An Evolutionary Investigation

AN EVOLUTIONARY INVESTIGATION OF DEPRESSED MOOD:
THE RELATIONSHIP BETWEEN ADVERSE LIFE EVENTS
AND DEPRESSIVE SYMPTOM PATTERNS
Dissertation presented to the Faculty of the
California School of Professional Psychology
Alliant International University
San Diego
In partial fulfillment of the requirements for the degree of
Doctor of Philosophy
by
Alissa Ann Maitino, M.A.
2015
Approved by:
Irwin Rosenfarb, Ph.D.
Jack Maser, Ph.D.
Matthew Keller, Ph.D.

UMI Number: 3708057
All rights reserved
INFORMATION TO ALL USERS

The quality of this reproduction is dependent upon the quality of the copy submitted.
In the unlikely event that the author did not send a complete manuscript
and there are missing pages, these will be noted. Also, if material had to be removed,
a note will indicate the deletion.
UMI 3708057
Published by ProQuest LLC (2015). Copyright in the Dissertation held by the Author.
Microform Edition © ProQuest LLC.
All rights reserved. This work is protected against
unauthorized copying under Title 17, United States Code
ProQuest LLC.
789 East Eisenhower Parkway
P.O. Box 1346
Ann Arbor, MI 48106 - 1346
Adverse Life Events and Depressive Symptom Patterns ii
Dedication
In memory of Susan Bonita Maitino, my mom and the most inspiring and influential
woman in my life.
Adverse Life Events and Depressive Symptom Patterns iii
Acknowledgments
I would like to acknowledge the people who helped me as I worked on this dissertation.
Professor Irwin Rosenfarb provided invaluable expertise in clinical psychology, and offered
constructive suggestions for refining my research methodology. Professor Matthew Keller
inspired my dissertation topic and gave crucial insight into navigating evolutionary psychology.
Professor Jack Maser provided thoughtful instruction, and helped me examine both clinical and
subthreshold depression through a more accurate lens. Professor Dale Glaser facilitated my
understanding and appreciation of multilevel modeling. My siblings, Sara, Bryan, and Andrew,
and my friends, especially Dina, Veronica, and Rachel, offered support that was persistent and
took many forms. Beginning on day one and continuing to the end, my father, John Maitino,
served as the vital source of inspiration through his encouragement and optimism.
Adverse Life Events and Depressive Symptom Patterns iv
Abstract
A major issue for depression researchers involves explaining the substantial variation in
symptom profiles of depression. Symptom profiles of depression vary between individuals and
across episodes within the same individual. Variation in symptom profiles across depressive
episodes within the same individual is more pronounced across noncontiguous episodes,
suggesting temporary state factors (i.e., environmental and/or physiological) may influence the
symptom profile expressed during an episode. Adverse life events (ALEs) often precede
depressive episodes and the types of ALEs that precede episodes vary. Research demonstrates a
causal relationship between ALE exposure and subsequent depression onset. These findings have
prompted a handful of researchers to investigate whether different types of ALEs are related to
different patterns of depressive symptoms. The situation-symptom congruence hypothesis
(SSCH) is grounded in evolutionary theory, and argues that different types of adverse situations
should lead to distinct patterns of depressive symptoms that help individual deal with the
adaptive challenges of the situation. Recent research supports the SSCH but has numerous
limitations. We tested the SSCH using an alternative methodology that addressed some
limitations of past research. Our sample (N = 265) included 197 females and 68 males with and
without major depressive disorder (MDD and non-MDD, respectively) between the ages of 18
and 63 (M = 27, SD = 10.9). We assessed depressive symptoms and ALEs daily for up to nine
days. We hypothesized that the relationships between ALEs and depressive symptom patterns
would be consistent with SSCH predictions, and that the relationships between ALEs and
depressive symptoms would be consistent for non-MDD and MDD participants. Results of
multilevel modeling and correlational analyses indicated that the relationships between ALEs
and depressive symptom patterns were largely consistent with SSCH predictions for four of six
ALEs, and that the relationships between ALEs and depressive symptoms were largely
Adverse Life Events and Depressive Symptom Patterns v
consistent across non-MDD and MDD participants. Our findings demonstrate that depressive
symptoms, expressed during both subthreshold and clinical episodes, may have evolved because
they helped our ancestors cope with the adaptive challenges of certain adverse situations.
Additional implications are discussed, along with limitations and directions for future research.
Adverse Life Events and Depressive Symptom Patterns vi
Table of Contents
Dedication.................................................................................................................................. ii
Acknowledgments..................................................................................................................... iii
Abstract .....................................................................................................................................iv
Chapter I: Introduction ................................................................................................................ 1
The Present Study ...................................................................................................................5
Chapter II: Literature Review ...................................................................................................... 7
Previous Approaches for Investigating the Relationship Between Adverse Life Events and the
Clinical Presentation of Depression .........................................................................................7
An Alternative Approach for Investigating the Relationship between Adverse Life Events and
the Clinical Presentation of Depression ................................................................................. 14
The social navigation hypothesis. ........................................................................... 19
The analytical rumination hypothesis. ....................................................................19
The social risk hypothesis. ..................................................................................... 20
The social competition hypothesis. ......................................................................... 21
The domain-independent approach to low mood. ...................................................21
The Situation-Symptom Congruence Hypothesis ...................................................................22
Research Support for the Situation-Symptom Congruence Hypothesis ..................................25
Keller and Nesse (2005). ........................................................................................ 25
Keller and Nesse (2006). ........................................................................................ 28
Keller, Neale, and Kendler (2007). ......................................................................... 33
Couyoumdjian et al. (2012). ................................................................................... 37
Limitations of Past Research ................................................................................................. 39
An Alternative Approach for Testing the Situation-Symptom Congruence Hypothesis ..........42
Hypotheses ............................................................................................................................ 44
Chapter III: Method .................................................................................................................. 48
Participants ........................................................................................................................... 48
Protection of Human Participants ..........................................................................................49
Procedures............................................................................................................................. 49
Adverse Life Events and Depressive Symptom Patterns vii
Measures ............................................................................................................................... 51
Demographic Questionnaire. .................................................................................. 51
Center for Epidemiologic Studies Depression Scale—Revised. .............................. 52
Depression module of the Structured Clinical Interview for DSM-IV Axis I
Disorders. .......................................................................................................................... 55
Depressive Symptoms Scale. ................................................................................. 56
Adverse Life Events Measure. ...............................................................................57
Research Design and Data Analysis....................................................................................... 59
Hypothesis 1 models. ............................................................................................. 62
Hypothesis 2 models. ............................................................................................. 65
Hypothesis testing. ................................................................................................. 66
Chapter IV: Results ................................................................................................................... 69
Sample Characteristics .......................................................................................................... 69

Attrition ................................................................................................................................ 71
Descriptive Statistics ............................................................................................................. 74
Frequency of observations. .................................................................................... 74
CESD-R and SCID scores. .....................................................................................75
Adverse Life Events Measure. ...............................................................................76
Adaptive symptom cluster and nonadaptive symptom cluster scores. .....................91
Depressive Symptoms Scale scores. ..................................................................... 105
Correlations. ........................................................................................................ 115
Data Screening .................................................................................................................... 120
Missing data......................................................................................................... 120
Leverage and influence. ....................................................................................... 121
Assumptions........................................................................................................................ 121
Hypothesis Testing .............................................................................................................. 123
Hypothesis 1. ....................................................................................................... 124
Hypothesis 2. ....................................................................................................... 133
Chapter V: Discussion............................................................................................................. 168
Summary of Findings .......................................................................................................... 170

Adverse Life Events and Depressive Symptom Patterns viii
Hypothesis 1: Findings, Explanations, and Implications ...................................................... 171

Failure. ................................................................................................................ 171
Death of a loved one. ........................................................................................... 172
Romantic loss. ..................................................................................................... 173
Chronic stress. ..................................................................................................... 173
Social isolation. ................................................................................................... 174
Winter. ................................................................................................................. 174
Hypothesis 1: Integration of Findings with Past Literature................................................... 174
Hypothesis 1: Convergent findings....................................................................... 174
Hypothesis 1: Explanations and implications of convergent findings. ................... 175
Hypothesis 1: Divergent findings. ........................................................................ 175
Hypothesis 1: Explanations and implications of divergent findings. ..................... 176
Hypothesis 2: Findings, Explanations, and Implications ...................................................... 184
Hypothesis 2: Integration of Findings with Past Literature................................................... 189
Hypothesis 2: Convergent findings....................................................................... 189
Hypothesis 2: Explanations and implications of convergent findings .................... 190
Additional Implications of Findings for Theory, Research, and Practice .............................. 190
Limitations and Future Directions for Research ................................................................... 196
Conclusion .......................................................................................................................... 201
References .............................................................................................................................. 203
APPENDIX A Informed Consent Agreement ........................................................................ 222
APPENDIX B Demographic Questionnaire .......................................................................... 229
APPENDIX C Center for Epidemiologic Studies Depression Scale - Revised ....................... 239
APPENDIX D Depressive Symptoms Scale: Instructions, Scales, and Items ......................... 241
APPENDIX E Modified Version of the Depressive Symptoms Scale .................................... 245
APPENDIX F Adverse Life Events Measure......................................................................... 256

Adverse Life Events and Depressive Symptom Patterns ix
List of Tables
Table 1 Predictions of the Situation-Symptom Congruence Hypothesis .......................... 24
Table 2 Adverse Life Events and Corresponding Adaptive and Nonadaptive Symptom
Clusters.............................................................................................................. 46
Table 3 Sociodemographic Characteristics of Sample: Frequencies and Percentages ...... 71
Table 4 Results of Attrition Analyses ............................................................................. 73
Table 5 Frequencies and Percentages of Days Completed ............................................... 74
Table 6 Frequencies and Percentages of Responses to Failure, Total and by Day and
Make-Up Day .................................................................................................... 78
Table 7 Descriptive Statistics of Responses to Failure, Total and by Day and Make-Up
Day .................................................................................................................... 79
Table 8 Frequencies and Percentages of Responses to Death of a Loved One, Total

and by Day and Make-Up Day ........................................................................... 80
Table 9 Descriptive Statistics of Responses to Death of a Loved One, Total and by

Day and Make-Up Day ...................................................................................... 81
Table 10 Frequencies and Percentages of Responses to Romantic Loss, Total and by

Table 11 Descriptive Statistics of Responses to Romantic Loss, Total and by Day and
Make-Up Day .................................................................................................... 83
Table 12 Frequencies and Percentages of Responses to Chronic Stress, Total and by

Table 13 Descriptive Statistics of Responses to Chronic Stress, Total and by Day and
Make-Up Day .................................................................................................... 85
Table 14 Frequencies and Percentages of Responses to Social Isolation, Total and by

Table 15 Descriptive Statistics of Responses to Social Isolation, Total and by Day and
Make-Up Day .................................................................................................... 87
Adverse Life Events and Depressive Symptom Patterns x
Table 16 Frequencies and Percentages of Responses to Winter, Total and by Day and
Make-Up Day .................................................................................................... 88
Table 17 Descriptive Statistics of Responses to Winter, Total and by Day and Make-Up
Day .................................................................................................................... 89
Table 18 Frequencies and Percentages of Responses to Adverse Life Events on Day 1 ..... 90
Table 19 Results of Analyses Comparing Participants With and Without Major

Depressive Disorder on Levels of Adverse Life Events for Day 1 ...................... 91
Table 20 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Scores for Failure, Total and by Day .................................................................. 93

Scores for Failure by Make-Up Day ................................................................... 94

Scores for Death of a Loved One, Total and by Day ........................................... 95

Scores for Death of a Loved One by Make-Up Day ........................................... 96

Scores for Romantic Loss, Total and by Day ...................................................... 97

Scores for Romantic Loss by Make-Up Day ...................................................... 98

Scores for Chronic Stress, Total and by Day ...................................................... 99

Scores for Chronic Stress by Make-Up Day ..................................................... 100

Scores for Social Isolation, Total and by Day ................................................... 101

Scores for Social Isolation by Make-Up Day.................................................... 102
Adverse Life Events and Depressive Symptom Patterns xi

Scores for Winter, Total and by Day ................................................................ 103

Scores for Winter by Make-Up Day ................................................................. 104
Table 32 Descriptive Statistics for Emotional Pain, Total and by Day and Make-Up
Day .................................................................................................................. 106
Table 33 Descriptive Statistics for Pessimism, Total and by Day and Make-Up Day ...... 107
Table 34 Descriptive Statistics for Fatigue, Total and by Day and Make-Up Day ........... 108
Table 35 Descriptive Statistics for Anhedonia, Total and by Day and Make-Up Day ...... 109
Table 36 Descriptive Statistics for Rumination, Total and by Day and Make-Up Day ..... 110
Table 37 Descriptive Statistics for Crying, Total and by Day and Make-Up Day ............ 111
Table 38 Descriptive Statistics for Guilt, Total and by Day and Make-Up Day ............... 112
Table 39 Descriptive Statistics for Increased Sleep, Total and by Day and Make-Up
Day .................................................................................................................. 113
Table 40 Descriptive Statistics for Desire for Social Support, Total and by Day and
Make-Up Day .................................................................................................. 114
Table 41 Correlations for Adaptive and Nonadaptive Symptom Clusters, ALEs, and
Diagnostic Group on Day 1 .............................................................................. 116
Table 42 Correlations for scores on Adverse Life Events, Depressive Symptoms Scale
Scales, and Diagnostic Group on Day 1 ........................................................... 119
Table 43 Hypothesis 1 Multilevel Models: Adverse Life Events, Gender, and Age
Predicting Adaptive and Nonadaptive Symptom Cluster Scores ....................... 126
Table 44 Correlation Matrix and Steiger’s Z Test Results for Adverse Life Events and
Adaptive/Nonadaptive Symptom Cluster Scores .............................................. 129
Table 45 Hypothesis 2a Multilevel Model Results for Failure ......................................... 135
Table 46 Hypothesis 2b Multilevel Model Results for Death of a Loved One ................. 140
Table 47 Hypothesis 2c Multilevel Model Results for Romantic Loss ............................ 145
Adverse Life Events and Depressive Symptom Patterns xii
Table 48 Hypothesis 2d Multilevel Model Results for Chronic Stress ............................. 150
Table 49 Hypothesis 2e Multilevel Model Results for Social Isolation ............................ 155
Table 50 Hypothesis 2f Multilevel Model Results for Winter ......................................... 162

