrated employee who is
therapy treatment gains, solve life problems, seeking a raise has a goal to receive higher pay and
build a life worth living also to avoid being fired; thus, she might regulate
Group skills Increase capabilities for mindfulness, the experience or expression of frustration through
training distress tolerance, interpersonal various means. Beauchaine (2015) has argued that
effectiveness, emotion regulation, and emotion regulation is difficult to study, as it is often
self-management/regulation defined as the absence of problematic responses. If
Telephone Generalize new behaviors to relevant the frustrated employee avoided yelling at the boss,
consultation situations the assumption is that she must have done some-
Consultation Maintain and improve therapist thing to regulate the experience or expression of
team motivation and capability frustration, and the researcher’s (or clinician’s) chal-
lenge is to determine specific markers of the em-
ployee’s emotion regulation in this situation.
have examined group DBT skills training. Findings In contrast, emotion dysregulation may be easier
from these studies provide strong support for the to identify, as it is characterized by the presence of
efficacy of standard DBT for BPD (and related observable behavior or emotional responses that are
problems), and emerging support for group DBT too prolonged, intense, labile, or situationally inap-
skills training for problems such as BPD, emotion propriate (Beauchaine, 2015). One working defini-
dysregulation, depression, anxiety, disordered eating tion of emotion dysregulation in DBT is “the in-
(bingeing and purging), and other difficulties ability, even when one’s best efforts are applied, to
(Neacsiu & Linehan, 2014; Valentine, Bankoff, change in a desired way emotional cues, experiences,
Poulin, Reidler, & Pantalone, 2015; McMain et al., actions, verbal responses, and/or nonverbal expres-
2018). A 2013 systematic review from the Cochrane sions under normative conditions” (p. 511). Similar
Database of Systematic Reviews on treatments for to other definitions of emotion dysregulation (e.g.,
BPD found moderate to large effects supporting see Beauchaine, 2015), this definition captures the
DBT over treatment as usual for reducing inappro- importance of goals (i.e., “in a desired way”).
priate anger, parasuicidal behavior, and improving Additionally, consistent with the skill deficit model,
mental health (Stoffers et al., 2013). Accordingly, this definition captures deficits in emotion regula-
both the Australian National Health and Medical tory capabilities. Within this framework, we would
Resource Council (NHMRC) and the United know that the employee is emotionally dysregulated
Kingdom’s National Collaborating Centre for by the presence of enduring or overly intense frus-
Mental Health (NICE) have concluded that DBT tration or the observable behaviors of yelling or
has the most evidence among current treatments threatening the boss, all of which interfere with her
for BPD (NHMRC, 2012; NICE, 2009). goal to remain employed and receive a raise.
Similarly, emotion dysregulation would be evident
Conceptualization of Emotion if the employee tries to dampen her frustration or
Dysregulation in Dialectical avoid yelling or threatening but is unable to do so.
Behavior Therapy A potential disadvantage of this view of emotion
In this volume, a key distinction is made between dysregulation (shared by contemporary definitions
emotion regulation and dysregulation. There are of emotion regulation) is its breadth and scope.
several extant definitions of emotion regulation, but Emotion dysregulation could be considered a key
a common theme is that emotion regulation in- etiological contributor to a broad range of dysfunc-
volves alterations to the form, frequency, experi- tion, from mood and anxiety disorders to gambling,
ence, or expression of emotions (Beauchaine, 2015; binge eating and substance use problems, aggres-
Gross, 1998). As such, emotion regulation could sion, suicidal self-injurious behaviors, and so forth.
occur through homeostatic physiological mecha- The breadth of the construct of emotion dysregula-
nisms, modifications in attention to or awareness tion (within and outside of DBT) makes it both
of emotional stimuli, cognitive reappraisal, actions a key transdiagnostic variable and a ubiquitous,
Chapman and Hope 465

somewhat amorphous contributor to a range of have examined emotional vulnerability in BPD
psychopathology. extensively, using a range of methods (subjective
self-report, physiological measures, neuroimaging,
Emotion Dysregulation in Borderline and so forth). It is beyond the scope of this chapter
Personality Disorder to provide an extensive, critical summary of this
According to Linehan’s (1993a) biosocial theory, research; however, a few consistent findings have
BPD results from a transaction between a biologi- emerged. First, emotional sensitivity and reactivity
cally based vulnerability to emotions and an invali- in BPD do not appear to be global, across positive
dating rearing environment. Given the focus of this and negative emotions or all contexts. Instead, emo-
chapter, we emphasize emotion vulnerability, but it tional vulnerability appears to be specific to negative
is important to recognize that emotion dysregula- emotions and particular emotional contexts, such
tion evolves within a social-developmental context. as those involving social rejection, negative perfor-
Within the biosocial theory, individuals with BPD mance feedback, and ambiguous or anger-related
are prone to three primary features of emotion vul- stimuli (e.g., Donegan et al., 2003; Gratz, Rosenthal,
nerability. The first is heightened emotional sensitiv- Tull, Lejuez, & Gunderson, 2010). Further, findings
ity, which involves a low threshold for emotional regarding emotional reactivity consistently show
responding, such that low-intensity stimuli (e.g., a heightened amygdala activity (Goodman et al.,
minor change in another person’s facial expression 2014; Silvers et al., 2016) and reduced connectivity
or voice tone) reliably elicit an emotional response. of the amygdala to frontal brain regions involved in
The second feature is heightened emotional reactivity, effortful emotion regulation (medial, dorsolateral,
consisting of a tendency to experience particularly and ventrolateral prefrontal cortex; Baczkowski et
intense emotional reactions. The third feature is al., 2017). Findings are more mixed with respect to
slow return to emotional baseline (sometimes referred subjectively reported and autonomic emotional re-
to as delayed recovery), consisting of a lengthy activity (e.g., subjectively reported mood reactivity
period before physiological and subjective arousal may be specific to negative emotions; see Rosenthal
intensity begin to dissipate following an emotion- et al., 2008 for review; Herpertz, Kunert, Schwenger,
ally evocative event. & Sass, 1999), possibly because these aspects of re-
Within the biosocial theory, repeated transac- activity are context dependent. Second, less research
tions between emotional vulnerability and an in- has examined a slow return to baseline, but some
validating environment ultimately contribute to findings suggest delayed recovery for subjectively
pervasive emotion dysregulation. An invalidating reported emotional responses and sympathetic ac-
environment is defined as one that indiscriminately tivity in BPD, although there is less evidence for
rejects the individual’s communication of emotions, delayed recovery on parasympathetic measures
intermittently reinforces extreme emotional expres- (Fitzpatrick & Kuo, 2015). In addition, researchers
sion, and oversimplifies the ease of problem solving have yet to carefully examine the specific features
(Linehan, 1993a). In a developmental context, emo- and emotional contexts associated with a slow return
tion vulnerability is thought to transact with the to baseline.
invalidating environment: high emotion vulnerabil- Emotion dysregulation and emotion vulnerabil-
ity (e.g., expressed through frequent, intense tan- ity are not the same, in that emotion dysregulation
trums; defiant behavior; emotional outbursts; and requires that the individual is unable to modulate
so forth) may require especially astute parenting and emotional responses or expression in a manner that
could occasionally evoke invalidating parental re- facilitates the attainment of needs or goals in par-
sponses. In turn, invalidation amplifies emotion ticular contexts. Heightened emotion vulnerability,
vulnerability and leaves the child bereft of the skills combined with a history of invalidation or trauma,
needed to regulate emotions. Moreover, emotion- can complicate effective emotion regulation. From a
ally vulnerable individuals are likely to require more DBT perspective, an emotionally vulnerable client
skills to navigate their emotions than individuals trying to regulate extreme emotions is much like
who have a less complex emotional profile, just as it someone with no training being asked to fly a
takes more skills to fly a fighter jet than it does to fighter jet in battle; pressing the eject button may
drive a Volkswagen.1 seem like the best option. Clinically, clients with
Since Linehan’s (1993a) publication of the bio- BPD often describe their emotions as out of con-
social theory (subsequently updated and expanded trol, destabilizing, or intolerable, and they often
by Crowell, Beauchaine, & Linehan, 2009), studies generate maladaptive options to regulate them (e.g.,

self-injury, drugs, suicidal behavior). In addition, Addressing Behavioral Aspects
researchers examining emotion regulation difficul- of Emotion Dysregulation
ties find that those with BPD and borderline per- Behavioral aspects of emotion dysregulation often
sonality features struggle with low emotional clar- include actions serving short-term functions (e.g.,
ity, awareness, and acceptance; difficulty engaging emotional relief ) but that hamper the pursuit of
in goal-directed behaviors when distressed; and use valued goals. Common examples include suicide
of avoidance or other maladaptive coping strategies attempts and nonsuicidal self-injury (NSSI), drug
(Aldao & Dixon-Gordon, 2014; Baer & Sauer, use, risky sex, and other self-damaging behaviors.
2011; Beblo et al., 2013; Chapman, Dixon-Gordon, These risky and life-threatening behaviors—which
& Walters, 2013; Dixon-Gordon et al., 2015; are a primary treatment target in Stage 1 of standard
Evans, Howard, Dudas, Denman, & Dunn, 2013; DBT—generally occur in emotional contexts and
Glenn & Klonsky, 2009; Leible & Snell, 2004; function to regulate emotions or to produce changes
Sauer-Zavala, Bentley, & Wilner, 2016). Therefore, in the environment that in turn regulate emotions.
despite being tasked with flying a fighter jet, those A client who engages in self-injury after a conflict
with BPD often, understandably, do not cope well with her partner might experience relief from aver-
with the situation. To solve this problem, DBT in- sive emotional states (e.g., tension, anger) or social
cludes a combination of skills training and other consequences that reduce painful emotion dysregu-
evidence-based interventions to address emotion lation (e.g., the partner soothing or providing com-
dysregulation. fort/reassurance or reducing demands or criticism).
Individual therapy involves a combination of self-
How Comprehensive Dialectical Behavior monitoring (via daily diary cards), functional/chain
Therapy Treats Emotion Dysregulation analyses of specific instances of the behaviors, and
DBT includes several interventions and strategies problem solving. In this context, “problem solving,”
that directly and indirectly target behavioral, cog- broadly defined, targets the factors maintaining
nitive, and physiological aspects of emotion dys- problem behaviors using a broad armamentarium
regulation. The most obvious way in which DBT of CBT- and DBT-oriented interventions, such as
addresses emotion regulation is by teaching clients commitment or motivational strategies, cognitive
emotion regulation skills, which is one of four skills modification, exposure, skills training and coach-
training modules in DBT (Linehan, 2015). Because ing, and contingency management, among others.
emotion regulation is such a broad and multifaceted Individually tailored modifications to the behav-
skill, the DBT emotion regulation skills module ioral aspects of emotion dysregulation often occur
(henceforth referred to as DBT-ER skills) is the within individual DBT therapy.
largest in the skills training manual, taking approxi- Group skills training can indirectly reduce be-
mately eight weeks to teach. Skills trainers first havioral aspects of emotion dysregulation by build-
teach clients how to understand emotions and their ing the client’s capacity to self-regulate and avoid
own emotional experience. Subsequently, clients harmful behavior. Based on a skill deficit model of
learn how to identify various components of emo- BPD, skills training aims to improve capacities that
tions, including cognitive (interpretations, percep- will help the client reduce out-of-control behavior
tions, attention/awareness), behavioral (action and work toward important goals. The crisis sur-
urges, emotional expressions, actions), and physio- vival subset of the distress tolerance skills, for ex-
logical components (physical sensations, neurobio- ample, helps clients manage intense emotions with-
logical changes). By studying a systemic model, cli- out engaging in actions that will make their situation
ents learn that changes in one component of an worse. Some examples of these skills include (1)
emotional response can affect other components of STOP, which involves stopping, taking a step back,
the system; thus, we can regulate our emotions by observing the crisis/stressful situation, and proceed-
changing cognitive, behavioral, or physiological as- ing mindfully; (2) pros and cons, which involves en-
pects of an emotion. In addition, as noted in the tertaining the pros and cons of engaging in a prob-
next section, DBT addresses emotion dysregulation lem behavior (e.g., self-injury) versus the pros and
in less structured ways in individual therapy, tele- cons of using a skill instead; and (3) distraction and
phone coaching, and group skills training. Next, we self-soothing activities that help the client delay or
discuss various ways in which DBT addresses the avoid problem behaviors (Linehan, 1993b, 2014).
behavioral, physiological, and cognitive aspects of Another DBT skill targeting behavioral aspects of
emotion dysregulation. emotion dysregulation is opposite action (from the

emotion regulation skills), which involves engaging Addressing Physiological Aspects
in actions that run counter to the urges accompany- of Emotion Dysregulation
ing dysregulated emotional states (particularly those Physiological aspects of emotion dysregulation
that are mismatched in either form or intensity with often include emotions that are overly intense rela-
the current context; Linehan, 2015). An example of tive to the situation, overwhelming, and involving
this is a client with road rage purposely slowing high physiological arousal and delayed recovery.
down, relaxing his grip on the steering wheel, and Intense physiological responses can make it difficult
trying to foster empathy or compassion for the slow for clients to process information, inhibit maladap-
driver in front of him (rather than gunning the tive actions, and engage effectively in therapy.
engine, gesticulating madly, and trying desperately Individual DBT therapists typically target physio-
to pass the other driver). Another example would be logical dysregulation as needed in therapy sessions
a client paralyzed with fear of social situations who or during telephone coaching, by teaching skills to
actively and mindfully attends and participates in reduce or better tolerate physiological arousal.
small talk at a party. In addition, the interpersonal Heightened physiological dysregulation on the
effectiveness skills include several concrete behav- phone or in therapy sessions may occur in response
ioral strategies for clients to assert their needs effec- to difficult discussions of emotionally evocative
tively and manage conflict without making situa- events, interactions between the client and thera-
tions worse. pist, memories or flashbacks occurring during ses-
Emotion dysregulation can occur behaviorally sion, or reactions to various therapeutic interven-
during individual DBT and group skills training tions (e.g., exposure therapy). As clients with BPD
sessions. Many of the in-session behaviors falling and other emotion-oriented disorders often are well
within the category of “therapy-interfering behav- practiced at suppressing emotional expression, the
ior” (Linehan, 1993a; see also Chapman & therapist must be mindful of emotional shifts oc-
Rosenthal, 2016) represent emotion dysregulation, curring in the moment. The first signs of physiolog-
such as yelling, refusing to talk, engaging in verbal ical dysregulation often are behavioral, such as the
aggression toward the therapist or other clients, sob- client who looks down, turns away, and fidgets
bing uncontrollably, leaving the room, and so forth. when experiencing intense anxiety or shame or be-
When these behaviors occur in session, this provides comes rigid and silent when experiencing intense
an opportunity for the therapist to help the client anger. The therapist also might attend to alterations
learn to act effectively, even when emotions are dys- in voice tone or visual signals (e.g., reddening face,
regulated. One common strategy to accomplish this perspiration).
aim is contingency management, often involving When the therapist observes signs of physiologi-
the therapist blocking or extinguishing undesirable cal dysregulation, it is helpful to start by bringing
behavior and eliciting and reinforcing more desir- these observations to the client’s attention (e.g.,
able behavior. A therapist might ask a client threat- “I notice that you seem to breathing more rapidly”;
ening suicide, for example, to start over, state what “Your face appears red, and you seem to be holding
he needs without the threat, and provide reinforce- a lot of tension in your arms”; “Your voice is steadily
ment for this alternative behavior (i.e., differential getting louder”). Clients may also benefit from
reinforcement of alternative behavior [DRA]; practicing the skill of mindfulness to current emo-
Farmer & Chapman, 2016; see Petscher, Rey, & tion (Linehan, 2015), which involves observing and
Bailey, 2009 for review of empirical support for describing physiological sensations. It can be help-
DRA). Over time and with repeated practice, the ful for clients to know that physiological aspects of
hope is that the client will develop a capacity to self- an emotional response (e.g., hormonal and neuro-
regulate, even in the presence of intense emotions. chemical changes) are typically fleeting, lasting no
Indeed, this is a common aim across individual, longer than a minute or so. Simply allowing the
telephone, and group modes of DBT (Lynch, physiological response to unfold without amplify-
Chapman, Rosenthal, Kuo, & Linehan, 2006; ing or retriggering it (i.e., through rumination, re-
Lynch, Trost, Salsman, & Linehan, 2007). Other exposure to emotional cues, or actions that worsen
strategies include skills coaching to help the client the situation) can help the client learn that the aver-
tolerate or regulate dysregulated emotional arousal, sive physiological wave of an emotion often ebbs
as discussed next. fairly quickly. In addition, the therapist may coach

the client in DBT skills addressing physiological labeling and awareness may also help clients reduce
arousal (see below). physiological arousal if they use this knowledge to
If a client is afraid to experience strong emotions, accurately label emotions (given evidence that emo-
informal exposure strategies (Farmer & Chapman, tion labeling may reduce activity in the amygdala;
2016; Linehan, 1993a) can help the client experi- Lieberman et al., 2007).
ence emotions in the absence of threatening events.
For example, some clients are afraid to experience Addressing Cognitive Aspects
sadness, likely because they have historically faced of Emotion Dysregulation
punishing consequences from their caregivers. As a Cognitive aspects of emotion dysregulation can
result, the physiological sensations of sadness and present in several ways, such as rumination, hyper-
associated urges (to cry, etc.) have become associ- vigilance to cues for threat, rejection sensitivity, fear
ated with threatening events, and the client avoids, of abandonment, rigid thinking, and/or difficulty
escapes, or sometimes experiences panic, anger, or disengaging attention from emotional content.
frustration when sadness arises. Informal exposure Further, intense physiological arousal can often
in these cases involves instructing the client to expe- impair information processing, such that trying to
rience sadness for prolonged periods without avoid- intervene cognitively is much like trying to converse
ing or escaping, while regularly assessing the client’s with someone across the street during a hurricane.
subjective units of distress. This work can also be Several studies have demonstrated that the narrow-
accomplished through formal exposure protocols, ing of attention and an emphasis on proximal goals
involving a hierarchy and regular within- and out- (i.e., to escape emotions) accompany highly intense,
of-session practice. Exposure protocols can address aversive emotional states (Tice, Bratslavsky, &
physiological, behavioral, and cognitive aspects of Baumeister, 2001). Baumeister (1990) coined the
emotion dysregulation. Indeed, recent research sug- term cognitive deconstruction to describe a cognitive
gests that DBT plus structured exposure protocols state occurring in the context of aversive emotions
may have more benefit for suicidal patients with and often preceding suicidal behavior. Although
BPD and posttraumatic stress disorder (PTSD) DBT includes the standard CBT armamentarium
than standard DBT alone, across assessed behaviors of strategies, these strategies often must be modified
(e.g., self-injury), symptoms (e.g., PTSD), and gen- stylistically or combined with other interventions
eral psychiatric outcomes (Harned, Korslund, & (e.g., behavioral methods or arousal regulation) for
Linehan, 2014). emotionally dysregulated clients.
DBT skills training also targets physiological as- The dialectical worldview underlying DBT in-
pects of emotion dysregulation. In particular, the forms cognitive approaches to emotion dysregula-
distress tolerance skill module includes the TIP tion. First, dialectical theory encourages DBT ther-
skills, designed to alter physiological arousal by apists to balance change-oriented interventions
changing body temperature (e.g., putting one’s face with validation. A common cognitively oriented
in a bowl of cold water; taking a bath, foot bath, or approach in DBT involves clarifying the contingent
shower), engaging in intense exercise, or using relax- relationship of the client’s behavior with some un-
ation strategies such as paired muscle relaxation, desirable consequence (often called “contingency
paced breathing, or other related strategies; Linehan, clarification,” e.g., “When you yell at me, I have a
2015). Some of these skills aim to activate the para- hard time focusing on what you’re saying”). A thera-
sympathetic nervous system, such as the face-in- pist combining this approach with validation would
cold-water strategy, which purportedly stimulates validate the client’s anger and frustration while also
the dive reflex. Similarly, paced breathing, which clarifying the effects of yelling on the therapist and
involves extending exhalations for approximately the therapy session. One key function of emotions
twice as long as inhalations, can reduce heart rate by is to communicate to others (Linehan, 2014); thus,
capitalizing on natural arrhythmias occurring across validation helps to convey that the emotion’s func-
the respiratory cycle (heart rate decreases during ex- tion has been fulfilled (i.e., the message has gotten
halation). Clients are often taught to use TIP skills through).
to alter physiological arousal when their emotions Second, dialectical theory encourages therapists
are too intense for clear thinking or more compli- to use a balance of different interpersonal styles,
cated skills use. In addition, training in emotional with the primary therapy styles being reciprocity and

irreverence. Reciprocity involves warmth and re- pressions of anger (see Neacsiu, Eberle, et al., 2014
sponsiveness to the client’s needs and wishes. for a review). This evidence has been reviewed exten-
Irreverence, in contrast, involves the therapist sively elsewhere (e.g., Neacsiu, Eberle, et al., 2014;
making unexpected statements, using humor or a Stoffers et al., 2013). As such, we focus on recent
matter-of-fact style, and oscillating intensity of innovative work on the relevance and treatment of
emotional expression, among other approaches. physiological aspects of emotion dysregulation.
Lynch and colleagues (2006) have argued that, A promising emergent area of DBT research is
because irreverent responses often are surprising, ir- focused on identifying physiological processes and
reverence in DBT may prompt an orienting re- examining how DBT may change these underlying
sponse, capturing the client’s attention. When a physiological mechanisms of emotion dysregula-
client is experiencing the cognitive effects of emotion. For example, functional magnetic resonance
tion dysregulation (e.g., narrowing of attention, ru- imaging (fMRI) captures patterns of neural activa-
minative self-focus), a key goal is to get his or her tion by measuring changes in blood oxygenation,
attention. In addition, irreverence may help the an indicator that is highly correlated with blood
client think more flexibly about upsetting situa- flow (e.g., Raichle, 1998). By pairing fMRI with
tions, and flexible thinking runs counter to the cog- longitudinal investigation, researchers can investi-
nitive rigidity often accompanying emotion dys- gate (1) unique patterns of brain activity associated
regulation. These approaches to cognitive aspects of with emotion dysregulation (e.g., in patients with
emotion dysregulation can be useful in both indi- BPD compared to other psychiatric groups and
vidual and group DBT. healthy controls) and (2) the effects of interven-
Third, a dialectical worldview suggests that there tions on physiological markers of emotion dysregu-
is no absolute truth, and that both client and thera- lation (e.g., changes in neural activation following
pist can benefit from considering opposing or alter- DBT). Mounting evidence suggests that BPD is
native perspectives. The therapist often models dia- associated with dysfunctions in the fronto-limbic
lectical thinking by showing how seemingly system (e.g., amygdala hyperactivity, reduced pre-
opposing ideas can go together. An example for a frontal connectivity with the amygdala, reduced ac-
client who is angry with her therapist for going on tivity in key frontal areas associated with emotion
vacation and being unavailable during that time and self-regulation) and that DBT may ameliorate
could be as follows: “It is understandable that you’re these dysfunctions.
angry. My being unavailable makes it a lot harder
for you to get the help and support you need. And, Neurobiological Factors Associated
at the same time, it’s reasonable for me to go on va- with Self-Injury
cation, and these periodic breaks put me in a better To better understand patients’ reasons for self-injury
position to help you in the long run.” Modeling or and implications for emotion regulation, research-
encouraging a dialectical worldview may be particu- ers have begun to study self-injury through innova-
larly useful for clients struggling with cognitive as- tive laboratory behavioral analogs. Some of this work
pects of emotion dysregulation. For example, abso- involves a paradigm where participants receive a
lute or “polarized” thinking (e.g., “The therapist is small incision.
awful and unprofessional for going away on vaca- Reitz and colleagues (2015) exposed a group of
tion. She/he doesn’t care about me at all!”; “I’m still self-injuring women with BPD and a group of
depressed; therefore, I’m failing in therapy”) may healthy controls to either a real incision or a sham
amplify negative emotions and provoke further ex- incision following stress induction. For the healthy
treme emotional and behavioral reactions. controls, receiving a real incision did not lead to
Encouraging dialectical thinking may help the stress-reducing effects on subjective or physiological
client expand his or her view of upsetting situations measures. In contrast, for women with BPD, receiv-
and reduce polarized and rigid thinking. ing an incision led to decreased aversive tension
(i.e., self-reported distress), decreased amygdala ac-
Evidence for Dialectical Behavior Therapy tivation, and increased prefrontal connectivity (to
in the Treatment of Emotion Dysregulation superior frontal gyrus). In essence, the incision was
Growing evidence supports use of DBT for prob- effective at “normalizing” the heightened amygdala
lems related to emotion dysregulation, which can response for the women with BPD, and the sham
include self-damaging behaviors, such as self-harm, was not. Such research supports a basic tenet of
substance use, suicide attempts, and dysregulated ex- DBT that individuals engage in behaviors like

