ANXIETY, STRESS, & COPING, 2016

VOL. 29, NO. 4, 335–351

http://dx.doi.org/10.1080/10615806.2015.1134788

INVITED ARTICLE

Depression and stressful environments: identifying gaps in

conceptualization and measurement
Constance Hammen
Department of Psychology, University of California, Los Angeles, Los Angeles, CA, USA

ABSTRACT ARTICLE HISTORY

Background and Objectives: Stress is well known as a trigger of depressive Received 17 December 2015
reactions, fear, anxiety, and behavioral disorders. However, there are many Accepted 17 December 2015
gaps in the conceptualization and measurement of environmental stress.
KEYWORDS
Results: Exciting developments in the neuroscience of stress have Stress; life events; chronic
increasingly expanded our knowledge of mechanisms by which stress may stress; early childhood
affect emotional and behavioral adjustment. Ironically, environmental adversity; stress sensitization;
stress has often been a silent player in human studies of stress processes. stress measures
There is a significant need for increased efforts to include environmental
stress variables in models of internalizing and other disorders.
Measurement and conceptualization issues are prominent, and this article
makes the case for improved methods of measuring acute, chronic, and
early life stress, and for additional conceptualization of the dynamically
changing and bidirectional effects of stress on disorder over time.
Conclusions: There is a critical need for greater focus on and better
measurement of the environment and its impact on emotional and other
disorders, with emphasis on developmentally informed hypotheses.
Empirical findings and new perspectives may contribute enormously to our
understanding of normal and abnormal outcomes, and also to the
challenge of effective interventions to promote mental health and optimal
functioning.

For decades, depression has been construed within a diathesis–stress model of vulnerability trig-
gered by stressful life events, and long before that, most cultures since the dawn of time have
observed associations between melancholic states and the perils of life such as bereavement, roman-
tic conflict, and economic turmoil. Descriptive studies have amply documented that the majority
(80%) of episodes of major depression occur within a few months or less of major negative life
events, with empirical evidence of stressors playing a triggering/causal role (e.g. Brown & Harris,
1989; Kendler & Gardner, 2010; Kendler, Karkowski, & Prescott, 1999). Yet, the great majority of indi-
viduals who experience stressors do not become depressed at levels and durations consistent with
diagnostic thresholds. Thus, for many years the key question in depression research has explicitly or
implicitly been “why do some people get depressed following stressors and others do not?” An enor-
mous research literature has documented the numerous predictors of and vulnerability factors for
depression (and anxiety) that are beyond the scope of this chapter to review: sociodemographic
characteristics, dysfunctional cognitive processes and appraisals, personality-temperament charac-
teristics, coping styles, clinical and family history, and interpersonal/relational styles (e.g. see
edited books such as Abela & Hankin, 2008; Gotlib & Hammen, 2014; Richards & O’Hara, 2014). To
a great extent, more recent research on genetic and neurobiological variables has turned toward

CONTACT Constance Hammen hammen@psych.ucla.edu

© 2016 Taylor & Francis
336 C. HAMMEN

exploration of risk mechanisms of stress reactivity. It could be said that nowadays the story of
depression is about the stress–depression link and how it operates (see reviews Gibb, Beevers, &
McGeary, 2013; Hing, Gardner, & Potash, 2014; McEwen & Morrison, 2013; Pariante & Lightman,
2008; Russo & Nestler, 2013; Slavich & Irwin, 2014).
Less research has been conducted on stress as such in relation to anxiety disorders (excepting
post-traumatic stress and related disorders), but there are important reasons to include anxiety dis-
orders within this discussion. Obviously, core anxiety mechanisms of threat appraisal and fear learn-
ing include detection and interpretation of stressful stimuli and situations and heightened emotional
reactivity. Vulnerability factors for both anxiety disorders and depressive disorders include exposure
to adverse early life events and dysfunctional family attachment processes that affect appraisal and
emotion regulation, as well as underlying vulnerability traits such as neuroticism (e.g. Barlow, Ellard,
Sauer-Zavala, Bullis, & Carl, 2014; Nolte, Guiney, Fonagy, Mayes, & Luyten, 2011). Furthermore, there is
considerable evidence of comorbidity of anxiety and depressive disorders (e.g. Mineka, Watson, &
Clark, 1998), and increasing evidence that depression and anxiety disorders load on the same
general latent factor, a transdiagnostic dimension of “internalizing” (Krueger, Caspi, Moffitt, & Silva,
1998; Krueger & Markon, 2006). The internalizing disorders may sometimes but not always be
further partialled into two subfactors, fear and distress (e.g. Slade & Watson, 2006). Thus, depression
and anxiety disorders share common features, and use of this transdiagnostic factor may help to
advance the study of mental disorders that heretofore has been weighted down and hindered in pro-
gress on etiology and treatment by the substantial heterogeneity and comorbidity inherent in diag-
nosis-based research, including the high degree of comorbidity between depressive and anxiety
disorders (e.g. Carragher, Krueger, Eaton, & Slade, 2015). For these reasons, this article’s focus on
stress and depression extends to a considerable extent to internalizing disorders generally.
Paradoxically, however, stressors – in the sense of environmental conditions – have often been the
silent player in contemporary stress–depression research. This article will briefly discuss how stress
experiences and exposure have been conceptually or empirically neglected or inadequately con-
ceived, or measured poorly, or measured narrowly in psychopathology research. Further, the
simple diathesis-–stress model of diatheses moderating the link between stress and depression
needs to be modified to include dynamic and bidirectional aspects.

What is stress and how should it be conceptualized?