Adverse Life Events and Depressive Symptom Patterns xiii
List of Figures
Figure 1. Results of correlational analyses and Steiger’s Z tests by adverse life event. ....... 130
Figure 2. The relationships between social isolation and DSS scales (i.e., anhedonia and
desire for social support) for non-MDD and MDD participants. .......................... 160
Figure 3. The relationships between winter and DSS scales (i.e., anhedonia, rumination,
and crying) for non-MDD and MDD participants.. .............................................. 167
Adverse Life Events and Depressive Symptom Patterns 1
Chapter I: Introduction
According to the current Diagnostic and Statistical Manual of Mental Disorders (5th ed.;
DSM-V; American Psychiatric Association, 2013), approximately 7% of the population will
experience major depressive disorder (MDD), the most severe form of clinical depression, over a
12-month period. However, this prevalence varies significantly by age group; the likelihood of
experiencing MDD for18- to 29-year-old individuals is three times that for individuals who are
60 years or older (American Psychiatric Association, 2013). Additionally, females are cited as
being 1.5 to 3 times as likely as males to develop MDD (American Psychiatric Association,
2013). The lifetime risk for MDD varies in community samples, with that for women ranging
from 10% to 25% and that for men ranging from 5% to 12% (American Psychiatric Association,
2000).
Clinical depression has many negative consequences for public health, society, and the
economy. In the United States (US), it is the primary source of disability for individuals between
the ages of 15 and 44; worldwide, it is the primary source of disability for individuals who are
above the age of four (World Health Organization, 2004). In the US, more than 90% of the
33,300 annual suicides are attributed to depression and/or substance abuse disorders (Centers for
Disease Control and Prevention, 2010; Moscicki, 2001). The impact of depression on US
business is estimated to be approximately “$70 billion in medical expenditures, lost productivity,
and other costs” (Tanouye, 2001, para. 1).
There are many different terms used to reference depressive disorders and concepts, and
they are often used in an imprecise manner in the literature. For example, depression might refer
collectively to the various depressive disorders recognized by the DSM, or specifically to MDD.
It can also refer to the general phenomenon of depression, which is defined by the APA
Dictionary of Psychology as “dysphoria that can vary in severity from a fluctuation in normal
mood to an extreme feeling of sadness, pessimism, and despondency” (American Psychological
Association, 2007, p. 269). This imprecise use of the term depression and other depression
terminology makes depression an elusive concept. In this dissertation, an effort will be made to
use the most specific terms possible to refer to different depressive disorders and depression
concepts. The specific disorder names recognized by the DSM-IV-TR such as major depressive
disorder or dysthymic disorder will refer to specific clinical depressive disorders. Clinical
depression/depressive disorders will refer collectively to the depressive disorders recognized by
the DSM-IV-TR. Subthreshold depression/depressive disorders will refer to dysphoric episodes
that do not meet DSM-IV-TR criteria for a clinical depressive disorder. Depression/depressive
disorders will refer collectively to both clinical and subthreshold depression/depressive
disorders, or to the general phenomenon of depression/depressive disorders. We relied on
diagnoses recognized by the DSM-IV-TR because we used the depression module of the
Structured Clinical Interview for DSM-IV-TR (SCID; First, M. D., Spitzer, R. L., Gibbon, M., &
Williams, J. B. W., 2002) to diagnose MDD, which is based on DSM-IV-TR diagnostic criteria.
Also, the DSM-IV-TR was more widely used than the DSM-V during our data collection.
Despite its far-reaching impact, many questions regarding the nature, etiology, and
treatment of depression remain unanswered. One major issue involves identifying the factors that
influence the clinical presentation of depression. Research indicates that the symptom profiles of
MDD vary across individuals (Baumeister & Parker, 2012) and across time in the same person
(Coryell et al., 1994; Oquendo at al., 2004). This variation is more pronounced across
noncontiguous episodes, suggesting that “impermanent state factors” (i.e., environmental and/or
physiological factors) may influence the symptom profile that is expressed during a particular
episode of MDD (Coryell et al., 1994). In addition, research consistently demonstrates a causal
relationship between exposure to adverse life events (ALEs) and subsequent MDD onset
(Kendler, Karkowski, & Prescott, 1999). Furthermore, the types of ALEs that precede episodes
of MDD vary, ranging from romantic loss or a loved one’s death to failure to reach a major goal
or chronic stress (Kendler et al., 2002).
These findings have prompted researchers to investigate the relationship between ALEs
and the clinical presentation of depression. Researchers have utilized a number of different
approaches for examining this relationship. One approach focused on whether ALEs are
associated with certain subtypes of MDD (hereinafter referred to as the subtype-based
approach). For example, many studies compared the rates of pre-onset ALEs (i.e., ALEs that
precede the onset of a depressive episode) in individuals with endogenous and nonendogenous
MDD (Bebbington et al., 1988; Brown, Harris, & Hepworth, 1994; Brown, Ni Brolchain, &
Harris, 1979; Brugha & Conroy, 1985; Dolan, Calloway, Fonag, deSouza, & Wakeling, 1985;
Monroe, Thase, Hersen, Himmelhoch, & Bellack, 1985; Paykel, Rao, & Taylor, 1984; Roy,
Breier, Doran, & Pickar, 1985; Thomson & Hendrie, 1972; Zimmerman, Coryell, & Phohl,
1986;). According to the APA Dictionary of Psychology (VandenBos, 2007), endogenous
depression is a type of depression that “occurs in the absence of a psychological stressor and in
which a biological or genetic cause is implied” (p. 330) while nonendogenous depression is
“apparently precipitated by a stressful event or situation, such as a career or relationship setback”
(p. 772). In the literature, endogenous depression has also been referred to as biological,
melancholic, and psychotic depression while nonendogenous depression has been referred to as
reactive, exogenous, and atypical depression. In an effort to be clear and consistent, we will use
the most common terms, endogenous and nonendogenous depression to reference these subtypes.
A second and slightly different approach for examining the relationship between ALEs
and the clinical presentation of depression has focused on whether ALEs are related to specific
classes of depressive symptoms in MDD rather than specific subtypes of MDD (hereinafter
referred to as the class-based approach). For instance, one study examined the association
between ALEs and classes of depressive symptoms (i.e., cognitive-affective symptoms versus
somatic symptoms) in individuals with endogenous nonpsychotic MDD (Monroe, Harkness,
Simons, & Thase, 2001). Another study compared cognitive and somatic symptoms in
individuals with MDD who did and did not endorse pre-onset ALEs (Muscatell, Slavich,
Monroe, & Gotlib, 2009).
Although the subtype- and class-based approaches have yielded some meaningful results
and represent necessary steps in moving toward a better understanding of the relationship
between ALEs and the clinical presentation of depression, they have a number of significant
limitations. One limitation is that both approaches have yielded inconsistent findings, leading
some researchers to conclude that there is a weak relationship between ALEs and the clinical
presentation of depression (Mazure, 1998), and others to argue that there are problems with the
manner in which stress (Monroe & Simon, 1997) and depressive subtypes (Gotlib & Hammen,
2009; Hammen, 2005; Mazure, 1998) have been defined. A second limitation is that these
approaches have limited their focus to the most severe form of depression by only including
research participants diagnosed with MDD. This diagnostic requirement prevents researchers
from detecting any stress-symptom associations that are not consistent with current diagnostic
criteria, and any stress-symptom associations that are specific to less severe forms of depression.
A third limitation is that these approaches are limited to examining the relationship between
ALEs and the clinical presentation of depression at a proximate level of analysis, thereby failing
to consider an ultimate level of analysis. A proximate examination aims to understand how the
relationship under investigation works while an ultimate examination aims to determine why the
relationship exists in the first place. Researchers and theorists increasingly recognize that a
comprehensive understanding of any psychological phenomenon requires examination at both

proximate and ultimate levels of analysis (Brune et al., 2012; Confer et al., 2010; Gilbert, 2013;
Siegert, 2003).
The Present Study
An alternative approach for examining the relationship between ALEs and the clinical
presentation of depression focuses on whether different types of ALEs are associated with
different patterns of depressive symptoms, and lacks the limitations cited above. Grounded in
evolutionary theory, Keller and Nesse’s (2006) situation-symptom congruence hypothesis
(SSCH) is consistent with this approach. Evolutionary psychology assumes that psychological
disorders arise from a set of adaptations that are, at some level, functional. Based on the
assumption that different depressive symptoms solve different problems, the SSCH argues that
different adverse situations should trigger different depressive symptom patterns that help the
individual deal with the adaptive challenges characteristic of the situation (Keller & Nesse,
2006).
A number of recent research studies support the SSCH (Couyoumdjian et al., 2012;
Keller, Neale, & Kendler, 2007; Keller & Nesse, 2005, 2006) but are limited in numerous ways.
Some of these limitations include the following: compared to concurrent reports, retrospective
reports about experiences that occurred a week or more in the past are less reliable and valid due
to increased potential for contamination caused by self-enhancement, faulty memory, and
anchoring bias (Henry, Moffitt, Caspi, Langley, & Silva, 1994; Ross & Fletcher, 1985; Schwarz
& Sudman, 1994; Smith, Leffingwell, & Ptacek, 1999); Keller et al. (2007) were the only
researchers who examined the relationship between ALEs and depressive symptom patterns in a
within-person sample and in a sample of participants diagnosed with MDD; studies that utilize
mood induction procedures have questionable external validity and an increased likelihood of
demand effects; sample characteristics that limit generalizability and external validity; asking
participants to choose a single ALE category to indicate the ALE they believe led to their
dysphoric episode may reduce validity of the predictor variable; and the utilization of statistical
procedures that limit what can be learned from the data. In the present study, we will test the
SSCH using an alternative approach that attempts to address these limitations.
In order to provide a strong foundation for exploring the relationship between different
types of ALEs and depressive symptom patterns, and testing specific evolutionary predictions of
the SSCH, we will examine a number of different areas of theory and research. First, we will
discuss previous approaches for examining the relationship between ALEs and the clinical
presentation of depression, along with the limitations of these approaches. Second, we will
introduce the SSCH as an alternative approach for investigating the relationship between ALEs
and the clinical presentation of depression, and discuss its advantages over previous approaches.
Third, we will introduce the evolutionary approach to depression followed by the major
evolutionary models of depression. Fourth, we will critically examine research that has tested the
SSCH or examined the relationship between ALEs and depressive symptom patterns. Fifth, we
will describe our study and hypotheses.

Chapter II: Literature Review
Previous Approaches for Investigating the Relationship Between Adverse Life Events and
the Clinical Presentation of Depression
From the late 1970s to the mid-1990s, researchers investigated the relationship between
adverse life events (ALEs) and the clinical presentation of depression by focusing on whether
ALEs are associated with specific subtypes of major depressive disorder (MDD). Researchers
who utilized this subtype-based approach restricted their investigations to the endogenous and
nonendogenous subtypes of MDD. Based on the biopsychosocial model of depression, the
subtype-based approach assumes that biological, psychological, and/or environmental/social
factors play key roles in the etiology of MDD, and that these factors can interact in a unique
manner that leads to different subtypes of MDD. For example, biological or genetic factors are
believed to play larger roles in the etiology of endogenous MDD while environmental or social
factors are believed to play larger roles in the etiology of nonendogenous MDD. Although
psychological factors such as cognitive vulnerabilities or personality variables are often
considered in research examining the general stress-depression relationship, they were not, to our
knowledge, a focus of research examining the relationship between ALEs and subtypes of MDD.
Researchers who utilized the subtype-based approach examined whether individuals
diagnosed with endogenous and nonendogenous MDD varied in their rates of pre-onset ALEs.
Most researchers found no significant difference in the rates of pre-onset ALEs for individuals
with endogenous and nonendogenous MDD (Bebbington et al., 1988; Brown, Harris, &
Hepworth, 1994; Brown et al., 1979; Brugha & Conroy, 1985; Dolan et al., 1985; Monroe et al.,
1985; Paykel et al, 1984; Roy et al., 1985; Thomson & Hendrie, 1972; Zimmerman et al., 1986).
However, some researchers found that individuals with nonendogenous MDD had
significantly higher rates of pre-onset ALEs than individuals with endogenous MDD (Cornell,
Milden, & Shrimp, 1985; Matussek & Neuner, 1981), and a normal control group (Fountoulakis,
Iacovides, S. Kaprinis, & Kaprinis, 2006). Frank, Anderson, Reynolds, Ritenour, and Kupfer
(1994) also found a significantly higher rate of pre-onset ALEs for individuals with
nonendogenous MDD than individuals with endogenous MDD, and this pattern was true for
individuals with and without histories of recurrent MDD. On the other hand, Mitchell et al.
(2003) found that ALEs were more likely to precede first rather than subsequent episodes of
MDD, particularly for individuals with endogenous MDD. Similarly, in a group of individuals
assessed with the Life Events and Difficulties Schedule (LEDS), Brown et al. (1994) found high
rates of pre-onset ALEs in individuals with endogenous MDD who were experiencing first
episodes and in individuals with nonendogenous MDD who were experiencing first or
subsequent episodes. However, in a sample of individuals diagnosed using a British diagnostic
category, Brown et al. found significantly lower rates in a small group of individuals with
endogenous MDD using a British diagnostic category who were experiencing subsequent
episodes. Finally, Paykel et al. (1984) found no significant difference in rates of pre-onset ALEs
for individuals with endogenous and nonendogenous MDD, but did find that individuals with
endogenous MDD had significantly lower rates of a more specific category of pre-onset ALEs,
chronic difficulties, than individuals with nonendogenous MDD.
These inconsistent findings led many researchers to conclude there is a weak relationship
between ALEs and subtypes of MDD (Mazure, 1998). On the other hand, Brown et al. (1994)
found that individuals with endogenous MDD experiencing first episodes and individuals with
nonendogenous MDD experiencing first or subsequent episodes had high rates of pre-onset
ALEs while individuals with endogenous MDD not experiencing their first episode had
significantly lower rates of pre-onset ALEs. Based on this finding, Brown et al. suggested that
episode recurrence may contribute to the weak relationship observed in some studies.
Other researchers have argued that the inconsistent findings resulted from the lack of a
standardized approach in defining and measuring ALEs (Hammen, 2005; Ingram & Siegle, 2009;
Mazure, 1998) and depressive subtypes across studies (Katschnig, Pakesch, & Egger-Zeidner,
1986). For example, some studies measured life events with checklists such as the Social
Readjustment Rating Scale (Cornell et al., 1985; Grant, Gerst, & Yager, 1976; Thomson &
Hendrie, 1972) or the Psychiatric Epidemiology Research Interview Life Events Scale
(Dohrenwend, Krasnoff, Askenasy, & Dohrenwend, 1978; Monroe et al., 1985) while other
studies assessed life events with semi-structured interviews such as the Recent Life Events
Interview (Paykel, 1997; Paykel et al., 1969; Roy et al., 1985) or the LEDS (Bebbington et al.,
1988; Brown & Harris, 1989; Brown et al., 1994; Brown et al., 1979; Dolan et al., 1985; Frank et
al., 1994). Checklists are limited to the events listed, and therefore, may overlook certain events
that would be detected by an interview method (Mazure, 1998; Paykel, 1983). Also, checklists
do not assess an event within the context of an individual’s life circumstances (Paykel, 1983).
For example, an unintended pregnancy can range from a somewhat stressful event to an
extremely stressful event, depending on a woman’s financial situation or the quality of her
marital relationship (Monroe and Depue, 1991).
In 2001, researchers began to examine the relationship between ALEs and the clinical
presentation of depression by focusing on whether ALEs are related to specific classes of
depressive symptoms rather than specific subtypes of depression. Based on the biopsychosocial
model of depression, the class-based approach assumes that biological, psychological, and/or
social factors play key roles in the etiology of depression, and that these factors can interact in a
unique manner that leads to specific depressive symptom profiles.
The few researchers who have utilized the class-based approach have restricted their
investigations to the following classes of depressive symptoms: cognitive/affective and somatic.

Monroe et al. (2001) examined these relationships in individuals with endogenous, nonpsychotic
MDD and found that pre- but not post-onset ALEs were associated with cognitive-affective
symptoms and suicidal ideation but not somatic symptoms. Muscatell et al. (2009) also examined
these relationships and found that ALEs were associated with both cognitive and somatic
symptoms in males and females with MDD. Again, the inconsistency in these findings may have
resulted from the different methodologies utilized across studies. For example, Monroe et al.
(2001) measured symptoms using the Beck Depression Inventory-1a (BDI-IA; Beck & Steer,
1993) and the interview version of the Hamilton Rating Scale for Depression (Hamilton, 1960)
while Muscatell et al. (2009) did so using the BDI-IA and Beck Depression Inventory-II (Beck,
Steer, & Brown, 1996). Muscatell et al. (2009) acknowledged that an interview-based symptom
measure may be a more sensitive method for detecting specific stress-symptom associations.
To date, most of the researchers who have examined the relationship between ALEs and
the clinical presentation of depression have utilized the subtype- or class-based approach.
Unfortunately, these approaches are characterized by numerous limitations. One limitation is that
both approaches have yielded inconsistent findings that probably resulted, at least in part, from
methodological issues (Hammen, 2005; Ingram & Siegle, 2009; Mazure, 1998). For example, the
majority of these studies have focused on broad categories of ALEs by including various types of
events in one category (Bebbington et al., 1988; Brown et al., 1979; Brown et al., 1994; Brugha
& Conroy, 1985; Dolan et al., 1985; Monroe et al., 1985; Monroe et al., 2001; Muscatell et al.,
2009; Paykel et al., 1984; Roy et al., 1985; Thomson & Hendrie, 1972; Zimmerman et al., 1986).
Monroe and Simons (1991) argue that “a comprehensive conceptualization of stress can lead to a
vague definition of the construct, which lacks the requisite theoretical specificity for powerful
prediction” (p. 409). In other words, it is possible that stress has been defined in a manner that is
too broad to detect stress-symptom associations. Monroe et al. (2001) suggests that “partitioning
severe events into more fine-grained classes of theoretical relevance” may lead to further
detection of stress-symptom associations” (p. 173).
A second limitation is that these approaches have limited their focus to MDD, the most
severe form of depression. A diagnosis of MDD requires that certain predefined symptoms are
present. At the time of data collection for our study, the DSM-IV-TR (American Psychiatric
Association, 2000) was considered the gold standard for making psychiatric diagnoses. The
DSM-IV-TR required the presence of at least five of nine predefined symptoms over a period of
at least two weeks. In research, these strict requirements increase the likelihood of homogeneous
symptom profiles and prevent researchers from detecting stress-symptom associations that are
inconsistent with the DSM-IV-TR’s diagnostic criteria for MDD.
Requiring a diagnosis of MDD also prevents researchers from detecting stress-symptom
associations that present in less severe forms of depression since they may not be the same as
those which present during MDD. Sadek and Bona (2000) found that many patients who no
longer met criteria for a DSM-IV-TR depressive disorder continued to present with depressive
symptoms that caused significant psychosocial impairment. In addition, Judd, Schettler, and
Akiskal (2002) examined the course of illness and symptom status in individuals with MDD and
found that their typical symptom status was characterized by subthreshold depressive symptoms
that were associated with psychosocial impairment. Based on these results, they argued that, over
the long-term, the symptomatic presentation of MDD is dimensional rather than categorical in
nature. These findings suggest that less severe forms of depression are a significant problem for
individuals with MDD and should not be overlooked in research.
A third limitation is that the subtype- and class-based approaches have limited their focus
to proximate as opposed to ultimate explanations of the relationship between ALEs and the
clinical presentation of depression. A proximate explanation focuses on how a psychological