self-injury to provide short-term relief from the date, three longitudinal investigations have been
physiological effects of emotion dysregulation.2 The conducted examining changes in neural activity
ongoing challenge for researchers and clinicians is to before and after receiving DBT in patients with
identify teachable skills that are as effective and ap- BPD. As discussed here and in Chapters 16 and 24
pealing to dysregulated patients without the long- of this volume, overactivity of the amygdala in re-
term consequences. sponse to emotional stimuli has been implicated as
Another laboratory study examined if painful a mechanism of emotion dysregulation in BPD
stimuli alone (without tissue injury) leads to amyg- (e.g., Schmahl et al., 2006; Donegan et al., 2003;
dala deactivation, or if painful stimuli plus tissue Herpertz et al., 2001).
injury (e.g., from incision) is necessary (Willis et al., One question examined by clinical neuroscien-
2016). Fifty-seven self-injuring participants with tists is whether there are identifiable neurobiological
BPD and 60 healthy control participants were ran- changes in response to DBT. Schnell and Herpetz
domly assigned to one of three conditions: painful (2007) conducted the first investigation of changes
incision (pain + incision), painful “noninvasive no- in neural activity following DBT. In a small pilot
ciceptive stimulus” (pain + no incision: a blade that study, six patients with BPD were scanned in an
hurt but did not cut participants), or a sham stimu- fMRI machine before treatment and following 12
lus (no pain + no incision). In each of the condi- weeks of DBT inpatient care. Patients were com-
tions, participants received the stimulus to their pared to five healthy controls who did not meet cri-
forearm following a stressful arithmetic task in teria for BPD. For all participants, negative emo-
which participants were told (using deception) they tions were induced through standardized images
were performing below average. This task was used that are reliably experienced as unpleasant and pro-
to simulate real-world stressful conditions, thereby duce negative emotions (e.g., picture of a soldier
prompting emotion dysregulation and self-injury. with a gun next to a dead body; picture of a cheetah
This stress induction led to increased heart rate for baring its teeth while eating flesh). The researchers
both groups of participants, and increased urges to found that after DBT, the patients with BPD dis-
self-injure for patients with BPD. To control for ex- played reduced activity in the anterior cingulate
pectations, participants were not told which of the cortex (ACC), temporal and posterior cingulate,
three conditions they would receive and were not and insula in response to unpleasant stimuli relative
able to see the stimulus that the researchers delivered to their pretreatment scans. The four patients who
to their forearm behind a shield screen. The research- were most responsive to DBT on clinical outcome
ers found that, for the BPD patients, immediate re- measures displayed a decreased hemodynamic re-
ductions in subjective arousal and heart rate oc- sponse, modulated by subjective emotional arousal.
curred in both the pain + incision and the pain + no Specifically, there was a decrease in the extent to
incision conditions. These findings suggested that which highly emotional unpleasant stimuli elicited
pain may be a primary mechanism underlying the a left amygdala response for those patients who did
emotion regulatory effects of injury. Moreover, pa- well in treatment. The authors suggest that this may
tients with BPD showed a significantly stronger de- represent improved emotion regulation at a physio-
crease in subjective arousal following either painful logical level. Moreover, differences in brain activa-
stimulus compared with healthy controls. Unlike tion (e.g., ACC activation) between patients and
patients with BPD, healthy controls did not show healthy controls were reduced after the patients un-
decreases in arousal or heart rate following the pain- derwent treatment. The researchers concluded that
ful stimuli compared to the sham stimuli. Consistent after 12 weeks of inpatient DBT, patients experi-
with patient self-reports that the regulating effects of enced decreased neural reactivity to negative stim-
self-injury are short-lived, reduced subjective arousal uli. Limitations of this study include a small sample
and heart rate did not persist when researchers reas- size, as well as the modified three-month version
sessed participants 30 minutes after the stimulus ap- of DBT.
plication (Willis et al., 2016). In the second study of neural changes in patients
who completed DBT, Goodman and colleagues
Neurobiological Changes Following (2014) improved upon limitations of the first study
Dialectical Behavior Therapy by increasing their sample size and providing
Researchers are beginning to turn to fMRI to deter- patients with 12-month standard, comprehensive
mine whether DBT can change neurobiological DBT. Before treatment and after 12 months, par-
processes underlying emotion dysregulation. To ticipants completed an fMRI task that involved

viewing pleasant, unpleasant, or neutral images damaging behaviors. This is especially important,
while amygdala activity was measured. In addition given that self-damaging and life-threatening be-
to investigating changes in amygdala activity fol- haviors are among the most alarming and urgent
lowing treatment, the researchers also investigated treatment targets for patients who receive DBT.
participants’ self-reported changes in emotion regu- Going forward, there are several important future
lation, as assessed by the Difficulties in Emotion directions to consider. In this section, we discuss the
Regulation Scale (DERS; Gratz & Roemer, 2004). following directions: (1) increasing multimethod,
As expected, healthy control participants, who did multicontext research on emotion dysregulation;
not receive DBT treatment, did not show signifi- (2) streamlining treatment; and (3) considering
cant changes in amygdala activity or self-reported frameworks for the transdiagnostic treatment of
emotion regulation strategies over the 12 months. In emotion dysregulation.
contrast, patients with BPD displayed significant
changes in both amygdala activity and emotion Increasing Multimethod, Multicontext
regulation following 12 months of treatment. Research on Emotion Dysregulation
Specifically, patients showed an overall decrease in To continue improving DBT, more basic/transla-
amygdala activity and decreased self-reported diffi- tional research is needed to specify the nature of
culties in emotion regulation. Moreover, change in emotion dysregulation and contexts in which it
amygdala activity was associated with improved emerges. To benefit from research on specific com-
emotion regulation, leading the authors to conclude ponents of emotion dysregulation and corre-
that acquisition of emotion regulation strategies in sponding interventions, it is important to estab-
DBT may account for reduced amygdala activity lish a common language of both subjective and
following treatment. Nonetheless, it remains un- physiological markers of emotion dysregulation.
known how “normalized” the BPD patients’ amyg- This requires more precise definitions and meas-
dala activity was posttreatment, and how long de- urement tools. Future research should continue
creased amygdala activation is maintained after the using multiple methods to assess emotion dysreg-
end of treatment. ulation (self-report, psychophysiological, neuro-
Niedtfeld and colleagues (2017) investigated imaging, etc.).
changes in amygdala response to pain over the In particular, researchers should seek to include
course of DBT (n = 28) compared with treatment as physiological markers of emotion dysregulation and
usual (n = 15). Prior to DBT, patients with BPD should examine changes in these measures over the
showed amygdala deactivation in response to pain- course of treatment. Psychophysiological and neu-
ful stimulation. Given that amygdala deactivation is robiological measurements of emotion dysregula-
associated with a dampening of negative emotions, tion should also be included as outcomes in RCTs
the authors suggest that this response to pain stim- (in addition to common outcomes, such as hospi-
uli may contribute to emotion-regulating effects of talization, severity of symptoms, self-injury, etc.).
self-injury. Following DBT treatment, the effect of Although there is promising research on neurobio-
pain on amygdala deactivation was reduced. That is, logical changes following DBT, more research is
patients with BPD who received DBT treatment needed to understand the long-term durability of
showed reduced coupling between pain and amyg- these treatment effects. Existing longitudinal studies
dala deactivation, compared to patients who re- have been short term (e.g., Goodman et al., 2014;
ceived treatment as usual. If this effect persists well Niedtfeld et al., 2017), so questions remain regard-
beyond the end of treatment, patients could be at ing the stability of the neurobiological effects of
sustained, lower risk of self-injury. DBT. Thus, it is important for researchers to assess
whether gains are maintained, by which clients, and
Future Directions whether there are downstream consequences of re-
Originally developed to treat complex, highly sui- duced physiological dysregulation following treat-
cidal patients, DBT systematically addresses emo- ment (e.g., does decreased amygdala activation or
tion dysregulation in several ways. Findings support increased prefrontal connectivity predict changes in
the effectiveness of DBT for reducing various as- likelihood of future hospitalization, self-injury, or
pects of emotion dysregulation. Further, recent re- substance use).
search has examined whether DBT affects potential Evidence reviewed in this chapter suggests that
neurobiological mechanisms associated with self- there may be particular patterns of emotion dysreg-

ulation in BPD, which appear to emerge in specific Considering Transdiagnostic Treatments
contexts. Further research using multiple methods for Emotion Dysregulation
to measure emotion dysregulation and designs that Along with other treatments addressing emotions
capture contextual influences on emotion dysregu- and emotion regulation (e.g., the Unified Protocol;
lation would be particularly illuminating (e.g., ex- Barlow et al., 2004), DBT may be a useful transdiag-
perimental manipulation of context, ecological mo- nostic approach. Increasingly, clinical researchers are
mentary assessment, etc.). Understanding these moving away from categorical segregation of disor-
patterns and contexts could help refine and stream- ders, identifying common underlying problems and
line treatment. Notwithstanding, even if this re- proposing transdiagnostic treatment for multiple dis-
search contributes to streamlined treatments focus- orders, such as Barlow and colleagues’ (2004) unified
ing on key contextual factors, clinicians would still protocol (UP) treatment of emotional and other dis-
need to conduct idiographic analyses of factors con- orders (e.g., transdiagnostic p rotocol for eating disor-
tributing to their clients’ emotion dysregulation. ders; Fairburn, Cooper, Shafran, & Wilson, 2008).
Initial research has yielded promising findings for use
Streamlining Treatment of DBT in non-BPD populations with emotion
Beyond translational research to inform increased dysregulation, including anxiety or depression (e.g.,
treatment efficiency, there is some evidence that Neacsiu, Eberle, et al., 2014), treatment-resistant de-
DBT may be streamlined for particular clinical pression (Harley, Sprich, Safren, Jacobo, & Fava,
problems. DBT is a comprehensive treatment, and 2008), binge-eating disorder (Safer & Jo, 2010),
evidence suggests that briefer or skills-only formats anger (see Frazier & Vela, 2014 for review), and sui-
might be effective (e.g., McMain, Guimond, cidal and nonsuicidal self-injury (Mehlum et al.,
Barnhart, Habinski, & Streiner, 2017; Neacsiu, 2014, 2016). Nonetheless, more research is warranted
Eberle, et al., 2014). Moreover, even specific skill to establish the efficacy of DBT as a transdiagnostic
modules (Dixon-Gordon, Chapman, & Turner, treatment for emotion dysregulation.
2015) or modified DBT interventions with specific DBT could fall along a continuum of transdiag-
targets (e.g., shame; Rizvi, Brown, Bohus & nostic interventions for disorders characterized by
Linehan, 2011) may have beneficial effects. This lit- emotion dysregulation. Treatments such as the UP,
erature is too young to make recommendations re- for example, might address emotional disorders of
garding the streamlining of DBT for treatment of lower severity, whereas comprehensive DBT (a higher
dysregulated patients, but given the resource burden intensity treatment) might address more complex
associated with comprehensive, long-term treat- and severe disorders. In light of limited resources for
ment, movement in this direction could be fruitful. mental health treatment and increasing demand,
Similarly, Internet-based or electronic applica- treatment guidelines are needed to identify who may
tions have promise for training patients to reduce require a higher intensity intervention. While DBT
emotion dysregulation. Based on the DBT skill was designed as a comprehensive 12-month treat-
deficit model, learning to reduce emotion dysregu- ment, there is growing evidence that the use of spe-
lation requires training and practice. Individual and cific modes of DBT, such as skills group only, may be
group therapy sessions, even in comprehensive beneficial for high-risk individuals awaiting compre-
DBT, make up approximately 3% of a client’s hensive DBT (e.g., McMain et al., 2017), or for pa-
waking hours, and realistically, dysregulated clients tients who do not meet criteria for BPD but who
with functional impairments likely spend a maxi- experience significant emotion dysregulation (e.g.,
mum of 1% to 2% more time practicing DBT skills. Neacsiu, Eberle, et al., 2014; Valentine et al., 2015).
In contrast, estimates suggest that people spend DBT has built-in flexibility to address less severe
many of their waking hours interacting with their treatment targets because DBT makes use of existing
smartphones or other computerized devices. evidence-based approaches that are effective for less
Applications that involve training and practice in severe clinical problems (Linehan, 1993a). Research
strategies to reduce the various aspects of emotion in this area is too nascent to offer guidelines regarding
dysregulation (behavioral, cognitive, physiological) a potential continuum of transdiagnostic treatments,
could have great potential when combined with but emerging findings suggest that lower intensities
standard therapy (evidence suggests generally that of DBT may be appropriate for clients with less com-
e-therapy is more effective when combined with plex clinical problems where emotion dysregulation
real-life therapy; e.g., Rogers et al., 2014). is still a primary concern.

A related, promising application of DBT is 2004), which suggest that pain and injury paradigms dampen
stepped-care models, beginning with lower inten- physiological markers of emotion dysregulation.
sity treatments and triaging patients to more inten-
sive doses of treatment during acute phases of References
illness. For example, Paris (2015) implemented a Aldao, A., & Dixon-Gordon, K. L. (2014). Broadening the
stepped-care model where clients with BPD receive scope of research on emotion regulation strategies and
short-term comprehensive DBT for 12 weeks during psychopathology. Cognitive Behavior Therapy, 43, 22–33.
Baczkowski, B. M., van Zutphen, L., Siep, N., Jacob, G. A.,
acute phases of illness (e.g., following referral from Domes, G., Maier, S., . . . & Arntz, A. (2017). Deficient
ER), followed by intermittent follow-up for pa- amygdala–prefrontal intrinsic connectivity after effortful
tients who have not achieved remission. Such ap- emotion regulation in borderline personality disorder.
plications of DBT also highlight a need for RCTs European Archives of Psychiatry and Clinical Neuroscience,
on short-term “doses” of comprehensive DBT, which 267, 551–565.
Baer, R. A., & Sauer, S. E. (2011). Relationships between
is most commonly studied as a 12-month treatment. depressive rumination, anger rumination, and borderline
Thus, the efficacy of briefer doses is unknown, al- personality features. Personality Disorders: Theory, Research,
though current studies are underway to address this and Treatment, 2, 142–150.
(e.g., McMain et al., 2018). Moreover, a stepped- Barlow, D. H., Allen, L. B., & Choate, M. L. (2004). Toward a
care treatment model parallels expected changes in unified treatment for emotional disorders. Behavior Therapy,
35(2), 205–230.
symptoms over time, with longitudinal research Baumeister, R. F. (1990). Suicide as escape from self. Psychological
showing that impulsive behaviors increase during Review, 97(1), 90–113.
acute phases of illness but remit more quickly than Beauchaine, T. P. (2015). Future directions in emotion
emotion dysregulation, which tends to be a more dysregulation and youth psychopathology. Journal of Clinical
chronic feature of BPD (Paris, 2003, 2015). In a Child and Adolescent Psychology, 44, 875–896.
Beblo, T., Fernando, S., Kamper, P., Griepenstroh, J.,
recent RCT, McMain et al. (2017) found that par- Aschenbrenner, S., Pastuszak, A., . . . & Driessen, M. (2013).
ticipation in a 20-week DBT skills group reduced Increased attempts to suppress negative and positive emotions
suicidal and self-injurious behavior for individuals in borderline personality disorder. Psychiatry Research, 210,
with BPD compared to waitlist, suggesting that an 505–509.
abbreviated skills group could be a helpful first step Chapman, A. L., Dixon-Gordon, K. L., & Walters, K. N. (2013).
Borderline personality features moderate emotion reactivity
for patients awaiting treatment. In conclusion, we and emotion regulation in response to a fear stressor. Journal
believe that multimethod translational research fur- of Experimental Psychopathology, 4, 451–470.
ther specifying problems with emotion dysregula- Chapman, A. L., Gratz, K. L., & Brown, M. Z. (2006). Solving
tion will inform improvements in the efficiency, the puzzle of deliberate self-harm: The experiential avoidance
effectiveness, and flexibility of DBT as a key trans- model. Behavior Research and Therapy, 44, 371–394.
Chapman, A. L., & Rosenthal, M. Z. (2016). Managing
diagnostic treatment. therapy-interfering behavior: Strategies from dialectical
behavior therapy. Washington, DC: American Psychological
Acknowledgments Association.
Work on this chapter was supported by a Michael Smith Crowell, S. E., Beauchaine, T. P., & Linehan, M. M. (2009). A
Foundation for Health Research Career Investigator Award and a biosocial developmental model of borderline personality:
Simon Fraser University FASS Dean’s Research Grant to the first Elaborating and extending Linehan’s theory. Psychological
author and a Canadian Institutes of Health Research Postdoctoral Bulletin, 135, 495–510.
Fellowship Award to the second author. Dixon-Gordon, K. L., Chapman, A. L., & Turner, B. J. (2015).
A preliminary pilot study comparing dialectical behavior
therapy emotion regulation skills with interpersonal
Notes effectiveness skills and a control group treatment. Journal of
1. Skilled DBT therapists employ a significant number of Experimental Psychopathology, 6(4), 269–828.
metaphors when working with clients. Metaphors are Dixon-Gordon, K. L., Weiss, N. H., Tull, M. T., DiLillo, D.,
especially important when teaching the biosocial theory Messman-Moore, T., & Gratz, K. L. (2015). Characterizing
because (1) the theory is presented early in treatment before emotional dysfunction in borderline personality, major
therapist-client trust has been established, and (2) a goal of depression, and their co-occurrence. Comprehensive
presenting the theory is to reduce blame and non-dialectical Psychiatry, 62, 187–203.
thinking (e.g., “it is my fault that I am this way” or “it is my Donegan, N. H., Sanislow, C. A., Blumberg, H. P., Fulbright,
family’s fault that I am suffering”). Thus, this is one example R. K., Lacadie, C., Skudlarski, P., . . . Wexler, B. E. (2003).
of a metaphor that a therapist might use when explaining the Amygdala hyperreactivity in borderline personality disorder:
biosocial theory and why some people may need explicit skills Implications for emotional dysregulation. Biological
training. Psychiatry, 54, 1284–1293.
2. This is also consistent with theoretical models of self-injury Evans, D., Howard, M., Dudas, R., Denman, C., & Dunn, B. D.
(e.g., Chapman, Gratz & Brown, 2006; Nock & Prinstein, (2013). Emotion regulation in borderline personality disorder:

Examining the consequences of spontaneous and instructed Linehan, M. M. (2015). DBT Ⓡ skills training manual. New York,
use of emotion suppression and emotion acceptance when NY: Guilford Press.
viewing negative films. Journal of Experimental Psychopathology, Linehan, M. M., Armstrong, H. E., Suarez, A., Allmon, D., &
4, 546–565. Heard, H. L. (1991). Cognitive-behavioral treatment of
Fairburn, C. G., Cooper, Z., Shafran, R., & Wilson, G. T. chronically parasuicidal borderline patients. Archives of
(2008). Eating disorders: A transdiagnostic protocol. In General Psychiatry, 48, 1060–1064.
D. H. Barlow (Ed.), Clinical handbook of psychological Lynch, T. R., Chapman, A. L., Rosenthal, M. Z., Kuo, J. K., &
disorders: A step-by-step treatment manual (pp. 578–614). New Linehan, M. M. (2006). Mechanisms of change in dialectical
York, NY: Guilford Press. behavior therapy: Theoretical and empirical observations.
Farmer, R. F., & Chapman, A. L. (2016). Behavioral activation. Journal of Clinical Psychology, 62, 459–480.
Washington, DC: American Psychological Association. Lynch, T. R., Trost, W. T., Salsman, N., & Linehan, M. M.
Fitzpatrick, S., & Kuo, J. R. (2015). A comprehensive (2007). Dialectical behavior therapy for borderline
examination of delayed emotional recovery in borderline personality disorder. Annual Review of Clinical Psychology, 3,
personality disorder. Journal of Behavior Therapy and 181–205.
Experimental Psychiatry, 47, 51–59. McMain, S., Chapman, A. L., Kuo, J. R., Guimond, T., Streiner,
Frazier, S. N., & Vela, J. (2014). Dialectical behavior therapy for D., Dixon-Gordon, K. L., .
.
.
Hoch, J. (2018). The
the treatment of anger and aggressive behavior: A review. effectiveness of 6 versus 12-months of dialectical behavior
Aggression and Violent Behavior, 19, 156–163. therapy for borderline personality disorder: The feasibility of
Glenn, C. R., & Klonsky, E. D. (2009). Emotion dysregulation a shorter treatment and evaluating responses (FASTER) trial
as a core feature of borderline personality disorder. Journal of protocol. BMC Psychiatry, 28, 1–16. https://doi.org/10.1186/
Personality Disorders, 23, 20–28. s12888-018-1802-z
Goodman, M., Carpenter, D., Tang, C. Y., Goldstein, K. E., McMain, S. F., Guimond, T., Barnhart, R., Habinski, L., &
Avedon, J., Fernandez, N., .
.
.
& Siever, L. J. (2014). Streiner, D. L. (2017). A randomized trial of brief dialectical
Dialectical behavior therapy alters emotion regulation and behavior therapy skills training in suicidal patients suffering
amygdala activity in patients with borderline personality from borderline disorder. Acta Psychiatrica Scandinavica, 135,
disorder. Journal of Psychiatric Research, 57, 108–116. 138–148.
Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment Mehlum, L., Ramberg, M., Tørmoen, A. J., Haga, E., Diep,
of emotion regulation and dysregulation: Development, L. M., Stanley, B. H., . . . Grøholt, B. (2016). Dialectical
factor structure, and initial validation of the Difficulties in behavior therapy compared with enhanced usual care for
Emotion Regulation Scale. Journal of Psychopathology and adolescents with repeated suicidal and self-harming behavior:
Behavioral Assessment, 26, 41–54. Outcomes over a one-year follow-up. Journal of the American
Gratz, K. L., Rosenthal, M. Z., Tull, M. T., Lejuez, C. W., & Academy of Child and Adolescent Psychiatry, 55, 295–300.
Gunderson, J. G. (2010). An experimental investigation of Mehlum, L., Tørmoen, A. J., Ramberg, M., Haga, E., Diep, L. M.,
emotional reactivity and delayed emotional recovery in Laberg, S., . . . Grøholt, B. (2014). Dialectical behavior therapy
borderline personality disorder: The role of shame. for adolescents with repeated suicidal and self-harming
Comprehensive Psychiatry, 51, 275–285. behavior: A randomized trial. Journal of the American Academy
Gross, J. J. (1998). The emerging field of emotion regulation: An of Child and Adolescent Psychiatry, 53, 1082–1091.
integrative review. Review of General Psychology, 2, 271–299. National Collaborating Centre for Mental Health (NICE).
Harley, R., Sprich, S., Safren, S., Jacobo, M., & Fava, M. (2008). (2009). Borderline personality disorder: Treatment and
Adaptation of dialectical behavior therapy skills training management. London, UK: British Psychological Society and
group for treatment-resistant depression. Journal of Nervous Royal College of Psychiatrists.
and Mental Disease, 196, 136–143. National Health and Medical Research Council (NHMRC).
Harned, M. S., Korslund, K. E., & Linehan, M. M. (2014). A 2012. Clinical practice guideline for the management of
pilot randomized controlled trial of Dialectical Behavior borderline personality disorder. Melbourne, Australia: Author.
Therapy with and without the Dialectical Behavior Therapy Neacsiu, A. D., Bohus, M., & Linehan, M. M. (2014). Dialectical
Prolonged Exposure protocol for suicidal and self-injuring behavior therapy: An intervention for emotion dysregulation. In
women with borderline personality disorder and PTSD. J. J. Gross (Ed.), Handbook of emotion regulation (pp. 491–507).
Behavior Research and Therapy, 55, 7–17. New York, NY: Guilford Press.
Herpertz, S. C., Dietrich, T. M., Wenning, B., Krings, T., Neacsiu, A. D., Eberle, J. W., Kramer, R., Wiesmann, T., &
Erberich, S. G., Willmes, K., . . . & Sass, H. (2001). Evidence Linehan, M. M. (2014). Dialectical behavior therapy
of abnormal amygdala functioning in borderline personality skills for transdiagnostic emotion dysregulation: A pilot
disorder: a functional MRI study. Biological Psychiatry, 50(4), randomized controlled trial. Behavior Research and Therapy,
292–298. 59, 40–51.
Leible, T. L., & Snell, W. E. (2004). Borderline personality Neacsiu, A. D., & Linehan, M. M. (2014). Dialectical behavior
disorder and multiple aspects of emotional intelligence. therapy for borderline personality disorder. In D. H. Barlow
Personality and Individual Differences, 37, 393–404. (Ed.), Clinical handbook of psychological disorders (5th ed., pp.
Lieberman, M. D., Eisenberger, N. I., Crockett, M. J., Tom, 394–461). New York, NY: Guilford Press.
S. M., Pfeifer, J. H., & Way, B. M. (2007). Putting feelings Neacsiu, A. D., Rizvi, S. L., & Linehan, M. M. (2010). Dialectical
into words. Psychological Science, 18, 421–428. behavior therapy skills use as a mediator and outcome of
Linehan, M. M. (1993a). Cognitive-behavioral treatment of treatment for borderline personality disorder. Behavior Research
borderline personality disorder. New York, NY: Guilford Press. and Therapy, 48, 832–839.
Linehan, M. M. (1993b). Skills training manual for treating Niedtfeld, I., Schmitt, R., Winter, D., Bohus, M., Schmahl, C.,
borderline personality disorder. New York, NY: Guilford Press. & Herpertz, S. C. (2017). Pain-mediated affect regulation is