Eminent researchers in the human depression field frequently do not include stress assessment in
their research paradigms, and as an example, one individual told me that it just took too much
time in the protocol loaded with neuroimaging, genetic analyses, and complex hypothalamic-
pituitary-adrenal (HPA) axis-based assays and dozens of questionnaires. For some teams, the
search for the causes of depression/anxiety seems to begin after the person is already symptomatic.
Further, for some research teams, environmental stress is best assessed not as what is going on in
the person’s world but is assumed to be what is going on in their minds about their world. Such
models start with the explicit, sometimes implicit, assumption that depressive reactions and
anxiety symptoms are the product of dysfunctional appraisal patterns such that molehills are inter-
preted as mountains because of inborn and acquired tendencies to exaggerate the threat, failure,
and loss stimulated by possibly minimally negative, harmless, or neutral events. Such misinterpreta-
tions then beget severe and enduring syndromes by genetically programmed, neurobiological
changes in the HPA axis and neural circuits. Such dysfunctional processes also are hypothesized
to impede “repair” processes allowing return to normal states. Actual stress experiences, thus, are
not as relevant in such perspectives as are the cognitive and biological mechanisms of stress.
In contrast, some perspectives on psychopathology including my own are vitally interested in the
observation that the lives of depressed and disordered individuals may be objectively challenging,
and from the beginning some infants may be exposed to adverse conditions in utero and postnatally,
and in the manner in which the primary caregiver mediates the impact of the environment. The
 ANXIETY, STRESS, & COPING 337

developing brain and neuroendocrine and hormonal systems are sculpted by the environment, and
by the success or failure of the caregivers to promote engaged, attentive, positive, warm, and stable
relationships to promote the child’s sense of self, others, and the world. Depending on what the child
learns and the resources she can command, she may be only partly successful in negotiating devel-
opmental demands and may occasionally be overwhelmed by the requirements and events of life,
including negotiating the increasingly complex demands of social engagement and life outside
the family. In these perspectives on internalizing psychopathology, the vulnerable developing indi-
vidual unwittingly not only experiences but contributes to the continuing occurrence of stressors
and challenges; such “stress generation” (Hammen, 1991) is due to the stable problematic environ-
mental situations in which she is mired, personal characteristics, maladaptive levels of learned
skills and coping mechanisms, dysfunctional (overreactive) neurobiological systems, and genetic
resources that promote maladaptive responses to stressors. In such approaches, environmental stres-
sors themselves partially shape the appraisal, neural, endocrine, and genetic mechanisms of symp-
toms and disorders in developmentally driven, complex ways that are essential for understanding
human differences. Models that are inclusive of environmental events and circumstances may also
contribute to devising effective interventions that include modifiable personal, interpersonal, com-
munity, and policy level variables.

Construing and measuring stressful experiences

This section describes three aspects of naturally occurring environmental stresses that are relevant to
depressive episodes and affect most forms of psychopathology: acute life events, chronic stressors,
and early childhood adversities.

Acute life events

The most commonly encountered stress variable in human research involves acute negative life
events occurring in the recent past. In most studies measurement has typically taken the form of inex-
pensively scored, easily administered questionnaires and checklists, varying in length and psycho-
metric soundness. While this strategy is cost-effective and a practical choice in the context of large
and expensive studies, the limitations of questionnaires are considerable. Scott Monroe has
written several excellent articles discussing the limitations and noting interview options (e.g.
2008). Among the pitfalls are that, by definition, questionnaires contain only limited numbers of poss-
ible events, and respondents might interpret the events in very different ways that could obscure
understanding of what really happened. It is also sometime quite difficult for individuals on their
own to accurately determine the date of the event – a critical issue if the purpose is to determine
whether an event actually preceded/triggered symptoms, or episodes. A fundamental problem, fur-
thermore, is that severity of stress is typically rated by subjective ratings of the impact of the event
that are highly colored by current emotional distress; depressed and anxious individuals exaggerate
threat or its actual role in their emotional reaction. Conversely, individuals who experienced signifi-
cant negative events but did not react with distress may fail to check off an item if they did not think it
was “stressful”. Thus, the ratings of “stressfulness” or severity are inherently confounded with distress
and/or appraisal biases, a circularity in which the dependent variable predicts the independent vari-
able. There is also an enormous amount of measurement noise due to erroneous reporting, failures of
recall or misinterpretation, and failure of the questionnaire to include personally relevant but poten-
tially rare or idiosyncratic events.
Overall, as Monroe (2008) reports, interview-based assessment of stressful life events has become
considered the gold-standard method, especially if based on the “contextual threat” approach. With
such methods, interviewers are trained to ask semi-structured questions to elicit information about
the circumstances and consequences of an event so that events of a similar nature but occurring in
very different contexts may be understood in terms of what is at stake in different circumstances. For
338 C. HAMMEN

example, there is a vast difference between the death of a beloved spouse unexpectedly, who was
also the primary earner in the family, versus death of an estranged and reviled spouse following a
long illness and extended separation due to incarceration. Brown and Harris (1978), British social
scientists, were the original creators of the Life Events and Difficulties Schedule (LEDS), and also
developed procedures for objective scoring of the severity of the impact of the event independent
of knowledge of how the person emotionally reacted to the event.
Influenced by the LEDS, Hammen developed a semi-structured interview for assessing acute life
events in the 1980’s that came to be called the UCLA Life Stress Inventory, and it has been used
in dozens of studies with diverse populations including adults, children, younger adolescents, and
older adolescents (e.g. Conway, Hammen, & Brennan, 2012; Hammen, 1991; Hammen, Henry, &
Daley, 2000; Hammen, Mayol, deMayo, & Marks, 1986; Rudolph & Hammen, 1999). It differs in
several ways from the LEDS: shorter to administer and makes use of independent rating teams to
determine objective scores. Further differences are noted below in the discussion of assessment of
chronic stress.
In general, interview measures perform better than questionnaires in studies of predictive validity.
For example, Monroe (2008) reviewed empirical support for the superiority of interviews over check-
lists for predicting outcomes such as depression. Interviews also have the flexibility of capturing per-
sonally relevant events not included on checklists, and of determining when they occurred, and how
several different related events should be characterized (e.g. as separate or all aspects of the same
event, such as an automobile accident that led to debt, injury, a lawsuit, and job loss). A recent con-
troversy in the depression field about gene–environment interactions is instructive, and emphasizes
quality of stress assessment. One group published a meta-analysis indicating nonsignificant evidence
of gene × environment interactions with the serotonin promotor variant 5-HTTLPR (Risch et al., 2009),
whereas another group’s larger meta-analysis resulted in analyses supporting evidence of gene–
environment interaction with this gene (Karg, Burmeister, Shedden, & Sen, 2011). Karg et al. (2011)
also provided evidence that the difference between the two meta-analyses was due in large part
to the inclusion of studies that used high-quality objective and/or interview measures of stress assess-
ment (see also Caspi, Hariri, Holmes, Uher, & Moffitt, 2010). Thus, investigators are encouraged to
make use of interview-based contextual threat measures of negative life events for testing
complex models of interactions and transactions among environmental, biological, and genetic
factors on psychopathology outcomes.