mechanism works while an ultimate or evolutionary explanation focuses on why the
psychological mechanism exists in the first place. Before elaborating on this limitation, we will
briefly discuss the value of explaining a phenomenon at both a proximate and ultimate level of
analysis. Researchers and theorists are increasingly recognizing that a full scientific
understanding of any phenomenon requires understanding at both a proximate and ultimate level
(Brune et al., 2012; Confer et al., 2010; Gilbert, 2013; Siegert, 2003). An ultimate level is also
referred to as an evolutionary or adaptationist level. As stated by MacDougall-Shackleton
(2011):
Consideration at one level can help generate novel hypotheses at the other, define
categories of behavior and set criteria that must be addressed. Taking an adaptationist
stance thus strengthens research on proximate mechanisms. Similarly, it is critical for
researchers studying adaptation and function to have detailed knowledge of proximate
mechanisms that may constrain or modulate evolutionary processes. (p. 2076)
Numerous evolutionary theorists use the example of fever to demonstrate the value of
explaining a phenomenon at both a proximate and ultimate level of analysis (Keller & Nesse,
2006; Nesse, 2005: Nesse & Williams, 1994). Fever was considered to be an abnormal response
for many years and doctors would often suppress it with drugs like acetaminophen. At a
proximate level, fever is an increase in body temperature that can be triggered by bacterial toxins
or other fever-producing agents. However, an ultimate level of analysis recognizes the significant
metabolic costs of fever and the fact that it is a universal capacity as clues that it might be
adaptive. Indeed, it is now clear that fever is often a normal physiological response to infection
or inflammation that aids in the survival of an individual by eliminating invading pathogens
(Soszynski, 2003).
Clearly, both levels of analysis are necessary for a comprehensive and accurate
understanding of fever. A proximate explanation provides invaluable information about the
mechanisms that produce and maintain a fever, and informs the ultimate level of analysis by
providing clues that it may be an evolved response. An ultimate explanation tells us that fever is
a normal response that evolved to protect against infection in certain instances, and informs the
proximate level of analysis by providing insight into specific situations in which it might be
adaptive, as well as those mechanisms which are providing the adaptive response. At a more
practical level, these complimentary explanations provide invaluable information about when
physicians should and should not suppress or treat fever.
It should now be clear why a proximate and ultimate explanation are necessary for a full
understanding of any phenomenon. We have discussed two approaches for examining the
relationship between ALEs and the clinical presentation of depression, namely, the subtype-and
class-based approaches. Again, a third limitation of these approaches is that they seek a
proximate as opposed to ultimate explanation of this relationship. Both approaches are based on
the biopsychosocial model of depression, which attempts to explain the relationship between
ALEs and the clinical presentation of depression at a proximate level by identifying and
describing the biological, psychological, and/or social factors that contribute to or maintain
depression.
More specifically, the subtype-based approach focuses on whether ALEs are associated
with specific subtypes of MDD, and attempted to show that social/environmental factors (i.e.,
ALEs) play a significant role in a subtype of MDD that is thought to be more
social/environmental in nature (i.e., nonendogenous MDD) but not in a subtype of MDD that is
believed to be more biological in nature (i.e., endogenous MDD). Similarly, the class-based
approach focuses on whether ALEs are related to specific classes of depressive symptoms, and
attempts to demonstrate that social/environmental factors (i.e., ALEs) are more strongly
associated with a class of depressive symptoms that is thought to be more social/environmental
in nature (i.e., cognitive-affective symptoms) than with a class of depressive symptoms that is
thought to be more biological in nature (i.e., somatic symptoms).
Both approaches are limited to providing a proximate explanation of the relationship
under investigation because they aim to describe proximate aspects of the relationship (i.e., the
extent to which environmental/social factors play a role in biological and non-biological
subtypes of MDD or specific classes of depressive symptoms). They fail to address why the
relationship may exist in the first place, and more specifically, whether the relationship between
ALEs and the clinical presentation of depression is an evolved response that provides a selective
advantage in certain situations.
In summary, both the subtype- and class-based approaches have been utilized to
investigate the relationship between ALEs and the clinical presentation of depression. The
subtype-based approach focused on whether ALEs are associated with specific subtypes of MDD
while the class-based approach focused on whether ALEs are related to specific classes of
depressive symptoms in MDD. Limitations of these approaches include the following:
inconsistent findings that are likely due to methodological issues; focus on MDD, which prevents
researchers from detecting stress-symptom associations that are not consistent with the DSM’s
current diagnostic criteria for MDD; and finally, failure to consider why the capacity for a
depressive response to ALEs might have evolved in the first place.
An Alternative Approach for Investigating the Relationship between Adverse Life Events
and the Clinical Presentation of Depression
An alternative approach for examining the relationship between ALEs and the clinical
presentation of depression focuses on whether different types of ALEs are related to different
patterns of depressive symptoms, and lacks the limitations cited above. Keller and Nesse’s
(2006) situation-symptom congruence hypothesis (SSCH) is consistent with this approach.
Grounded in evolutionary theory, the SSCH aims to explain why human beings experience
symptoms of depression in the first place. Based on the assumption that certain depressive
symptoms serve certain adaptive functions, the SSCH hypothesizes that different types of
adverse situations should trigger different depressive symptom patterns that help the individual
deal with the adaptive problems characteristic of the adverse situations (Keller & Nesse, 2006).
For example, the SSCH argues that crying often causes others to offer social support and should
be adaptive in situations that involve a loss of social support such as a loved one’s death or
romantic breakup.
The SSCH lacks the limitations of previous approaches for examining the relationship
between ALEs and the clinical presentation of depression. To begin with, the SSCH does not
suffer from the aforementioned methodological issues of the subtype- and class-based
approaches. Rather than including all different types of ALEs within one construct, which may
prevent detection of more specific ALE-symptom associations, the SSCH separates ALEs into
different categories based on evolutionary theory. For example, the subtype- and class-based
approaches would have assigned failure at an important goal, social isolation, and other ALEs to
a single construct encompassing all ALEs. However, the SSCH argues that ALEs such as failure
at an important goal and social isolation are characterized by different adaptive challenges, and
therefore, would lead to different symptoms that provide some advantage given the adaptive
challenges of the situation.
For example, when an individual fails at a significant goal, they have likely invested a
large amount of valuable resources (i.e., time, psychological, energy, or money) that did not
result in any return. Depressive symptoms such as fatigue (i.e., feeling of physical or mental
exhaustion) should help an individual stop investing resources in a goal they are unlikely to
reach. On the other hand, social isolation involves a lack of social resources and should lead to
depressive symptoms such as crying, which often leads others to offer social support and
strengthens interpersonal connections. Given that failure at an important goal and social isolation
are predicted to be associated with different adaptive challenges and different symptoms, it
makes sense to place them in separate theoretical categories. As mentioned previously, doing so
may provide “sufficient statistical power for detecting differential effects” (Monroe et al., 2001,
p. 174).
Additionally, unlike previous approaches for examining the relationship between ALEs
and the clinical presentation of depression, the SSCH does not limit its focus to MDD. Instead,
the SSCH makes predictions about subthreshold depression, and is based on the assumption that
understanding subthreshold depression will inform our understanding of clinical depression. In
doing so, it does not require the strict diagnostic criteria of MDD, which may increase the
likelihood of homogeneous symptom profiles and prevent detection of stress-symptom
associations that are not in line with current diagnostic criteria. It also takes the dimensional
nature of the long-term symptomatic presentation of MDD into consideration, thereby allowing
researchers to investigate subthreshold forms of depression that are often overlooked despite
their significant negative impact and frequent expression over the course of MDD.
Finally, the SSCH is not limited to examining the relationship between ALEs and the
clinical presentation of depression at a proximate level of analysis. Proximate explanations tell us
how a mechanism works. While previous approaches have sought a proximate explanation for
the relationship between ALEs and depressive symptom patterns, the SSCH pursues and ultimate
explanation, which attempts to explain why the relationship under investigation exists in the first
place. An ultimate explanation is not only necessary for a full understanding of any
psychological phenomenon, it also informs research seeking proximate explanations, tells us
whether certain depressive symptoms are a normal response to particular ALEs, and provides
insight into when depressive symptoms should be treated.
Evolutionary Models of Depression
As discussed previously, the SSCH is grounded in evolutionary theory. In general,
evolutionary approaches to psychopathology assume that psychological disorders arise from a set
of adaptations that are, at some level, functional. These adaptations evolved because they helped
our ancestors cope more effectively with adaptive challenges they faced repeatedly over
evolutionary time. Evolutionary theorists have acknowledged that it is sometimes difficult to
understand how a negative state may be adaptive, and have used the following examples to
facilitate understanding: it is often assumed that negative states like fever and pain are abnormal
despite evidence that they are regulated by evolved systems which are activated in certain
unfavorable situations (Keller & Nesse, 2006; Nesse, 2005; Nesse & Williams, 1994). Nesse
(1990) argued that the same is true for affect states, describing them as:
specialized modes of operation shaped by natural selection to adjust the physiological,
psychological, and behavioral parameters of the organism in ways that increase its
capacity and tendency to respond adaptively to the threats and opportunities characteristic
of specific kinds of situations (p. 268).
In other words, emotions are controlled by evolved systems and help individuals deal more
effectively with the particular situations in which they are aroused. When expressed in
appropriate situations, they provide the individual with a selective advantage (Nesse, 2009a).
A substantial amount of theoretical research and some empirical research supports this
argument. Leading theorists have agreed that the emotions are expressed as a set of organized
changes in biological, cognitive, and behavioral systems (Arnold, 1960; Izard, 1977; Lazarus,
Konner, & Folkman, 1980; Plutchik, 1980; Strongman, 1987; Tomkins, 1980; Young, 1979).
Likewise, evolutionary theorists have agreed that evolved systems control and regulate these
depressive symptoms (Beck, 1967; Gilbert, 1992; Hill, 1968; Lewis, 1934; Nesse, 1990; Powles,
1992).
In addition, researchers and theorists have asserted that depressive symptoms are reliably
elicited in specific unfavorable situations (Brown & Harris, 1978, 1986; Cooke & Hole, 1983;
Finlay-Jones & Brown, 1981; Lloyd, 1980; Monroe & Simons, 1991; Monroe, 1990; Paykel,
1982). A study by Finlay-Jones and Brown (1981) provides empirical support for this assertion.
They examined the relationship between recent ALEs and three types of psychiatric disorders
(anxiety, depression, and mixed anxiety/depression), and found that significant loss, grave
danger, and combined significant loss-grave danger contributed to these three types of
psychiatric disorders, respectively. To summarize, evolutionary theorists argue that depressive
symptoms are not necessarily abnormal or maladaptive, and may have evolved to help human
beings deal more effectively with certain unfavorable situations.
Although all major evolutionary models of depression view depression as arising from a
set of adaptations that are, at some level, functional, they vary on two important dimensions. One
dimension involves what depressive state is considered to be adaptive. Adaptation models view
clinical depression as an adaptation while dysregulation models view clinical depression as the
product of an adaptive mechanism (i.e., the capacity for depressed mood) that has stopped
functioning properly. Dysregulation models assume understanding the capacity for low mood is
necessary for a comprehensive understanding of clinical depression. Another dimension on
which evolutionary models vary is the domain in which the depressive state is hypothesized to
function. Domain-specific models limit the functionality of depressive symptoms to particular
types of situations such as those that involve social interactions (Allen & Badcock, 2003), social
competition (Price, Sloman, Gardner, Gilbert, & Rohde, 1994), or social problem-solving
(Watson & Andrews, 2002) while domain-independent models argue that symptoms of
depression can be adaptive in various types of situations that involve fitness challenges (Nesse,
2000).
Evolutionary models of depression represent a relatively recent movement in psychology.
These models have not only succeeded in providing a strong theoretical foundation for
explaining and exploring depression, but also in generating many testable hypotheses. However,
empirical investigations of these models remain limited (Kennair, 2003). We will discuss some
of the major evolutionary models of depression.
The social navigation hypothesis. Watson and Andrews’ (2002) social navigation
hypothesis (SNH) views clinical depression as an adaptation that functions in the domain of
social problem-solving. According to the SNH, depression serves a social rumination and social
motivation function. The social rumination function triggers psychological changes that help the
individual examine and solve important adaptive problems in fitness-relevant social situations.
For example, anhedonia prevents the individual from being distracted by pleasurable activities,
and therefore, preserves energy and resources for examining and solving fitness-relevant social
problems. The social motivation function involves the fitness costs produced by depressive
symptoms such as anhedonia, which are consciously and unconsciously signaled to members of
the depressed individual’s social group and motivate group members to provide various forms of
support that may improve the depressed individual’s situation.
The analytical rumination hypothesis. Andrews and Thomson’s (2009) analytical
rumination hypothesis (ARH) asserts that clinical depression is an adaptation that functions in
the domain of complex problem-solving. According to the ARH, clinical depression evolved
because it helped individuals engage in sustained analysis of complex problems by triggering