reduced after dialectical behavior therapy in borderline Safer, D. L., & Jo, B. (2010). Outcome from a randomized
personality disorder: A longitudinal fMRI study. Social controlled trial of group therapy for binge eating disorder:
Cognitive and Affective Neuroscience, 12, 739–747. Comparing dialectical behavior therapy adapted for binge
Nock, M. K., & Prinstein, M. J. (2004). A functional approach eating to an active comparison group therapy. Behavior
to the assessment of self-mutilative behavior. Journal of Therapy, 41, 106–120.
Consulting and Clinical Psychology, 72, 885–890. Sauer-Zavala, S., Bentley, K. H., & Wilner, J. G. (2016).
Paris, J. (2003). Personality disorders over time. Washington, DC: Transdiagnostic treatment of borderline personality disorder
American Psychiatric Publishing. and comorbid disorders: A clinical replication series. Journal
Paris, J. (2015). Stepped care and rehabilitation for patients of Personality Disorders, 30, 35–51.
recovering from borderline personality disorder. Journal of Schmahl, C., Bohus, M., Esposito, F., Treede, R. D., Di Salle, F.,
Clinical Psychology, 71, 747–752. Greffrath, W., . . . Hennig, J. (2006). Neural correlates of
Petscher, E. S., Rey, C., & Bailey, J. S. (2009). A review antinociception in borderline personality disorder. Archives
of empirical support for differential reinforcement of of General Psychiatry, 63, 659–666.
alternative behavior. Research in Developmental Disabilities, Schnell, K., & Herpertz, S. C. (2007). Effects of dialectic-
30, 409–425. behavioral-therapy on the neural correlates of affective
Raichle, M. E. (1998). Behind the scenes of functional brain hyperarousal in borderline personality disorder. Journal of
imaging: A historical and physiological perspective. Psychiatric Research, 41(10), 837–847.
Proceedings of the National Academy of Sciences, 95, 765–772. Silvers, J. A., Hubbard, A. D., Biggs, E., Shu, J., Fertuck, E.,
Reitz, S., Kluetsch, R., Niedtfeld, I., Knorz, T., Lis, S., Paret, C., Chaudhury, S., . . . Brodsky, B. S. (2016). Affective lability and
. . . Bohus, M. (2015). Incision and stress regulation in difficulties with regulation are differentially associated with
borderline personality disorder: Neurobiological mechanisms amygdala and prefrontal response in women with Borderline
of self-injurious behavior. British Journal of Psychiatry, 207, Personality Disorder. Psychiatry Research: Neuroimaging, 254,
165–172. 74–82.
Ritschel, L. A., Lim, N. E., & Stewart, L. M. (2015). Stoffers, J. M., Völlm, B. A., Rücker, G., Timmer, A., Huband, N.,
Transdiagnostic applications of DBT for adolescents and & Lieb, K. (2013). Psychological therapies for people with
adults. American Journal of Psychotherapy, 69, 111–128. borderline personality disorder. Cochrane Library, 8, 1–25.
Rizvi, S. L., Brown, M. Z., Bohus, M., & Linehan, M. M. Tice, D. M., Bratslavsky, E., & Baumeister, R. F. (2001).
(2011). The role of shame in the development and treatment Emotional distress regulation takes precedence over impulse
of borderline personality disorder. In R.L. Dearing (Ed.), control: If you feel bad, do it! Journal of Personality and Social
Shame in the therapy hour (pp. 237–260). Washington, DC: Psychology, 80, 53–67.
American Psychological Association. Valentine, S. E., Bankoff, S. M., Poulin, R. M., Reidler, E. B., &
Rogers, K., Banis, M., Falkenstein, M. J., Malloy, E. J., Pantalone, D. W. (2015). The use of dialectical behavior
McDonough, L., Nelson, S. O., . . . Haaga, D. A. (2014). therapy skills training as stand-alone treatment: A systematic
Stepped care in the treatment of trichotillomania. Journal of review of the treatment outcome literature. Journal of Clinical
Consulting and Clinical Psychology, 82, 361–367. Psychology, 71, 1–20.
Rosenthal, M. Z., Gratz, K. L., Kosson, D. S., Cheavens, J. S., Willis, F., Kuniss, S., Kleindienst, N., Naoum, J., Reitz, S., Boll,
Lejuez, C. W., & Lynch, T. R. (2008). Borderline personality S., . . . Schmahl, C. (2016). The role of nociceptive input and
disorder and emotional responding: A review of the research tissue injury on stress regulation in Borderline Personality
literature. Clinical Psychology Review, 28, 75–91. Disorder. Pain, 158, 479–487.

CH A PTE R
Future Directions in Research and
32 Treatment of Emotion Dysregulation
Theodore P. Beauchaine, Hunter Hahn, and Sheila E. Crowell
Abstract
This chapter discusses themes that emerged while editing the Oxford Handbook of Emotion Dysregulation
and outlines directions for future research. Although the term emotion dysregulation has at times
been used amorphously in the literature, most authors now define the phenomenon as experiences
and expressions of emotion that interfere with situationally appropriate, goal-directed behavior. Situational
embedding of emotion dysregulation is important given very different expectations of appropriate
emotional expression across contexts and cultures. Despite emerging consensus regarding emotion
dysregulation as a construct, several challenges lie ahead. Major tasks for the field are to (1) abandon
implicit notions of emotion dysregulation in favor of formally operationalized definitions, such as
that provided earlier; (2) maintain a clear distinction between emotion dysregulation versus mood
dysregulation; (3) map transdiagnostic features of emotion dysregulation across functional domains
of behavior such as those instantiated in the Research Domain Criteria matrix and, where appropriate,
syndromes in the Diagnostic and Statistical Manual of Mental Disorders; (4) further develop prevention
and treatment programs that systematically target emotion dysregulation across development; and
(5) extend emotion dysregulation research to stigmatized groups in an effort to identify mechanisms
of mental health disparities. Chapters in this volume address these issues and advance the science
of emotion dysregulation in new and exciting ways.
Keywords: emotion dysregulation, emotion regulation, prevention, intervention, treatment, Research

Domain Criteria, transdiagnostic, development
Introduction emotion. Objectives of this chapter are to briefly

Over the past decade or so, emotion dysregulation synthesize key themes that emerged and offer sugges-
has emerged as a construct of critical interest to neu- tions for future research on emotion dysregulation
roscientists, developmental psychologists, develop- across the lifespan, including translational implica-
mental psychopathologists, and psychiatrists, in- tions for prevention and intervention.
cluding those who seek to prevent and intervene on
psychopathology (see, e.g., Beauchaine, 2015a, 2015b, Concepts, Definitions, and Themes
in press; Beauchaine & Cicchetti, 2019; Beauchaine, Several conceptual, definitional, and thematic issues
Hinshaw, & Bridge, 2019; Crowell, Beauchaine, & cut across chapters in this volume. In sections to
Linehan, 2009; Lin et al., 2019; Neacsiu, Bohus, follow, we summarize a number of these issues. More
& Linehan, 2014; Thompson, 2019; Weinberg & detailed coverage can be found in specific chapters.
Klonsky, 2009). While editing this unique volume
on emotion dysregulation, we had the privilege of Emotion Versus Mood
reviewing cutting-edge theory and research, includ- As outlined throughout this volume, progress in
ing novel perspectives, methods, and transdiagnostic emotion dysregulation research will almost certainly
treatment approaches designed to target dysregulated be facilitated by more consistent differentiation
477
among constructs that are sometimes conflated, Ackerman, & Izard, 1995; John & Gross, 2004);
including emotion, mood, emotion regulation, and and (3) research on development of emotion regula-
emotion dysregulation. Although contributing au- tion, including normative trajectories and family
thors were careful in this regard, it remains common dynamics that support or disrupt emergence of
in the field to use the terms emotion and mood inter- healthy regulation (e.g., Morris, Silk, Steinberg,
changeably. Notably, however, emotions differ from Myers, & Robinson, 2007; Pang & Beauchaine,
mood in terms of both eliciting events and duration 2013; Vasilev, Crowell, Beauchaine, Mead, & Gatzke-
(Beauchaine & Cicchetti, 2019). Emotions (e.g., Kopp, 2009). These examples highlight a small frac-
desire, anger, disgust) last for short intervals (seconds tion of the voluminous literature on emotion reg-
to minutes), are elicited by specific stimuli, and ulation and emotion regulatory processes. Readers
motivate behavioral action or inaction (see Fox, who are interested in expended discussion regarding
2018). In contrast, moods (e.g., anhedonia, depres- theory, definitions, and measurement of emotion
sion, mania) are more persistent (hours to weeks), regulation are referred to comprehensive reviews
are imbued by broader internal and external milieus, (e.g., Adrian, Zeman, & Veits, 2011; Cole, Martin,
and bias behavior, cognition, and emotion over time & Dennis, 2004; Sheppes et al., 2015).
(Fox, 2018). Although emotions can affect mood In contrast to the situationally functional nature
and mood can bias the valence of emotions, mood of emotion regulation, emotion dysregulation im-
and emotion are distinguishable phenomena. For plies failure to dampen strong emotional responses
example, depressed individuals sometimes show less to achieve situational objectives. This may include
emotional reactivity to sadness-eliciting stimuli than inappropriate/ineffective use of emotion regulation
healthy controls (Rottenberg, 2005). Thus, mood skills and strategies. Thus, emotion dysregulation is
dysregulation is not synonymous with emotion dys- often conceptualized at least in part by difficulties
regulation (see also Sheppes, Suri, & Gross, 2015). with emotion regulation (e.g., Gratz & Roemer,
For this reason and others, consistent definitions 2004). A common result of this conceptualization is
are critical when distinguishing between mood a view of emotion regulation and dysregulation as
and emotion. distinct endpoints along a single dimension, which
oversimplifies both constructs.
Emotion Regulation Versus Dysregulation In this volume, we urged authors to use a single
The study of emotion regulation dates back further definition of emotion dysregulation to provide con-
in time than the study of emotion dysregulation. sistency across chapters. According to this perspec-
Consequently, there are widely used definitions of tive, emotion dysregulation is characterized by “a
emotion regulation that are well established and pattern of emotional experience and/or expression
guide scientific inquiry. Thompson (1994) defined that interferes with appropriate goal-directed be-
emotion regulation as “extrinsic and intrinsic pro- havior” (Beauchaine, 2015a, p. 876). This defini-
cesses responsible for monitoring, evaluating, and tion, which we discuss in further detail elsewhere
modifying emotional reactions, especially their in- (Beauchaine & Cicchetti, 2019; Beauchaine &
tensive and temporal features, to accomplish one’s Haines, 2019), underscores several important as-
goals” (pp. 27–28). Similarly, Gross (1998) defined pects of emotion dysregulation, beginning with an
emotion regulation as “processes by which individu- emphasis on emotion rather than mood, as outlined
als influence which emotions they have, when they earlier. A critical aspect of this definition is its ag-
have them, and how they experience and express nostic stance vis-à-vis evolutionary functions of
these emotions” (p. 275). These definitions form the emotions. Instead, it focuses on “appropriate” goal-
foundation of several intersecting lines of research directed behavior. Thus, the definition is embedded
on emotion regulation, including (1) laboratory emo- in situational functionalism—not evolutionary func-
tion elicitation research in which participants are tionalism. Many emotions and behaviors that may
directed to regulate or not regulate emotions accord- have conferred selective advantages in our evolution-
ing to specific instructions (e.g., Ehring, Tuschen- ary environments of adaptation have no bearing on
Caffier, Schnülle, Fischer, & Gross, 2010; Gross & fitness in our contemporary environments (Mead,
Levenson, 1993; Gyurak, Gross, & Etkin, 2011); (2) Beauchaine, & Shannon, 2010). In fact, certain be-
explorations of individual differences in emotion haviors such as impulsivity may have been adaptive
regulation and its associations with temperament, in specific evolutionary contexts but place individu-
personality, and/or psychopathology (e.g., Aldao, als at situational disadvantage in classrooms, work
Nolen-Hoeksema, & Schweizer, 2010; Cicchetti, environments, and so forth.
478 Future Directions in Research and Treatment

Our definition also accommodates cultural dif- emotional responses—especially as children mature
ferences in the situationally functional value of (e.g., Ball, Ramsawh, Campbell-Sills, Paulus, & Stein,
emotion. This is important because appropriate emo- 2013; Beauchaine, Zisner, & Hayden, 2019; Gold et
tional responses to specific situations often differ al., 2016; Korponay et al., 2017; Kujawa et al., 2016;
across cultures (Boiger et al., 2018). For example, Prater, Hosanagar, Klumpp, Angstadt, & Phan, 2013;
those who are reared in Japanese culture are more Qing et al., 2012; Shannon, Sauder, Beauchaine, &
likely to respond with anger to individuals who are Gatzke-Kopp, 2009). At the psychophysiological
seen as inconsiderate, whereas Americans show little level of analysis, low respiratory sinus arrhythmia
emotional response to similar behaviors (Boiger, (RSA)—a putative peripheral biomarker of prefron-
Mesquita, Uchida, & Feldman Barrett, 2013). Thus, tal cortex function (Thayer, Hansen, Saus-Rose, &
emotional reactions that are normative in some cul- Johnsen, 2009)—marks emotion dysregulation across
tures may elicit social rejection, reprisals, and other an impressively broad list of psychiatric conditions
consequences that impede goal-directed behavior in (e.g., Beauchaine, 2015b; Beauchaine & Thayer,
other cultures. Therefore, cultural context must be 2015; Bell et al., 2019). As most readers are likely
considered when evaluating the situational appro- aware, an extensive literature links top-down pre-
priateness and value of expressed emotions (e.g., frontal control to effective behavior, emotion, and
Bhugra & McKenzie, 2003; Mauss & Butler, 2010). self-regulation (e.g., Dixon, Thiruchselvam, Todd,
Finally, our definition implicitly acknowledges & Christoff, 2017; Heatherton & Wagner, 2011;
the afunctional nature of at least some emotions. For Palacios-Barrios & Hanson, 2019; Zelazo, 2015).
example, expressions of sadness, anger, and other Identifying biomarkers of emotion dysregulation
emotions at the cinema may hold no functional is important for several reasons. Carefully selected
or dysfunctional value whatsoever (Beauchaine & biomarkers can index treatment response (e.g.,
Cicchetti, 2019). Taken together, eliciting contextual Beauchaine, Zisner, et al., 2019; Bell et al., 2018),
events and match or mismatch between intensity of may be used to evaluate allostatic effects on biological
expression and context often determine whether an systems following extreme and protracted stress (e.g.,
emotional reaction is situationally functional, dys- Thayer, Åhs, Fredrikson, Sollers, & Wager, 2012),
functional, or afunctional; regulated, dysregulated, and are useful as indices of emotion dysregulation
or unregulated (Aldao, 2013). in populations who either self-report inaccurately,
such as very young children, or cannot self-report at
Multiple Levels of Analysis all, such as those with certain developmental delays
Another theme we promoted across chapters is the and disabilities (see Zisner & Beauchaine, 2016).
importance of considering transactional processes Social and environmental factors are also critical
across multiple levels of analysis toward understand- to understanding development of emotion dysregu-
ing development and maintenance of emotion dys- lation. An impressive literature describes how emo-
regulation. As a transdiagnostic vulnerability to dition dysregulation is often socialized within families
verse forms of psychopathology (e.g., Beauchaine, through adverse attachment relationships, coercive
2015a, 2015b; Fairholme et al., 2013; Hofmann, and invalidating parent–child relationships, and other
Sawyer, Fang, & Asnaani, 2012), emotion dysregu- untoward experiences including abuse and maltreat-
lation is represented in multiple elements/cells of ment (e.g., Beauchaine, Gatzke-Kopp, & Mead,
the Research Domain Criteria (RDoC) matrix 2007; Beauchaine, & Zalewski, 2016; Cole, Hall, &
(Beauchaine, 2015a; Bradley et al., 2011; Insel, 2014; Hajal, 2017; Crowell et al., 2013; Morris et al., 2007;
National Institute of Mental Health, 2019). In Thompson & Meyer, 2007). Thus, emotion dysreg-
terms of traditional syndromes defined in the ulation emerges not only from lack of support for
Diagnostic and Statistical Manual of Mental Disorders competent self-regulation but also from family pro-
(DSM-5, 2013), although different classes of psychi- cesses that reinforce emotional lability, hinder chil-
atric disorder are characterized by different forms of dren’s self-regulation attempts, and/or invalidate,
emotion dysregulation, such as unregulated impul- dismiss, or ignore their feelings entirely (Bridgett,
sivity (desire, wanting, enthusiasm) in externalizing Burt, Edwards, & Deater-Deckard, 2015; Buckholdt,
disorders and unregulated anxiety (fear, distress, ap- Parra, & Jobe-Shields, 2014; Crowell et al., 2009).
prehension) in internalizing disorders, both show Dysregulated emotional responses, such as anxious
patterns of aberrant connectivity between subcorti- avoidance, anger, and hypervigilance, often repre-
cal neural structures and functional subdivisions of sent endpoints of complex interactions between
the prefrontal cortex that ordinarily suppress strong heritable vulnerabilities and adverse environmental
Beauchaine, Hahn, and Crowell 479

experiences (see Beauchaine, in press; Beauchaine a treatment target follows from its transdiagnostic
et al., 2019; Crowell et al., 2009). associations with a wide range of psychiatric disor-
The important role that parent–child relationship ders that span the internalizing and externalizing
dynamics play in socializing self-regulation, emo- spectra and other forms of psychopathology includ-
tion dysregulation, and related processes is specified ing personality disorders (e.g., Beauchaine, 2015a, in
in painstaking research on dyadic interaction pat- press; Beauchaine, Zisner, & Sauder, 2017; Fairholme
terns between mothers and vulnerable children et al., 2013; McLaughlin, Hatzenbuehler, Mennin,
(e.g., Beauchaine, 2015a; Crowell et al., 2014, 2017; & Nolen-Hoeksema, 2011). Some predispositions
Shipman & Zeman, 2001). This work demonstrates toward emotion dysregulation may be rooted in
how family social dynamics shape emotional, be- temperament, including negative affectivity and
havioral, and physiological dysregulation described soothability. Infants and young children who score
in this chapter and throughout this volume. Self- high on negative affectivity and low on soothability
injuring adolescent girls, for example—a population show emotional distress that is more intense, pro-
characterized by extreme emotion dysregulation longed, and resistant to parental attempts at inter-
(Beauchaine et al., 2019; Crowell et al., 2005)—are personal down-regulation (e.g., Blandon, Calkins, &
exquisitely sensitive to their mothers’ aversive and Keane, 2010; Schmidt, Fox, Perez-Edgar, & Hamer,
invalidating behaviors, as evidenced by both sympa- 2009). Such temperaments also evoke negative emo-
thetic and parasympathetic nervous system reactiv- tional reactivity from caregivers—particularly less
ity during dyadic interactions (Crowell et al., 2014, skilled caregivers (e.g., Micalizzi, Wang, & Saudino,
2017). Importantly, such patterns of autonomic 2017). Such bidirectional, evocative processes may
activity and reactivity are sensitive to early interven- lead to long-term disruptions in parent–child coreg-
tions that reduce negative parenting practices (e.g., ulation of emotion, which in turn escalates emotion
Beauchaine et al., 2015; Bell et al., 2018). dysregulation across development (cf. Crowell et al.,
Given practical limitations in computing power, 2014; Lunkenheimer, Olson, Hollenstein, Sameroff,
analytic methods, and coding time, evaluations of & Winter, 2011).
family dynamics have been conducted almost exclu- In general, both prevention and intervention
sively with dyads (for an exception see Hollenstein, strategies focus on (1) altering social contingencies
Allen, & Sheeber, 2016). Yet in everyday settings, that support/reinforce emotional lability and emo-
family interactions—including those that support tion dysregulation while (2) teaching effective
effective emotion and self-regulation or reinforce emotion regulation strategies. Among children and
emotional lability—occur among more than two adolescents, many prevention efforts include parent
people, such as both parents and siblings. With rapid training. These efforts teach parents to engage in less
advances in computing power, including automated negative emotional reactivity and interact with their
computer vision and machine learning (ACVM), children and respond to their emotions in ways that
emotion dysregulation research with two, three, or foster development of healthy emotion regulation
more individuals is possible. In our own work, we (e.g., Beauchaine et al., 2013; Havighurst & Harley,
recently demonstrated how ACVM technology can 2007; Havighurst, Harley, Kehoe, & Pizarro, 2012).
capture moment-to-moment dependencies in facial Prevention and intervention programs that reduce
expressions of affective valence (positive, negative) coercive parenting styles with children, for example,
and arousal in mother–daughter dyads (Haines, reduce rates of psychopathology and criminality in
Bell, et al., 2019). ACVM captures emotional dy- adolescence and adulthood (e.g., Conduct Problems
namics in real time compared with hundreds of Prevention Research Group, 2015; Scott, Briskman,
hours required for human coders (see Haines, & O’Connor, 2014). Among children at lower risk,
Southward, Cheavens, Beauchaine, & Ahn, 2019). school-based prevention programs, such as mind-
Given this advantage, we expect research on family fulness training (e.g., Flook et al., 2010; Mendelson
dynamics of emotion dysregulation to proliferate in et al., 2010) and cognitive skills training (e.g.,
upcoming years. Domitrovich, Cortes, & Greenberg, 2007), both of
which foster healthy emotion regulation develop-
Treating Emotion Dysregulation ment into adulthood, reduce the likelihood of psy-
Several chapters in this volume address prevention chopathology with age.
and treatment implications of understanding emo- Many empirically supported treatments target
tion dysregulation and its development. As de- emotion dysregulation across the lifespan. Intervention
scribed earlier, interest in emotion dysregulation as programs for children and adolescents include parent