Chronic stress
Chronic stress has been an important focus of animal models of depression/anxiety, considered as
best characterizing naturalistic experiences involving physical deprivation, predator conditions,
and social defeat. Although even in animal studies the experimental paradigms of chronic stress
are considered difficult and costly, they are viewed as essential for modeling analogs of depression
and anxiety (e.g. Krishnan & Nestler, 2008).
Ironically, however, chronic stress in humans has been substantially less studied than acute life
events in depression/anxiety contexts. Chronic stress in humans refers to stressful, challenging, or
threatening ongoing conditions that typically affect everyday life. Chronic stressors range in severity,
from mild (such as an intermittent medical issue with symptoms that require attention and may
slightly modify life style) to severe (living in a dangerous neighborhood visited by violence and
wretched living conditions). Generally, research on the effects of such chronic circumstances on
symptoms and disorders has focused on the impact of individual situations, such as marital distress
(Robles, Slatcher, Trombello, & McGinn, 2014), poverty (Evans, Li, & Whipple, 2013), caretaking for an
ill family member (Adelman, Tmanova, Delgado, Dion, & Lachs, 2014; Revenson et al., 2015), and iden-
tity discrimination (Schmitt, Branscombe, Postmes, & Garcia, 2014). Evidence invariably shows that
such chronic stressors are associated with higher levels of distress including depression and
anxiety and potentially a myriad of health and behavioral problems.
 ANXIETY, STRESS, & COPING 339

Several features of chronic stress in relation to depression and anxiety are conceptually and
empirically noteworthy. First, there is commonly a bidirectional effect between stress and symptoma-
tology. Virtually all psychological disorders are embedded in chronic stress, and studies of clinical
populations, whether descriptive or neurobiological, invariably confound effects of stress and symp-
toms. Chronically stressful conditions promote depressive reactions and anxiety, and depression/
anxiety contributes to chronically stressful situations, such as conflictual close relationships, work per-
formance difficulties, and problems in family life and health. The bidirectional effect is often predic-
tive of chronic or recurrent depressive episodes and anxiety. Individuals who are demoralized and
fearful, experiencing reduced energy, poor concentration, low motivation, and diminished self-con-
fidence, for example, are less able to mount effective and active coping strategies that promote effec-
tive problem-solving and engage useful social and material support. Their symptoms likely worsen
stressful conditions that in turn prolong or deepen emotional distress, a vicious cycle of stress and
distress. However, chronic stress makes it difficult to understand the “timing” of an episode of
major depressive disorder, and more research is needed. For example, Hammen, Kim, Eberhart,
and Brennan (2009) found a potentiating effect in which high chronic stress makes it more likely
that an episode will be triggered following an acute negative life event.
Second, chronic stress in one area of life is commonly accompanied by additional sources of stress,
a pile-up of adverse conditions. Someone with marital conflict and instability, for example, may be
likely to experience difficulty in parenting relationships with children. Individuals with ongoing
chronic health problems may experience employment stress. Certainly low income is likely to be
associated with a variety of chronic difficulties in housing, relationship stability, poor health and
less access to health care, and the like (e.g. Evans et al., 2013). An example of potentially multiple
chronic stressors is single mother status. Two large-scale studies have shown that the association
between single parent status and depression is entirely or largely mediated by higher chronic and
acute stress and low social support typically due to low income, lack of co-parent support, and
employment and child care strains (Cairney, Boyle, Offord, & Racine, 2003; Targosz et al., 2003).
Third, chronic stress is chronic and may persist continuously. Although obviously some negative
situations are relatively time-limited and resolve, a good many chronically stressful circumstances
are continuous even if fluctuating in severity over time. For example, individuals’ life situations
may be constrained to a great extent by education, income, and other barriers such as racial discrimi-
nation, and by the multiple innate and acquired personality and socioemotional, as well as genetic
and neurobiological factors that shape reactions to stress. Individuals may be “stuck” in low socioe-
conomic and family conditions that restrict access to marital, employment, and neighborhood situ-
ations that offer pathways to greater comfort and security, and socioemotional satisfaction and
adjustment. They may also be “stuck” in their maladaptive stress reaction styles and coping strategies,
including limited sources of support. As an example of the continuity of chronic stress, in 15 years of
follow-up of a large sample of depressed and never-depressed women and their children, Hazel,
Hammen, Brennan, and Najman (2008) found substantial correlations between several areas of
maternal life (income, marital satisfaction, and mental health issues) in the first 5 years of the
child’s life and at child’s age 15. For example, women who reported marital distress in the child’s
early life tended to report marital distress 10–15 years later even if married to different men;
mental health problems continued often despite treatment, and financial hardship also persisted.
The implications of the characteristics of chronic stress affect how we need to think about and
measure it. First, most research on stress reactivity and stress mechanisms in depression and
anxiety focuses solely on acute, stressful life events. This means that an important predictor and
potential mechanism (chronic stress) is present and operational, even if it is not being measured.
Thus, what has been attributed solely to acute stress and explored as psychological and neurobiolo-
gical mechanisms of acute stress is confounded by the unmeasured effects of chronic stress. More-
over, efforts to measure single chronic stressors, such as marital distress, while commendable, may
not go far enough in capturing the common occurrence of different levels of chronic stress in mul-
tiple domains – for example, the pile-up of economic difficulties with marital, and health issues.
340 C. HAMMEN