psychological and physical changes in the individual. These changes involve preserving
cognitive resources for examining the complex problem, preventing the individual from wanting
to engage in other pleasurable activities, and lessening the number of distractions experienced by
the individual. Together, these changes provide a fitness advantage by helping the individual
solve complex social problems that represent adaptive challenges faced repeatedly by our
ancestors over evolutionary time.
The social risk hypothesis. Allen and Badcock’s (2003) social risk hypothesis (SRH) of
depressed mood argues that depressed mood is an adaptation that functions to minimize risk in
social situations. More specifically, the theorists state that depressed mood “evolved to minimize
risk in social interactions in which individuals perceive that the ratio of their social value to
others, and their social burden on others, is at a critically low level” (p. 887). The SRH is based
on the assumption that each member of a social group has a certain cost-benefit ratio for the
group. The individual’s cost to the group, or social burden, involves the amount of resources they
take from the group while the individual’s benefit to the group, or social value, involves the
amount of resources they provide the group. When the individual’s cost and benefit to the group
are nearly equivalent, he or she is in danger of being excluded from the group. Because the social
group has provided many fitness-relevant resources (e.g., reproductive opportunities) over
evolutionary time, a mechanism that reduced the likelihood of exclusion from the group evolved
because it provided a fitness advantage.
Allen and Badcock (2003) argue that certain features of depressed mood states are
mechanisms that reduce social risk for an individual at risk for social exclusion. These
mechanisms include “(a) hypersensitivity to signals of social threat from others, (b) sending
signals to others that reduce social risk, and (c) inhibiting risk-seeking (e.g., confident,
acquisitive) behaviors” (p. 887). For example, increased sensitivity to others’ socially threatening
communications occurs because the depressed individual’s attention is focused on threatening
social cues, and the depressed individual interprets such cues as more socially threatening than
they actually are. This mechanism reduces social risk by allowing the depressed individual to
avoid taking actions that might result in social losses or exclusion.
The social competition hypothesis. The social competition hypothesis asserts that
depressed mood allows individuals to concede when they are involved in competitions in which
they are likely to lose social rank (Price, et al., 1994). More specifically, depressed mood is an
“involuntary subordinate strategy” (ISS) that helps the individual settle a social conflict while
reducing or preventing injury and other negative consequences (p. 309). This comes about
through three adaptive functions. One function involves producing a psychological state of
powerlessness in which the individual stops behaving aggressively toward competitors they are
unlikely to defeat. A second function involves conveying to one’s social group and competitors
that one has given up. A third function involves inducing a psychological state of submission,
which helps the individual accept the loss and communicate his or her position to others. A
maladaptive depressive disorder may result if the ISS is unable to function properly (e.g., the
individual is unwilling to accept the loss)
The domain-independent approach to low mood. Nesse’s (2000, 2009a) domain-
independent approach to low mood argues that depressed mood can be adaptive in many
domains, and draws from Klinger’s (1975) work on goal disengagement. Nesse sees the capacity
for low mood as an adaptive mechanism but views clinical depression as either a low mood
mechanism that is not functioning properly or a brain abnormality. Additionally, his approach
can be characterized as domain-independent because he believes the capacity for low mood can
be adaptive in many different types of situations. Nesse argues that mood is an adaptation that
regulates how resources are invested in environments that vary on level of propitiousness. A
propitious environment is one in which an individual is behaving in a manner that is likely to
make progress toward an important goal while an unpropitious environment is one in which an
individual is behaving in a manner that is unlikely to do so.
According to Nesse, certain features of depressed mood increase the individual’s “ability
to cope with the adaptive challenges characteristic of unpropitious situations in which effort to
pursue a major goal will likely result in danger, loss, bodily damage, or wasted effort” (2000, p.
14). For example, Nesse argues that decreased motivation may block behaviors related to goal
pursuit and is adaptive when an individual is pursuing a major goal they don’t have the resources
to reach; low mood is also adaptive in this situation because it encourages the individual to
consider investing valuable resources in alternative pursuits. Low mood can transform into
clinical depression if the individual continues to invest resources in a pursuit that will not pay off
(Klinger, 1975; Nesse, 2009a). Nesse identifies numerous reasons that an individual might not be
willing or able to abandon an unattainable goal, including but not limited to anxiety or excessive
desire to succeed (Nesse, 2009a). Clinical depression may also result from a brain abnormality,
or a low mood mechanism that is not functioning properly.
The Situation-Symptom Congruence Hypothesis
Keller and Nesse’s (2006) situation-symptom congruence hypothesis (SSCH) represents
a testable evolutionary hypothesis that draws from Nesse’s domain-independent approach to low
mood (2000, 2009). As mentioned earlier, the SSCH argues that different types of ALEs may
result in different patterns of depressive symptoms which serve to solve the fitness problems
characteristic of the situation in which they are triggered. Unlike many evolutionary models of
depression, the SSCH focuses on subthreshold depression as opposed to clinical depression.
Keller and Nesse chose this focus because a diagnosis of clinical depression may conceal
relevant depressive symptom patterns that are inconsistent with current diagnostic criteria for
depression (Judd, Akiskal, & Paulus, 1997; Keller & Nesse, 2006), and because clinical forms of
depression are often maladaptive. The SSCH also differs from many other evolutionary models
by asserting that depressive symptoms serve different functions and can be adaptive across many
types of situations.
Based on the assumption that specific depressive symptoms may help solve adaptive
problems characteristic of the situations in which they are triggered, the SSCH argues that
certain depressive symptoms are likely to be more pronounced following particular unfavorable
situations. For example, Keller and Nesse (2006) state that
Fatigue refers to physical or mental weariness. Normally fatigue results from exertion
and motivates conserving energy and disengaging motivation. It is parsimonious to
assume that fatigue serves the same functions when continued striving is unlikely to be
rewarded, such as following failures (given that continued striving at failed goals is
maladaptive), when one is unable to cope with all they are attempting to do, or when
physical exertion should be minimized to conserve energy, such as might have occurred
during ancestral winters. (p. 318)
The SSCH also makes predictions about situations in which the following symptoms should be
adaptive: crying, desire for social support, pessimism, guilt, rumination, anhedonia, anxiety,
appetite changes, and sleep increases/decreases. Based on predictions made by Keller and Nesse
(2006), Table 1 lists each depressive symptom, its proposed function, and the unfavorable
situations in which it is likely to be adaptive. Some depressive symptoms may be consequences
of physiological events that occur in the nervous system during depression (Keller & Nesse,
2006). It should be mentioned that the SSCH does not make predictions about the presence or
absence of certain depressive symptoms in certain situations; instead, the SSCH makes
predictions about how pronounced certain symptoms are in specific situations.

Table 1
Predictions of the Situation-Symptom Congruence Hypothesis
Symptom Proposed function of symptom Situation in which symptom should

be prominent
Emotional pain To make situations in which there is a Death of a loved one, romantic loss,
loss of fitness-relevant resources failure at important goal, social
painful isolation
Crying To strengthen social bonds Death of a loved one, romantic loss,
social isolation
Desire for To create new social bonds or Death of a loved one, romantic loss,
social support strengthen deficient social bonds social isolation
Fatigue To decrease effortful behavior in Failure at important goal, chronic
unfavorable situations stress/difficulty coping, ancestral
winters
Pessimism To stop investing resources in Failure at important goal, chronic
unattainable goals stress/difficulty coping
Guilt To gain insight into one’s role in Romantic loss, failure at important
problematic situations goal, chronic stress/difficulty
coping
Rumination To learn from a current situation in Romantic loss, failure at important
order to avoid similar ones in the goal, chronic stress/difficulty
future coping
Anhedonia To decrease approach and risk-taking Failure at important goal, chronic
behaviors in unfavorable situations stress/difficulty coping, ancestral
winters
Anxiety To increase one’s attention to and Threatening situations
vigilance against potential threats
High appetite To increase caloric intake when food is Ancestral winters
scarce
Low appetite To decrease caloric intake in order to *
reduce energy expenditure or
exposure to risk in unfavorable
situations
Increased sleep To conserve energy in unfavorable Ancestral winters
situations
Decreased To maintain hypervigilance in *
sleep dangerous or risky situations
* The SSCH does not make any specific predictions about this symptom.
Research Support for the Situation-Symptom Congruence Hypothesis
Unlike most evolutionary models of depression, numerous researchers have tested the
SSCH over the last decade (Couyoumdjian et al., 2012; Keller et al., 2007; Keller & Nesse,
2005, 2006).
Keller and Nesse (2005). Keller and Nesse conducted the first of these studies in 2005.
They investigated why certain depressive symptoms may present during a particular depressive
episode by examining the relationship between types of ALEs and depressive symptom patterns.
Unlike the majority of researchers examining depressed mood from an evolutionary perspective,
Keller and Nesse did not argue that depressed mood has a single function that is expressed in a
single domain, such as a minimizing risk in social situations (Allen & Backcock, 2003). Instead,
they hypothesized that various subtypes of depression may have developed over evolutionary
time because they helped individuals solve adaptive problems characteristic of different types of
unfavorable situations.
Given that Keller and Nesse (2005) viewed depressed mood as an adaptation, part of their
research involved determining the most probable functions of specific depressive symptoms in
different adverse situations. They identified functions for the following depressive symptoms:
sadness, crying, guilt, fatigue, pessimism, changes in appetite, and sleep disturbance. For
example, they cited research that indicated that people often comfort and empathize with
individuals who are crying (Cornelius, 1997; Labbot, Martin, Eason, & Berkey, 1991); and other
research that suggested that crying may lead to stronger interpersonal connections (Frijda, 1986).
Based on these research findings, Keller and Nesse argued that “one function of crying in adults
is to solicit help and to strengthen weakened social networks” (p. 29), and hypothesized that
crying is likely to be exhibited in situations characterized by interpersonal losses or limited
interpersonal support. Another example involves fatigue, which Keller and Nesse described as a
state that warns the individual that he or she has minimal energy and should use energy resources
sparingly. In addition, individuals experiencing depressed mood become fatigued more easily
and resting does not ameliorate this symptom. They argued that fatigue most likely helps
individuals to preserve energy resources and stop working toward unattainable goals, and
therefore, may serve an adaptive function in situations in which an individual’s additional
striving will probably not help him or her reach a goal (i.e., failure), or in unfavorable situations
or environments (i.e., ancestral winters).
Keller and Nesse (2005) asked 2,791 undergraduate students if they had gone through a
2-week period in which they experienced low mood during the previous 12 months. Nine
hundred and twenty students reported such an experience. Oversampling for rare ALEs, the
researchers asked 542 of the 920 eligible students to participate in their study. The final sample
included 337 students, of which 62% were female. The sample had a median age of 20.
Keller and Nesse (2005) assessed ALEs by asking participants to think of the 7-day
period during which they felt the most down over the previous 12 months, and write about
anything they believed might have caused this episode. Participants were asked not to include
any symptoms they experienced during this period of low mood in their response to ensure that
Keller and two research assistants were unaware of participants’ symptoms when reviewing
participants’ responses and attempting to agree on ALE categories. Based on Keller and the
research assistants’ coding, ALE categories included death of a loved one (n = 34), romantic loss
(n = 34), social isolation (n = 64), failure at an important goal (n = 33), stress (n = 38),
wintertime (n = 33), and other cause (n = 44). The researchers used the 20-item Center for
Epidemiologic Studies Depression Scale (CES-D; Radloff, 1977) to assess the depressive
symptoms participants experienced during their periods of low mood. The researchers reworded
this scale so that it was in the past tense. Based on face validity of the CES-D items, the
researchers identified the following symptom scales: sadness, crying, guilt, fatigue, pessimism,
decreased appetite, and disturbed sleep. ALEs served as the (between-person) predictor variables
and the depressive symptoms served as the (within-person) response variables.
Keller and Nesse (2005) conducted a MANOVA profile analysis with an ALE x
Symptom omnibus interaction term to examine the relationships between ALEs and depressive
symptom patterns. In addition, the researchers conducted one planned interaction contrast for
each of the six ALEs to examine whether depressive symptom patterns were consistent with their
predictions. Each planned interaction contrast examined a particular ALE compared to the other
ALEs on the predicted symptom compared to all other symptoms for that ALE. Finally, the
researchers statistically controlled for gender, weeks since ALE was experienced, number of
depressive episodes experienced in the past, use of antidepressants, and mood during the last
seven days.
Keller and Nesse (2005) found the ALE x Symptom interaction term to be significant,
demonstrating that the patterns of depressive symptoms varied across ALEs. The results of the
six planned interaction contrasts indicated that for all ALEs except stress, depressive symptom
patterns were consistent with their hypotheses. More specifically, sadness and crying were
prominent after romantic losses and deaths of loved ones; sadness, crying, and self-reproach after
social isolation; self-reproach, fatigue, and pessimism after failures; fatigue, pessimism, and
increased eating and sleeping during the winter season.
Overall, Keller and Nesse (2005) found support for their hypothesis. Individuals’
depressive symptom patterns varied across ALEs. In addition, depressive symptom patterns were
consistent with their predictions about the symptoms that would be most adaptive for each ALE.
For example, higher levels of crying were adaptive during situations characterized by
interpersonal loss because it led to stronger interpersonal connections. Higher levels of

pessimism and fatigue were adaptive during situations characterized by failures, stress, and
wintertime because they helped the individual conserve energy in unfavorable environments in
which investing resources and expending energy will probably not be effective or lead to
success. Keller and Nesse’s theoretical argument and hypothesis in this study are consistent with
and led to the SSCH, which they introduced in their 2006 study.
Keller and Nesse (2006). In 2006, Keller and Nesse conducted three additional studies
that explored whether different ALEs lead to distinct depressive symptom patterns that might be
useful in dealing with the adaptive problems characteristic of the different ALEs. In the first
study, the researchers developed a measure called the Depressive Symptoms Scale (DSS) that
could measure the depressive symptoms about which the SSCH makes predictions. The
researchers were interested in subthreshold depressive reactions following ALEs in a nonclinical
sample. As a result, their validation of the DSS was based on a nonclinical sample (i.e.,
undergraduate students in an introductory psychology class who earned course credit for
participating in the study). The researchers asked 2,664 introductory psychology students (57%
female) if they had gone through a period of low mood that lasted at least two weeks over the
previous 12 months. One thousand one hundred and twenty seven reported that they had. The
researchers asked these individuals whether there were any events or situations they believed had
led to their period of low mood. Participants identified the following events or situations: chronic
stress (46.7%), romantic loss (25.4%), social isolation (39.5%), death of a loved one (13.0%),
failure at an important goal (19.7%), the winter (9.7%), no cause (8.4%), and other cause
(18.9%).
Keller and Nesse (2006) prescreened and oversampled for rare ALEs, including death of
a loved one, failure, and winter, in order to make sure that sample sizes for these ALEs would be
sufficient. Of the 1,127 individuals who endorsed a period of low mood, 623 were asked to
participate. Four hundred and seventy-three of these individuals agreed to participate, of which
456 finished the study. Due to incomplete data or procedural violations, 11 of these individuals
were dropped from the study. The final sample included 445 participants between the ages of 18
and 23 (M = 18.8, SD = 9.9), including 283 females and 162 males. The researchers cross-
validated this exploratory sample with a sample of individuals (n = 311) who volunteered
through a website used for online psychological studies.
Participants in both samples were asked to complete a brief demographic questionnaire.
Next, participants were asked to think of the most emotionally painful 7-day period over the
previous year, and write about any situations or incidents they believed led to the period of low
mood. Participants were also asked to write about their emotional experience during the period
of low mood. Participants were then asked to complete the DSS, the CES-D, and the Beck
Depression Inventory (BDI: Beck, Steer, & Garbin, 1988) based on the symptoms they
experienced during the period of low mood. Finally, participants were asked to indicate how
seriously they took the study and were then debriefed.
Keller and Nesse (2006) developed the DSS in a series of steps. First, they conducted
exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) on data they collected
from the exploratory sample to determine the latent structure of the DSS items, dropping any
items and factors that were inconsistent with this structure. This step resulted in a primary model
that consisted of 11 factors (i.e., depressive symptoms) made up of 47 items. Two factors were
dropped due to having less than three items. Second, they conducted CFA to cross-validate the
primary model using the cross-validation sample. Results indicated that the exploratory and
cross-validation samples had the same latent structures but slightly different factor loadings.
Third, they evaluated the primary model by comparing it with competing models. The results of
these comparisons indicated that the factor structure of the DSS was superior to three other
models and equivalent to a fourth model.
In their second study, Keller & Nesse (2006) used the DSS to examine whether different
ALEs were associated with distinct depressive symptom patterns that were consistent with SSCH
predictions. Participants included the exploratory sample from Study 1. The procedure was the
same as that for Study 1 except that participants had to provide more information in certain
areas. For example, after participants wrote about what events or incidents they believed had led
to their period of low mood, they identified the most likely cause from a list of eight ALEs. The
list included the following ALEs: “death of a loved one (n = 44), romantic loss (n = 92), social
isolation (n = 112), failure at an important goal (n = 44), stress or difficulty coping (n = 83),
wintertime (n = 30), no cause (n = 13), and other cause (n = 27)” (p. 323). Participants answered
additional questions about the properties of the ALEs they had identified. For example, they
were asked about the extent to which the ALE involved losing a person they were close to, and
how long ago the ALE had occurred. Finally, participants provided information on their present
mood, use of antidepressants, and history of depression.
Keller and Nesse (2006) tested whether patterns of depressive symptoms varied across
ALES in a repeated measure MANOVA that included a Precipitant x Symptom interaction term.
The within-person response variables were the 11 depressive symptoms from the DSS while the
between-person predictor variables were the 7 categorical ALEs. Keller and Nesse conducted
between- and within-person follow-up ANOVA contrasts to test specific predictions of the
SSCH. Using structural equation modeling (SEM), they tested whether participants’ responses
about the extent to which their self-identified ALEs were related to social loss and failed effort
varied in their associations with the 11 depressive symptoms.