management training (e.g., Kazdin, 1997; Webster- als experience high rates of discrimination and
Stratton & Reid, 2010; Webster-Stratton, Reid, & significant mental health disparities (Bostwick et al.,
Beauchaine, 2011), dialectical behavior therapy (DBT) 2014; González, Tarraf, Whitfield, & Vega, 2010;
for children (Perepletchikova & Goodman, 2014), McLaughlin, Hatzenbuehler, & Keyes, 2010; Pieterse,
and mindfulness-based approaches (e.g., Burke, 2010; Todd, Neville, & Carter, 2012). In discussion to
Semple, Lee, Rosa, & Miller, 2010), among others. follow, we focus on these groups.
In adulthood, interventions that target emotion Mental health disparities may be driven in part
dysregulation often include emotion regulation by chronic stress resulting from discrimination and
classes, cognitive-behavioral strategies for managing stigma (e.g., Hatzenbuehler, 2009; Berger & Sarnyai,
emotions, and strategies for mending disrupted at- 2015). In the United States, both Blacks and sexual
tachment relationships, establishing trust, and boost- minorities experience high rates of discrimination
ing interpersonal effectiveness, crisis survival skills, across the lifespan (e.g., Balsam, Rothblum, &
and management of psychiatric symptoms (e.g., Beauchaine, 2005; McLaughlin et al., 2010), which
Linehan, Bohus, & Lynch, 2007; Neacsiu, Bohus, & increases risk for psychopathology and other adverse
Linehan, 2014). More recently, mindfulness-based outcomes. Yet despite increased exposures to dis-
interventions have gained significant attention (Farb, crimination, not all minority individuals develop
Anderson, Irving, & Segal, 2015; Gu, Strauss, Bond, mental health problems (e.g., Burt & Simons, 2015;
& Cavanagh, 2015). Despite some success of these Hatzenbuehler, 2009). This suggests potential me-
and other treatments, many individuals see no benefit diating variables between stigmatization and mental
from treatment or do not attain full remission of health (Hatzenbuehler, 2009).
symptoms, highlighting the need for new and en- Emotion dysregulation appears to be one such
hanced therapeutic approaches. mediator (e.g., Hatzenbuehler, 2009; McLaughlin
Modern, transdiagnostic conceptualizations of et al., 2010; Rogers et al., 2017). Exposure to dis-
psychopathology such as RDoC may eventually crimination predicts emotion dysregulation among
advance treatment development. Traditionally, em- both Blacks and sexual minorities (Hatzenbuehler
pirically supported psychotherapies have been et al., 2009). Among Blacks, exposure to discrimina-
disorder-specific based on DSM categorizations. More tion is associated with reduced connectivity between
recently, however, treatments targeting transdiag- the prefrontal cortex and subcortical structures
nostic vulnerabilities and risk factors for psychopa- (Berger & Sarnyai, 2015), a common feature of emo-
thology have grown in popularity. Emotion dysregu- tion dysregulation, as described in detail earlier (see
lation has received attention as a critical intervention “Multiple Levels of Analysis”; Beauchaine, 2015a;
target, with early success. Transdiagnostic treatments Beauchaine & Cicchetti, 2019). More work is needed
that affect emotion dysregulation, such as the unified to assess developmental effects of stigma on mental
protocol (UP) for transdiagnostic treatment of emo- health at additional levels of analysis (e.g., epigenetic,
tional disorders (Barlow, Farchione, Sauer-Zavala, neurohormonal, etc.).
et al., 2017) and DBT (Linehan, 1993; Neacsiu, Adapting existing empirically supported treat-
Eberle, Kramer, Wiesmann, & Linehan, 2014), are ments for specific cultural groups may be one
at least somewhat effective for a broad range of dis- method to reduce mental health disparities (Hall,
orders, and may be as effective as disorder-specific Ibaraki, Huang, Marti, & Stice, 2016). Although
treatments (Barlow, Farchione, Bullis, et al., 2017). little work has examined interventions targeting
emotion dysregulation specifically, there is growing
Stigma and Emotion Dysregulation evidence of the value of adapting treatments to
A growing literature focuses on health disparities cultural groups (Hall et al., 2016). For example,
across demographic groups that may benefit from Pachankis, Hatzenbuehler, Rendina, Safren, and
adapted prevention and intervention approaches. For Parsons (2015) modified the UP for use with gay
example, some researchers have examined relations and bisexual men, including a transdiagnostic focus
between emotion dysregulation and health dispari- on emotion dysregulation resulting from stigma,
ties among individuals with stigmatized identities with moderate success.
(Hatzenbuehler, 2009; Hatzenbuehler, Nolen- To date, most studies of emotion dysregulation
Hoeksema, & Dovidio, 2009). Although society among stigmatized groups have been cross-sectional,
stigmatizes many such identities (Rodriguez-Seijas, relying exclusively on self-reports of emotion dysreg-
Burton, Adeyinka, & Pachankis, 2019), Black and ulation. Although these studies represent an impor-
sexual minority (e.g., lesbian, gay, bisexual) individu- tant starting point, future work that examines

evelopment of emotion dysregulation across
d References
multiple levels of analysis (e.g., psychophysiological, Adrian, M., Zeman, J., & Veits, G. (2011). Methodological
neural, self-report) is needed to advance prevention implications of the affect revolution: A 35-year review of
emotion regulation assessment in children. Journal of
and intervention science. Racial minorities and sexual Experimental Child Psychology, 110, 171–197. doi:10.1016/j.
minorities report changes in discrimination and jecp.2011.03.009
group identity across the lifespan, both of which relate Aldao, A. (2013). The future of emotion regulation research:
to psychopathology (e.g., Balsam et al., 2005; Cox, Capturing context. Perspectives on Psychological Science, 8,
Dewaele, Van Houtte, & Vincke, 2010; Yip, Seaton, 155–172. doi:10.1177/1745691612459518.
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010).
& Sellers, 2006). This highlights the need for lifes- Emotion-regulation strategies across psychopathology: A
pan developmental approaches in the future. Finally, meta-analytic review. Clinical Psychology Review, 30, 217–237.
inclusion of appropriate comparison groups may doi:10.1016/j.cpr.2009.11.004
help to identify commonalities and differences be- American Psychiatric Association. (2013). Diagnostic and statistical
tween stigmatized and nonstigmatized groups, aiding manual of mental disorders (5th ed.). Arlington, VA: Author.
Ball, T. M., Ramsawh, H. J., Campbell-Sills, L., Paulus, M. P., &
in identification of treatment targets for adapted Stein, M. B. (2013). Prefrontal dysfunction during emotion
therapies. regulation in generalized anxiety and panic disorders.
Psychological Medicine, 43, 1475–1486. doi:10.1017/
Conclusion S0033291712002383
We hope this Oxford Handbook serves as a useful Balsam, K. F., Rothblum, E. D., & Beauchaine, T. P. (2005).
guide for future research on emotion dysregulation. Victimization over the life span: A comparison of lesbian,
gay, bisexual, and heterosexual siblings. Journal of Consulting
Contributing authors address various important
and Clinical Psychology, 73, 477. doi:10.1037/0022-
topics, including conceptual and definitional issues; 006X.73.3.477
transdiagnostic associations of emotion dysregula- Barlow, D. H., Farchione, T. J., Bullis, J. R., Gallagher, M. W.,
tion with diverse forms of psychopathology; cog- Murray-Latin, H., Sauer-Zavala, S., . . . & Ametaj, A. (2017).
nitive, social, behavioral, and neurobiological ap- The unified protocol for transdiagnostic treatment of emotional
disorders compared with diagnosis-specific protocols for
proaches to construing emotion dysregulation; and
anxiety disorders: A randomized clinical trial. JAMA Psychiatry,
assessment and treatment of emotion dysregulation. 74, 875–884. doi:10.1001/jamapsychiatry.2017.2164
Organization of the Handbook is also explicitly de- Barlow, D. H., Farchione, T. J., Sauer-Zavala, S., Latin, H. M.,
velopmental, which is essential if we wish to prevent Ellard, K. K., Bullis, J. R., . . . Cassiello-Robbins, C. (2017).
emotion dysregulation from emerging. Unified protocol for transdiagnostic treatment of emotional
disorders: Therapist guide. New York, NY: Oxford University
Indeed, a focus on development of emotion dys-
Press.
regulation is especially important. As already de- Beauchaine, T. P. (2015a). Future directions in emotion
scribed, early childhood and adolescence are partic- dysregulation and youth psychopathology. Journal of Clinical
ularly important periods during which neurobiological Child and Adolescent Psychology, 44, 875–896. doi:10.1080/15
systems that subserve emotion regulation are vulner- 374416.2015.1038827
Beauchaine, T. P. (2015b). Respiratory sinus arrhythmia: A
able to long-lasting structural and functional changes
transdiagnostic biomarker of emotion dysregulation and
that may persist throughout the lifespan (Hair, psychopathology. Current Opinion in Psychology, 3, 43–47.
Hanson, Wolfe, & Pollak, 2015; Nguyen-Louie, doi:10.1016/j.copsyc.2015.01.017
2018; Palacios-Barrios & Hanson, 2019; Pfefferbaum Beauchaine, T. P. (in press). A developmental psychopathology
et al., 2018). In addition, social and environmental perspective on the emergence of antisocial and borderline
personality pathologies across the lifespan. In C. W. Lejuez
factors may render individuals of stigmatized mi-
& K. L. Gratz (Eds.), Handbook of personality disorders. New
nority groups highly vulnerable to psychopathol- York, NY: Cambridge University Press.
ogy, particularly in adolescence (Balsam et al., 2005; Beauchaine, T. P., & Cicchetti, D. (2019). Emotion dysregulation
Berger & Sarnyai, 2015; Hatzenbuehler, 2009). and emerging psychopathology: A transdiagnostic,
Many treatments exist that address these and other transdisciplinary perspective. Development and Psychopathology.
Advance online publication. doi:10.1017/S0954579419000671
concerns, and future developments will likely make
use of multiple methods for assessing emotion dys- Polyvagal theory and developmental psychopathology:
regulation across multiple levels of analysis, includ- Emotion dysregulation and conduct problems from
ing biological, cognitive/behavioral, and familial/ preschool to adolescence. Biological Psychology, 74, 174–184.
social. Emotion dysregulation is a complex and mul- doi:10.1016/j.biopsycho.2005.08.008
Beauchaine, T. P., Gatzke-Kopp, L. M., Neuhaus, E., Chipman,
tidimensional construct that changes across the lifes-
J., Reid, M. J., & Webster-Stratton, C. (2013). Sympathetic-
pan and remains a promising focus of research on and parasympathetic-linked cardiac function and prediction
the etiology and treatment of nearly all psychiatric of externalizing behavior, emotion regulation, and prosocial
disorders. behavior among preschoolers treated for ADHD. Journal of

Consulting and Clinical Psychology, 81, 481–493. doi:10.1037/ Boiger, M., Mesquita, B., Uchida, Y., & Feldman Barrett, L.
a0032302 (2013). Condoned or condemned: The situational affordance
Beauchaine, T. P., & Haines, N. (2019). Functionalist and of anger and shame in the United States and Japan.
constructionist perspectives on emotion dysregulation. In Personality and Social Psychology Bulletin, 39, 540–553.
T. P. Beauchaine & S. E. Crowell (Eds.), The Oxford handbook doi:10.1177/0146167213478201
of emotion dysregulation. New York, NY: Oxford University Bostwick, W. B., Meyer, I., Aranda, F., Russell, S., Hughes, T.,
Press. Birkett, M., & Mustanski, B. (2014). Mental health and
Beauchaine, T. P., Hinshaw, S. P., & Bridge, J. A. (2019). suicidality among racially/ethnically diverse sexual minority
Nonsuicidal self-injury and suicidal behaviors in girls: The youths. American Journal of Public Health, 104, 1129–1136.
case for targeted prevention in preadolescence. Clinical doi:10.2105/AJPH.2013.301749
Psychological Science. Advance online publication. Bradley, B., DeFife, J. A., Guarnaccia, C., Phifer, J., Fani, N.,
doi:10.1177/2167702618818474 Ressler, K. J., & Westen, D. (2011). Emotion dysregulation
Beauchaine, T. P., Neuhaus, E., Gatzke-Kopp, L. M., Reid, and negative affect: Association with psychiatric symptoms.
M. J., Brekke, A., Olliges, A., . . . Webster-Stratton, C. (2015). Journal of Clinical Psychiatry, 72, 685–691. doi:10.4088/
Electrodermal responding predicts responses to, and may be JCP.10m06409blu
altered by, preschool intervention for ADHD. Journal of Bridgett, D. J., Burt, N. M., Edwards, E. S., & Deater-Deckard, K.
Consulting and Clinical Psychology, 83, 293–303. doi:10.1037/ (2015). Intergenerational transmission of self-regulation: A
a0038405 multidisciplinary review and integrative conceptual framework.
Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as Psychological Bulletin, 141, 602–654. doi:10.1037/a0038662
a transdiagnostic biomarker of psychopathology. International Buckholdt, K. E., Parra, G. R., & Jobe-Shields, L. (2014).
Journal of Psychophysiology, 98, 338–350. doi:10.1016/j. Intergenerational transmission of emotion dysregulation
ijpsycho.2015.08.004 through parental invalidation of emotions: Implications for
Beauchaine, T. P., & Zalewski, M. (2016). Physiological and adolescent internalizing and externalizing behaviors. Journal
developmental mechanisms of emotional lability in coercive of Child and Family Studies, 23, 324–332. doi:10.1007/
relationships. In T. J. Dishion & J. J. Snyder (Eds.), The s10826-013-9768-4
Oxford handbook of coercive relationship dynamics (pp. 39–52). Burke, C. A. (2010). Mindfulness-based approaches with
New York, NY: Oxford University Press. children and adolescents: A preliminary review of current
Beauchaine, T. P., Zisner, A. R., & Hayden, E. P. (2019). research in an emergent field. Journal of Child and Family
Neurobiological mechanisms of psychopathology and Studies, 19, 133–144. doi:10.1007/s10826-009-9282-x
treatment action. In T. H. Ollendick, S. W. White, & Burt, C. H., & Simons, R. L. (2015). Interpersonal racial
B. A. White (Eds.), The Oxford handbook of clinical child and discrimination, ethnic-racial socialization, and offending:
adolescent psychology (pp. 699–723). New York, NY: Oxford Risk and resilience among African American females. Justice
University Press. Quarterly, 32(3), 532–570. doi:10.1080/07418825.2013.781
Beauchaine, T. P., Zisner, A., & Sauder, C. L. (2017). Trait 205
impulsivity and the externalizing spectrum. Annual Review of Cicchetti, D., Ackerman, B. P., & Izard, C. E. (1995). Emotions
Clinical Psychology, 13, 343–368. doi:10.1146/annurev- and emotion regulation in developmental psychopathology.
clinpsy-021815-093253 Development and Psychopathology, 7, 1–10. doi:10.1017/
Bell, Z., Knapton, E., McDonough-Caplan, H., Shader, T., Zisner, S0954579400006301
A., & Beauchaine, T. P. (2019). Respiratory sinus arrhythmia Cole, P. M., Hall, S. E., & Hajal, N. (2017). Emotion
reactivity across empirically-based structural categories of dysregulation as a vulnerability to psychopathology. In
psychopathology: A meta-analysis. Psychophysiology, 56, T. P. Beauchaine & S. P. Hinshaw (Eds.), Child and adolescent
e13329. doi:10.1111/psyp.13329 psychopathology (3rd ed., pp. 346–386). Hoboken, NJ: Wiley.
Bell, Z., Shader, T., Webster-Stratton, C., Reid, M. J., & Cole, P. M., Martin, S. E., & Dennis, T. A. (2004). Emotion
Beauchaine, T. P. (2018). Improvements in negative parenting regulation as a scientific construct: Methodological challenges
mediate changes in children’s autonomic responding following and directions for child development research. Child
a preschool intervention for ADHD. Clinical Psychological Development, 75, 317–333. doi:10.1111/j.1467-8624.2004.
Science, 6, 134–144. doi:10.1177/2167702617727559 00673.x
Berger, M., & Sarnyai, Z. (2015). “More than skin deep”: Stress Conduct Problems Prevention Research Group. (2015). Impact
neurobiology and mental health consequences of racial of early intervention on psychopathology, crime, and well-
discrimination. Stress, 18, 1–10. doi:10.3109/10253890.2014.9 being at age 25. American Journal of Psychiatry, 172, 59–70.
89204 doi:10.1176/appi.ajp.2014.13060786
Bhugra, D., & McKenzie, K. (2003). Expressed emotion across Cox, N., Dewaele, A., Van Houtte, M., & Vincke, J. (2010).
cultures. Advances in Psychiatric Treatment, 9, 342–348. Stress-related growth, coming out, and internalized
doi:10.1192/apt.9.5.342 homonegativity in lesbian, gay, and bisexual youth. An
Blandon, A. Y., Calkins, S. D., & Keane, S. P. (2010). Predicting examination of stress-related growth within the minority
emotional and social competence during early childhood stress model. Journal of Homosexuality, 58, 117–137. doi:10.10
from toddler risk and maternal behavior. Development and 80/00918369.2011.533631
Psychopathology, 22, 119–132. doi:10.1017/ Crowell, S. E., Baucom, B. R., Potapova, N. V., McCauley, E.,
S0954579409990307 Fittleson, M., Barth, H., . . . Beauchaine, T. P. (2013).
Boiger, M., Ceulemans, E., De Leersnyder, J., Uchida, Y., Mechanisms of contextual risk for adolescent self injury:
Norasakkunkit, V., & Mesquita, B. (2018). Beyond Emotion invalidation and conflict escalation in mother-child
essentialism: Cultural differences in emotions revisited. interactions. Journal of Clinical Child and Adolescent
Emotion, 18, 1142. doi:10.1037/emo0000390 Psychology, 42, 467–480. doi:10.1080/15374416.2013.785360

Crowell, S. E., Baucom, B. R., Yaptangco, M., Bride, D., Hsiao, emotion regulation scale. Journal of Psychopathology and
R., McCauley, E., & Beauchaine, T. P. (2014). Emotion Behavioral Assessment, 26, 41–54. doi:10.1023/B:JOBA.
dysregulation and dyadic conflict in depressed and typical 0000007455.08539.94
adolescents: Evaluating concordance across psychophysiological Gross, J. J. (1998). The emerging field of emotion regulation: An
and observational measures. Biological Psychology, 98, 50–58. integrative review. Review of General Psychology, 2, 271–299.
doi:10.1016/j.biopsycho.2014.02.009 doi:10.1037/1089-2680.2.3.271
Crowell, S. E., Beauchaine, T. P., & Linehan, M. (2009). A Gross, J. J., & Levenson, R. W. (1993). Emotional suppression:
biosocial developmental model of borderline personality: Physiology, self-report, and expressive behavior. Journal
Elaborating and extending Linehan’s theory. Psychological of Personality and Social Psychology, 64, 970–986.
Bulletin, 135, 495–510. doi:10.1037/a0015616 doi:10.1037/0022-3514.64.6.970
Crowell, S. E., Beauchaine, T. P., McCauley, E., Smith, C., Gu, J., Strauss, C., Bond, R., & Cavanagh, K. (2015). How do
Stevens, A. L., & Sylvers, P. (2005). Psychological, autonomic, mindfulness-based cognitive therapy and mindfulness-
and serotonergic correlates of parasuicidal behavior in based stress reduction improve mental health and wellbeing?
adolescent girls. Development and Psychopathology, 17, A systematic review and meta-analysis of mediation studies.
1105–1127. doi:10.1037/0022-006X.73.3.371 Clinical Psychology Review, 37, 1–12. doi:10.1016/j.
Crowell, S. E., Butner, J., Wiltshire, T. J., Munion, A. K., cpr.2015.01.006
Yaptangco, M., & Beauchaine, T. P. (2017). Evaluating Gyurak, A., Gross, J. J., & Etkin, A. (2011). Explicit and implicit
emotional and biological sensitivity to maternal behavior emotion regulation: A dual-process framework. Cognition and
among depressed and self-injuring adolescent girls using Emotion, 25, 400–412. doi:10.1080/02699931.2010.544160
nonlinear dynamics. Clinical Psychological Science, 5, 272–285. Haines, N., Bell, Z., Crowell, S., Hahn, H., Kamara, D.,
doi:10.1177/2167702617692861 McDonough-Caplan, H., . . . Beauchaine, T. P. (2019). Using
Dixon, M. L., Thiruchselvam, R., Todd, R., & Christoff, K. (2017). automated computer vision and machine learning to code
Emotion and the prefrontal cortex: An integrative review. facial expressions of affect and arousal: Implications for emotion
Psychological Bulletin, 143, 1033. doi:10.1037/bul0000096 dysregulation research. Development and Psychopathology.
Domitrovich, C. E., Cortes, R. C., & Greenberg, M. T. (2007). Advance online publication. doi:10.1017/S0954579419000312
Improving young children’s social and emotional competence: Haines, N., Southward, M. W., Cheavens, J. S., Beauchaine,
A randomized trial of the preschool “PATHS” curriculum. T. P., & Ahn, W.-Y. (2019). Using computer-vision and
Journal of Primary Prevention, 28, 67–91. doi:10.1007/ machine learning to automate facial coding of positive and
s10935-007-0081-0 negative affect intensity. PLoS One, 14, e0211735. doi:10.1371/
Ehring, T., Tuschen-Caffier, B., Schnülle, J., Fischer, S., & journal.pone.0211735
Gross, J. J. (2010). Emotion regulation and vulnerability to Hair, N. L., Hanson, J. L., Wolfe, B. L., & Pollak, S. D. (2015).
depression: Spontaneous versus instructed use of emotion Association of child poverty, brain development, and
suppression and reappraisal. Emotion, 10, 563–572. academic achievement. JAMA Pediatrics, 169, 822–829.
doi:10.1037/a0019010 doi:10.1001/jamapediatrics.2015.1475
Fairholme, C. P., Nosen, E. L., Nillni, Y. I., Schumacher, J. A., Hall, G. C. N., Ibaraki, A. Y., Huang, E. R., Marti, C. N., &
Tull, M. T., & Coffey, S. F. (2013). Sleep disturbance and Stice, E. (2016). A meta-analysis of cultural adaptations of
emotion dysregulation as transdiagnostic processes in a psychological interventions. Behavior Therapy, 47, 993–1014.
comorbid sample. Behaviour Research and Therapy, 51, doi:10.1016/j.beth.2016.09.005
540–546. doi:10.1016/j.brat.2013.05.014 Hatzenbuehler, M. L. (2009). How does sexual minority stigma
Farb, N. A. S., Anderson, A. K., Irving, J. A., & Segal, Z. V. “get under the skin”? A psychological mediation framework.
(2015). Mindfulness interventions and emotion regulation. Psychological Bulletin, 135, 707. doi:10.1037/a0016441
In J. J. Gross (Ed.), Handbook of emotion regulation (2nd ed., Hatzenbuehler, M. L., Nolen-Hoeksema, S., & Dovidio, J.
pp. 548–568). New York, NY: Guilford. (2009). How does stigma “get under the skin”? The mediating
Flook, L., Smalley, S. L., Kitil, M. J., Galla, B. M., Kaiser- role of emotion regulation. Psychological Science, 20,
Greenland, S., Locke, J., . . . Kasari, C. (2010). Effects of 1282–1289. doi:10.1111/j.1467-9280.2009.02441.x
mindful awareness practices on executive functions in Havighurst, S. S., & Harley, A. (2007). Tuning into kids:
elementary school children. Journal of Applied School Emotionally intelligent parenting program manual. Melbourne,
Psychology, 26, 70–95. doi:10.1080/15377900903379125 Australia: University of Melbourne.
Fox, E. (2018). Perspectives from affective science on Havighurst, S. S., Harley, A. H., Kehoe, C. E., & Pizarro, E.
understanding the nature of emotion. Brain and Neuroscience (2012). Tuning in to teens: Emotionally intelligent parenting
Advances, 2, 1–8. doi:10.1177/2398212818812628 program manual. Melbourne, Australia: University of
Gold, A. L., Shechner, T., Farber, M. J., Spiro, C. N., Leibenluft, Melbourne.
E., Pine, D. S., & Britton, J. C. (2016). Amygdala-cortical Heatherton, T. F., & Wagner, D. D. (2011). Cognitive
connectivity: Associations with anxiety, development, and neuroscience of self-regulation failure. Trends in Cognitive
threat. Depression and Anxiety, 33, 917–926. doi:10.1002/ Sciences, 15, 132–139. doi:10.1016/j.tics.2010.12.005
da.22470 Hofmann, S. G., Sawyer, A. T., Fang, A., & Asnaani, A. (2012).
González, H. M., Tarraf, W., Whitfield, K. E., & Vega, W. A. Emotion dysregulation model of mood and anxiety
(2010). The epidemiology of major depression and ethnicity disorders. Depression and Anxiety, 29, 409–416. doi:10.1002/
in the United States. Journal of Psychiatric Research, 44, da.21888
1043–1051. doi:10.1016/j.jpsychires.2010.03.017 Hollenstein, T., Allen, N. B., & Sheeber, L. (2016). Affective
Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment patterns in triadic family interactions: Associations with
of emotion regulation and dysregulation: Development, adolescent depression. Development and Psychopathology, 28,
factor structure, and initial validation of the difficulties in 85–96. doi:10.1017/S0954579415000309