Finally, the chronicity and continuity of stress over long periods of life require models of effects that
capture the different contributions of early, recent, and continuous exposure, and that are develop-
mentally informed in order to capture processes activated at certain times of life and as a function of
individual trajectories of stress and disorder (e.g. Lupien, McEwen, Gunnar, & Heim, 2009). These
points are elaborated more fully below.
Measurement of individual chronic conditions. There are multiple questionnaire methods of measur-
ing individual domains of chronic stress. Some of the most common are marital distress (e.g. Dyadic
Adjustment Scale; DAS, Spanier, 1976 and its many revisions); the Parenting Stress Index (PSI; Abidin,
1986) is the most commonly used self-report measure of ongoing parenting difficulties. Caregiver
stress may be measured using the Relatives’ Stress Scale (RSS; Greene, Smith, Gardiner, & Timbury,
1982), a measure of the perception of stresses associated with caring for an elderly relative. There
are multiple measures of job stress, neighborhood conditions, and economic strain. Several of
these measures are reviewed in Hammen, Dalton, and Thompson (2015). As with questionnaires
assessing acute life events, such measures of ongoing stressors are subject to the limitations of
mood-related bias in reporting of the impact or severity of such experiences.
Measurement of multiple domains of chronic conditions. In the 1980’s, influenced by the LEDS
(Brown & Harris, 1978), we developed an interview assessment that evaluated both acute life
stress and chronic conditions (e.g. Hammen et al., 1987). As noted earlier, the interview for acute
life events is based on the contextual threat approach in which interviewers probe the occurrence
of life events in the prior year (or less, depending on the design), using semi-structured questions
to elicit sufficient detail about the occurrence and consequences of the event to permit an indepen-
dent rating team to evaluate the “objective” threat or impact of the event (“how the typical person in
the same circumstances would experience the impact”). The UCLA Life Events Interview (or LSI) as it
became known, also introduced a semi-structured interview assessment of chronic stress in each of
multiple domains that affect the typical person. The domains may vary slightly by population, and
typically include the following if relevant: romantic/intimate relationship, relationships with children,
relationships with primary relatives (parents and siblings), close friends, social life, finances, work or
relevant vocation, school, health of self, and health of family. The entire LSI including eliciting acute
events is organized around probes of these domains. Scoring of the severity of the chronic stress in
each domain is rated by the interviewer, based on objective, factual information, based on a five-
point scale for each domain, with each score anchored by behaviorally specific information. For
example, for the domain of work, a score of “2” represents good working conditions in all or
nearly all areas (workload, rewards, safety, stability, relations with boss and coworkers) and a “4” rep-
resents poor circumstances in three or four of these conditions.
The UCLA LSI (both acute and chronic) has been adapted for use with young adults, older adults,
children, young adolescents, and older adolescents, and modified slightly according to project-
specific goals (e.g. low income, Hispanics, and pregnant adolescents). Data on the reliability and val-
idity of the chronic stress assessments have been reported in studies with different ages (e.g.
Hammen et al., 2009; Hammen & Brennan, 2001; Hammen, Brennan, Keenan-Miller, & Herr, 2008;
Rudolph & Hammen, 1999).
Heretofore, the only interview-based assessment of chronic stressors of which we are aware is the
“ongoing difficulties” aspect of the LEDS. “Ongoing difficulties” persisting over a period of time (in
most studies operationally defined as at least four weeks) are elicited along with acute stressors, in
a series of interview probes across different areas of life. Unfortunately, however, very little psycho-
metric information has been provided about issues of reliability and validity of these methods of
chronic stress assessment. The “ongoing difficulties” approach is event-based, and is the continuation
of a stressful life event and its sequelae, but the LEDS does not systematically assess and score mul-
tiple domains across all respondents.
Dutch investigators developed a questionnaire termed the Long-Term Difficulties Instrument
which was recently tested for validation in a community sample over the past year and also over
their lifetimes (Rosmalen, Bos, & de Jonge, 2012). Consisting of 12 items, the questionnaire
 ANXIETY, STRESS, & COPING 341

showed good test–retest reliability, and significant correlations with questionnaire measures of dis-
tress, perceived stress, and neuroticism. However, retrospective reporting of such long intervals com-
pounds the potential biasing effects of memory, mood, and interpretation on self-ratings of
stressfulness. Turner, Wheaton, and Lloyd (1995) also published a chronic stress questionnaire asses-
sing subjective perceptions of ongoing sources of stress; however, psychometric data supporting use
of the measure were not located.