Keller and Nesse (2006) found the ALE x Symptom interaction term to be significant for
all depressive symptoms, demonstrating that different ALEs were associated with distinct
depressive symptom patterns. Controlling for gender, time since ALE, use of antidepressants,
depression history, and current mood did not alter these findings. The results of the between-
person follow-up ANOVA contrasts indicated that 4 of 10 symptoms had significantly higher
mean levels for the predicted ALEs. The number of symptoms with significantly higher mean
levels rose to 8 after they controlled for overall dysphoria. The results of the within-person
follow-up ANOVA contrasts indicated that depressive symptom patterns were consistent with
SSCH predictions for all ALEs except chronic stress. Controlling for gender, time since ALE,
use of antidepressants, depression history, and current mood did not alter these findings. Results
from the SEM tests of the SSCH indicated that failed effort was significantly related to the
following symptoms (in descending order in terms of relationship strength): “guilt, rumination,
pessimism, fatigue, anxiety, sleepiness, anhedonia, and emotional pain” (p. 325). In addition,
there was a significant relationship between social loss and desire for social support, emotional
pain, and crying, and a negative relationship between social loss and guilt. Controlling for three
potential mediating variables (i.e., Lack of Control, Suddenness, and Shamed) did not alter these
results, demonstrating that these variables were not mediators in the failed effort-depressive
symptom pattern or social loss-depressive symptom pattern relationships.
Overall, the results of Study 2 (Keller & Nesse, 2006) supported the SSCH. The
depressive symptom patterns experienced by individuals varied depending on the pre-onset
ALEs. In addition, the depressive symptom patterns that followed different ALEs were largely
consistent with SSCH predictions. For example, pessimism was prominent following failure and
inability to cope while desire for social support was prominent following death, romantic loss,
and social isolation. Furthermore, these findings did not result from individuals’ perceptions
about what caused the depressive episode. Keller and Nesse argued that pessimism is adaptive
for individuals after failure because it can help them to give up on a goal which they are unlikely
to achieve while desire for social support is adaptive after death, romantic loss, and social
isolation because it can facilitate making or reforming social bonds.
In their third study (Keller & Nesse, 2006), they replicated the results from Study 2 in an
analogue study. They randomly assigned 113 participants to imagine failing at a major goal
(failure condition) or death of a loved one (death condition). This design allowed them to assess
the direction of causation, which was not possible with the retrospective design used in Study 2.
Because imagining a situation is likely to elicit less intense emotions than actually experiencing
it, participants who had indicated that goal accomplishment and social attachments were
important or very important to them were preselected. The final sample included 116 psychology
students (64 female) who earned course credit. Participants’ were 18- to 22-year-olds, with an
average age 18.5 (SD = 0.93).
Keller and Nesse (2006) asked participants in the death condition to write a story about a
loved one who dies within a few months of being diagnosed with brain cancer. They asked
participants in the failure condition to write a story about their failure to reach a goal that was
very important to them. Both conditions required participants to follow specific guidelines that
removed potential confounds and avoided methodological issues. After writing the story,
participants in both conditions completed the DSS questionnaire (modified to be in the present
tense), answered 2 probing questions, and were debriefed.
Keller and Nesse (2006) tested whether there was a relationship between different ALEs
and distinct depressive symptom patterns with the Precipitant x Symptom interaction term in a
repeated measure MANOVA. The within-person response variables were 8 of the depressive
symptoms from the DSS while the between-person predictor variables were the 2 ALEs (i.e.,
death of a loved one and major failure). SSCH predictions were tested using between- and
within-person follow-up ANOVA contrasts.
Keller and Nesse (2006) found the Precipitant x Symptom interaction term to be
significant for all depressive symptoms, demonstrating that a different pattern of depressive
symptoms resulted from imagining the death of a loved one than imagining a major failure.
These findings did not change after controlling for the level of emotional involvement in writing
the story. The results of the between-person follow-up ANOVA contrasts indicated that
depressive symptom patterns caused by death of loved one and failure were consistent with
SSCH predictions. Imagining a loved one’s death resulted in more pronounced emotional pain,
crying, and desire for social support while imagining a major failure led to more pronounced
fatigue, pessimism, anhedonia, and guilt.
Overall, the results of Study 3 (Keller & Nesse, 2006) supported the SSCH. Similar to the
results of Study 2, the depressive symptom patterns experienced by an individual varied
depending on the ALE that preceded them, and the patterns of depressive symptoms that
followed different ALEs were largely consistent with the predictions of the SSCH. However,
unlike the results of Study 2, the results of study 3 were not subject to the limitations of
retrospective reports, including the third variable problem and reverse causation. By asking
participants to imagine the ALE rather than think about a past ALE, Keller and Nesse were able
to assess the direction of causation. Therefore, these results provided some evidence that death of
a loved one and failure actually led to the predicted depressive symptom patterns.
Keller, Neale, and Kendler (2007). In 2007, Keller et al. investigated the associations
between ALEs and depressive symptom patterns in participants with and without a diagnosis of
major depressive disorder (MDD). In addition, they addressed whether the pattern of depressive
symptom patterns resulted from stable intrapersonal differences as opposed to ALEs by

conducting within-person analyses with participants who had experienced multiple ALEs.
Participants were Caucasian twin pairs who were part of the Virginia Adult Twin Study of
Psychiatric and Substance Use Disorders, which is part of the population-based Mid-Atlantic
Twin Registry (Kendler & Prescott, 2006). Twin pairs completed between one and four
interviews, and endorsed one or more depressive episodes during at least one wave of the study.
The sample included 2,595 females and 2,261 males. The average age of females was 33.9 years
(SD = 8.5) while the average age of males was 35.5 years (SD = 8.8).
During interviews, participants were asked questions to determine if they had
experienced a depressive episode of five or more days over the previous year. A participant who
reported experiencing such an episode was asked questions about which symptoms he or she had
experienced using criterion A of the DSM-III-R. A participant was recognized as experiencing a
depressive episode if he or she endorsed two or more of the nine symptoms of MDD listed under
criterion A of the DSM-III-R. Requiring any two of the nine MDD symptoms made sense
because Keller et al. (2007) were interested in examining subthreshold depressive episodes, and
because requiring specific symptoms would obscure relevant symptom patterns. They assessed
symptom severity by asking participants to indicate on a 5-point scale how much the symptom
affected their daily life. Data collected using the DSM-III-R was also used to determine whether
a participant met criteria for MDD.
Next, participants were asked whether they believed any event or situation led to their
depressive episode, and if so, to describe the event or situation. Participants who indicated more
than one event or situation were asked to order them in terms of causal importance. The
researchers then assigned the most causally important event or situation to one of nine ALE
categories. The ALE categories included failure, death of a loved one, chronic stress, romantic
loss, health problems, scare, interpersonal conflict, other, and nothing. Finally, participants
completed the depression and anxiety subscales of the Revised Symptom Checklist-90
(Derogatis, 1983) in order to account for mood during the month prior to the study, and were
interviewed with an adapted version of the Structured Clinical Interview for the DSM-III-R
(SCID; Spitzer & Williams, 1985) in order to assess for MDD during year prior to the study.
Keller et al. (2007) completed three statistical analyses. Their first analysis involved a
between-person sample that included participants who had experienced a single depressive
episode or multiple episodes that they believed resulted from the same ALE. They examined the
association between different ALEs and depressive symptom patterns in a MANOVA that
included an ALE x Symptom interaction term. The predictor variables were the nine ALEs and
the response variables were the 12 standardized symptom scale scores. Their second analysis
involved a within-person sample that included participants who had experienced more than one
depressive episode that they believed resulted from more than one ALE. They examined the
association between different ALE categories and depressive symptom patterns using a
MANOVA omnibus test. The predictor variables were the nine ALEs and the response variables
were the 12 within-person symptom deviations. A symptom deviation was a participant’s
symptom levels subtracted from his or her mean symptom levels across all episodes. Their third
analysis involved participants from the between- and within-person analyses who were
diagnosed with MDD. For participants who had experienced multiple ALEs they believed
resulted from the same ALE, Keller et al. selected one episode at random to include in the
analysis. They investigated the association between different ALE categories and depressive
symptom patterns in this sample using a MANOVA that included an ALE x Symptom
interaction term. All three analyses included an omnibus test and follow-up contrast tests.
The ALE x Symptom interaction term was significant for the between-person analyses
that included participants who experienced a single depressive episode or more than one
depressive episode they believed resulted from the same ALE. These results demonstrated
distinct depressive symptom patterns for different ALEs. This was true for all ALE categories
except failure and interpersonal conflict. For example, in the case of death and romantic breakup,
levels of insomnia, emotional pain, loss of appetite, and anhedonia were higher than those of
psychomotor retardation, fatigue, and appetite increase.
The ALE x Symptom interaction term was significant for within-person analyses that
included participants who experienced more than one depressive episode they believed resulted
different ALEs. Because these analyses compared different depressive symptom patterns among
different ALEs within the same individual, they indicate that depressive symptom patterns were
not a product of stable interpersonal differences rather than the ALEs. This was true for four of
the nine ALEs. The depressive symptom patterns for romantic loss, death, nothing, and chronic
stress were consistent with those of the between-person analysis.
The ALE x Symptom interaction term was significant for the within- and between-person
analyses that investigated the association between different ALE categories and depressive
symptom patterns among individuals with an MDD diagnosis. These results indicated that the
relationship between different ALEs and different depressive symptom patterns was present for
both subthreshold and clinical depressive episodes. The results of the follow-up contrasts were
highly consistent across the three analyses, indicating that the relationships between ALEs and
depressive symptom patterns were similar across the three samples.
Overall, Keller et al.’s (2007) findings suggest that different ALEs are associated with
distinct depressive symptom patterns. These findings were true for individuals with and without
a diagnosis of MDD. Following death of a loved one, appetite loss, decreased appetite, and
emotional pain were more pronounced while increased sleep and guilt were not. After a romantic
breakup, sadness, appetite loss, difficulty concentrating, and guilt were more pronounced while
fatigue, psychomotor retardation, restlessness, hypersomnia, and increased appetite were not.
Following chronic stress and failure, fatigue, hypersomnia, and appetite gain were more
pronounced while sadness, anhedonia, and loss of appetite were not. The fact that depressive
symptom patterns were similar for participants who experienced one or multiple depressive
episodes increased confidence that these findings were not due to chance or to stable
interpersonal differences.
Couyoumdjian et al. (2012). In 2012, Couyoumdjian et al. examined the relationship
between ALEs and depressive symptom patterns in a nonclinical sample. They also looked at
personal goals as a possible mediator in this relationship. They recruited participants online using
professional mailing lists. Participants included 328 women whose average age was 38.8 years
and 128 men whose average age was 42.7 years. All participants were Italian Caucasians. Most
participants were employed and had completed vocational or university education.
The entire study was completed online and lasted approximately 45 minutes. Participants
answered demographic questions and then completed an Italian version of the Center for
Epidemiologic Studies Depression Scale (CES-D; Fava, 1983) to assess and control for mood
during the previous week. Following the same method used by Keller et al. (2007), participants
then answered questions about the symptoms they experienced during the worst, if any, period of
depressed mood they had experienced over the previous year that lasted at least 5 days.
Symptoms included those identified in criterion A for MDD in the DSM-IV-TR (American
Psychiatric Association, 2000). Participants also indicated whether or not they believed any
event may have caused the depressive episode. If they believed there was an event, they wrote
about the event and then identified it in Keller et al.’s (2007) list of ALEs. Finally, participants
indicated how much the identified event disrupted their ability to achieve numerous personal
goals (e.g., having a rewarding and satisfying job).

Couyoumdjian et al. (2012) conducted three statistical analyses. In the two analyses, they
attempted to replicate the results of Keller et al. (2007). In the first analysis, they examined the
relationship between specific ALEs and patterns of depressive symptoms by testing an ALE x
Symptom “interaction term in a repeated measures multivariate analysis of variance”
(MANOVA) that controlled for current mood (p. 3). The predictor variable was the event
category while the response variable was the standardized symptom score. In the second
analysis, they examined the relationship between ALEs and different depressive symptom
patterns by computing one-way analyses of variance (ANOVAS) on depressive symptom scores
for each ALE. The third analysis examined whether personal goals mediated the relationships
between ALEs and depressive symptom patterns through mediational analyses. The predictor
and response variables were ALE and depressive symptom score, respectively, while the
mediating variable was personal goal appraisal.
Results of the Couyoumdjian et al. (2012) study indicated that different ALEs were
related to different patterns of depressive symptoms. The ALE x Symptom interaction term was
significant for all of the symptoms when controlling for age and current mood. Symptom levels
differed by ALE category for 5 of the 12 symptoms, including sadness, appetite loss,
worthlessness, poor concentration, and anhedonia. A series of one-way ANOVAS indicated that
average symptom levels were significantly different for no ALE and stress, and approaching
significance for interpersonal conflict, health problems, and failure. Post hoc analyses showed
that higher levels of appetite loss and feeling blue and lower levels of emotional pain and
appetite loss were associated with no ALE while higher levels of insomnia and restlessness were
associated with stress.
Also consistent with their hypotheses, Couyoumdjian et al. (2012) found that personal
goal appraisal partially mediated the relationship between affective loss (i.e., romantic loss and
death of a loved one) and sadness, and the relationships between failure and worthlessness, and
between failure and anhedonia. The results of a principal component analysis yielded two
factors, including lovableness (i.e., family, sex and romance, and marriage) and success (i.e.,
career, finances, social recognition and approval, career, leadership, positive social qualities,
social approval, belonging, and achievement). These factors predicted 59% of the total variance,
and were used as mediators in subsequent analyses. Lovableness partially mediated the
relationship between affective loss and sadness while success partially mediated the relationships
between failure and worthlessness, and between failure and anhedonia. These results did not
change when they controlled for mood.
Overall, Couyoumdjian et al.’s (2012) results indicated that different ALEs are associated
with specific depressive symptom patterns, and that this relationship was partially mediated by
personal goal appraisal. Levels of sadness, appetite loss, worthlessness, poor concentration, and
anhedonia differed by ALE category. Higher levels of hypersomnia and appetite gain and lower
levels of decreased appetite and emotional pain were associated with no ALE while higher levels
of restlessness and insomnia were associated with stress. Lovableness partially mediated the
relationship between affective loss and sadness while success partially mediated the relationships
between failure and worthlessness, and between failure and anhedonia. These findings extended
those of previous studies by suggesting that a particular ALE is associated with a specific
depressive symptom pattern when that ALE impedes an important personal life goal.
Limitations of Past Research
Taken together, past studies by Keller and others (i.e., Couyoumdjian et al., 2012; Keller
et al., 2007; Keller & Nesse, 2005, 2006) demonstrate that there is relationship between type of
precipitant and depressive symptom patterns, and suggest the possibility that different
precipitants lead to certain patterns of depressive symptoms. However, these past studies have
numerous limitations.
First, all but one past study (i.e., Study 3, Keller & Nesse, 2006) involved collecting self-
report information about ALEs and depressive symptoms that occurred over the past year.
Research indicates that retrospective reports about experiences that occurred a week or more in
the past are less valid and reliable, and more biased when compared to concurrent reports
(Henry, Moffitt, Caspi, Langley, & Silva, 1994; Ross & Fletcher, 1985; Schwarz & Sudman,
1994; Smith, Leffingwell, & Ptacek, 1999). An individual’s report about a period of low mood
and what they believe may have led to it may change over time and become contaminated for a
number of reasons, including but not limited to the tendency to distort the past in a way that
reflects better on the self, faulty memory, and the inclination to give excessive weight to a
particular aspect of the experience.
Second, Keller et al. (2007) conducted the only study that investigated the relationships
between ALEs and depressive symptom patterns in a within-person sample. However, it should
be mentioned that they did not test the SSCH or examine many of the ALEs (i.e., social isolation
and winter) and depressive symptoms (i.e., crying, desire for social support, pessimism, and
rumination) about which the SSCH makes predictions.
Third, Keller et al. (2007) conducted the only study that included participants with a
diagnosis of MDD. As a result, only one study investigated whether the relationship between
ALEs and patterns of depressive symptoms that existed for a non-MDD participants would be
consistent with the relationship for MDD participants. But again, it should be mentioned that
they did not test the SSCH or examine many of the ALEs (i.e., social isolation and winter) and
depressive symptoms (i.e., crying, desire for social support, pessimism, and rumination) about
which the SSCH makes predictions.