Insel, T. R. (2014). The NIMH research domain criteria (RDoC) Micalizzi, L., Wang, M., & Saudino, K. J. (2017). Difficult
project: Precision medicine for psychiatry. American Journal of temperament and negative parenting in early childhood: A
Psychiatry, 171, 395–397. doi:10.1176/appi.ajp.2014.14020138 genetically informed cross-lagged analysis. Developmental
John, O. P., & Gross, J. J. (2004). Healthy and unhealthy emotion Science, 20, e12355. doi:10.1111/desc.12355.
regulation: Personality processes, individual differences, and Morris, A. S., Silk, J. S., Steinberg, L., Myers, S. S., & Robinson,
life span development. Journal of Personality, 72, 1301–1334. L. R. (2007). The role of the family context in the
doi:10.1111/j.1467-6494.2004.00298.x development of emotion regulation. Social Development, 16,
Kazdin, A. E. (1997). Parent management training: Evidence, 361–388. doi:10.1111/j.1467-9507.2007.00389.x
outcomes, and issues. Journal of the American Academy National Institute of Mental Health. (2019). Research Domain
of Child and Adolescent Psychiatry, 36, 1349–1356. Criteria matrix. Retrieved from https://www.nimh.nih.gov/
doi:10.1097/00004583-199710000-00016 research/research-funded-by-nimh/rdoc/constructs/rdoc-
Korponay, C., Pujara, M., Deming, P., Philippi, C., Decety, J., matrix.shtml
Kosson, D. S., . . . Koenigs, M. (2017). Impulsive-antisocial Neacsiu, A. D., Bohus, M., & Linehan, M. M. (2014). Dialectical
dimension of psychopathy linked to enlargement and behavior therapy skills: An intervention for emotion
abnormal functional connectivity of the striatum. Biological dysregulation. In J. J. Gross (Ed.), Handbook of emotion
Psychiatry: Cognitive Neuroscience and Neuroimaging, 2, regulation (Vol. 2). New York, NY: Guilford.
149–157. doi:10.1016/j.bpsc.2016.07.004 Neacsiu, A. D., Eberle, J. W., Kramer, R., Wiesmann, T., &
Kujawa, A., Wu, M., Klumpp, H., Pine, D. S., Swain, J. E., Linehan, M. M. (2014). Dialectical behavior therapy skills for
Fitzgerald, K. D., . . . Phan, K. L. (2016). Altered development transdiagnostic emotion dysregulation: A pilot randomized
of amygdala-anterior cingulate cortex connectivity in anxious controlled trial. Behaviour Research and Therapy, 59, 40–51.
youth and young adults. Biological Psychiatry Cognition doi:10.1016/j.brat.2014.05.005
Neuroscience Neuroimaging, 1, 345–352. doi:10.1016/j. Nguyen-Louie, T. T., Simmons, A. N., Squeglia, L. M.,
bpsc.2016.01.006 Alejandra Infante, M., Schacht, J. P., & Tapert, S. F. (2018).
Lin, B., Kaliush, P. R., Conradt, E., Terrell, S., Neff, D., Allen, Earlier alcohol use onset prospectively predicts changes in
A. K., . . . Crowell, S. E. (2019). Intergenerational transmission functional connectivity. Psychopharmacology, 235, 1041–1054.
of emotion dysregulation: Part I. Psychopathology, self- doi:10.1007/s00213-017-4821-4.
injury, and parasympathetic responsivity among pregnant Pachankis, J. E., Hatzenbuehler, M. L., Rendina, H. J., Safren,
women. Development and Psychopathology. Advance online S. A., & Parsons, J. T. (2015). LGB-affirmative cognitive-
publication. doi:10.1017/S0954579419000336 behavioral therapy for young adult gay and bisexual men: A
Linehan, M. M. (1993). Cognitive-behavioral treatment of randomized controlled trial of a transdiagnostic minority
borderline personality disorder. New York, NY: Guilford Press. stress approach. Journal of Consulting and Clinical Psychology,
Linehan, M. M., Bohus, M., & Lynch, T. R. (2007). Dialectical 83, 875. doi:10.1037/ccp0000037
behavior therapy for pervasive emotion dysregulation. In Palacios-Barrios, E. E., & Hanson, J. L. (2019). Poverty and self-
J. J. Gross (Ed.), Handbook of emotion regulation. New York, regulation: Connecting psychosocial processes, neurobiology,
NY: Guilford. and the risk for psychopathology. Comprehensive Psychiatry,
Lunkenheimer, E. S., Olson, S. L., Hollenstein, T., Sameroff, 90, 52–64. doi:10.1016/j.comppsych.2018.12.012
A. J., & Winter, C. (2011). Dyadic flexibility and positive Pang, K. C., & Beauchaine, T. P. (2013). Longitudinal patterns of
affect in parent–child co-regulation and the development of autonomic nervous system responding to emotion evocation
child behavior problems. Development and Psychopathology, among children with conduct problems and/or depression.
23, 577–591. doi:10.1017/S095457941100006X Developmental Psychobiology, 55, 698–706. doi:10.1002/
Mauss, I. B., & Butler, E. A. (2010). Cultural context moderates dev.21065
the relationship between emotion control values and Perepletchikova, F., & Goodman, G. (2014). Two approaches to
cardiovascular challenge versus threat responses. Biological treating preadolescent children with severe emotional and
Psychology, 84, 521–530. doi:10.1016/j.biopsycho.2009.09.010 behavioral problems: Dialectical behavior therapy adapted
McLaughlin, K. A., Hatzenbuehler, M. L., & Keyes, K. M. for children and mentalization-based child therapy. Journal
(2010). Responses to discrimination and psychiatric disorders of Psychotherapy Integration, 24, 298. doi:10.1037/a0038134
among Black, Hispanic, female, and lesbian, gay, and Pfefferbaum, A., Kwon, D., Brumback, T., Thompson, W. K.,
bisexual individuals. American Journal of Public Health, 100, Cummins, K., Tapert, S. F., . . . Sullivan, E. V. (2018). Altered
1477–1484. doi:10.2105/AJPH.2009.181586 brain developmental trajectories in adolescents after initiating
McLaughlin, K. A., Hatzenbuehler, M. L., Mennin, D. S., & drinking. American Journal of Psychiatry, 175, 370–380.
Nolen-Hoeksema, S. (2011). Emotion dysregulation and doi:10.1176/appi.ajp.2017.17040469
adolescent psychopathology: A prospective study. Behavior Pieterse, A. L., Todd, N. R., Neville, H. A., & Carter, R. T.
Research and Therapy, 49, 544–554. doi:10.1016/j. (2012). Perceived racism and mental health among Black
brat.2011.06.003 American adults: A meta-analytic review. Journal of
Mead, H. K., Beauchaine, T. P., & Shannon, K. E. (2010). Counseling Psychology, 59, 1–9. doi:10.1037/a0026208
Neurobiological adaptations to violence across development. Prater, K. E., Hosanagar, A., Klumpp, H., Angstadt, M., &
Development and Psychopathology, 22, 1–22. doi:10.1017/ Phan, L. K. (2013). Aberrant amygdala–frontal cortex
S0954579409990228 connectivity during perception of fearful faces and at rest in
Mendelson, T., Greenberg, M. T., Dariotis, J. K., Feagans Gould, generalized social anxiety disorder. Depression and Anxiety,
L., Rhoades, B. L., & Leaf, P. J. (2010). Feasibility and 30, 234–241. doi:10.1002/da.22014
preliminary outcomes of a school-based mindfulness Qing, L., Haoran, L., Luo, G., Wang, Y., Tang, H., Han, L., &
intervention for urban youth. Journal of Abnormal Psychology, Yao, Z. (2012). Impaired prefrontal-amygdala effective
38, 985–994. doi:10.1007/s10802-010-9418-x connectivity is responsible for the dysfunction of emotion

process in major depressive disorder: A dynamic causal Thayer, J. F., Hansen, A. L., Saus-Rose, E., & Johnsen, B. H.
modeling study on MEG. Neuroscience Letters, 523, 125–130. (2009). Heart rate variability, prefrontal neural function,
doi:10.1016/j.neulet.2012.06.058 and cognitive performance: The neurovisceral integration
Rodriguez-Seijas, C., Burton, C. L., Adeyinka, O., & Pachankis, perspective on self-regulation, adaptation, and health. Annals
J. E. (2019). On the quantitative study of multiple of Behavioral Medicine, 37, 141–153. doi:10.1007/s12160-009-
marginalization: Paradox and potential solution. Stigma and 9101-z
Health. Advance online publication. doi:10.1037/sah0000166 Thompson, R. A. (1994). Emotion regulation: A theme in
Rogers, A. H., Seager, I., Haines, N., Hahn, H., Aldao, A., & search of definition. Monographs of the Society for Research in
Ahn, W. Y. (2017). The indirect effect of emotion regulation Child Development, 59, 25–52. doi:10.1111/j.1540-5834.1994.
on minority stress and problematic substance use in lesbian, tb01276.x
gay, and bisexual individuals. Frontiers in Psychology, 8, 1881. Thompson, R. A. (2019). Emotion dysregulation: A theme in
doi:10.3389/fpsyg.2017.0188 search of definition. Development and Psychopathology.
Rottenberg, J. (2005). Mood and emotion in major depression. Advance online publication. doi:10.1017/S0954579419000282
Current Directions in Psychological Science, 14, 167–170. Thompson, R. A., & Meyer, S. (2007). Socialization of emotion
doi:10.1111/j.0963-7214.2005.00354.x regulation in the family. In J. J. Gross (Ed.), Handbook of
Schmidt, L. A., Fox, N. A., Perez-Edgar, K., & Hamer, D. H. emotion regulation (pp. 249–268). New York, NY: Guilford.
(2009). Linking gene, brain, and behavior: DRD4, frontal Vasilev, C. A., Crowell, S. E., Beauchaine, T. P., Mead, H. K., &
asymmetry, and temperament. Psychological Science, 20, Gatzke-Kopp, L. M. (2009). Correspondence between
831–837. doi:10.1111/j.1467-9280.2009.02374.x physiological and self-report measures of emotion dysregulation:
Scott, S., Briskman, J., & O’Connor, T. G. (2014). Early A longitudinal investigation of youth with and without
prevention of antisocial personality: Long-term follow-up of psychopathology. Journal of Child Psychology and Psychiatry, 50,
two randomized controlled trials comparing indicated and 1357–1364. doi:10.1111/j.1469-7610.2009.02172.x
selective approaches. American Journal of Psychiatry, 171, Webster-Stratton, C., & Reid, M. J. (2010). The Incredible Years
649–657. doi:10.1176/appi.ajp.2014.13050697. parents, teachers and children training series: A multifaceted
Semple, R. J., Lee, J., Rosa, D., & Miller, L. F. (2010). A treatment approach for young children with conduct
randomized trial of mindfulness-based cognitive therapy for problems. In J. Weisz & A. Kazdin (Eds.), Evidence-based
children: Promoting mindful attention to enhance social- psychotherapies for children and adolescents (2nd ed.,
emotional resiliency in children. Journal of Child and Family pp. 122–141). New York, NY: Guilford.
Studies, 19, 218–229. doi:10.1007/s10826-009-9301-y Webster-Stratton, C., Reid, M. J., & Beauchaine, T. P. (2011).
Shannon, K. E., Sauder, C., Beauchaine, T. P., & Gatzke-Kopp, Combining parent and child training for young children
L. (2009). Disrupted effective connectivity between the with ADHD. Journal of Clinical Child and Adolescent
medial frontal cortex and the caudate in adolescent boys with Psychology, 40, 191–203. doi:10.1080/15374416.2011.546044
externalizing behavior disorders. Criminal Justice and Weinberg, A., & Klonsky, E. D. (2009). Measurement of emotion
Behavior, 36, 1141–1157. doi:10.1177/0093854809342856 dysregulation in adolescents. Psychological Assessment, 21,
Sheppes, G., Suri, G., & Gross, J. J. (2015). Emotion regulation 616–621. doi:10.1037/a0016669
and psychopathology. Annual Review of Clinical Psychology, Yip, T., Seaton, E. K., & Sellers, R. M. (2006). African American
11, 379–405. doi:10.1146/annurev-clinpsy-032814-112739 racial identity across the lifespan: Identity status, identity
Shipman, K. L., & Zeman, J. (2001). Socialization of children’s content, and depressive symptoms. Child Development, 77,
emotion regulation in mother–child dyads: A developmental 1504–1517. doi:10.1111/j.1467-8624.2006.00950.x
psychopathology perspective. Development and Psychopathology, Zelazo, P. D. (2015). Executive function: Reflection, iterative
13(2), 317–336. doi:10.1017/S0954579401002073 reprocessing, complexity, and the developing brain.
Thayer, J. F., Åhs, F., Fredrikson, M., Sollers III, J. J., & Wager, Developmental Review, 38, 55–68. doi:10.1016/j.dr.2015.07.001
T. D. (2012). A meta-analysis of heart rate variability and Zisner, A., & Beauchaine, T. P. (2016). Psychophysiological
neuroimaging studies: Implications for heart rate variability methods and developmental psychopathology. In D. Cicchetti
as a marker of stress and health. Neuroscience and (Ed.), Developmental psychopathology. Vol. 2: Developmental
Biobehavioral Reviews, 36, 747–756. doi:10.1016/j. neuroscience (3rd ed., pp. 832–884). Hoboken, NJ: Wiley.
neubiorev.2011.11.009 doi:10.1002/9781119125556.devpsy222

INDEX
Note: Figures and tables are indicated by an italic “f ” and “t” respectively, following the page numbers.
A region-of-interest analysis in 6, 189 amygdala