Early life adversity

There has been an explosion of interest in recent years on the effects of exposure to adverse events in
childhood (often termed early childhood adversity, ECA or EA). Methods of measurement in humans
are discussed below. The construct itself may refer narrowly to abuse/maltreatment or more broadly
to a variety of challenging situations affecting a child’s family and living environment. A wealth of
information from animal and human studies indicates that exposure to abnormal stress levels
and patterns during critical childhood periods of brain development may lead to long-term
changes in neural circuitry and neuroregulatory mechanisms that can have significant negative
effects on brain structure and function, thereby affecting many functions and behaviors (Anda
et al., 2006; Shonkoff et al., 2012). Such impairments are predictive of numerous negative health
outcomes (e.g. Miller & Chen, 2010; Scott et al., 2011; Shonkoff et al., 2012), and cognitive difficul-
ties (e.g. Pechtel & Pizzagalli, 2011) as well as behavioral and emotional disorders. With regard to
depression and anxiety disorders, Green et al. (2010) found that ECAs predicted 32.4% of all anxiety
disorders and 26.2% of mood disorders in the National Comorbidity Survey Replication, with most
onsets in childhood. Similar analyses in the World Health Organization World Mental Health
Surveys reported the population attributable risk proportions of 31% anxiety disorders and
22.9% mood disorders (see also Anda et al., 2006; Kessler et al., 2010; St. Clair et al., 2015). In a
study of adolescent first onsets, when internalizing disorders were also sub-classified as “fear dis-
orders” (e.g. specific and social phobias, panic disorder) versus “distress disorders” (generalized
anxiety disorder, major depressive disorder, PTSD, and separation anxiety disorder), McLaughlin
et al. (2012) found population attributable risks proportions of 15.7% for fear disorders and
32.2% for distress disorders. In all these studies, ECAs were associated strongly with substance
use and behavioral disorders as well.
As with chronic stressors, there are important facts from the empirical literature that have concep-
tual and methodological implications. As is well-documented across numerous studies, the effects of
early adversity exposure are general, with little evidence that specific adversity types are uniquely
predictive of particular disorders (e.g. parental death predicting depression; Green et al., 2010).
Early adversity exposures predict a wide range of psychiatric disorders. Also notable is that individuals
who experience any adversity likely experience more than one; clustering is typical. This is particularly
true of what Kessler and colleagues term “maladaptive family functioning” (parental mental illness,
substance misuse, criminality, domestic violence, physical and sexual abuse, and neglect; for
example, Green et al., 2010; Kessler et al., 2010). Thus, it is difficult to attribute outcomes to single
adversities, and increasingly the field (of human research) has moved away from measuring single
negative childhood events, such as parental death, divorce, or sexual/physical abuse, because nega-
tive outcomes may be erroneously attributed to events that actually occur within a context of mul-
tiple negative conditions. Such considerations lead to three issues: what types of adversity should be
included and how should they be assessed, how best to model the impact of multiple events, and
whether further differentiation of the content or nature of the events may have implications for
causal processes.
Assessment of childhood adversities. There is considerable room for improvement and develop-
ment of this construct and the way it is measured. A standard definition of what should be included
as a childhood adversity is lacking, and indeed, there is no standard definition of what “childhood”
exposure means (measures commonly include youth through 16 or 18). By definition, the assessment
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of adversity exposure in childhood is virtually always by retrospective report (although occasionally

contemporaneously obtained information is available in longitudinal studies (e.g. Phillips, Hammen,
Brennan, Najman, & Bor, 2005) or through records of legal and social welfare reports (Cicchetti & Toth,
2005). The retrospective nature is generally not considered to be a serious liability, inasmuch as val-
idity studies generally have supported the accuracy of reporting of abuse as verified by community
records or by informant/witness concurrence (Bifulco, Brown, Lillie, & Jarvis, 1997; Hardt & Rutter,
2004). Individuals rarely erroneously report abusive situations that did not occur, but there is some
concern about under-reporting by individuals who do not wish to admit or may not recall sensitive
information. Nevertheless, even if somewhat underreported, patterns of association between adverse
conditions and mental health issues are clearly strong and replicated across many samples, with sig-
nificant proportions of the population reporting one or more adverse conditions in the childhood and
teenage years.
Most of the earliest childhood adversity research was conducted on samples in which the respon-
dent reported maltreatment in the form of sexual, physical, or emotional abuse, and sometimes
exposure to domestic violence (maternal battery), but it soon became clear that these conditions
commonly overlapped with each other and thus should be assessed collectively (e.g. Edwards,
Holden, Felitti, & Anda, 2003). Most recent studies have employed checklists covering a variety of
negative experiences of childhood before age 18 with specific questions drawn from existing ques-
tionnaires such as the Conflict Tactics Scale (Straus, 1990). For example, Anda et al. (2006) assessed
exposure to eight domains: sexual, emotional, physical abuse, witnessing domestic violence, sub-
stance abuse, mental illness, incarceration, and parental separation/divorce. Kessler et al. (2010) in
the WHO study included 12 adversities, including the above plus parental death, neglect, life-threa-
tening illness of the child, and family economic adversity (and did not include emotional abuse). An
earlier study in the National Cormorbidity Survey included 26 items experienced by age 16 (Kessler,
Davis, & Kendler, 1997). Generally most studies have administered the checklists as structured inter-
views, although sometimes they are administered as questionnaires. Bifulco, Brown, and Harris (1994)
developed a contextual interview assessment to evaluate the link between ECA and depression, the
Childhood Experiences of Care and Abuse covering parental care, sexual and physical abuse, with
excellent reliability and validity but it is labor-intensive and requires training. A self-report question-
naire version has also been developed that has adequate reliability and validity (Bifulco, Bernazzani,
Moran, & Jacobs, 2005).
Clearly the measurement of childhood adversity is at a developing stage, with content largely
shaped by literature reviews indicating various risk factors for maladjustment. Additional research
is needed to address the following critical issues.
First, what content should be included? As noted, there is considerable nonspecificity between
adverse conditions and outcomes, with clustering or aggregation of negative circumstances as the
norm. One group used factor analyses to define content clusters, with the clearest associations of
mental disorders with a “maladaptive family functioning” factor (parental substance abuse, crimi-
nality, domestic violence, abuse, and neglect; Green et al., 2010; McLaughlin et al., 2012 in the
National Comorbidity Survey Replication and the NCS Adolescent survey). St. Clair et al. (2015) also
focused on family quality, using an interview to probe items about the caregiver’s perceptions of
the family environment, including family relationships, economic conditions, health, abuse, crime,
and chronic social impairments. The investigators then used the person-oriented strategy of latent
class analysis (LCA) to identify groups sharing similar profiles. Four groups were distinguished by par-
enting quality, labeled optimal, aberrant, discordant (distinguished by marital conflict), and hazar-
dous (high marital conflict plus high proportion of maltreatment and/or parent criminality). All
three of the nonoptimal groups were associated with depressive symptoms in girls, two associated
with depression in boys, and over time girls’ association of nonoptimal family conditions with
depression was more stable than boys’ depression. It seems clear that poor quality of caretaking is
a critical predictor of maladjustment but we know relatively little about the specific ingredients
and mechanisms.
 ANXIETY, STRESS, & COPING 343