Fourth, Keller and Nesse’s (2006) analogue study utilized a mood induction procedure.
Such studies have questionable validity and may be prone to demand effects. Asking a
participant to imagine what it would be like to lose a loved one is very different from actually
losing a loved one. It is difficult to know whether the effects of the two would be comparable.
Additionally, asking a participant to imagine such an experience may influence or bias their
behavior in a way that affects the results of the study.
Fifth, each of the samples utilized in the research studies described above had one or
more characteristics that resulted in limited generalizabilty and external validity. The samples
used in Keller and Nesse’s (2005, 2006) studies were made up of college students from a
Midwestern university with ages ranging from approximately 18 to early 20’s, making it
impossible to determine whether the results would be the same for individuals who are not
college students, or of a similar age. The sample used in the Keller et al.’s (2007) study was
made up of Caucasian twins, again making it difficult to generalize the results to individuals
outside of this specific population. Finally, Couyoumdjian et al. (2012) used a sample of
participants recruited through professional mailing lists, also reducing generalizability.
Sixth, past studies required participants to choose a single ALE category to indicate the
ALE they believed led to their dysphoric episode. As a result, a participant who believed two or
more different ALEs contributed equally to their dysphoric episode was forced to leave
important information out. In other words, there may have been some inaccuracy in the
measurement of ALEs in the studies, resulting in reduced validity of the predictor variable.
Support for this claim comes from the fact that participants reported that multiple precipitants
caused their depressive symptoms 21% of the time in Keller et al.’s (2007) study.
Seventh, the research by Keller and colleagues (Couyoumdjian et al., 2012; Keller et al.,
2007; Keller & Nesse, 2005, 2006) described above was limited by the statistical procedures they
utilized. Although these statistical procedures were able to test their hypotheses, there are more
up-to-date, though more complicated statistical techniques, such as multilevel modeling (MLM).
MLM is superior to more traditional statistical techniques numerous reasons. For example, one
advantage of MLM is that it can flexibly handle missing data, thereby preventing the loss of
relevant data that might influence the results. Such data would have had to be discarded in the
research by Keller and colleagues.
An Alternative Approach for Testing the Situation-Symptom Congruence Hypothesis
In our study, we tested the SSCH using an alternative approach to investigate the
relationship between ALEs and depressive symptom patterns. This approach addressed some of
the limitations of past research, and increased our understanding of the relationship between
ALEs and depressive symptom patterns.
First, our study involved a daily diary design in which we collected self-report
information about events or issues that occurred over the past day rather than the past year.
Participants completed daily measures for up to nine days. While both our design and the designs
utilized in past research relied on retrospective self-report information, our design allowed self-
report information to be collected closer in time to when it actually occurred. This increased
reliability and validity by decreasing contamination caused by the impact of self-enhancement,
faulty memory, and anchoring bias.
Second, our study involved a repeated measure design in which each participant had one
or more observations. This allowed us to focus on within- as well as between-person variation.
This was an important next step because only one past study (Keller et al., 2007) examined
within-person variation. Additionally, Keller et al. did not test the SSCH and did not examine
many of the ALEs and depressive symptoms about which the SSCH makes predictions.
Third, our study included a sample of participants with a diagnosis of MDD, allowing for
an investigation of whether the relationship between ALEs and depressive symptoms that exist
for non-MDD participants is consistent with the relationship that exists for MDD participants.
While Keller et al. (2007) also included a sample of participants with a diagnosis of MDD, they
did not test the SSCH and did not examine some ALEs and depressive symptoms about which
the SSCH makes predictions.
Fourth, we investigated ALEs and depressive symptoms that occurred naturally and were
not the result of mood induction procedures that attempted to simulate this phenomenon. In
doing so, our study was not plagued by the validity and demand effect issues that may have
limited Keller and Nesse’s (2006) analogue study.
Fifth, our study involved a community sample while past studies involved samples
limited to college students (Keller & Ness, 2005, 2006) and Caucasian twin pairs (Keller et al.,
2007), and participants recruited through professional mailing lists (Couyoumdjian et al., 2012).
As such, our participants covered a wider range of ages, ethnicities, occupations, and
socioeconomic backgrounds, resulting in increased generalizability and external validity.
Sixth, participants in our study could endorse multiple ALE categories, and indicate the
degree to which their self-identified ALE involved each ALE category. As a result, we were able
to examine the association between a participant’s level or degree of ALE and level of different
symptoms. Past researchers asked participants to choose a single ALE category to indicate the
ALE they believed led to their dysphoric episode. As a result, a participant who believed two or
more different ALEs contributed equally to his or her dysphoric episode was forced to leave
important information out, possibly resulting in reduced validity of the predictor variable. In
support of this claim, Keller et al. (2007) found that participants attributed their symptoms to
multiple causes/precipitants 21% of the time. By allowing participants to endorse multiple ALE
categories and indicate the degree to which their self-identified ALE involved each ALE
category rather than forcing participants to choose a single ALE category, we made finer
quantitative distinctions in the measurement of ALEs. As a result, we likely measured ALEs
more accurately in our study, thereby increasing the internal validity of our predictor variables.
Seventh, we utilized multilevel modeling (MLM) to test our hypotheses. MLM is a
modern statistical technique that is superior to many traditional techniques for numerous reasons.
MLM was able to accommodate the nested nature of our data (i.e., observations nested within
days). Because MLM can handle data in which the number of observations varies across
participants, we did not lose a large amount of data that might have influenced our results.
Hypotheses
One major goal of this study was to determine whether there is a relationship between
ALEs and depressive symptom patterns that is consistent with the SSCH in individuals who have
experienced one or more ALEs. More specifically, are different ALEs associated with distinct
patterns of depressive symptoms in such a way that certain symptom clusters (hereinafter
referred to as adaptive symptom clusters) are more prominent than other symptom clusters
(hereinafter referred to as nonadaptive symptom clusters) depending on the ALE they follow?
In general, Hypothesis 1 states that the relationship between a particular ALE and its adaptive
symptom cluster (ASC) will be positive in direction, and significantly stronger than the
relationship between that ALE and its nonadaptive symptom cluster (NSC). An ASC score was
calculated by taking the average of the DSS scale scores that the SSCH predicted to be
prominent following a particular ALE. Similarly, an NSC score was calculated by taking the
average of the DSS scale scores that the SSCH did not predict to be prominent following a
particular ALE. Table 2 lists the six ALEs and their corresponding ASCs and NSCs.
x Hypothesis 1a. The correlation between failure at an important goal and its ASC will be
positive in direction and significantly stronger than the correlation between failure at an
important goal and its NSC.
x Hypothesis 1b. The correlation between death of a loved one and its ASC will be positive
in direction and significantly stronger than the correlation between death of a loved one
and its NSC.
x Hypothesis 1c. The correlation between romantic loss and its ASC will be positive in
direction and significantly stronger than the correlation between romantic loss and its
NSC.
x Hypothesis 1d. The correlation between chronic stress and its ASC will be positive in
direction and significantly stronger than the correlation between chronic stress and its
NSC.
x Hypothesis 1e. The correlation between social isolation and its ASC will be positive in
direction and significantly stronger than the correlation between social isolation and its
NSC.
x Hypothesis 1f. The correlation between winter and its ASC will be positive in direction
and significantly stronger than the correlation between winter and its NSC.
Table 2
Adverse Life Events and Corresponding Adaptive and Nonadaptive Symptom Clusters
Adverse life event Adaptive symptom cluster Nonadaptive symptom cluster

Failure Emotional pain, pessimism, fatigue, Crying, increased sleep, desire for
anhedonia, rumination, guilt social support
Death Emotional pain, crying, desire for Pessimism, fatigue, anhedonia,
social support rumination, guilt, increased sleep
Romantic loss Emotional pain, rumination, crying, Pessimism, fatigue, anhedonia,
guilt, desire for social support increased sleep
Chronic stress Pessimism, fatigue, anhedonia, Emotional pain, crying, increased
rumination, guilt sleep, desire for social support
Social isolation Emotional pain, crying, desire for Pessimism, fatigue, anhedonia,
social support rumination, guilt, increased sleep
Winter Fatigue, anhedonia, increased sleep Emotional pain, pessimism,
rumination, crying, guilt, desire
for social support
A second major goal of this study was to determine whether there is a consistent
association between ALEs and depressive symptom for individuals without MDD and
individuals with MDD. In general, Hypothesis 2 states that the relationship between a particular
ALE and each depressive symptom will be consistent for non-MDD and MDD participants.
x Hypothesis 2a. The relationship between failure and each depressive symptom will be
consistent for non-MDD participants and MDD participants.
x Hypothesis 2b. The relationship between death of a loved one and each depressive
symptom will be consistent for non-MDD participants and MDD participants.
x Hypothesis 2c. The relationship between romantic loss and each depressive symptom will
be consistent for non-MDD participants and MDD participants.
x Hypothesis 2d. The relationship between chronic stress and each depressive symptom
will be consistent for non-MDD participants and MDD participants.

x Hypothesis 2e. The relationship between social isolation and each depressive symptom
will be consistent for non-MDD participants and MDD participants.
x Hypothesis 2f. The relationship between failure and each depressive symptom will be
consistent for non-MDD participants and MDD participants.