Aase, H. 238–239 terminology related to 184–185 activation across anxiety 186–188
abuse. See childhood abuse traditional approach in 183, 185–189 age-related changes in 69–70
ACC. See anterior cingulate cortex variability in emotion and diagnostic in associative learning 4
acceptance and commitment therapy categories 194 in autism 288–289
(ACT) 401, 451–452 affective variability 353, 415, 417, in borderline personality disorder
Achenbach, T. M. 237 419–420 365–367, 370, 466, 470–472
Achenbach System of Empirically Based affect regulation model of binge eating/ in cognitive control 72
Assessment for School-Age Children bulimia nervosa 328 in cognitive reappraisal 42, 302, 320
(ASEBA) 429–430 affiliative bonds 142–143, 145–149 in core limbic group 191
ACS (Affective Control Scale) 401–402 affiliative emotions 2, 3 in fear conditioning 43, 186
ACVM (automated computer vision and afunctional displays of emotion 2, 3, 479 habituation to emotional stimuli in
machine learning) 480 aging 69–80 fMRI 209
adaptive-basins model 29–34, 34f cognitive control and 71–73 in internalizing spectrum disorders 256
addiction 313–321. See also substance use decision making and 77, 79, 80 in motivated behavior 17, 20
disorders duration of emotion and 78, 80 in psychosis spectrum disorders 304
allostatic load models of 314, 316 emotional modulation of LPPs in reward pathway 315, 317
brain regions related to 20 and 170–171 in self-regulation 349
drivers of 313 emotional well-being and 69–72, serotonin expression in 225
emotion dysregulation and 316–317, 75–77, 79, 80 startle response and 287
320 emotion dysregulation and 75–80 in suppression 302, 318
future research directions 321 emotion regulation and 70–75 trait anxiety and 87, 192, 193
neurobiological models of 174–175 future research directions 80 trauma exposure and 268
reward pathway and 315–317 memory and 78 analog observation tasks 379, 385–387
volitional regulation of emotion psychopathology and 78–79 anhedonia
and 317–321 regulatory strategies and 71, 73–76 addiction and 316–318, 321
vulnerability to 314–315 relationships and 77, 99 assessment of 8
ADHD. See attention-deficit/hyperactivity respiratory sinus arrhythmia and 161n2 depression and 135, 402, 452
disorder sequences of emotion and behavior in dopaminergic function and 227, 239,
adolescents. See children and adolescents 76–78 349
Adrian, Molly 377, 430 aging brain model 69–70 psychosis spectrum disorders and 303,
affect-as-information hypothesis 30, 44–45 AIM (Affect Intensity Measure) 399 305
Affect Intensity Measure (AIM) 399 Albein-Urios, N. 319–320 anorexia nervosa (AN) 327–338
affective chronometry 176 alcohol abuse. See substance use disorders characteristics of 327
Affective Control Scale (ACS) 401–402 Aldao, A. 332 ecological momentary assessment
Affective Lability Scale (ALS) 399–400 alexithymia of 332–335, 419
affective neuroscience 183–195. See also autism and 286 experimental research on 335–338
functional magnetic resonance eating disorders and 332, 336, 338 late positive potentials and 175–176
imaging; neuroimaging methamphetamine use and 320 self-report assessments and 329–332
basic emotions in 185 psychosis spectrum disorders and 302, socioemotional processing and 335,
constructionist approach in 183–184, 304 336, 338
189–194 Allard, E. S. 72–73 theoretical models related to 328–329
defined 183 alleles 33, 90, 109–110, 120, 208–211, ANS. See autonomic nervous system
future research directions 193–194 226–227 antecedent-focused regulatory
on internalizing spectrum disorders Allen, Kenneth J. D. 411 strategies 73, 88, 301, 447, 448, 455
255–256 Allen, N. B. 119, 386–387 anterior cingulate cortex (ACC)
interplay of networks in 193–194 allostasis 27, 28, 30 addiction and 319
on neural bases of emotion 185–189, allostatic load 228, 266, 275, 314, 316 age-related changes in use of 72, 73, 78
191–193 ALS (Affective Lability Scale) 399–400 in borderline personality disorder 366,
overview 183–184 Amstadter, Ananda B. 203 370
487
anterior cingulate cortex (ACC) (Continued ) attention core affect and 190
in cognitive control 72 defined 15 individual differences in arousal 61
in depression 256 emotion in relation to 40–44 internalizing spectrum disorders
in emotion regulation 91, 137 late positive potentials and 169, 170, and 256
in motivated behavior 20 170f psychosis spectrum disorders and
overmodulation and 271 motivated behavior and 17 304–306
in reappraisal of negative emotion 4 psychosis spectrum disorders and 300 synchrony during conflict
respiratory sinus arrhythmia and 155 salience network and 187 conversations 105
trait anxiety and 87 selective 73 avoidance emotions 2–4, 6, 88
undermodulation and 271 attentional biases
antidepressant medications 47, 142, addiction and 316, 318–319 B
161n1, 173 autism and 30 Babkirk, S. 171
antisocial behavior 238–242, 436 borderline personality disorder Babuscio, T. 319
antisocial personality disorder (ASPD) and 365, 370 BAM (Becoming a Man) program 434
92, 227, 239 childhood maltreatment and 251–252 Bardeen, J. R. 274
anxiety disorders. See also specific conditions congruent mood state and 43 Barlow, D. H. 447, 473
addiction and 314 emotion regulation and 41, 213 Barrett, Lisa Feldman 5–6, 28–30
attentional biases and 41 vulnerability to 208 BAS (behavioral activation system) 414
autism and 283, 285, 286 attentional deployment 40, 73, 132–133, BASC (Behavioral Assessment System
brain regions related to 20, 188, 189, 135, 302, 447 for Children) 429
192–193 attention-deficit/hyperactivity disorder basic emotions
emotion dysregulation and 47, 254 (ADHD) in affective neuroscience 185
family influences on 102–103, 251–253 delinquency associated with 242, 243 eating disorders and recognition of 335
functional connectivity deficits and 4, developmental progression from 238, hyperactivation of 19
188 241, 243, 428 locationist perspective on 7
gender differences and 92, 443 dopaminergic function and 227, 228 LPP potentiation to 170
late positive potentials and 173 emotional lability and 58 motivated behavior directed by 17–18
maladaptive motivated behavior environmental influences on 242 neural structures in promotion of 3, 6
and 21–22 ontogenic process perspective on 238, Pankseppian model of 15–16, 20
in older adults 78, 79 242, 243f regulatory strategies vs. 93–94
predictive factors 19 parent training interventions for 431 basic emotion theory 6, 28, 185
prenatal exposure to 143 prefrontal cortex development and 240 Baumeister, R. F. 30, 469
prevalence of 443 respiratory sinus arrhythmia and 156 Bayley Scales of Infant Development 385
regulatory strategies and 136 risk factors for 87 BDNF (brain-derived neurotrophic factor)
respiratory sinus arrhythmia and 156, trait impulsivity and 238–240, 242 gene 209, 257
157, 257 treatments for 431, 434, 435 Beauchaine, Theodore P. 1, 87, 89–90,
serotonergic function and 225 Attention Network Task 411 128, 153, 227, 237, 465, 477
trait anxiety and 78, 85, 87, 89 attributional biases 5, 102, 104, 434 Becerra, R. 398
treatments for 173, 203, 432, 449–452 attunement 143–145 Bechara, A. 69–70
approach emotions 2–4, 6, 88, 227 Atzil, S. 149 Becker, S. P. 271
Armey, Michael F. 352–353, 411 autism spectrum disorder (ASD) 283–292 Beckes, Lane 27, 32
arm restraint task 386 attentional biases in 30 Becoming a Man (BAM) program 434
ASD. See autism spectrum disorder behavioral difficulties and 284 BED (binge eating disorder) 327–333,
ASEBA (Achenbach System of Empirically comorbidity and 283, 285, 290, 291 336–338
Based Assessment for School-Age diagnostic formulation of 283, behavioral activation system (BAS) 414
Children) 429–430 285–286 behavioral assessments 377–389.
ASPD (antisocial personality disorder) 92, electrophysiology and 288 See also behavioral observation;
227, 239 emotional lability and 58, 283, 286 specific assessments
Aspinwall, L. G. 93 future research directions 291–292 computerized 387–389
Asselbergs, J. 420 genetic influences on 289–290 of externalizing spectrum
associative learning 3, 4, 227 methodology for study of 286–292 disorders 429–430
Atchley, Rachel M. 313 neuroimaging studies and 288–289 future research directions 389
attachment figures 31 psychophysiology and 287–288 multiple levels of analysis in 63, 380
attachment theory respiratory sinus arrhythmia and 156 for schizophrenia 303
adaptive-basins model and 31–32, 34 theoretical models of emotion theoretical perspectives on 378–379
development of 141 dysregulation in 284–286 Behavioral Assessment System for
disorganized attachments 32, 100–101, autobiographical memory 46, 170, 176, Children (BASC) 429
108, 252, 363 192, 412, 420 behavioral expression 14–16, 19, 21, 90, 133
elements of 31 automated computer vision and machine behavioral inhibition system (BIS) 414
on emotion dysregulation 100–101 learning (ACVM) 480 behavioral observation
insecure attachments 100, 120, 144, 252 autonomic nervous system (ANS) advantages of 55, 378
internalizing spectrum disorders activation without emotion 33 analog tasks 379, 385–387
and 252 autism and 287 analytic approach to 62–63
488 index
of children and adolescents 56–62 borderline personality disorder C
coding systems for 117, 387 (BPD) 361–372 Cabanac, M. 17
of context-inappropriate emotion brain regions related to 20, 91, 365–367, Cacioppo, J. 69–70
57–58, 62 370, 466, 470–472 Caffier, D. 337
of duration of emotion 59–60 characteristics of 361–362, 429, Calkins, S. D. 120
of emotional lability 58–59, 63 466–467 callous-unemotional (CU) traits 58–59,
of emotion dysregulation 55–63, comorbidity and 367, 372 156, 271–272
205, 253, 430 ecological momentary assessment Campbell-Sills, L. 447
length and number of 60–61 of 367, 417–418 Campitelli, G. 398
limitations of 63, 290, 378, 412 emotional responding in 364–368 candidate epigenetic studies 224–225, 231
methodology for 380, 381–384t emotion dysregulation within 58, 129, candidate gene studies 109, 207t,
naturalistic 380, 385 225, 466–467 208–210, 214
structured tasks 385 future research directions 371–372 Cannon, T. D. 212
Bell, Spencer 313 gender differences and 92 Carroll, K. M. 319
Bell, Ziv E. 153 graphical depiction of emotion Carter, J. C. 331
Benight, C. C. 273 dysregulation in 371, 371f cascading systems 30–33, 34f
Bennett, D. C. 271, 275 late positive potentials and 176 Castaldo, R. 156
Bents, H. 331 parent–child interactions and 120 catechol-0-methyltransferase (COMT)
Berg, K. C. 334 posttraumatic stress disorder and 367 gene 90, 208, 209
Beri, S. 226 regulatory strategy use in 364, categorization, in theory of constructed
Berk, Michele 377 368–370 emotion 190, 192
Berner, L. A. 334 respiratory sinus arrhythmia and 156 Cavanagh, M. 428
Bernston, G. 69–70 self-inflicted injury in 361, 363, 416, CBT. See cognitive-behavioral therapy
biases. See also attentional biases 417, 470–471 CD. See conduct disorder
attributional 5, 102, 104, 434 serotonergic function and 225–226 Cecil, C. A. M. 269
in brain development 29 theoretical perspectives on 362–364 central nervous system 15, 155, 185, 225,
in heritability estimates 205 treatments for 367, 370, 451, 463–471 287, 444
information processing 378, 449 Bowlby, J. 31, 32, 100, 141, 266 Chaplo, S. D. 275
in older adults 72, 73, 75, 77 Boyle, C. L. 123 Chapman, Alexander L. 463
Pavlovian 5 BPD. See borderline personality disorder Chentsova-Dutton, Y. E. 93
recall 333, 418 Bradley, B. 265 Child Behavior Checklist (CBCL) 429,
self-referential 171, 172, 176 brain. See also affective neuroscience; 434, 436
binge eating disorder (BED) 327–333, neuroimaging; specific parts childhood abuse
336–338 of brain dissociation and 55
Binion, Grace 115, 118 evolution of 186 epigenetics and 269
biological pathways. See also limbic- functional patterns of activity in 187 internalizing spectrum disorders
hypothalamic-pituitary-adrenal axis neurodevelopment 29, 35, 239–241, and 251–252
alteration through DNA 285, 292, 349 invalidating environment and 122
methylation 224 triune brain concept 185–186 orbitofrontal cortex and 241
candidate epigenetic studies of 225 brain-derived neurotrophic factor (BDNF) respiratory sinus arrhythmia and 158
epigenetic studies with 224–230 gene 209, 257 risk factors for 144
neurotransmitter systems 225–228, Brammer, S. 429 self-regulation and 103
267 Brazelton Neonatal Behavioral Assessment childhood maltreatment. See also
biometrical model 204–206, 207t, 212 Scale (BNBAS) 385 childhood abuse
biosocial theory 117, 176, 362–363, 432, Bremner, J. D. 267 allostatic load and 228
466, 474n1 Brennan, Patricia A. 427 context-inappropriate emotion
bipolar disorder. See also depression; mania Bridgett, D. J. 156 and 57–58
context-inappropriate emotion and 57 Brockmeyer, T. 331 emotion dysregulation in aftermath
ecological momentary assessment Brody, G. H. 231 of 273–274
of 415 Brown, April L. 427 familial dysfunction and 89, 270
genetic influences on 212 Brown, E. J. 122 genetic interactions with 209, 257, 258
L-HPA axis dysfunction and 228 Brown, Mindy 221 internalizing spectrum disorders
valuation of emotion in 134 Buckner, J. D. 419 and 251, 253, 254
BIS (behavioral inhibition system) 414 bulimia nervosa (BN) 327–338 salience network activation and 256
BN. See bulimia nervosa characteristics of 327 childhood trauma 265–276. See also
BNBAS (Brazelton Neonatal Behavioral ecological momentary assessment posttraumatic stress disorder
Assessment Scale) 385 of 332–335, 418 biopsychosocial processes in 268–270
Boden, M. T. 276 experimental research on 335–338 callous-unemotional traits and 271–272
body–mind training 435 self-report assessments and 329–332 conceptualizations of 266–268
body regard 353–354 socioemotional processing and Developmental Trauma Disorder
Bohlmeijer, E. T. 452 335–336 proposal and 272–273
Boker, S. M. 213 theoretical models related to 328 emotion dysregulation in aftermath
Bolger, N. 413 Butler, E. A. 92 of 265, 273–275
index 489
childhood trauma (Continued ) DERS score improvement computerized behavioral tasks 387–389
future research directions 275–276 following 401 COMT (catechol-0-methyltransferase)
over-/undermodulation subtypes for eating disorders 331 gene 90, 208, 209
and 271 late positive potentials and 173 conduct disorder (CD)
children and adolescents. See also family; limitations of 464 characteristics of 428
parent–child interactions for maladaptive motivated behavior 22 developmental pathway to 238, 241
abuse of (see childhood abuse) for posttraumatic stress disorder 276 dopaminergic function and 227
attachment theory and 31–32, 100–101 principles of 432, 444, 449 environmental influences on 242
autistic (see autism spectrum disorder) for psychosis spectrum disorders 307 functional connectivity deficits
cognitive control in 42 cognitive change 40–42, 73, 132, 133, and 240
context-inappropriate emotion in 301–302, 447 gender differences and 92
57–58 cognitive control. See also executive neural deficits related to 91
dissociation among 55 functioning prefrontal cortex development
duration of emotion in 59–60 age-related changes in 71–73 and 240, 241f
eating disorders among 327 borderline personality disorder respiratory sinus arrhythmia and 156,
emotional lability in 58–59, 253, 350 and 368–369 257
emotional modulation of LPPs in brain regions related to 72–73, 185, risk factors for 87, 89
170–171 255–256 trait impulsivity and 239
in environments of adaptation 3 emotion in relation to 45–46, 72–73 treatments for 434
gender-specific socialization in socioemotional selectivity theory 70 conflict
practices and 92 cognitive deconstruction 469 adaptation to 45, 46
maltreatment of (see childhood cognitive-interpersonal maintenance coercion theory and 117
maltreatment) model of anorexia nervosa 329 escalation of 58, 88, 93, 119
motivated behavior in 18 cognitive motor group 192, 195n5 externalizing spectrum disorders
observation of (see behavioral cognitive reappraisal and 242
observation) addiction and 318–320 in interaction models 119
prefrontal cortex response in 4 age-related changes in use of 74 marital 101, 104
respiratory sinus arrhythmia in borderline personality disorder and 368 resolution of 46, 87, 350
156–158 brain regions related to 42, 318 in romantic relationships 145–146
self-inflicted injury by 345–346, 352 defined 41, 133, 254, 301 skills for management of 463, 468
self-regulation by 56, 102–104 detached 74 conflict discussion task 93, 146, 148, 386
trauma and (see childhood trauma) eating disorders and 332 Conkey, Lindsey C. 361
treatment strategies for 432–435, 449, effectiveness of 59 Conners’ Rating Scales (CRS) 429
480–481 in emotion coaching 457 Conradt, Elisabeth 108, 221
Children’s Emotion Management late positive potentials and 169–170, constructed emotion theory 5, 183–184,
Scales 430 170f, 172–176 189–194
chromatin 222, 230 limitations of 42, 135 constructionism
Cicchetti, Dante 249, 273, 274 operant reinforcement and 118 in affective neuroscience 183–184,
cigarettes 175, 313–315, 317–319 positive 74, 79 189–194
Clement, P. F. 328 psychosis spectrum disorders and 301, convergence and divergence with
Clore, G. L. 30 302 functionalism 6–8
Coan, J. A. 32 as therapeutic technique 41, 46–47, implications for emotion
cocaine 175, 313–314, 319–320 437 dysregulation 5–6
Coccaro, E. F. 205 cognitive reframing. See cognitive innateness vs. 29
coercion theory 117, 121 reappraisal principles of 4–5
cognition Cohn, A. M. 429 psychological 188, 189, 191
attention (see attention) Cole, Pamela M. 53 theory of constructed emotion 5,
constructionist accounts of 4 common pathway model 206 183–184, 189–194
decision making (see decision making) comorbidity context, in emotion dysregulation 2, 27,
eating disorders and 330 of anxiety and depression 173 35, 75–76
emotion in relation to 39–47, 72 autism and 283, 285, 290, 291 context-inappropriate emotion 57–58, 62
learning (see learning) borderline personality disorder Cooper, J. L. 330
memory (see memory) and 367, 372 core affect theory 5, 7, 28, 54, 190
psychopathology and 136–137 emotion dysregulation as 285 coregulation 88, 350, 444, 448
in psychosis spectrum disorders genetic and environmental core limbic group 191, 192, 195n3
304–305 influences 212 Corner, Geoffrey W. 141
serotonin and 225 internalizing–externalizing 62, 158, 285 C-PTSD (complex posttraumatic
spontaneous 55 psychosis spectrum disorders and 299 stress disorder) 267
cognitive-behavioral therapy (CBT) regulatory deficits and 206 Cross, D. 265, 269
ACS score improvement competitive games with peer Crowell, Sheila E. 85, 119, 158, 209, 221,
following 402 confederates 386 225, 345, 363, 477
for children and adolescents 434, 449 complex posttraumatic stress disorder Crowther, J. H. 352–353
cognitive reappraisal in 41, 46–47, 437 (C-PTSD) 267 CRS (Conners’ Rating Scales) 429
490 index
Csikszentmihalyi, M. 413, 414 regulatory strategies and 135 emotion dysregulation as
Cukrowicz, K. C. 147 respiratory sinus arrhythmia and 156, conceptualized in 465–467
Culbert, K. M. 335 161n1, 257 empirical support for 464–465,
cultural influences 2, 90, 93, 479, rumination and 41 470–472
481–482 salience network dysregulation in 193 future research directions 472–474
Cummings, E. M. 104 serotonergic function and 225, 226 interpersonal processes and 149
CU (callous-unemotional) traits 58–59, suicidal ideation and 79, 172 metaphor use in 474n1
156, 271–272 symptoms of 171, 227, 254 modes and functions of 464, 465t
Cyders, M. A. 332 treatments for 432, 450–452 neurobiological changes following
DERS. See Difficulties in Emotion 470–472
D Regulation Scale for parent–child interactions 124
Damasio, A. R. 30 detached reappraisal 74 physiological issues addressed by
DAPP-BQ (Dimensional Assessment development. See also socioemotional 468–469
of Personality Pathology–Basic development principles of 432, 450–451
Questionnaire) 396–397 brain-related 29, 42, 88 for psychosis spectrum disorders 307
Darwin, Charles 6, 101, 141 defined 15 for self-inflicted injury prevention 354
Davidson, R. J. 176 of emotion dysregulation 100–103, skills training component of 433, 434,
Davies, P. T. 104 116–121 463–464, 467–469
Davis, B. 386–387 motivated behavior and 18 stepped-care models of 474
DBT. See dialectical behavioral therapy neurodevelopment 29, 35, 239–241, streamlining 473
DeBaryshe, B. 117 285, 292, 349 Diamond, L. M. 93
decision making normative patterns of 230 diathesis-stress model 108, 109
age-related changes in 77, 79, 80 developmental perspective differential susceptibility 103, 108–110
emotion in relation to 30, 31, 44–45 on behavior assessment 379 Difficulties in Emotion Regulation
improvement strategies 434 on emotion dysregulation 88, 89, Scale (DERS)
maladaptive 183 251–253, 349–351 age-related effects and 77
somatic marker hypothesis on 30–31, on externalizing spectrum alternate versions of 401, 411
45 disorders 429 in behavioral observation 56
systemic biases in 44 on internalizing spectrum borderline personality disorder and 472
Decker, S. E. 319 disorders 251–253, 259 core emotion difficulties assessed by
Deckersbach, T. 398 on psychopathology 86, 87, 89, 257 348, 430
DeClaire, J. 453, 457 resilience in 86 eating disorders and 329–331, 338
default mode network (DMN) 192–194, on treatment strategies 431 empirical support for 400–401
289 Developmental Trauma Disorder phenotype assessment and 213
defensive regulation model 272 (DTD) 272–273 posttraumatic stress disorder and
DeGarmo, D. S. 242 DeWall, N. C. 30 274–275
degeneracy 28, 29, 194 Diagnostic and Statistical Manual of Mental self-inflicted injury and 354
Delahanty, D. L. 273 Disorders, 5th edition (DSM-5) digital phenotyping 420
delusions 300, 304–306 discrete order approach of 237 Dimaggio, G. 225
deoxyribonucleic acid (DNA) eating disorders in 327 Dimensional Assessment of Personality
composition of 208, 222 emotional symptoms of Pathology–Basic Questionnaire
double helix structure of 222, 223f psychopathology in 71, 127 (DAPP-BQ) 396–397
methylation 208, 222–231, 269 internalizing spectrum disorders in 251, disappointing gift paradigm 118, 386
transcription 208, 222, 269 445 discrete emotion theories 54
depression. See also bipolar disorder on nonsuicidal self-injury disorder 348 discrimination 266, 481–482
addiction and 314 on psychosis spectrum disorders 299, disorganized symptoms 300, 301
autism and 283, 285 306 dissociation 55, 267, 271, 272, 361, 367
brain regions related to 20, 256 on suicidal behavior disorder 348 distraction
cognitive control deficits and 45 trauma and PTSD in 195n2, 266, cognitive resources and 73–74
ecological momentary assessment 267, 270 effectiveness of 40, 59, 133
of 414–415 dialectical behavioral therapy late positive potentials and 177
emotional lability and 58 (DBT) 463–474 limitations of 41
family influences on 102, 104, 251–253 ACS score improvement following 402 operant reinforcement and 118
gender differences in 92, 443 behavioral issues addressed by distress tolerance
genetic influences on 212 467–468 assessment of 389
late positive potentials and 171–173 for borderline personality borderline personality disorder and 369
learned helplessness and 134 disorder 370 invalidating environment and 118
L-HPA axis dysfunction and 228 for children and adolescents 433–435, laboratory-based assessment of 213
medications for 47, 142, 161n1, 173 481 serotonergic function and 90, 208, 209
in older adults 78–79 cognitive issues addressed by 469–470 strategies for 451, 463, 467
postpartum 147, 149 DERS score improvement distress tolerance test (DTT) 389
prenatal exposure to 142 following 401, 472 Ditzen, B. 148
prevalence of 443 for eating disorders 331 Dixon-Gordon, Katherine L. 361
index 491
DMN (default mode network) 192–194, socioemotional processing and dual-process model of 30
289 335–336, 338 evolutionary perspective on 2–3, 6–8
DNA. See deoxyribonucleic acid state–trait emotion interactions in 335 functionalist accounts of 2–4, 6–8,
Docherty, Anna R. 299 theoretical models related to 328–329 54, 60
domain-relevant approach to treatments for 329, 331 generation of (see emotion generation)
emotion 27–31, 33–35, 34f ECI (Emotion Context-Insensitivity) as information 30–34, 44–45
domain specificity of emotion 27–29, model 171 interpersonal levels of 92–93
31, 35 ecological momentary assessment intrapersonal levels of 89–92
domestic violence. See intimate (EMA) 411–420 measurement challenges 250
partner violence of addictive behavior 321 mechanistic perspective on 13–14
dopamine advantages of 412–413 modal model of 41
anhedonia and 227, 239, 349 of bipolar disorder 415 mood vs. 33, 445, 447–478
autism and 289–290 of borderline personality disorder 367, motivated behavior and 14, 20, 21
in developmental theory 89 417–418 neural bases of 185–189, 191–193
in emotion dysregulation 227–228 of cognitive reappraisal 302 overmodulation of 270–272, 275, 276
in reward processing 7, 228 of depression 414–415 Pankseppian model of 15–17
trait impulsivity and 239 of eating disorders 328, 332–335, 338, regulation of (see emotion regulation)
variation in receptor genes 32, 109 418–419 social behavior regulation through
Doussard-Roosevelt, J. A. 154 of emotional inertia 213 27–35
Doyle, C. 273 of emotion socialization 119 socialization of (see emotion
Drabant, E. M. 90 incorporation in multimethod socialization)
DRD4 gene 109, 110, 227–228 research 214 theories of (see emotion theories)
drug abuse. See substance use disorders of individual differences in emotional undermodulation of 270–272, 275,
DSM-5. See Diagnostic and Statistical trajectory 413–414 276
Manual of Mental Disorders, limitations of 413 Emotion-Affect Regulation Interview 430
5th edition overview 411 emotional awareness
DTD (Developmental Trauma psychophysiological measures and 414 borderline personality disorder
Disorder) 272–273 of self-inflicted injury 352–354, and 368, 467
DTT (distress tolerance test) 389 416–417 default mode network and 289
dual-generation interventions 121–123 self-report assessments and 116 individual variations in 134
dual-process model of emotion 30 of specific emotions over time 414 lack of 274, 330, 348, 362
Dudeney, J. 104 of stress response 413–414 parenting interventions for 454
Duncan, L. E. 211 of substance use craving 419–420 psychosis spectrum disorders and 301,
duration of response metric 176 unobtrusive 420 304, 305, 307
Dvorak, R. D. 403 ecological momentary interventions emotional behavior
dyadic processes. See also parent–child (EMIs) 420 abrupt changes in 58–59, 62–63
interactions Edelbrock, C. 237 afunctional 2, 3, 479
emotion in 63, 141 EDs. See eating disorders age-related changes in 76–78
at interpersonal level of emotion 92–93 Edwards, Weston Layne 27 in children and adolescents 32
romantic relationships 145–148 EFT (emotion-focused therapy) 449–450, context-inappropriate 57–58, 62
in self-regulation development 433 455 duration of emotion 59–60, 78, 80
dynamic systems theory 54, 55, 60 Egeland, B. 120 organism-wide 17
Ehrmantrout, N. 386–387 emotional clarity
E Eimer, M. 170 borderline personality disorder and
eating disorders (EDs) 327–339. Eisenberg, N. 104 363, 368, 467
See also anorexia nervosa; Elbert, T. 272 eating disorders and 330, 331, 336
bulimia nervosa elderly persons. See aging lack of 272, 274, 275, 348, 354
binge eating disorder 327–333, electroencephalography (EEG) 19, 184, schizophrenia and 305
336–338 193, 288, 291, 319 emotional competence 57, 122, 430,
in DSM-5 327 electrophysiology 153–154, 288, 317 444–447, 453
ecological momentary assessment Elliot, A. J. 414 emotional go/no-go tasks 388–389, 411
of 328, 332–335, 338, 418–419 EMA. See ecological momentary emotional inertia 213
emotion dysregulation in prediction assessment emotional lability
of 254 EMIs (ecological momentary autism and 58, 283, 286
experimental research on 335–338 interventions) 420 behavioral observation of 58–59, 63
future research needs 339 emotion callous-unemotional traits and 58–59
gender differences in 327 basic (see basic emotions) in children and adolescents 58–59,
integrative model for 338–339 cognition in relation to 39–47, 72–73 253, 350
mood manipulation and 337–338 constructionist accounts of 4–8, 29 defined 58
prevalence of 327 definitions of 14–15, 33, 167, 184, 445 functional connectivity deficits and 4
psychophysiology and 336–337 domain-relevant approach to 27–31, negative reinforcement of 157, 158
regulatory strategy use in 332 33–35, 34f psychopathology and 58, 59, 397
self-report assessments and 329–332 domain specificity of 27–29, 31, 35 respiratory sinus arrhythmia and 116
492 index
emotional reactivity constructionist accounts of 5–6 definitions of 39–40, 70, 87, 154, 204,
addiction and 317, 319, 320 context in 2, 27, 35, 75–76 300, 362, 411, 478
age-related changes in 70, 75 cultural influences on 93, 479, executive functioning and 72
borderline personality disorder 481–482 functionalist accounts of 4, 101–103
and 363, 365–368, 371, 372, 466 definitions of 3, 39, 71, 128, 154, genetics (see genetic influences)
cultural influences on 93, 479 250, 411, 478–479 implicit vs. explicit 70, 80, 137
defined 128 developmental perspective on 88, 89, interpersonal (see interpersonal
depression and 213 251–253, 349–351 processes)
family influences on 104 eating disorders and (see eating molecular genetics and 208–212, 257
late positive potentials and 172, disorders) motivations for engagement in 128
174–176 functionalist accounts of 4, 101–103, parenting interventions for 455–456
posttraumatic stress disorder and 271 110, 348 process model of (see process model of
psychosis spectrum disorders and genetics and (see genetic influences) emotion regulation)
300, 303 intergenerational transmission of 143, socioemotional development and 431
reduction of 448 146, 149, 221 stages of 88, 130–136, 131f
startle response and 287 interpersonal processes and strategies for (see regulatory strategies)
to stressors 257, 317 (see interpersonal processes) validity of construct 250
temperament and 284 motivated behavior and 18–19 as valuation system 129–130, 130f
emotional responding multidimensional model of 362 Emotion Regulation Checklist 56, 58,
addiction and 316–317, 320, 321 neuroimaging of (see neuroimaging) 274, 430
blunting of 57 patterns of behavior indicative of Emotion Regulation Questionnaire 74,
in borderline personality disorder 56–60 276, 302
364–368, 371, 372 personality disorders (see specific emotion socialization
cognitive control over 42 disorders) childhood maltreatment and 270
in decision making 44 reinforcement of (see operant ecological momentary assessment
in depression 171 reinforcement) of 119
dopamine pathways and 227 in relationships (see relationships) family processes in 61, 117, 479–480
in dyadic interactions 63 self-injury (see self-inflicted injury) internalizing spectrum disorders
maladaptive 18–19, 71 stigma and 304, 305, 481–482 and 104, 257
manipulation of 40–42 trauma (see trauma) invalidating environment and 122–123
quantification of 176 treatments for (see treatment training interventions 121, 453
socioemotional development and 453 strategies) emotion theories
emotional security hypothesis 104 emotion-enhanced memory 43 basic emotion theory 6, 28, 185
emotional sensitivity 349, 350, 363–365, Emotion Expression Scale for constructed emotion theory 5,
396–398, 451, 466 Children 430 183–184, 189–194
emotional stop-signal tasks 412 emotion-focused therapy (EFT) 449–450, core affect 5, 7, 28, 54, 190
emotional systems 15–20, 30, 46 455 discrete 54
emotional well-being emotion generation domain-relevant approach in 29
aging and 69–72, 75–77, 79, 80 integrated theory of 87 dynamic systems 54, 55, 60
autism and 283 models of 8, 86–87, 128 future research directions 35
cognitive reappraisal and 133 psychopathology and 250 EMSP (emotion-modulated startle
defined 69 regulation processes during 40, 73 paradigm) 337
self-care for 455, 456 situation–attention–appraisal–response endophenotypes 32, 212, 214, 239, 415
supportive interactions and 148 perspective on 86 Engel, S. G. 333, 335, 419
emotion-as-social-information model 31 subcortically mediated 4, 86, 87, 91, English, T. 448
emotion avoidance model of anorexia 320 environmental influences
nervosa 328–329 as valuation system 129–130, 130f differential susceptibility to 103,
emotion coaching 104, 121, 157, 270, emotion induction procedures 387 108, 109
444–445, 453–457 Emotion Management Scales 56 epigenetics and 221, 224
Emotion Context-Insensitivity (ECI) emotion misregulation 47, 129 on externalizing spectrum disorders
model 171 emotion-modulated startle paradigm 241–243
emotion dysregulation. See also (EMSP) 337 on phenotypes 206
psychopathology emotion paradox 303 on prefrontal cortex
in addiction (see addiction) Emotion Reactivity Scale (ERS) 398 neuromaturation 240–241
aging and (see aging) emotion regulation on respiratory sinus arrhythmia 156
assessment of (see behavioral addiction and 317–321 epigenetics 221–231
assessments; ecological momentary aging and 70–75 biological pathways in 224–230
assessment; self-report assessments) brain regions related to 91 childhood trauma and 268–269
attachment theory on 100–101 cognitive control and 72–73 controversies and challenges to
in autism (see autism spectrum disorder) conceptualizations of 55, 167, 428, study of 230–231
as comorbidity 285 446, 465 defined 29, 221, 258
conceptualizations of 53–55, 88, 167, context in 2, 27, 35, 128 DNA modifications and 208, 221
300, 396–397, 428, 446, 465–466 cultural influences on 93, 479 history of 224
index 493
epigenetics (Continued ) first-order syndromes 238 Froeliger, Brett 313, 316
in intergenerational transmission of functional connectivity deficits and 4 frontoparietal network 190, 192, 193
emotion dysregulation 143, 221 gender differences in 92, 291 frustration tasks 120, 252, 386
internalizing spectrum disorders genetic influences on 90, 142–143, 206 Fruzzetti, A. E. 329
and 258, 259 prefrontal cortex neuromaturation functionalism
methodology for study of 224–225, and 239–241 on behavior assessment 378–379
229–231 prevention strategies for 435–436 convergence and divergence with
overview of processes in 222–224 resilience against 91 constructionism 6–8
stress and 106, 107 respiratory sinus arrhythmia and critiques of 5–8
temperament and 86 156–160 on emotion dysregulation 4, 101–103,
epigenome-wide association studies trait impulsivity and 87, 89, 238–240, 110, 348
(EWASs) 224, 225, 229, 230 242–243 evolutionary 2–3, 6–8
equifinality 19, 429 treatments for 430–437 locationist basic emotion perspective
error-related negativity (ERN) 193 of 7
ERS (Emotion Reactivity Scale) 398 F on relational processes of emotion
escape model of binge eating/bulimia face-to-face still-face paradigm 54, 60
nervosa 328 385–386 situational 478–479
essentialism 185 facial expressions variant uses of term 2–4
event-related potentials (ERPs) 168, 176, amygdala in perception of 186–187 functional magnetic resonance
193. See also late positive potentials deficits in processing 283, 304, 446 imaging (fMRI)
evolution emotion transmission through 144 addiction and 317, 319
of brain 186 evolutionary role of 141 advantages of 184
conservation of emotion across 15, 16 mood states influenced by 448 amygdala habituation to emotional
facial expressions and 141 of negative emotion 63, 85 stimuli in 209
innate processes and 29, 30 in somatic marker hypothesis 30 in behavioral observation 430
natural selection in 6 family. See also children and adolescents; history of neural studies with 6
of social behavior 155 parent–child interactions internalizing spectrum disorders
teleological misconceptions of 5, 6 appraisal processes influenced by 102 and 255, 256
evolutionary functionalism 2–3, 6–8 in emotional socialization processes 61, limitations of 7
EWASs (epigenome-wide association 117, 479–480 mechanisms of 184
studies) 224, 225, 229, 230 emotion dysregulation influenced by on neural activation changes following
executive functioning 103–104, 479–480 DBT 470–472
brain regions related to 4, 192, 431 in genetic studies of emotion overmodulation and 271
defined 45 regulation 204–206, 212 functional neuroimaging 19, 21, 184
emotion regulation and 72 internalizing spectrum disorders and functional polymorphisms 208
environmental influences on 241 251–253, 444
in overriding motivational marital conflict within 101, 104 G
tendencies 19 Family Stress Model 101, 104 Gable, S. L. 414