Recently, a novel approach to content was proposed by McLaughlin and Sheridan (McLaughlin,
Sheridan, & Lambert, 2014; Sheridan & McLaughlin, 2014), who argued that the manifest content
may not be as important as the functional content of adversities, especially in terms of brain devel-
opment. The authors argued that studies of the impact of adversity by counting the number or types
of adversities have done little to identify the mechanisms that account for psychopathology and
impairment. They note that the majority of research on abnormal neural development has been
framed in terms of the neuroendocrine consequences of stress and the concept of allostatic load
(e.g. Burghy et al., 2012; McEwen & Morrison, 2013). McLaughlin and colleagues argue, however,
that such models based on stress physiology do not fully capture the extensive neurodevelopmental
disruptions associated with stressors. They propose framing the mechanisms in cognitive neuro-
science-based constructs that have been amply studied in experimental studies of animals and in
some human research. Specifically, they review evidence on dimensions of “threat” and “deprivation”,
and suggest that while not a perfect fit for certain ECAs and noting that they certainly co-occur in
many children’s experiences, the dimensions are associated with particular facets of brain develop-
ment, and should be assessed and evaluated in models of ECAs and outcomes. McLaughlin and
colleagues suggest that additional functional dimensions of experience could similarly help to
shed light on the mechanisms of early stress exposure, and specifically note that absence of or
loss of attachment figures may represent experiences with distinct implications for brain develop-
ment (e.g. Tottenham, 2012). Additionally, investigators have begun to explore the links between
early adversity experiences and the development of other risk factors for depression and anxiety
such as dysfunctional reward processing, negative and positive affectivity and affect regulation,
and various additional domains and putative endophenotypes for disorders (e.g. reviews in
Bogdan, Nikolova, & Pizzagalli, 2013; Hankin, 2015; Pizzagalli, 2014).
How should the impact of childhood adversities on emotional disorders be modeled? Basic analyses of
the predictive effects of ECAs have generally been exploratory and descriptive. Bivariate analyses are
commonly reported, but the high degree of clustering makes use of individual associations not
meaningful when multiple adversities are present. More typically, multivariate analyses of various
types may be presented (e.g. Green et al., 2010; Kessler et al., 2010), attempting to determine the rela-
tive contributions of each controlling for others, or controlling for number, or including interactions
among variables. In general those analyses have indicated “subadditive” effects. In contrast, other
investigators have specifically hypothesized dose–response relationships between number of adver-
sities and severity of outcomes, based on neurobiological models of the cumulative deleterious
impact on the developing brain of exposure to stressors. For example, Anda et al. (2006) reported
evidence of a dose–response effect on all 18 outcomes including symptomatology, social adjustment,
and memory impairment (but see also St. Clair et al., 2015). Clearly the conceptual issues concerning
type of relationship between disorder and adversities are in a nascent state of development, and
must be more fully informed going forward by specific hypotheses regarding timing and sequencing
of maturation of neural processes in light of timing of environmental stressors and their interactions
with genetic programming.
What aspects of ECAs are causally relevant? The suggestions of McLaughlin and Sheridan noted
above (McLaughlin et al., 2014; Sheridan & McLaughlin, 2014) represent one aspect of functionally
meaningful attributes of ECAs to investigate. A further conceptual/assessment gap that needs to
be addressed is the general failure of current methods to evaluate the context in which ECAs
occur, just as we recommend for assessment of negative (acute) life events. Such information
would be needed to determine basic and important issues of ECA occurrence such as the temporal
sequence, timing in relation to child age/development, and persistence or recurrence of the adverse
condition (e.g. Green et al., 2010).
Furthermore, also related to additional information about context is the critical question of
whether quality of maternal care is best considered as a buffer (e.g. Tang, Reeb-Sutherland,
Romeo, & McEwen, 2014) or poor care as an adverse condition. Harris, Brown, and Bifulco (1986),
for example, in their classic study of effects of parental loss on depression, determined that it was
344 C. HAMMEN

not the childhood loss itself but the resulting “loss of care” especially maternal loss, that accounted
for depression. Unfortunately, the significance of this finding has been largely overlooked in recent
studies. Most studies of ECA do not specifically determine critical features of caretaking present
during each adverse experience and whether effects are heightened or mitigated by the quality of
care. There are doubtless other mediators and moderators of the effects of ECAs, as the long
history of research on the mediators/moderators of the effects of acute stress on depression tells
us. Conceptually and empirically, attachment processes and caregiver qualities would be expected
to exert important influences on the child’s ability to manage challenging circumstances, but also
other moderators and mediators concerning resources, child attributes, and environmental features
should be explored (e.g. St. Clair et al., 2015).
The basic issue of timing is also conceptually critical. It is important to know not only when does
the adversity occur in relation to age and development (e.g. Lupien et al., 2009), but also, for example,
whether some adversities were present during prenatal development. Prenatal stress, operating
through a variety of neurobiological and behavioral mechanisms is clearly related to a variety of mala-
daptive outcomes in infants and children (e.g. Goodman & Lusby, 2014; Monk, Spicer, & Champagne,
2012; O’Connor, Monk, & Fitelson, 2014; Stein et al., 2014). Prenatal stress is often associated with
maternal depression and anxiety, but it is highly likely that for many stressed and distressed
women, such conditions persist beyond pregnancy, and therefore, studies focused on exposure to
adversities during early life should evaluate prenatal effects as well. It would seem that many of
these critical questions are best answered in studies with longitudinal designs commencing in preg-
nancy, rather than retrospective studies of older adolescents and adults.