Chapter III: Method
Participants
A power analysis (Cohen, 1992) based on a repeated measure, between- and within-
person design (effect size of .5, error probability of .05, 2 groups) indicated the need for 62
participants, including 31 participants for the non-major depressive disorder (non-MDD) group
and 31 participants for the major depressive disorder (MDD) group. Because recruiting
participants with MDD took significantly longer than recruiting participants without MDD, the
final sample size included more non-MDD participants than was indicated by the power analysis.
The final sample included 265 participants, including 233 non-MDD participants and 32 MDD
participants. Participants included 197 females (74%) and 68 males (26%) between the ages of
18 and 63 (M = 27, SD = 10.9).
In order to participate in our study, individuals had to be at least 18 years of age.
Individuals who endorsed the following pre-existing Axis I diagnoses were excluded from the
study: current substance dependence, schizophrenia, schizoaffective disorder, and/or psychotic
disorders. In addition, individuals who endorsed more than passive suicidal thoughts were
excluded from participating after appropriate steps were taken to ensure their safety. More
specifically, individuals who indicated that they had suicidal thoughts but would not act on them
could participate. However, individuals were excluded if they endorsed either of the following
statements: “I want to kill myself,” or “If I was given the chance, I would kill myself.” Finally,
individuals who did not currently reside in the United States (US) were excluded from the study,
along with those who did not have a US mobile telephone number or adequate text-message
capability.
Protection of Human Participants
Our study was designed and conducted in accordance with the ethical and legal
guidelines of the California School of Professional Psychology at Alliant International
University, San Diego (CSPP AIU SD), the American Psychological Association, and other
relevant agencies. The methods and procedures utilized in this study were reviewed and
approved by the Institutional Review Board at CSPP AIU SD.
Procedures
Data collection took place from early January to late June of 2013. Participants were
recruited through advertisements on various websites (e.g., Craigslist, Facebook, Reddit,
Backpage, Twitter, and Google), and through advertisements at various universities and colleges
in southern California. All advertisements consisted of a brief description of the study, including
requirements, incentives, instructions for participating, and procedures.
The incentive for participating in this study was entrance into a raffle in which
participants could win up to four $100 cashier’s checks. Participants' chances of winning the
raffle prizes increased with continued participation. More specifically, a participant who
completed Days 1 – 5 of the study received two raffle tickets; a participant who completed Days
6 – 7 received a third raffle ticket; a participant who completed Days 8 – 9 received a fourth
raffle ticket. Therefore, a participant who completed all nine days of the study and thus earned a
total of four raffle tickets, had the potential to win up to four $100 cashier’s checks. The total
number of raffle tickets entered into the raffle was determined by the number of raffle tickets that
each participant earned during their participation. At the end of data collection, 13 winning raffle
tickets were drawn from the raffle. Each winning raffle ticket was worth one $100 cashier’s
check.
Interested individuals were asked to visit the study website to carefully review and
electronically sign an informed consent agreement (see Appendix A). The informed consent
agreement included relevant information about the following topics: study investigators, purpose
of the research, research procedures, risks and costs of participating, incentives and benefits of
participating, alternatives to participating, confidentiality, psychological treatment requests while
participating, questions about the research, mandatory reporting requirements, participant rights
and research withdrawal, and acknowledgement and consent to participate.
In order to reduce participant bias, it was necessary to conceal the full purpose of the
study and the names of the measures that were administered. Participants were told that the
purpose of the study was to look at the relationship between daily events and mood in order to
increase our understanding of how the two are related. Participants were informed that they
would be provided with a copy of the informed consent agreement upon request. Participants
were also informed that their participation was voluntary and that they could end their
participating at any time without penalty. Before signing the consent form, individuals were
instructed to contact the investigators with any questions they had about the study. Those who
met criteria and wanted to participate were asked to digitally sign the consent form, and proceed
to intake measures.
Intake measures were a demographic questionnaire, a suicidality screening question, and
the Center for Epidemiologic Studies Depression Scale Revised (CESD-R; Eaton, W. W., Smith,
C., Ybarra, M., Muntaner, C., & Tien, A.). The principal investigator (PI) contacted participants
who scored above 15 on the CESD-R to complete an interview (over the phone) with the
depression module of the Structured Clinical Interview for DSM-IV-TR (SCID; First, M. D.,
Spitzer, R. L., Gibbon, M., & Williams, J. B. W., 2002). Participants’ responses on the SCID
determined whether they were included in the MDD or non-MDD group. The MDD group
consisted of participants who met requirements for MDD according to the SCID while the non-
MDD group consisted of participants who did not meet criteria for MDD according to the SCID.
The day after completing intake measures, participants began receiving daily text
prompts at randomly selected times between 8:00 a.m. and 10:00 p.m.. Daily text prompts were
sent from the P.I.’s personal mobile telephone. Text messages were sent at randomly selected
times that were determined by a program on a website called Random.Org
(http://www.random.org/clock-times/). Upon receiving a text prompt, participants were asked to
complete daily measures within three hours. However, measures completed within four hours
were accepted.
Daily measures included the Depressive Symptoms Scale (DSS; Keller & Nesse, 2006),
and Adverse Life Events Measure (ALEM). Compliance with study procedures was checked by
examining submission times of all measures submitted by participants. Submission times were
recorded by Qualtrics (www.qualtrics.com) on the study website. After participants completed
their Day 9 measures, they completed a post-study CESD-R, answered the post-study suicidality
screening question, and were debriefed. During debriefing, participants were informed about the
full purpose of the study, and were given the opportunity to request information and ask
questions about to the study. Because we expected many participants to miss some daily
measures, we contacted participants who missed one or more daily measures and offered them
the opportunity to make-up missed days. More specifically, participants were offered one make-
up day for each missed day. This will be discussed in more detail in the Results section.
Measures
Demographic Questionnaire. We used a demographic questionnaire (see Appendix B)
to collect relevant background information and screen for suicidality. The demographic
questionnaire was comprised of a suicidality screening question and questions about relevant
background information, including contact information, ethnicity, cultural background,
nationality, education, occupation, history of mental illness, and family history of mental illness.
Center for Epidemiologic Studies Depression Scale—Revised. We used the Center for
Epidemiologic Studies Depression Scale—Revised (CESD-R; Eaton et al., 2004; see Appendix
C) to screen for potential MDD. More specifically, we administered the depression module of the
Structured Clinical Interview for DSM-IV Axis I Disorders (SCID; First et al., 2002) to
participants who scored above 15 on the CESD-R.
The original Center for Epidemiologic Studies Depression Scale (CESD; Radloff, 1977)
is a 20-item self-report scale that was developed by incorporating several established depression
inventories, including the following: Zung’s depression scale (Zung, 1965), the Beck Depression
Inventory (Beck, Ward, Mendelson, Mock, & Erbaugh, 1961), and the Depression Scale of the
Minnesota Multiphasic Personality Inventory (Hathaway & McKinley, 1942). The CESD is
based on DSM-II criteria for MDD, with items covering mood, interpersonal interactions,
somatic complaints, and motor functioning (Radloff, 1977). For example, the first item reads “I
was bothered by things that don’t usually bother me” (p. 387). Respondents report how
frequently they have felt this way over the past week with one of the following responses:
“Rarely or None of the time (Less than 1 Day), Some or a Little of the Time (1-2 Days),
Occasionally or a Moderate Amount of Time (3-4 Days), [or] Most or All of the Time (5-7
Days)” (p. 387). Scores range from zero to 60. More elevated scores indicate more depressive
symptoms.
Research has demonstrated good reliability for the CESD as evidenced by moderate test-
retest correlations between .45 and .70, along with high internal consistency (Cronbach’s α =
.85) in a general population sample and even higher internal consistency (Cronbach’s α = .90) in
a psychiatric sample (Radloff, 1977). Research has also shown the CESD to be a valid measure
of depressive symptomatology as evidenced by good discriminant and concurrent validity. For
example, a general population sample had significantly lower average CESD scores than a
psychiatric inpatient sample (Radloff, 1977).
The Center for Epidemiologic Studies Depression Scale—Revised (CESD-R; Eaton et
al., 2004) was introduced in 2004. The purpose of the revision was to reflect the current
diagnostic criteria for MDD based on the DSM-IV (1994), as well as improve its reliability in
identifying general dysphoria (Eaton et al., 2004). To this end, the revision involved dropping
eight items that did not reflect DSM-IV diagnostic criteria for MDD; adding new items to reflect
DSM-IV diagnostic criteria, including suicidal ideation, anhedonia, and psychomotor
agitation/retardation; and adding a new response category (i.e., “Nearly every day for two
weeks”) to more closely reflect the DSM-IV criteria.
Similar to the CES-D, the CESD-R is a 20-item self-report that screens for possible MDD
based on DSM-IV criteria in adults in the general population (Eaton et al., 2004). The CESD-R
has some advantages over other depression measures, including availability in the public domain
and lack of a theoretical basis. Each item covers a symptom in one of the following depressive
symptom categories: dysphoria, anhedonia, appetite loss, disturbed sleep, thinking/concentration,
guilt/worthlessness, fatigue, psychomotor retardation/agitation, and suicidal ideation. For
example, the first item reads “My appetite was poor.” Instructions are the same as for the CES-D
with the exception of the additional response category mentioned above. Like the CES-D, scores
range from zero to 60, and higher scores indicate more depressive symptoms. (The additional
response category is given a value of three in order to maintain the zero to 60 score range.) An
algorithm determines how probable (i.e., definite, probable, possible, subthreshold, unlikely) it is
that the respondent is experiencing a major depressive episode. A typical cutoff score of 16 or
greater is used to identify an individual who may be experiencing some level of depression. To
be conservative, we used a cutoff score of 15 in our study to identify participants who may have
been experiencing a major depressive episode.
Research by Eaton et al. (2004) indicated excellent internal consistency reliability and
good to excellent face and construct validity for the CESD-R. They also expected the CESD-R to
have very good test-retest reliability and criterion validity based on its high correlation with the
CESD, and how similar its form and response values are to those of the CESD. Using a
community sample (N = 7,389) and student sample (N = 245), Van Dam and Earlywine (2011)
investigated the psychometrics of the CESD-R, and found it to have excellent reliability. In terms
of internal consistency, Cronbach’s alphas were .92 and .93 for the community and students
samples, respectively. In our study, we conducted a reliability analysis to examine the internal
consistency of the CESD-R. Cronbach’s alpha coefficient for the CESD-R completed at intake
was .94 (n = 265) while that for the CESD-R completed at the end of the study was .93 (n =
174).
Van Dam and Earlywine (2011) also found the CESD-R to have strong convergent and
divergent validity. In the community sample, the correlation between the CESD-R and State-
Trait Inventory for Cognitive and Somatic Anxiety (STICSA; Ree, Macleod, French, & Locke,
2000), which measures state- and trait-based anxiety symptoms, was positive and strong (r =
0.737, p < 0.01). The correlation between the CESD-R and Schizotypal Personality
Questionnaire—Brief (SPQ-B; Raine & Benishay, 1995), which screens for schizotypal
personality disorder, was positive and moderate (r = 0.436, p < 0.01). For the student sample, the
correlation between the CESD-R and STICSA was also positive and strong (r = 0.653, p < 0.01)
while the correlation between the CESD-R and SPQ-B was positive and moderate (r = 0.426, p <
0.01). Correlations between the CESD-R, STICSA, and Positive and Negative Affect (PANAS;
Watson, Clark, & Tellegen, 1988), a measure of positive affect (PA) and negative affect (NA),
were also examined. The correlation between the PANAS-NA and the CESD-R was moderate
and positive (r = 0.576, p < 0.01) and the correlation between PANAS-NA and the STICSA was
positive and strong (r = 0.663, p < 0.01). The correlation between the PANAS-PA and the
CESD-R was negative and weak (r = - 0.263, p < 0.01) as was the correlation between the
STICSA and the CESD-R (r = - 0.233, p < 0.01).
Depression module of the Structured Clinical Interview for DSM-IV Axis I
Disorders. We administered the depression module of the Structured Clinical Interview for
DSM-IV Axis I Disorders (SCID-I; First et al., 2002) participants who scored above 15 on the
CESD-R in order to determine whether a participant was experiencing an episode of MDD. The
SCID-I semi-structured interview utilized by researchers and clinicians to make the most
common Axis I DSM-IV-TR diagnoses for individuals who are 18 and older. The interview takes
between 45 and 90 minutes to complete. The depression module of the SCID incorporates the
full diagnostic criteria of depressive disorders. Research suggests, for the most part, adequate to
excellent reliability. In one study, two raters conducted approximately 50 SCID-I interviews and
determined whether MDD diagnoses were appropriate with a mixed sample of 151 inpatients,
outpatients and non-patient controls (Lobbestael, Leugrans, & Arntz, 2011). Results indicated
fair inter-rater reliability (Kappa = .66) Using 84 pairs of raters, Zanarini et al. (2000) found
excellent inter-rater reliability (Kappa = .80) in a convenience sample of 19 outpatients. In the
same study, Zanarini et al. also found fair to good test-retest reliability (Kappa = .61, n = 38)
based on two interviews of 52 participants conducted 7 – 10 days apart.
In our study, SCID interviews were conducted by the P.I., who completed Steps 1 - 4 of
the SCID training steps presented on the official SCID website (retrieved from
http://www.scid4.org/training/overview.html on 11/16/2011). The PI recorded these interviews
so that a fellow graduate student who was also using the SCID in her dissertation could
determine whether MDD diagnoses were appropriate. Inter-rater reliability analysis (Kappa =
.88; p < .001) indicated excellent agreement (Landis & Koch, 1977).
It is difficult to comment on the validity of the SCID in a completely straightforward
manner because a gold standard for psychiatric diagnoses is not firmly established, and using the
clinical diagnoses as the standard is somewhat inappropriate due to the fact that structured
interview such as the SCID have been designed specifically to improve upon unstructured
clinical interviews (retrieved from http://www.scid4.org/psychometric/scidI_validity.html on
03/12/09). However, it should be mentioned that numerous studies actually identify the SCID as
the gold standard for diagnosing MDD (Shear et al., 2000; Steiner, Tebes, Sledge, & Walker,
1995). Also, a number of other studies that utilized approximations of the Spitzer’s LEAD
procedure (Spitzer, 1983) found that the SCID had superior validity in comparison to standard
clinical interviews (Basco et al., 2000; Fennig, Naisberg-Fennig, Craig, Tanenberg-Karant, &
Bromet, 1996; Kranzler, Kadden, Babor, Tennen, & Rounsaville, 1996; Kranzler et al., 1995)
Depressive Symptoms Scale. We used the Depressive Symptoms Scale (DSS; Keller &
Nesse, 2006) to measure depressive symptoms. The DSS requires participants to indicate the
extent to which they are experiencing various depressive symptoms by choosing one of the
following responses: rarely or none of the time = 1; some of the time = 2; a moderate amount of
the time = 3; most or all of the time = 4. The DSS is made up of 11 subscales, each of which is
composed of three or four items measuring a particular depressive symptom. Some of the
subscales include emotional pain, pessimism, anhedonia, and increased sleep. Some DSS items
include “I felt really sad,” “Things seemed hopeless,” “Everything seemed like such an effort,”
“I thought about how I could have done things differently,” “I felt ashamed,” and “I wanted to be
with close friends or family for support.” Appendix D presents the DSS instructions, scales, and
items. We modified the DSS items for our study to reflect the present tense. For example, the
item “I felt really sad” was changed to “I feel really sad.” See Appendix E for our modified
version of the DSS.
Keller and Nesse (2006) developed the DSS for their 2006 study in which they examined
the patterns of depressive symptoms that followed different adverse life events (ALEs). Please
see the Keller and Nesse (2006) subsection in Chapter II for a detailed description of how and
why the DSS was developed. As mentioned, based on their analyses, Keller and Nesse concluded
that the DSS should generalize to nonclinical populations. The 11 DSS symptom scales had an
average coefficient alpha of .86.
In our study, we conducted a pilot study to discover problems with this measure and the
amount of time required to complete it. The results of our pilot study indicated that the measure
accurately assessed the variable of interest, and took approximately 5 minutes to complete. On
Days 1 through 9 of our official (not pilot) study, the DSS was completed by participants to
measure depressive symptoms. A composite score was calculated for each of the 11 symptom
scales by taking the average of all the responses that make up a particular scale. We examined
nine of the 11 DSS symptom scales in our analyses, leaving out anxiety and increased appetite.
Because our study involved repeated measures completed daily for nine days, we examined
internal consistency of the DSS on Day 1, which had the largest sample. The nine scales had an
average coefficient alpha (Cronbach, 1951) of .84 (n = 239) on Day 1.
Adverse Life Events Measure. We developed the Adverse Life Events Measure
(ALEM; see Appendix F) to assess depressive symptoms. The principle investigator wrote the
ALEM items based on ALE categories examined in prior investigations of the relationship
between ALEs and depressive symptom patterns (Couyoumdjian et al., 2012; Keller et al., 2007;
Keller & Nesse, 2005, 2006). The event categories from prior investigations were derived from
free responses in which participants wrote about ALEs they believed led to depressive episodes
during the previous year. Event categories from Keller et al.’s (2007) study can be found at
Matthew Keller’s website (http://matthewckeller.com/EventCodingBook.xls). Keller and Nesse
found the test-retest reliability of the event categories to be adequate, with a kappa coefficient of
.51.
Item 1 of the ALEM asked participants to identify and write about the most stressful
event/issue they had experienced or focused on since they last completed daily measures, or in
the past 24 hours if they had not completed daily measures in the past 24 hours. Item 2 asked
participants to indicate the extent to which their self-identified stressful event/issue negatively
affected them using a 5-point Likert scale (1 = not at all or N/A, 2 = a little bit, 3 = moderately, 4
= quite a bit, and 5 = entirely). Items 3 through 13 asked participants to indicate the extent to
which their self-identified stressful event/issue involved a particular ALE category using the
same 5-point Likert scale. For example, one question read “To what extent does this event/issue
represent a failure or a disappointment that is final (not ongoing)?” Event categories included
failure, health/physical functioning, interpersonal conflict, death of a loved one, romantic loss,
chronic stress, social isolation, winter, other stressful event not mentioned here, and no stressful
event. We examined six of these event categories in our analyses, including failure, death of a
loved one, romantic loss, chronic stress, social isolation, and winter.
We conducted a pilot study to discover problems with the ALEM, the amount of time
required to complete it, and the frequency of different ALEs. The results of our pilot study
indicated that the ALEM accurately assessed the variables of interest. Pilot study participants
completed the ALEM in approximately five minutes, and endorsed a range of ALEs.
Furthermore, participants’ most elevated responses to Items 3 through 13 (i.e., those items that
addressed the extent to which their self-identified stressful event/issue involved a particular ALE
category) corresponded to their self-identified stressful event/issue and written description in
Items 1, respectively.
Research Design and Data Analysis
This study utilized a between- and within-person, repeated measures design to test
multilevel models. These models examined the relationship between ALEs and depressive
symptom patterns over 9 days of repeated measures. Multilevel modeling was the most
appropriate analytic strategy for this study for a number of reasons.
First, multilevel modeling is able to account for violations of independence. In this study,
time was nested within individuals, and individuals were nested within groups. It would have
been inappropriate to assume that individuals from the same diagnostic group did not behave
similarly; and to assume that an individual’s response on one occasion was independent from his
or her responses on the same measure on subsequent occasions. Violating the assumption of
independence leads to an increased rate of Type I error (i.e., the probability of detecting a
difference when one does not exist). Second, multilevel modeling employs full information
maximum likelihood estimation (FIML), which allows parameter estimates to vary at more than
one level. Given that one of our hypotheses involved examining whether ALE-symptom
relationships varied by diagnostic group, it was necessary to use a technique that allowed
parameter estimates to vary by group membership.
Third, multilevel modeling has the ability to flexibly handle missing data, and to work
with data in which participants have varying numbers of measurements over time. Traditional
repeated measures analysis treats time as a fixed factor in which all respondents have completed
the same number of measurements at the same time. In our study, a substantial number of
participants failed to complete all nine measurement occasions, resulting in varying numbers of
measurements across participants. Additionally, participants did not necessarily complete

measurements at the same time, or have the same duration between measurements. Using
multilevel modeling allowed us to retain all participants who completed at least one occasion,
thereby increasing sample size and power, and allowing us to retain data that may have
influenced our results. In addition, multilevel modeling accounted for the variability in
measurements and time. Fourth, by allowing multiple correlated response variables to be entered
into the same model, multilevel modeling allows for a comparison of effect sizes for each
predictor variable across multiple response variables (Hoffman & Rovine, 2007).
Data were collected online at the Qualtrics website ([http://www.qualtrics.com];
Qualtrics, 2013). Data were downloaded from the Qualtrics website into the Statistical Package
for the Social Sciences Version 21 (SPSS v21), which was used to perform data cleaning and
preliminary data analyses. Data were also transported from SPSS into Mplus Version 7.11
(Mplus v7.11; Muthén & Muthén, 2008-2012). Mplus is capable of performing multilevel
modeling (MLM) that involves analyzing multilevel data sets with repeated measures.
We conducted preliminary analyses to examine the structure of our data. We screened for
outliers and examined our data to identify and address assumption violations. MLM assumptions
are similar to those of traditional multiple regression, and include the following: linearity,
homoscedasticity, and normality of residuals (Maas & Hox, 2004).
Multilevel modeling is a form of regression in which parameters can vary at more than
one level. In the case of repeated measures multilevel modeling, which was utilized in this study,
Level 1 data consists of observations of individuals at multiple time points (i.e., repeated
measures of ALEs and depressive symptoms) while Level 2 data consists of attributes of
individuals that are not expected to change over time (i.e., gender, age, and diagnostic group
membership). In multilevel modeling, a separate regression model for each individual examines
the influence of Level 1 or time-varying predictors and Level 2 or time-invariant attributes on

outcomes. More specifically, at Level 1, the model examines how a series of within-person
predictors are associated with an outcome over time. At Level 2, the model examines how
between-person predictors and/or individual attributes are associated with that outcome.
In our study, we created a separate regression equation for each participant in order to do
the following: at Level 1, examine how an individual’s experience of a particular ALE over one
or more days was associated with depressive symptoms; and at Level 2, examine or control for
the influence diagnostic group membership and certain attributes (i.e., gender and age) on the
relationship between a particular ALE and depressive symptoms. For example, Hypotheses 1a
predicted that failure would be positively associated with the failure-adaptive symptom cluster
score (failure-ASC; i.e., the average symptom score for emotional pain, pessimism, fatigue,
anhedonia, rumination, and guilt); and the correlation between failure and the failure-ASC would
be significantly stronger than the relationship between failure and the failure-nonadaptive
symptom cluster (failure-NSC; i.e., the average symptom score for crying, increased sleep, and
desire for social support). Hypothesis 2a predicted that relationship between a particular ALE
(e.g., failure) and each depressive symptom (e.g., emotional pain) would be consistent for non-
MDD and MDD participants. We controlled for gender and age at Level 2 in all of our multilevel
models.
In our study, each multilevel model included time-varying predictor variables and
response variables at Level 1, and time-invariant predictor variables and attributes at Level 2.
Time-varying predictor variables included an ALE in our Hypothesis 1 models, and time and an
ALE in our Hypothesis 2 models. Time-varying response variables included an ASC and an NSC
in our Hypothesis 1 models, and nine depressive symptoms (derived from nine DSS scales) in
our Hypothesis 2 models. Time-invariant predictor variables included gender and age in our
Hypothesis 1 models, and gender, age, and diagnostic group (i.e., non-MDD versus MDD) in our
Hypothesis 2 models.
Each ALE was determined by a participant’s score on a particular ALEM item, with each
item representing one ALE category. Each ASC was calculated by taking the average of the
participant’s DSS scale scores that the SSCH predicted to be prominent following a particular
ALE. Each NSC was calculated by taking the average of the participant’s DSS scale scores that
the SSCH predicted not to be prominent following a particular ALE. Time was determined by
which day number or make-up day number a participant completed. Diagnostic group was
determined by a participant’s score(s) on the CESD-R and/or depression module of the SCID-I.
Each depressive symptom was determined by a participant’s score on a particular DSS scale.
As mentioned previously, testing Hypotheses 1a – 1f involved comparing the differences
in the effects of an ALE on ASCs and NSCs while Hypothesis 2a – 2f involved examining
whether the effects of an ALE on depressive symptoms varied by diagnostic group We estimated
12 multilevel models, each of which contained the variables necessary to test one of the twelve
hypotheses. The first 6 models tested Hypotheses 1a – 1f while the second 6 tested Hypotheses
2a – 2f. We will discuss the components of our Hypothesis 1 and 2 models below.
Hypothesis 1 models. Because our Hypothesis 1 models were identical with the
exception of a different ALE, we will focus this discussion on our model for Hypothesis 1a.
Hypotheses 1a predicted that failure would be positively associated with failure-adaptive
symptom cluster (failure-ASC; i.e., the average symptom score for emotional pain, pessimism,
fatigue, anhedonia, rumination, and guilt); and the correlation between failure and the failure-
ASC would be significantly stronger than the relationship between failure and failure-
nonadaptive symptom cluster (failure-NSC; i.e., the average symptom score for crying, increased
sleep, and desire for social support).