in psychosis spectrum disorders 300, Fani, N. 265 GAD (generalized anxiety disorder) 89,
305 Fast Track program 436 156, 173, 192–193, 256, 285
respiratory sinus arrhythmia and 155, fear conditioning 43, 186 Garland, Eric L. 313, 316
156 Feldman, R. 105, 149 GCTA (genome-wide complex trait
in theory of constructed emotion felt security 31, 34 analysis) 207t, 211–212
190–191 females. See gender differences GEDM (General Emotion Dysregulation
trauma exposure and 268 Fields-Olivieri, Margaret A. 53 Measure) 397–398
experience sampling 56, 58, 306, 353, Filene, J. H. 123 gender differences
412–413, 448 Filipp, S. H. 148 in anxiety disorders 92, 443
experimental research 105, 145, 335–339, Fischer, S. 332 in depression 92, 443
419 Fitzgerald, J. M. 174 in eating disorders 327
exposure therapy 173, 449 5-HTTLPR. See serotonin transporter- in interaction models 119
The Expression of the Emotions in Man linked polymorphism in internalizing and externalizing
and Animals (Darwin) 141 FKBP5 gene 209, 229, 269 disorders 92, 291
expressive suppression 40, 73–75, 78, flashbulb memories 43 in schizophrenia 299
133, 301 fMRI. See functional magnetic resonance socialization and 92
externalizing spectrum disorders 237–244. imaging in supportive interactions 148
See also specific conditions Forbes, Courtney N. 395 in treatment strategies 436–437
behavioral assessments of 429–430 Forest, M. 230 Gene–Environment interaction
characteristics of 427–428 Fox, D. 147 theory 363
context-inappropriate emotion in 57 Fraga, M. F. 230 General Emotion Dysregulation Measure
developmental perspective on 429 Franklin, J. C. 352 (GEDM) 397–398
dopamine pathway and 227–228 French, L. 211 generalized anxiety disorder (GAD) 89,
duration of emotion in 59 Fresco, D. M. 446 156, 173, 192–193, 256, 285
environmental influences on 241–243 Frewen, P. A. 271 genes, defined 208
494 index
genetic influences 203–214. See also Haynos, A. F. 329, 331, 334 functional connectivity deficits and 4
epigenetics; molecular genetics heart rate variability. See respiratory prefrontal cortex development and 156,
on autism 289–290 sinus arrhythmia 240
differential susceptibility and 108, 109 Heleniak, C. 274 trait impulsivity and 85, 87, 89
DNA methylation and 230–231 Heller, A. S. 135 Incredible Years program 121, 431, 432
on emotional modulation of LPPs 168 Hellhammer, D. H. 148 infant cry, emotion transmission
on externalizing spectrum disorders 90, Hendler, T. 149 through 143–144
142–143, 206 heritability. See genetic influences inferior frontal gyrus (IFG) 4, 91, 192,
future research directions 206, 212–214 Herman, J. L. 267 256, 271, 320
in intergenerational transmission of Herpertz, S. C. 471 informal exposure strategies 469
emotion dysregulation 143, 221 hidden regulators 31 information processing biases 378, 449
on internalizing spectrum disorders 90, Hierarchical Taxonomy of Psychopathology insular cortex 4, 20, 91
142–143, 205, 206, 257–258 (HiTOP) initiative 306 integrative body–mind training 435
at intrapersonal level of emotion 89–90 hippocampus integrative cognitive-affective therapy
on psychosis spectrum disorders activation across anxiety 189 (ICAT) 331
299–300, 306 in addiction 320 interaction models 116, 119–120
temperament and 85 amygdala influences on 43 internalizing spectrum disorders
twin studies on 204–206, 212, glucocorticoid receptors in 228 249–260. See also specific conditions
230–231, 269, 290, 415 in internalizing spectrum disorders 256 affective neuroscience on 255–256
genome-wide association studies septo-hippocampal system 3, 6, 90, 349 characteristics of 445
(GWASs) 207t, 210–211, 214 histone modification 208, 222, 223 developmental perspective on 251–253,
genome-wide complex trait analysis Hofer, Myron 31 259
(GCTA) 207t, 211–212 Hofmann, S. G. 448 in DSM-5 251, 445
genomic imprinting 222–223 Hogendoorn, S. M. 449 duration of emotion in 59
genotypes 29, 90, 208, 253, 257, 289 Holliday, Robin 224 economic burden of 443
Gibson, E. L. 414 Holmes, A. 170 emotion socialization and 104, 257
Giorda, R. 226 Holzman, J. B. 156 epigenetics and 258, 259
glucocorticoid receptor genes 31–33, 107, homeostasis family influences on 251–253, 444
224–225, 228–229, 258, 269 defined 15 first-order syndromes 238
goal-corrected behavioral systems 31 hedonic 316 functional connectivity deficits and 4, 91
Goldstein, R. Z. 169–170 as innate process 30 gender differences in 92, 291
Good, G. E. 429 motivated behavior and 15, 17 genetic influences on 90, 142–143,
Goodman, M. 471–472 regulation of 28, 32, 34f, 86, 190 205, 206, 257–258
Gottman, J. M. 105, 145, 453, 457 Hope, Nora H. 463 late positive potentials and 172
Gratz, Kim L. 120, 329, 348, 354, 395, Horowitz, M. J. 270 methodology for study of 253–254
396, 400, 403, 411, 446 Horvath, Sarah A. 327 overview 249–251
Gray, J. A. 90–91, 272, 414 Hostinar, Camelia E. 249 peer influences on 253
Gross, James J. 33, 59, 73, 87–88, 127, Houben, M. 353 psychophysiology and 256–257
141, 203–204, 378, 446–449, 478 Hubbard, J. A. 386 regulatory strategies and 254
Grosse, M. 331 Hunkele, K. 319 resilience against 91, 259–260
Gruber, J. 307 Hunter, J. 413, 414 respiratory sinus arrhythmia and
GWASs (genome-wide association Huntington’s disease 222 156–160
studies) 207t, 210–211, 214 hypothalamic-pituitary-adrenal (HPA) trait anxiety and 87, 89
axis 209, 210, 225, 256–258, treatments for 444, 448–458
H 287–288 International Classification of Diseases-11
Haedt-Matt, A. A. 333 hypothalamus 16, 191, 225, 228 (ICD-11) 266, 267, 270, 273
Hahn, Hunter 477 interpersonal levels of emotion 92–93
Haines, Nathaniel 1 I interpersonal processes 141–149.
Hajcak, Greg 167, 169–170 ICAT (integrative cognitive-affective See also parent–child interactions
Halberstadt, A. G. 446 therapy) 331 affiliative bonds and 142–143, 145–149
Haliczer, Lauren A. 361 ICD-11 (International Classification of age-related changes in 77
hallucinations 300, 305 Diseases-11) 266, 267, 270, 273 behavioral observation of 61
Ham, J. 105 identification stage of emotion borderline personality disorder and 363
Hamer, M. 414 regulation 88, 130–131, 131f, 134 in coregulation 88, 350, 444, 448
Harlow, H. F. 28, 141 IFG (inferior frontal gyrus) 4, 91, 192, cultural influences on 93
Harrison, A. 331 256, 271, 320 dyadic interactions 92–93
Hatzenbuehler, M. L. 481 illness, partner support during 147 in emotion transmission 143–145
Havighurst, Sophie S. 122, 443 implementation stage of emotion future research directions 149
Hawes, D. J. 104 regulation 88, 131, 131f, 135 maladaptive 183
Hawkins, R. C. 328 impulse control. See also addiction overview 141–142
Hawkley, L. 69–70 in borderline personality disorder 429 regulatory strategies and 55
Hawn, Sage E. 203 dialectical behavioral therapy for 434 in romantic relationships 145–148
Hayes, S. C. 452 eating disorders and 330 in socioemotional development 142
index 495
intimate partner violence 57, 107, depression 171–173 Maiti, A. K. 154
144–146, 429 distraction and 177 major depressive disorder. See depression
intrapersonal levels of emotion 89–92 duration of 168–169 males. See gender differences
invalidating environment model 117–118, eating disorders and 175–176 maltreatment. See childhood maltreatment
122–123, 363, 466 emotional modulation of 168–171, 175 mania 53, 134, 156, 227. See also bipolar
irreverence therapy style 470 future research directions 175–177 disorder
memory and 170, 176 Maniaci, M. R. 148
J posttraumatic stress disorder and Martin, Christina Gamache 115
Jazaieri, Hooria 127, 378 173–174 MASC (Multidimensional Anxiety
Jenness, J. L. 274 potentiation by stimuli 168, 169f Scale for Children) 290–291
Johansen, E. B. 238–239 substance use disorders and 174–175 Mattson, Whitney I. 13
Johnson, A. M. 104 suicidal ideation and 172 Maxwell, S. E. 214
lateral paralimbic group 191, 195n4 Mazefsky, C. A. 286
K Latzman, R. D. 120 McCauley, E. 274
Kadosh, K. C. 29 Lavender, J. M. 329, 330, 333 McGlone, F. P. 170
Kaliush, Parisa R. 85 LD (linkage disequilibrium) 207t, 211 McHugh, R. K. 317
Kaminski, J. W. 123 learned helplessness 134 McLaughlin, K. A. 274
Kämmerer, A. 331 learning. See also operant reinforcement McMain, S. F. 474
Kanakam, N. 205 associative 3, 4, 227 McRae, A. F. 230–231
Karmiloff-Smith, A. 29 defined 15 McRae, Kateri 39
Karnik, Niranjan S. 427 emotion as learning signal 30, 31 Meaney, M. J. 224
Kaufman, Erin A. 345 motivated behavior and 17 medial PFC group 191–192
Kaye, K. 385 observational 252 medial posterior group 191–192
Kayser, J. 171 social 100, 259, 449 memory
Keane, S. P. 120 LeDoux, J. 30, 448 age-related changes in 78
Keel, P. K. 333 Lee, S. H. 212 autobiographical 46, 170, 176, 192,
Kehoe, Christiane 443 Leshin, Joseph C. 183 412, 420
Keller, M. C. 212 Leve, C. 386–387 defined 15
Kendler, K. S. 206 Levenson, R. W. 105, 145 emotion-enhanced 43
Kensinger, E. A. 72–73 LiKamWa, R. 420 late positive potentials and 170, 176
Kerig, Patricia K. 265, 271, 275 limbic-hypothalamic-pituitary-adrenal mood-congruent 43–44
Khaled, Mona 141 (L-HPA) axis motivated behavior and 17
Kiel, E. J. 120 autism and 287 in psychosis spectrum disorders 303,
Kieras, J. 385 dysfunction of 228, 287 305
Kim, H. 90 epigenetic bases of functioning working 45–46, 78, 169, 241, 268, 300
Kim, J. 274 228–229 men. See gender differences
Kirschbaum, C. 148 glucocorticoid receptor and 224 Mence, M. 104
Klauer, T. 148 hyperresponsivity of 269 Mendelson, T. 436
Kleiman, E. M. 416 measurement of functioning 110 Menin, D. S. 446
Knutson, N. M. 242 physiological synchrony and 105 Merwin, R. M. 331
Kober, H. 192 stress and 106–107, 144–145, 228, 268 mesolimbic system 14, 87, 90, 227,
Kohlhoff, J. 104 trauma-related effects on 265, 275–276 239, 349
Kostaras, D. 147 Lindquist, Kristen A. 183 meta-emotion philosophy (MEP) 454,
Kostaras, X. 147 Linehan, Marsha M. 117, 129, 176, 349, 455
Kovacs, M. 104 363, 429, 432, 464, 466 methamphetamine 313, 314, 319, 320
Krause, E. D. 147 linkage disequilibrium (LD) 207t, 211 Miller, D. J. 413
Kring, A. M. 307 Links, P. S. 416 Miller, M. A. 414
Kumpula, M. J. 274 Liu, Y. 420 mind–brain correspondence 189
Kuppens, P. 213 Livesley, W. J. 396 mindfulness-based interventions 321,
load sharing 32–33 432–438, 450, 456, 480–481
L Lobo, I. 174 mirror tracing persistence task
Ladouceur, C. D. 119 locationist basic emotion perspective 7 (MTPT) 388
Lane, N. D. 420 Lonsdorf, T. B. 209 Misri, S. 147
Lane, R. D. 155 LPPs. See late positive potentials modal model of emotion 41
Lanius, R. A. 271 Lynam, D. R. 413 Modrowski, C. 275
late positive potentials (LPPs) 168–177 Lynch, T. R. 147, 470 modularity hypothesis 29
affective chronometry and 176 molecular genetics
anxiety disorders and 173 M emotion regulation studies in
attention and 169, 170, 170f MacDonald, D. E. 331 208–212, 257
borderline personality disorder and 176 Mackler, J. S. 120 methodology for study of 206, 207t,
cognitive reappraisal and 169–170, MacLean, P. D. 185–186 208–211
170f, 172–176 MacNamara, A. 169–170, 173, 174 overview 207–208
cultural influences on 93 main-effects models 118–121, 124, 352 specific gene variants in 206, 208
496 index
monitoring stage of emotion regulation Nelson, Eric E. 13 theoretical perspectives on 117–118
88, 131–132, 131f, 136 Nelson-Gray, R. O. 434 transactional models and 117, 120–121,
Montirosso, R. 226 nervous system. See specific branches 123
mood-congruent memory 43–44 Neuhaus, Emily 283 opioids 313–318, 351
mood disorders. See also specific conditions neuroconstructivism 29 opposite action strategy 467–468
autism and 285 neurodevelopment 29, 35, 239–241, 285, oppositional defiant disorder (ODD)
emotion dysregulation and 47 292, 349 characteristics of 428
family influences on 251 neuroimaging. See also affective developmental pathway to 238, 241
predictive factors 19 neuroscience; functional magnetic dopaminergic function and 227
regulatory strategies and 136 resonance imaging environmental influences on 242
serotonergic function and 225 addiction and 317 gender differences and 92
treatments for 450–451 age-related changes and 70 risk factors for 89
mood vs. emotion 33, 445, 447–478 autism and 288–289 treatments for 431, 434
Moore, K. E. 435 on cognitive reappraisal 42 orbitofrontal cortex (OFC)
Moore, S. A. 120 cortical subdivisions identified by 4 in addiction 318
Morie, K. 319 defined 184 age-related changes in use of 72, 73
Morningstar, Michele A. 13 emotion-specific patterns in 20 in borderline personality disorder 366
morphological systems 30–33, 34f functional 19, 21, 184 childhood abuse and 241
Morris, A. S. 118 psychosis spectrum disorders and 302, in cognitive control 72, 73
motivated behavior 13–22 304 conduct disorder and 240, 241f
attention and 17 neuroticism 41, 192, 205–208, 304, in emotion regulation 91
controversies regarding 20–21 338, 413 impulsivity inhibition by 240
defined 14 neurotransmitter systems 225–228, 267. in lateral paralimbic group 191
development and 18 See also specific neurotransmitters in motivated behavior 17
emotion and 14, 20, 21 neurovisceral integration theory in reappraisal of negative emotion 4
future research directions 21–22 (NIT) 155 in reward pathway 315, 317
homeostasis and 15, 17 Nicholson, A. A. 271 in self-regulation 349
learning and 17 nicotine use. See cigarettes Orcutt, H. K. 274
maladaptive 18–19, 21–22 Niedtfeld, I. 472 overmodulation of emotion 270–272,
memory and 17 Nieuwenhuis, S. 169 275, 276
methods for study of 19–20 NIMH (National Institute of Mental Overstreet, Cassie 203
overview 13–14 Health) 53–54, 212, 255, 306 oxytocin receptor (OXTR) gene 33,
in Pankseppian model 15, 16 Nock, M. K. 352, 417 90, 209
social behavior and 17–18 Nolen-Hoeksema, S. 332, 436
MTPT (mirror tracing persistence nonfunctional polymorphisms 208 P
task) 388 nonsuicidal self-injury. See self-inflicted paced auditory serial addition task
Muehlenkamp, J. J. 352–354 injury (PASAT) 336, 388
Multidimensional Anxiety Scale for Nugent, N. R. 352–353 Pachankis, J. E. 481
Children (MASC) 290–291 Pagliaccio, D. 209
multifinality 267, 429 O pain-offset relief hypothesis 351
multiple levels of analysis Oberlander, T. F. 224 panic disorder 134, 156, 157, 256
advancements in 348, 480 Obradović, J. 120 Panksepp, Jaak 8, 13, 15–17, 20, 21,
for age-related changes 80 O’Brien, Jacqueline 115 86–87, 91
in behavioral assessments 63, 380 observational learning 252 paranoia 303, 305, 361
in developmental processes 86, 94 observational research. See behavioral parasympathetic nervous system (PNS).
for endophenotypes 212 observation See also respiratory sinus arrhythmia
importance of 479 obsessive-compulsive disorder activation in DBT 469
interpersonal 92–93 (OCD) 156, 173, 193, 285 addiction and 316
intrapersonal 89–92 ODD. See oppositional defiant disorder autism and 287
Multisystemic Therapy 430 OFC. See orbitofrontal cortex phylogenetic account of 155, 157
multivariate pattern-based analyses Oland, A. A. 104 physiological synchrony of 259
(MVPA) 187 older adults. See aging in stress response 272, 448
mutuality in romantic relationships 147 On the Origin of Species (Darwin) 6 withdrawal to unthreatening social
ontogenic process perspective 238, 242, stimuli 157
N 243f paraventricular nucleus 4, 228
Nanney, D. L. 224 operant reinforcement 115–124 parent–child interactions. See also emotion
National Institute of Mental Health clinical interventions for 121–123 socialization
(NIMH) 53–54, 212, 255, 306 future research directions 123–124 affiliative bonds and 142–143
naturalistic observation 380, 385 interaction models and 116, 119–120 aversive 104, 117, 119, 120
natural selection 6 main-effects models and 118–120 behavioral observation of 57–59,
negative symptoms 300, 301 measurement tools 116–117 61–62
negative urgency 332, 335, 338, 339, in parent–child interactions 115–116 clinical interventions for 121–123
417, 420 replication across lifespan 116 coercion theory and 117, 121
index 497
parent–child interactions (Continued ) phobias 156, 173, 285 in cognitive control 72, 73, 185,
differential susceptibility and 108, 110 physical touch, emotion transmission 255–256
disorganized attachments 32, 100–101, through 143 in cognitive reappraisal 42
108, 252, 363 physiological hyperreactivity in emotion regulation 91, 137
emotion transmission in 143–145 hypothesis 144 impulsivity inhibition by 240
insecure attachments 100, 120, 144, physiological stress 143–145, 148, 149 in internalizing spectrum disorders 256
252 physiological synchrony (PS) 104–106, medial PFC group 191–192
interaction models for 116, 119–120 109, 110, 259 motivated behavior and 14
in invalidating environment 117–118, Plomin, R. 211 neuromaturation of 42, 88, 239–241
122–123 PMT (parent management training) in reappraisal of negative emotion 4
main-effects models for 118–120 432–434, 437, 480–481 respiratory sinus arrhythmia and
operant reinforcement in 115–124 PNS. See parasympathetic nervous system 155–156
physiological synchrony and 105–106 polygenic risk score (PRS) 207t, 211, 304, in reward pathway 315
self-regulation and 349–350, 433, 480 306 in self-regulation 349
in socioemotional development 350 polymorphisms trait anxiety and 87
transactional models for 117, 120–121, in candidate gene studies 208–210 process model of emotion regulation
123 defined 208 129–137
traumatic events and 269–270 DRD4 gene 109, 227–228 future research directions 136–137
parenting interventions 121, 431–434, 5-HTTLPR 90, 120, 208–209, regulatory strategies in 40, 132–133,
444–445, 452–458, 480–481 226–227, 257, 289 204, 362, 447
parent management training (PMT) FKBP5 gene 209, 229, 269 stages of regulation in 88, 130–136,
432–434, 437, 480–481 functional 208 131f
Paris, J. 474 nonfunctional 208 valuation system within 129–130, 130f
Parsons, J. T. 481 single nucleotide 208–211, 222, Promoting Alternative THinking
Parvaz, M. A. 169–170 223f, 231 Strategies (PATHS) program 436
PASAT (paced auditory serial addition polyvagal theory 155, 291 prospect theory 44
task) 336, 388 population stratification 210 Provenzi, L. 226
PATHS (Promoting Alternative THinking Porges, S. W. 154–155, 291 PRS (polygenic risk score) 207t, 211,
Strategies) program 436 positive reappraisal 74, 79 304, 306
Patterson, G. R. 117, 242 positive symptoms 300, 301 PS (physiological synchrony) 104–106,
Paul, S. 173 Posner, M. I. 385 109, 110, 259
Pavlovian bias 5 postpartum depression 147, 149 PSDs. See psychosis spectrum disorders
peers posttraumatic stress disorder (PTSD) psychoanalytic theory 203, 455
deviant affiliations 241, 242 amygdala activation in 188 psychological constructionism 188,
emotional responses to acceptance by 18 biopsychosocial processes in 268–270 189, 191
internalizing spectrum disorders borderline personality disorder and 367 psychological flexibility 133, 451–452
and 253 brain regions related to 193 psychopathology. See also emotion
operant reinforcement and 116 clinical interventions for 122 dysregulation; specific conditions
in reinforcement of gender-specific complex 267 aging and 78–79
processes 92 dissociation and 267, 271 brain regions related to 20
rejection by 253, 274 in DSM-5 195n2, 267, 270 classification of 237
social difficulties with 241 emotion dysregulation and 274–275 cognition and 136–137
periaqueductal gray 20, 191, 271 FKBP5 gene expression in 229, 269 developmental perspective on 86, 87,
peripheral nervous system 15, 28, 190, functional connectivity deficits and 188 89, 257
191, 257 in ICD-11 267, 270, 273 diagnostic criteria for 71, 127
Perry, N. B. 120 late positive potentials and 173–174 duration of emotion and 59
personality disorders. See specific disorders respiratory sinus arrhythmia and 156, emotional lability and 58, 59, 397
Perth Emotional Reactivity Scale 269 externalizing (see externalizing spectrum
(PERS) 398–399 symptoms of 173–174, 267 disorders)
PFC. See prefrontal cortex theoretical models of emotion factor analysis of symptoms 237–238
phasic dysregulation model 270 dysregulation in 270–273 gender-specific trajectories 92
phenotypes treatments for 276, 469 genetics (see genetic influences)
behavioral 29, 224 vulnerability to 269–270, 274 Hierarchical Taxonomy of
defined 204 Potenza, M. N. 319 Psychopathology initiative 306
differential susceptibility factors Pots, W. T. M. 452 internalizing (see internalizing spectrum
and 108 Powers, A. 265 disorders)
DNA methylation 231 Prader-Willi syndrome 223 late positive potentials and 171–175
of early-onset depression 172 Prakash, Ruchika Shaurya 69 psychosis (see psychosis spectrum
endophenotypes 32, 212, 214, 239, 415 prefrontal cortex (PFC) disorders)
environmental influences on 206 in addiction 318, 320 recovery from 41
genetic-related variances 29, 204–208 age-related changes in use of 72, 73 respiratory sinus arrhythmia and
infant 89 in borderline personality disorder 155–161, 257, 269
rise of 222, 224 365, 366 theoretical models for 153–154
498 index
psychophysiology. See also event-related internalizing spectrum disorders psychopathology and 155–161, 257, 269
potentials; respiratory sinus and 254 in psychophysiological assessments 412
arrhythmia maladaptive use of 135, 254, 362, quantification of 154, 155f, 159–160,
autism and 287–288 368–370, 447 160f
behavioral observation of 61 in process model 40, 132–133, 204, self-inflicted injury and 158, 257, 351
childhood trauma and 272, 276 362, 447 social and developmental influences
cognitive reappraisal and 41 in psychosis spectrum disorders on 156–158
eating disorders and 336–337 301–302, 305–306 task selection and 158–159
ecological momentary assessment response-focused 73, 88, 301, 447, 448 theoretical models for 154–156
and 414 response modulation 73, 132, 133, 447 response-focused regulatory strategies 73,
hyperreactivity to children’s distress situation modification 40, 73, 132–133, 88, 301, 447, 448
and 144 447 response modulation 73, 132, 133, 447
internalizing spectrum disorders situation selection 40, 73–74, 132, 135, reward pathway 227, 315–317
and 256–257 136, 447 ribonucleic acid (RNA) 208, 222, 223
measurement guidelines in 160 spontaneous use of 60, 368 Richmond, Julia R. 395
psychosis spectrum disorders stopping 136 Richter, Curt 17
(PSDs) 299–307. See also specific switching 45, 46, 132, 136 Riggs, Arthur 224
conditions Reis, H. T. 148, 414 Rini, C. 147
cognitive deficits in 304–305 Reitz, S. 470 rise time to peak metric 176
in DSM-5 299, 306 relationships 99–110. See also family; risk-as-feeling hypothesis 44
emotion abnormalities in 300–304 parent–child interactions; peers risk distribution 32–33
future research directions 307 age-related changes in 77, 99 Roemer, L. 329, 348, 354, 396, 400,
genetic influences on 299–300, 306 in attachment theory 32, 100–101 411, 446
methodology for study of 306 differential susceptibility and 108–110 Rogge, R. D. 148
neuroimaging studies of 302, 304 dyadic interactions and 92–93, ROI (region-of-interest) analysis 6, 189
prevalence of 299 145–148 romantic relationships 40, 116, 145–148
regulatory strategy use in 301–302, in functionalist emotions theory 93, Rothbart, M. K. 385
305–306 101–103 Rottenberg, J. 171
symptom dimensions of 300, 302–306 future research directions 109–110 Rowsell, M. 331
treatments for 307 as hidden regulators 31 RSA. See respiratory sinus arrhythmia
psychotropic medications 272, 367 physiological synchrony and 104–106, rumination
PTSD. See posttraumatic stress disorder 109, 110 borderline personality disorder and 369
romantic 40, 116, 145–148 childhood maltreatment and 251
R stress neurobiology and 106–107, defined 41, 302
Racine, Sarah E. 327, 330, 331 109, 110 eating disorders and 332, 334
Rains, J. C. 452 Rendina, H. J. 481 effectiveness of 133
Rajappa, K. 354 Repetti, R. 145, 146 as emotion misregulation 47
Ramsey, E. 117 Research Domain Criteria (RDoC) functionalist view of 102
Ramsook, K. Ashana 53 53–54, 212, 255, 306, 479, 481 older adults and 78
Rappaport, Lance M. 203 resilience psychosis spectrum disorders and 302,
Rasmussen, A. M. 268 in aftermath of trauma 275 305–306
rationalization strategy 447 in developmental perspective 86 Russell, V. A. 238–239
Raz, G. 192 promotion of 259–260
RDoC (Research Domain Criteria) respiratory sinus arrhythmia and 91, S
53–54, 212, 255, 306, 479, 481 156 Saarni, C. 446
reappraisal. See cognitive reappraisal social mechanisms of 94 Safren, S. A. 481
recall bias 333, 418 respiratory sinus arrhythmia (RSA) Sagvolden, T. 238–239
reciprocity therapy style 469–470 153–161 salience network (SN) 5–6, 187–188,
recovery time metric 176 addiction and 316 191–194, 256
region-of-interest (ROI) analysis 6, 189 age-related changes in 161n2 Satpute, A. 5–6
regulatory strategies. See also cognitive autism and 287, 291 SAVI (strength and vulnerability
reappraisal; distraction; in behavioral observation 430 integration theory) 70–71, 79
self-regulation; suppression defined 91, 154, 350, 479 Saxbe, Darby 141, 145, 146
age-related changes in use of 71, 73–76 differential susceptibility and 108–109 SBT (social baseline theory) 32–33
antecedent-focused 73, 88, 301, 447, emotional lability and 116 Schachter, S. 86
448, 455 in interaction models 119 Schatten, Heather T. 411
attentional deployment 40, 73, measurement issues related to Schauer, M. 272
132–133, 135, 302, 447 160–161 Schilling, E. A. 413
behavioral observation of 55, 59–60 methodological considerations in schizophrenia
cognitive change 40–42, 73, 132, 133, study of 158–161 cognitive deficits in 304–305
301–302, 447 neural substrates of 155–156 dopaminergic function and 227
coregulation 88, 350, 444, 448 overview 153–154 emotion abnormalities in 300, 301, 303
ineffectiveness of 60, 135 physiological synchrony and 105–106 gender differences in 299
index 499
schizophrenia (Continued ) loss through trauma 268 SOC-ER (selection, optimization, and
genetic influences on 299–300 neurological influences on 91, 156 compensation with emotion
methodology for study of 306 parent–child interactions and 349–350, regulation) framework 70, 71, 79
polygenic risk for 211 433, 480 social anxiety disorder 136, 173, 188,
regulatory strategy use in 305 reward pathway and 315–316 193, 285
respiratory sinus arrhythmia and 156 self-regulation shift theory (SRST) 273 social baseline theory (SBT) 32–33
salience network dysregulation in 193 self-report assessments 395–404. social behavior
symptom dimensions of 300, 303–305 See also specific assessments antisocial behavior 238–242, 436
schizotypal personality disorder 305 advantages of 56, 167, 395 defined 15
Schnell, K. 471 age considerations for 116, 253, 379 elicitation of prosocial behavior 2
Schreurs, K. M. G. 452 autism and 290, 292 emotion as regulator of 27–35
Schröder-Abé, M. 146 eating disorders and 329–332 evolution of 155
Schwarz, N. 30 future research directions 403–404 motivated behavior and 17–18
Schweizer, S. 332 in genetic studies 205, 213 social-ecological niche 28, 32–33
Selby, E. A. 334, 419 limitations of 74, 377–378, 395–396, socialization
selection, optimization, and compensation 412 emotion (see emotion socialization)
with emotion regulation (SOC-ER) of maladaptive responses to emotions gender and 92
framework 70, 71, 79 400–402 of RSA reactivity 158
selection stage of emotion regulation 88, overreliance on 275, 438 of stress neurobiology 106–107, 109
131, 131f, 134–135 parent–child interactions and 117, 119, social learning 100, 259, 449
selective attention 73 123 socioemotional development
self-care behaviors 451, 455–457 psychosis spectrum disorders and 302 adaptive-basins model on 30–32
self-inflicted injury (SII) 345–355. regulatory strategy use and 72, 75 attachment theory on 31
See also suicide and suicidal ideation of temperamental emotional emotional responding and 453
autism and 286 vulnerability 397–400 emotion regulation and 431
in borderline personality disorder 361, Seligowski, A. V. 274 future research directions 34–35
363, 416, 417, 470–471 separation anxiety disorder 89, 285, 445 heuristic view of 28
categorical conceptualizations of separation distress 31, 34 individual differences in 85–86
346–348 septo-hippocampal system 3, 6, 90, 349 interpersonal processes in 142
by children and adolescents 345–346, serotonin 225–227, 289 parent–child interactions in 350
352 serotonin transporter-linked physiological synchrony in 106
conflict escalation and 58, 119 polymorphism (5-HTTLPR) 90, socioemotional selectivity theory
development perspective on 349–351 120, 208–209, 226–227, 257, 289 (SST) 70, 71, 79
ecological momentary assessment of Shader, Tiffany M. 159, 237 somatic marker hypothesis 30–31, 45
352–354, 416–417 Shalev, A. Y. 266, 268 Speed, Brittany C. 167
emotional interaction patterns and 93 Sharma-Patel, K. 122 SRET (self-referential encoding task) 171,
future research directions 355 Shaw, D. S. 104 172, 176
L-HPA axis dysfunction and 228 Sheeber, L. 386–387 SRST (self-regulation shift theory) 273
methodology for study of 352–354 Shipman, K. L. 270 startle responses 267, 287, 317, 337, 367
moderating and mediating influences Shoji, K. 273 stepped-care treatment models 474
on 353–354 SII. See self-inflicted injury Steptoe, A. 414
motivations for 346, 351 Silk, J. S. 104 stigma 304, 305, 481–482
neurobiological factors associated Singer, J. 86 stimulants 313–314, 319–320
with 470–471 single nucleotide polymorphisms (SNPs) stop codon 208
prevention efforts 354–355 208–211, 222, 223f, 231 STOP skills 451, 467
respiratory sinus arrhythmia and 158, situated conceptualization 5 Stoycos, Sarah A. 141
257, 351 situational functionalism 478–479 strange situation paradigm 120, 252, 385
serotonergic function and 90, 209 situation–attention–appraisal–response strength and vulnerability integration
terminology related to 346, 347t perspective 86, 447 theory (SAVI) 70–71, 79
theoretical perspectives on 348–352 situation modification 40, 73, 132–133, stress. See also posttraumatic
treatments for 450–451 447 stress disorder
self-medication hypothesis 314 situation selection 40, 73–74, 132, 135, age-related changes in 75–76
self-referential biases 171, 172, 176 136, 447 buffers against 101, 143
self-referential encoding task (SRET) 171, Skowron, E. A. 158 cigarette use and 315
172, 176 Skuban, E. M. 104 diathesis-stress model 108, 109
self-regulation Smith, G. T. 332 EMA of response to 413–414
active coaching of 104 smoking. See cigarettes emotion regulation and 55, 75–76
by children and adolescents 56, SN (salience network) 5–6, 187–188, Family Stress Model 101, 104
102–104 191–194, 256 L-HPA axis in response to 228
constructive forms of 100 SNPs (single nucleotide polymorphisms) neurobiology of 106–107, 109, 110,
cortical structures in 4, 186, 349 208–211, 222, 223f, 231 257, 268
environmental influences on 241 SNS. See sympathetic nervous system of overriding motivational
improvement strategies 435 Snyder, J. J. 117 tendencies 19
500 index
physiological effects of 143–145, 148, overreliance on 302, 303 treatment strategies
149 psychosis spectrum disorders and acceptance and commitment
in postpartum period 147 301–302, 305 therapy 401, 451–452
psychotic symptoms related to 306 as PTSD coping strategy 270 CBT (See cognitive-behavioral
of separation distress 31, 34 of thoughts 73–75, 447 therapy)
Trier Social Stress Test 148, 317, 412 Surguladze, S. A. 209 for children and adolescents 432–435,
stress contagion 106, 145, 146 Svaldi, J. 337 449, 480–481
stria terminalis 4, 315 Swart, M. 209 DBT (See dialectical behavioral
Stroop tests 193, 336, 365–366, 402, switching 45, 46, 132, 136 therapy)
411, 436 sympathetic nervous system (SNS) developmental perspective on 431
structured observation 385 activation without emotion 34 emotion-focused therapy
substance use disorders (SUDs) assessment of activity in 105 449–450, 455
brain regions related to 227 autism and 287 exposure therapy 173, 449
dopaminergic function and 227 hyperreactivity in 268 for externalizing behavior
ecological momentary assessment mobilization in response to problems 430–437
of 419–420 threats 157 future research directions 437–438
environmental influences on 242 physiological synchrony of 259 integrative cognitive-affective
late positive potentials and 174–175 psychosis spectrum disorders and 303 therapy 331
maladaptive motivated behavior suppression and 63, 133 for internalizing spectrum
and 21–22 synchrony 142–144, 148–149. disorders 444, 448–458
in older adults 78 See also physiological synchrony mindfulness-based interventions 321,
prefrontal cortex development and 240 432–438, 450, 456, 480–481
respiratory sinus arrhythmia and 156 T Multisystemic Therapy 430
risk factors for 89 Tager, D. 429 parenting interventions 121, 431–434,
trait impulsivity and 239 Tchanturia, K. 331 444–445, 452–458, 480–481
treatments for 452 teleological explanations 3, 5, 6 special considerations for 436–437
suicide and suicidal ideation temperamental emotional stepped-care models 474
autism and 283, 285 vulnerability 363, 397–400 transdiagnostic 473–474, 481
behavioral observation and 63 Thayer, J. F. 155 Trickey, D. 269
borderline personality disorder theory of constructed emotion (TCE) 5, Trier Social Stress Test 148, 317, 412
and 361, 416 183–184, 189–194 triune brain concept 185–186
depression and 79, 172 Thiruchselvam, R. 177 Trompetter, H. R. 452
ecological momentary assessment Thompson, M. 271 Tronick, E. 105
of 416 Thompson, Ross A. 58, 99, 101, 478 Trupin, Eric 434–435
late positive potentials and 172 Thorp, S. R. 147 tryptophan hydroxylase-2 (TPH2)
L-HPA axis dysfunction and 228 thought suppression 73–75, 447 gene 209
serotonergic function and 90, 225, TIK (Tuning into Kids) program 122, Tull, Matthew T. 120, 395
226 444–445, 453–458 Tuning into Kids (TIK) program 122,
suicide and 283 TIP skills 451, 469 444–445, 453–458
treatments for 450–451 tobacco use. See cigarettes Tuschen-Caffier, B. 337
Sunderland, M. 456 touch, emotion transmission twin studies 204–206, 212, 230–231,
support through 143 269, 290, 415
behaviors related to 148 TPH2 (tryptophan hydroxylase-2)
during illness 147 gene 209 U
mobilization of 102, 291 trait anxiety 45, 78, 85–90, 192–193 Uhlmann, A. 320
parental 101–107, 117–122, 270 trait impulsivity 85–89, 238–243, 451 undermodulation of emotion 270–272,
in romantic relationships 145–148 Tranel, D. 69–70 275, 276
for self-inflicted injury prevention 354 transactional models 117, 120–121, 123, unified protocol (UP) treatment 473, 481
self-regulatory 106, 350 329 Uusberg, Andero 127
in transition to parenthood 147–148 transcription 208, 222, 269 Uusberg, Helen 127
suppression translational research 276, 301, 307,
addiction and 318, 319 472–474 V
age-related changes in use of 74–75 trauma Vachon, D. D. 413
borderline personality disorder childhood (see childhood trauma) vagal tone. See respiratory sinus
and 369 conceptualizations of 266–268, 272 arrhythmia
brain regions related to 302, 318 Developmental Trauma Disorder Valle, L. A. 123
cultural influences on 93 proposal 272–273 van der Kolk, B. A. 268
defined 74, 254, 301 evidence-based treatments for 122 van der Oord, S. 434
eating disorders and 332 late positive potentials and 173–174 Vander Stoep, A. 274
expressive 40, 73–75, 78, 133, 301 physiological effects of 265 Van Kleef, G. A. 31
functionalist view of 102 PTSD (See posttraumatic stress Vansteelandt, K. 417
genetic influences on 41 disorder) variable number tandem repeats
observability of 63 Treasure, J. 331 (VNTRs) 208
index 501
Vater, A. 146 W working memory 45–46, 78, 169, 241,
ventral striatum Wallace, Gemma T. 299 268, 300
components of 90 Walton, E. 230
in core limbic group 191 Wardle, J. 414 Y
motivated behavior and 14, 16 Waters, Sara F. 99, 105–106 Yap, M. B. 119
in reward pathway 227 Webster-Stratton, Carolyn H. 121, 431 Yates, T. M. 120
trait impulsivity and 239 Weinberg, A. 172, 205 Yehuda, R. 229
upregulation of responses in 318 Weisman, O. 143 Yerkes-Dodson Law 130
ventral tegmental area (VTA) 3, 6, 16, 20, West, J. 435
90, 227–228, 315 Wheeless, Linnie E. 395 Z
video-recall procedures 378, White, S. W. 286 Zajonc, R. B. 27
386–387 Whitmoyer, Patrick 69 Zalewski, Maureen 115, 118
violence. See childhood abuse; intimate Wichers, M. 415 Zarolia, Paree 39
partner violence Wildes, J. E. 330, 331 Zettle, R. D. 452
Vlisides-Henry, Robert D. 85 Winiarski, Dominika A. 427, 436 Zhang, L. 30
VNTRs (variable number tandem Winnicott, D. W. 100 Zhong, L. 420
repeats) 208 Wolz, I. 330 Zisner, A. 87, 89–90
Vohs, K. D. 30 women. See gender differences Zwi, M. 431
502 index