Nature of the associations between stress and depression/anxiety

As initially stated, most research involving stressors generally has been conceptualized within a
simple diathesis–stress paradigm (which many researchers invoke even if they do not include
measures of stress exposure). However, over the past couple of decades it has become clear that
this relationship is certainly not simple – nor is it unidirectional. Also, it is not stable but instead is
a dynamic relationship changing over time, experiences, and development. Briefly, key points of
the elements will be discussed.

Multiple levels of analysis

Unsurprisingly the quest to understand why some people become depressed following stress but
most do not has fueled numerous studies of moderators and mediators of the stress–depression
link. Increasing emphasis on mechanisms that account for depression has resulted in complex
models integrating at the molecular, cellular, systemic, and behavioral levels, including genetic,
neural, endocrine, and other biological variables as well as personal and environmental character-
istics that mold and shape neural, genetic, and behavioral functioning. Many investigators have
used the term “multiple levels of analysis” in calls for integrative research (e.g. Cicchetti & Dawson,
2002; Hankin, 2015). Importantly, this theme emphasizes developmentally informed conceptualiz-
ations that capture the dynamic, transactional nature of interacting systems, the effects of prior
development on subsequent normal and abnormal development, and the idea of multiple pathways
to disordered and resilient behaviors (e.g. Cicchetti, 1989).

Bidirectional associations between symptoms and stress

The stress–depression link is also increasingly understood to be bidirectional. Individuals with
psychological disorders often have stressful lives because their disorders and coping characteristics
contribute to dysfunction in major life roles. The term “stress generation” coined by Hammen (1991)
refers particularly to the hypothesis and initial empirical support for a pattern of elevated rates
 ANXIETY, STRESS, & COPING 345

among women with depression histories compared to those with no depression, of stressful life
events which they had at least partly contributed to, a pattern that has been replicated in child,
adolescent, and adult samples, male and female samples (reviewed in Liu, 2013). In the original
study, women with depressive disorders were especially likely to experience interpersonal events
that are “dependent” on their characteristics and behaviors. The tendency to contribute to the occur-
rence of stressful life events does not simply reflect impairments due to depression symptoms them-
selves, but occurs even when individuals are not currently depressed. Studies have suggested
numerous mechanisms, but the fundamental processes appear to affect close relationships, with
elevated levels of conflict, disruptions, and impairments in interpersonal functions such as excessive
reassurance-seeking, insecure attachment, oversensitivity, and lower positive affectivity and higher
negative affectivity, and decrements in social problem-solving (Eberhart & Hammen, 2006; Liu,
2013). Numerous temperament, personality, and family quality factors likely predict stress generation
as reviewed in Hammen & Shih, 2008; Liu, 2013). Recently, Starr, Hammen, Brennan, and Najman
(2012) also found a genetic predictor of stress generation: among youth with past depression,
those with short alleles of the 5-HTTLPR polymorphism in the promoter region of the serotonin trans-
porter gene are more likely to have elevated rates of stress generation.
Stress generation was initially studied in the context of occurrence of acute events, but more
recently we have extended the concept to apply to the idea that individuals may create or select
themselves into chronically stressful situations. We have shown, for example, that adolescents with
histories of depression compared to never-depressed youth are more likely to get into romantic
relationships before age 20 that have high levels of severe intimate partner violence (Keenan-
Miller, Hammen, & Brennan, 2007). Hammen, Brennan, and Le Brocque (2011) found that formerly
depressed young women compared with never-depressed women gave birth before age 20 and
reared their babies largely in the context of lack of marital or financial stability; early child-rearing
was associated with high levels of current depression in the young mothers. Katz, Hammen, and
Brennan (2013) found that young adults who had depressed mothers and personal histories of
depression were more likely to have less positive stable romantic relationships (judged by both
the youth and the partner) than their never-depressed counterparts. Thus, risk factors for depression
and depressive experiences appear to promote characteristics that predict maladaptive close
relationships that in turn increase the likelihood of enduring stress and the potential for recurring
depression.
Stress generation may occur in all forms of psychopathology, but major depressive disorder may
be unique. A recent study in our research team showed that even when transdiagnostic factors of
internalizing disorders and externalizing disorders plus individual diagnoses are statistically con-
trolled, major depressive episode contributed incrementally to the occurrence of life events with
interpersonal content (Conway et al., 2012). Interestingly, externalizing disorders were associated
with greater occurrence of non-interpersonal events (such as work, school, and accidents). For indi-
viduals with histories of depression, the increased levels of interpersonal stressors imply further
depression in a vicious depression–stress–depression cycle.
Stress generation highlights another phenomenon: the continuity of stressful experiences poten-
tially over a lifetime among those with depression. For example, Hammen, Hazel, Brennan, and
Najman (2012) and Hazel et al. (2008) found evidence of the continuity of stress occurrence from peri-
natal development through early adulthood. Consistent high levels of stressors suggests that psycho-
logical maladjustment attributed to recent stressors may also reflect the unknown effects of three
sources: early stress exposure, chronic stress, and recent stressors. Overall, the implications of
stress generation are notable – a vicious and recurrent cycle of stress and depression. It is a
pattern of stress exposure and stress generation that portends not only recurrent or chronic
depression, but also, likely intergenerational transmission of depression, as demonstrated in longi-
tudinal analyses of stress and depression over a 20-year period (Hammen et al., 2012).The continuity
of stress also has implications for mechanisms by which the stress–depression relationship changes
over time, as discussed in the following section.
346 C. HAMMEN

Changes in the link between stress and depression over time and experiences
Individual differences in vulnerability factors such as genetic and temperament factors are well-estab-
lished sources of differences between individuals in emotional responses to stress (e.g. Barlow et al.,
2014). Differences within-individuals require further study, and speak to a growing awareness of the
Additional ways in which characteristics of individuals’ appraisals of the self and world, and neurobio-
logical and behavioral processes change with development and the impact of many transacting influ-
ences. In the depression field, it has been argued with some suggestive evidence, that number of
prior episodes of depression portends increasing susceptibility to episodes. Solomon et al. (2000)
observed patterns of progressively briefer intervals between recurrences. Post (1992) was one of
the first to propose that recurrent mood disorders displayed features of kindling and sensitization
often seen in experimental animal studies as the result of repeated exposure to particular kinds of
stimuli. He argued that sensitivity to develop depressive episodes increases with number of prior epi-
sodes (especially compared to first onset) as episodes become progressively decoupled from stress
precipitants, consistent with genetic and neurobiological changes over time due to episodes and
stress. Other investigators have refined the model but report evidence for “sensitization”, the increas-
ing impact of stressors with less severity over the course of depression (e.g. Monroe & Harkness, 2005;
Stroud, Davila, Hammen, & Vrshek-Schallhorn, 2011).
Additionally, several studies have shown that exposure to early childhood adversities has a sensi-
tizing effect, such that the level of recent life stress needed to provoke a depressive episode is less for
those with adversity than those without (Hammen et al., 2000), and the probability of depression and
anxiety among those with early adversity exposure increases following exposure to recent acute life
events (McLaughlin, Conron, Koenen, & Gilman, 2010). Further, Starr, Hammen, Conway, Raposa, and
Brennan (2014) demonstrated a gene × environment × environment interaction. Greater depressive
reactions to proximal stress in young adulthood were greater among those with more early exposure
to adversity by age 5, and these effects were more pronounced among those with genetic character-
istics hypothesized to reflect heightened HPA axis reactivity and greater emotional responsiveness to
the environment (Corticotropin Releasing Hormone CRHR1 A alleles and serotonergic 5-HTTLPR short
alleles, respectively). While the mechanisms by which sensitization due to early stress exposure is not
fully known, it is likely due to profound effects of environmental experiences in shaping genetic and
neurobiological processes relevant to the stress response system (e.g. Lupien et al., 2009), as well as
possible psychological sensitization to personally meaningful experiences signaling perceptions of
loss, failure, and rejection.
Clearly, therefore, the stress–depression relationship is not static, with considerable implications
not only for theories of developmental psychopathology but also for clinical interventions. Future
research should be based on conceptualizations of stress reactivity that can also evaluate its chan-
ging nature over experience and development, and determine what kinds of interventions delivered
at different points in the lives of those at risk may be optimally effective.

Conclusions and future directions

This article has highlighted some emerging issues in the psychopathology of depression – and by
extension, anxiety disorders with which depression often co-occurs, and also with many other
psychological disorders involving affective, social, and behavioral maladjustment. The focus on
stress conceptualization and stress measurement is intended to emphasize the need for fuller
inclusion of the environment as a central player in psychopathology and human functioning, requir-
ing better conceptualization and better measurement.
Acute life events may be precipitants of depressive episodes and exacerbations of emotional and
behavioral problems, but they are commonly ignored in favor of other cognitive, genetic, neurobio-
logical and neuroendocrine risk factors and mechanisms, or measured poorly with checklists. Inter-
view methods have the advantage of careful probing for aspects of the context of the event that
 ANXIETY, STRESS, & COPING 347

permit reasonably objective judgments of severity of impact independent of the individual’s likely
biased perceptions. Nevertheless, acute stress is the tip of the iceberg, and has to be construed in
the context of a life history of stress exposure and the influence of potentially chronically stressful
conditions affecting daily life. Symptoms/disorders and chronic and acute stress are invariably inter-
twined so that it is difficult to disentangle multiple interacting processes and underlying mechanisms.
Many individuals with severe or recurrent psychological disorders also have histories of exposure
to adverse childhood conditions as far back as conception. Emerging research on the neurodevelop-
mental and epigenetic processes sculpted by the environment clearly requires improved methods of
measuring environmental exposures and the many moderating and mediating relationships of stress
exposures with outcomes. There is much to be improved in assessment of early childhood adversities,
including contextual assessment and developmentally informed methods and hypotheses. Both
manifest and functional content of stressor exposure may yield greater refinements in understanding
of mechanisms. Moreover, additional research on the role of caretaking and attachment relationships
as mediators and moderators of early stress exposure is critically important. Given the continuity of
stress experiences over years, it is important to address basic issues of what effects are due to early
exposure compared with continuing and proximal exposures, and changes in stress reactivity and
stress sensitivity as a function of development and experience. These dynamic aspects of the
stress–depression relationship challenge static models, and require more complex research
designs of individuals in their environmental contexts.
Finally, two additional observations point to the need for additional study: sex differences and
interpersonal content, two extensive bodies of research that require us to refine questions relating
to stress. These two themes apply largely to depression and internalizing disorders but may have
general implications. Sex differences in rates of depressive disorders have required that attention
be paid to gender-related processes including stress exposure and mechanisms of reactivity.
Women’s higher rates of depression are paralleled by higher rates of exposure to stressors, both per-
sonal and from exposure to those in the social network (“the cost of caring”; Hilt & Nolen-Hoeksema,
2014) as well as women’s greater reactivity to stressors when males and females have the same objec-
tive levels of exposure (e.g. Shih, Eberhart, Hammen, & Brennan, 2006). Similarly, a strong case can be
made for negative interpersonal events and circumstances as uniquely causative/triggering mechan-
isms in depression, perhaps especially for women. A full discussion is beyond this scope of this article,
but see Hammen and Shih (2014). It is worth pursuing if, and why, depression is especially related to
disruptions in close social bonds, and how such processes can be integrated into complex multifa-
ceted models of stress and depression.

Disclosure statement
No potential conflict of interest was reported by the author.

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