(Oxford Library of Psychology) Theodore P. Beauchaine, Sheila E. Crowell - The Oxford Handbook of Emotion Dysregulation-Oxford University Press (2020)

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

(Oxford Library of Psychology) Theodore P. Beauchaine, Sheila E. Crowell - The Oxford Handbook of Emotion Dysregulation-Oxford University Press (2020)

Uploaded by

Copyright:

Available Formats

The Oxford Handbook of Emotion Dysregulation

Oxford Library of Psychology

Methods and Measurement

Personality and Social Psychology

The Oxford Handbook

Published in the United States of America by Oxford University Press

© Oxford University Press 2020

All rights reserved. No part of this publication may be reproduced, stored in

You must not circulate this work in any other form

Library of Congress Cataloging-in-Publication Data

Molly Adrian, PhD Patricia A. Brennan, PhD

About the Editors vii

Theodore P. Beauchaine, PhD, earned his undergraduate degree in ­psychology

1. Functionalist and Constructionist Perspectives on Emotion

xiv Table of Contents

Two theoretical perspectives—functionalism and constructionism—predominate modern research on

Keywords: constructionism, emotion, emotion dysregulation, functionalism, psychopathology

Introduction editing this volume, Sheila Crowell and I (TPB)

2 Functionalist and Constructionist Perspectives

Beauchaine and Haines 3

4 Functionalist and Constructionist Perspectives

Beauchaine and Haines 5

6 Functionalist and Constructionist Perspectives

Beauchaine and Haines 7

8 Functionalist and Constructionist Perspectives

Beauchaine and Haines 9

10 Functionalist and Constructionist Perspectives

Beauchaine and Haines 11

Eric E. Nelson, Michele A. Morningstar, and Whitney I. Mattson

Keywords: affect, neuroscience, psychopathology, bottom-up, translational

This chapter is dedicated to Jaak Panksepp (1943–2017), a mentor, scholar, and

Introduction attention, facilitate memory, and guide decision

14 Emotions as Regul ators of Motivated Behavior

Nelson, Morningstar, and Mat tson 15

16 Emotions as Regul ators of Motivated Behavior

Nelson, Morningstar, and Mat tson 17

18 Emotions as Regul ators of Motivated Behavior

Nelson, Morningstar, and Mat tson 19

20 Emotions as Regul ators of Motivated Behavior

Nelson, Morningstar, and Mat tson 21

22 Emotions as Regul ators of Motivated Behavior

Nelson, Morningstar, and Mat tson 23

24 Emotions as Regul ators of Motivated Behavior

Nelson, Morningstar, and Mat tson 25

Lane Beckes and Weston Layne Edwards

Introduction ing emotion as emergent information about the

28 Emotions as Regul ators of Social Behavior

Beckes and Edwards 29

30 Emotions as Regul ators of Social Behavior

Beckes and Edwards 31

32 Emotions as Regul ators of Social Behavior

Beckes and Edwards 33

34 Emotions as Regul ators of Social Behavior

Beckes and Edwards 35

36 Emotions as Regul ators of Social Behavior

Beckes and Edwards 37

Kateri McRae and Paree Zarolia

Introduction being regulated, while cognitive neural systems are

40 Cognition and Emotion in Emotion Dysregul ation

M c Rae and Zarolia 41

42 Cognition and Emotion in Emotion Dysregul ation

M c Rae and Zarolia 43

44 Cognition and Emotion in Emotion Dysregul ation

M c Rae and Zarolia 45

Theodore P. Beauchaine, PhD, earned his undergraduate degree in psychology