The Level 1 equation for our Hypothesis 1a model was expressed as:
yti = π0i + π1i (FAILUREti) + eti
In this equation, yti represents each of the two response variables (i.e., the adaptive symptom
cluster score and the nonadaptive symptom cluster score) for person i at time t; π0i represents the
intercept of the response variable for person i; π1i (FAILUREti) represents the slope relationship
between failure and the response variable for person i at time t; and finally, eti represents the
unexplained variance for the intercept for person i at time t.
Given that our data consisted of within-person observations over multiple days, we could
have included time as a predictor variable in the model. However, we elected not include time in
the model for two reasons. First, Hypothesis 1, which was determined a priori, involved
comparing the relationships between a single ALE and each of the response variables and did not
involve examining the influence of time on the response variables. Second, including time in the
model would have prevented us from being able to test Hypothesis 1 because we would have
been limited to examining a coefficient of multiple determination rather than a simple coefficient
of determination. Coefficients of multiple determination provide information about the
proportion of variance in the response variable that is explained by the combined influence of
multiple predictor variables. In this study, such coefficients of multiple determination would
have provided information about the proportion of variance in the response variable (i.e., failure-
ASC or failure-NSC) explained by the combined influence of two predictor variables (i.e., time
and failure). Partialling out the influence of a single predictor variable (e.g., failure) is not
possible. As a result, including time would have prevented us from being able to test Hypotheses
1a – 1f.
In multilevel modeling, the Level 1 equation accounts for the nested structure of the data
(i.e., Level 1 within-person observations nested within the Level 2 between-person attributes,
gender and age) through Level 2 equations. The Level 2 equations incorporate the effects of
between-person attributes into the intercept and slope components [π0i and π1i (FAILUREti),
respectively] of the Level 1 equation. More specifically, the equation for the intercept
component, π0i, captures the influence of all the individual attributes (i.e., gender and age) on the
Level 1 intercept. Additionally, the equation for the slope component, π1i (FAILUREti), captures
the influence of all the individual attributes (i.e., gender and age) on the Level 1 slope. Our Level
2 equation for the Level 1 intercept was expressed as:
π0i = β00 + β01(GENDERi) + β02(AGEi) + u0i
In this equation, π0i represents the intercept of the response variables; β00 represents the value of
the intercept for person i when gender, age, and MDD are set to 0; β01(GENDERi) represents the
change in the value of the intercept for person i when gender goes from 0 to 1; β02(AGEi)
represents the change in the value of the intercept for person i when age increases by one year;
and finally, u0i represents the unexplained variance for the intercept.
Our Level 2 equation for the Level 1 slope relationship between failure and the response
variables was expressed as:
π1i = β10 + β11(GENDERi) + β12(AGEi) + u1i
In this model, π1i represents the slope of the response variables; β10 represents the intercept/value
of the slope relationship between failure and the response variable for person i when gender and
age are set to 0; β11(GENDERi) is the change in the slope relationship between failure and the
response variable for person i when gender goes from 0 to 1; β12(AGEi) represents the change in
the slope relationship between failure and the response variable for person i when age increases
by one year; and finally, u1i represents the unexplained variance for the slope relationship
between failure and the response variable for person i.

We have described our model for Hypothesis 1a, which focused on the relationship
between failure and the response variables (i.e., failure-adaptive symptom cluster score and
failure-nonadaptive symptom cluster score). Our models for Hypotheses 1b – 1f were identical to
those for Hypothesis 1a except that failure was replaced by a different ALE for each hypothesis,
and the response variables were replaced by the ASC and NSC specific to the ALE included in
each hypothesis. For example, Hypothesis 1b examined the association between death of a loved
one and the following response variables: death-ASC and death-NSC.
Hypothesis 2 models. Because our Hypothesis 2 models were identical with the
exception of a different ALE, we will focus this discussion on our model for Hypothesis 2a.
Again, Hypotheses 2a predicted that the relationship between failure and depressive symptoms
for participants without major depressive disorder (non-MDD) would be consistent with the
relationship between failure and depressive symptoms for participants with major depressive
disorder (MDD). We tested this hypothesis by examining whether each failure-depressive
symptom relationship (e.g., failure-emotional pain) varied by diagnostic group (non-MDD versus
MDD). The nine depressive symptoms included emotional pain, pessimism, fatigue, anhedonia,
rumination, crying, guilt, increased sleep, and desire for social support.
The Level 1 equation for the Hypothesis 2a model was expressed as:
yti = π0i + π1i (TIMEti) + π2i (ALEti) + eti
In this equation, yti represents each of the two response variables (i.e., the adaptive symptom
cluster score and the nonadaptive symptom cluster score); π0i represents the intercept of the
response variable; π1i (TIMEti) represents the slope relationship between time and the outcome
for person i at time t; π2i (ALEti) represents the slope relationship between ALE and outcome for
person i at time t; and finally, eti represents the unexplained variance for the intercept. We
included time in our Hypothesis 2 models because including a second predictor variable at Level
1 did not interfere with our ability to test Hypotheses 2a – 2f.
Including cross level interaction terms at Level 2 allowed us to examine whether the
association between ALE and each depressive symptom varied significantly by diagnostic group
(Aguinas, 2013). The cross level interaction terms for the intercept and slope relationships were
β03(DXGROUPi), β13(DXGROUPi), and β23(DXGROUPi), respectively. As a result, the Level 2
equations for the Level 1 intercept and slope relationships were expressed as:
π0i = β00 + β01(GENDERi) + β02(AGEi) + β03(DXGROUPi) + u0i
In these equations, the intercept component, β03(DXGROUPi), represents the change in the value
of the intercept for person i when diagnostic group goes from 0 to 1. The first slope component,
β13(DXGROUPi), represents the change in the slope relationship between time and outcome for
person i when diagnostic group goes from 0 to 1. The second slope component, β23(DXGROUPi),
represents the change in the slope relationship between ALE and the response variables for
person i when diagnostic group goes from 0 to 1.
Hypothesis testing. Hypothesis 1a predicted that the relationship between failure and
failure-ASC would be positive in direction, and would be significantly stronger than the
relationship between failure and failure-NSC. We tested this hypothesis in a series of steps. First,
we estimated the Hypothesis 1, Level 1 model for failure
yti = π0i + π1i (FAILUREti) + eti
while controlling for gender and age at Level 2. In this model, yti was the two response variables
(i.e., the failure-ASC and the failure-NSC); π0i was the intercept of the response variables; π1i
(FAILUREti) was the slope relationship between failure and the response variables for person i at
time t; and finally, eti was the unexplained variance for the intercept. See the Hypothesis 1
Models subsection for more detailed information about the Hypothesis 1, Level 2 models.
By estimating this model, we were able to examine the direction of the slope relationship
between failure and failure-ASC, and the slope relationship between failure and failure-NSC.
Additionally, we examined the coefficients of determination, r2s, for each of the response
variables. We then took the square root of each coefficient of determination in order to compute
the correlations, rs, between failure and each of the response variables. Next, we used Fisher’s r-
to-z transformation (Fisher, 1921) to standardize each correlation by transforming them to z
scores. Standardization was necessary because we wanted to compare two correlations that we
could not assume to be based on equivalent scales. Finally, given the dependency of the
correlations being compared (i.e., they were based on data from the same sample), we used
Steiger’s Z test (Steiger, 1980) to determine whether the correlation between failure and the
failure-ASC was significantly stronger than the correlation between failure and the failure-NSC.
Hypotheses 1b – 1f made the same predictions as Hypothesis 1a except that each one
corresponded to a different ALE and its corresponding ASC and NSC. For example, Hypothesis
1b predicted that the relationship between death and death-ASC would be positive in direction,
and would be significantly stronger than the relationship between death and death-NSC.
Likewise, Hypotheses 1b – 1f were tested in exactly the same manner as Hypothesis 1a.
Hypothesis 2a predicted that the relationship between failure and each depressive
symptom would be consistent for non-MDD and MDD participants. We tested this hypothesis in
a series of steps. First, we estimated the Hypothesis 2, Level 1 model for failure
yti = π0i + π1i (TIMEti) + π2i (FAILUREti) + eti
while controlling for gender and age at Level 2, and modeling diagnostic group as a cross level
interaction term (Aguinas, 2013). In this model, yti was the nine response variables (i.e.,
emotional pain, pessimism, fatigue, anhedonia, rumination, crying, guilt, increased sleep, and
desire for social support); π0i was the intercept of the response variables; π1i (TIMEti) is the slope
relationship between time and the response variables for person i at time t; π2i (FAILUREti) was
the slope relationship between failure and the response variables for person i at time t; and
finally, eti was the unexplained variance for the intercept. (See the Hypothesis 2 Models
subsection for more detailed information about the Hypothesis 2, Level 2 models.) By estimating
this model, we were able to examine whether or not there was a significant Failure x Diagnostic
Group interaction for each of the response variables. If there were significant Failure x
Diagnostic Group interactions for any of the outcomes, simple effects analyses were completed
to examine the difference in the failure-outcome relationships for each diagnostic group (i.e.,
non-MDD and MDD).
Hypotheses 2b – 2f made the same predictions as Hypothesis 2a except that each one
corresponded to a particular ALE. For example, Hypothesis 2b predicted that relationship
between death of a loved one and each depressive symptom would be consistent for non-MDD
and MDD participants. Likewise, Hypotheses 2b – 2f were tested in exactly the same manner as
value Hypothesis 2a.

Chapter IV: Results
The aim of our study was to examine the relationship between adverse life events (ALEs)
and depressive symptom patterns from an evolutionary perspective. To this end, we tested the
situation-symptom congruence hypothesis (SSCH) using a methodology that addressed many of
the limitations of past research. In this chapter, we will discuss the results of our research in the
following sections: sample characteristics, attrition, descriptive statistics, data screening,
assumptions, and hypothesis testing.
Sample Characteristics
Three hundred and twenty-five individuals attempted to participate in our study. A total
of 16 individuals were excluded, including ten individuals for significant suicidal ideation, four
individuals for a psychological diagnosis that involved psychosis, and two individuals for a
diagnosis of current substance dependence. An additional 36 individuals were disqualified for
failing to complete any repeated measures. In other words, these individuals completed intake
measures the day prior to what was supposed to be their first day of repeated measures; however,
they failed to complete their first or any subsequent repeated measure(s), which assessed the
variables of interest. The final sample included 265 participants, including 233 non-major
depressive disorder (non-MDD) participants and 32 major depressive disorder (MDD)
participants.
Table 3 provides a summary of our sample’s sociodemographic characteristics. Of the
265 participants, 197 (74%) were female while 68 (26%) were male. Participants’ ages ranged
from 18 to 63, with an average age of 27 (SD = 10.9), median age of 24, and modal age of 19.
The largest portion of the sample was non-Hispanic White/Caucasian/European American (48%)
followed by Latino/Hispanic American (18%), African American/Black (14%), Asian American
(13%), Other (3%), Middle Eastern/Arab/Arab American (2%), Native Hawaiian/Other Pacific
Islander (< 1%), and finally, Native American/American Indian/Alaskan Native (< 1%).
Seventy-one percent of the sample was single, 22% was married, 5% was divorced, 1% was
separated, and 1% was widowed. The sample varied in terms of education level. Approximately
16% had less than a high school degree and about 42% had a high school degree. Approximately
33% had completed some college, a vocational or professional certification program, or an
associate’s degree. About 7% had a college degree and approximately 2% had a graduate degree.
Fifty-two percent of the sample was employed, and 53% were students.
Table 3
Sociodemographic Characteristics of Sample: Frequencies and Percentages
Sociodemographic characteristic Frequency Percent

Ethnicity
African American/Black 38 14.3
Latino/Hispanic American 48 18.1
Non-Hispanic White/Caucasian/European American 128 48.3
Middle Eastern/Arab/Arab American 4 1.5
Asian/Asian American 35 13.2
Native Hawaiian/Other Pacific Islander 2 .8
Indian/Asian Indian/East Indian/Indian American 0 0.0
Native American/American Indian/Alaskan Native 2 .8
Other 8 3
Marital/Relationship Status
Single 188 70.9
Married/Civil Union/Domestic Partnership 58 21.9
Separated 4 1.5
Divorced 12 4.5
Widowed 3 1.1
Education
Less than high school 42 15.8
High school graduate 111 42
Some college or specialized training 87 32.8
College graduate 18 6.8
Graduate degree 7 2.6
Employment Status
Employed 137 51.7
Not employed 128 48.3
Student Status
Student 139 52.5
Not a student 126 47.5
Attrition
This study consisted of nine repeated measures that took place over nine days.
Participants began completing repeated measures the day after they completed intake measures
and were cleared for participation. In order to participate in the study, an individual was required
to complete at least one day of repeated measures. Individuals who failed to complete at least
one day of repeated measures were considered to have dropped out. A total of 44 individuals
dropped out of our study, leaving a total of 265 participants.
We examined whether dropouts differed from participants on gender, ethnicity, age, and
CESD-R total scores (see Table 4). Dropouts differed from participants on gender. Forty-three
percent of dropouts were male while 57% were female. On the other hand, 26% of participants
were male while 74% were female. Dropouts did not differ from participants on ethnicity.
Because neither age nor CESD-R data were normally distributed and did not improve following
transformation, we conducted Mann-Whitney U tests, which compare the medians of two
independent groups with the same distributions. Dropouts did not differ from participants on age
or CESD-R total score.
Because participants were permitted to complete anywhere from one to nine days of the
study, those who missed between one and eight days were not considered to have dropped out.
Instead, such participants were considered to have engaged in non-participation. Non-
participation will be discussed in the Data Screening section of this chapter.

Adverse Life Events and Depressive Symptom Patterns
Table 4
Results of Attrition Analyses
Dropouts Participants
(N = 44) (N = 265)
Frequency (%) Frequency (%) χ2 (df, N) p* phi
Gender 5.73 (1, 309) .02 .14
Male 19 (43.2) 68 (25.7)
Female 25 (56.8) 197 (74.3)
Ethnicity 10.03 (7, 309) .19 .18
African American/Black 11 (25.0) 38 (14.3)
Latino/Hispanic American 3 (6.8) 48 (18.1)
Non-Hispanic White/Caucasian/European 24 (54.5) 128 (48.3)
American
Middle Eastern/Arab/Arab American 0 (0.0) 4 (1.5)
Asian American 3 (6.8) 35 (13.2)
Native Hawaiian/Other Pacific Islander 0 (0.0) 2 (0.8)
Native American/American Indian/Alaskan 0 (0.0) 2 (0.8)
Native
Indian/Asian Indian/East Indian/Indian 0 (0.0) 0 (0.0)
American
Other 3 (6.8) 8 (3.0)
Median (IQR) Median (IQR) Mann-Whitney U p* r
Age 24.5 (21– 29) 24 (30 - 32) 5755.50 .89 -.0077
CESD-R total score 20.5 (6 – 34) 18 (8 – 27.5) 5624.00 .71 -.0213
Note: Because there were no participants who endorsed the “Indian/Asian Indian/East Indian/Indian American” category for
ethnicity, it was not included in the Pearson chi-square test, resulting in 7 degrees of freedom.
* two-tailed
73
Descriptive Statistics
Frequency of observations. As mentioned earlier, this was a nine-day study that
consisted of nine repeated measures. Participants began completing repeated measures the day
after they completed intake measures and were cleared for participation. In order to participate in
the study, an individual was required to complete at least one day of repeated measures.
Individuals who failed to complete at least one day of repeated measures were considered to
have dropped out. As a result, participants completed one to nine days of the study, or one to
nine repeated measures. The average number of days completed was 6.80 (SD = 2.73). Table 5
provides a comprehensive list of the frequencies for each number of days completed.
Table 5
Frequencies and Percentages of Days Completed
Number of days completed Frequency Percentage

1 23 8.7
2 15 5.7
3 8 3.0
4 11 4.2
5 12 4.5
6 16 6.0
7 27 10.2
8 42 15.8
9 111 41.9
Because many participants missed days of the study and had the option of making them
up, days of participation did not necessarily take place on consecutive days or within a nine-day
period. Additional reasons that days of participation did not necessarily take place on
consecutive days or within a nine-day period include participants’ failure to respond to the
principle investigator’s (PI’s) attempts to reach them to determine if they had missed their initial
repeated measures due to technical issues related to their mobile phone carrier, or failure to
respond to the PI’s attempts to reach them to complete the depression module of the Structured
Clinical Interview for the DSM-IV Axis I Disorders: Research Version (SCID-I: I/NP; First et
al., 2002).. The duration of individuals’ participation ranged from 1 to 27.11, days, with the
average duration being 8.93 (SD = 0.36).
CESD-R and SCID scores. Participants’ average total score on the pre-study Center for
Epidemiologic Studies Depression Scale Revised (CESD-R; Eaton et al., 2004) was 19.51 (N =
265, SD = 13.44). Some participants did not complete their final day of the study, which is when
they would have completed their post-study CESD-R. As a result, 175 of the 265 participants
completed the post-study CESD-R; these participants’ average total score was 18.16 (SD =
12.52). Participants’ pre-study CESD-R total scores were positively correlated with their post-
study CESD-R total scores, Pearson’s r(175) = .591, p < .001.
The principal investigator (PI) attempted to administer the depression module of the
Structured Clinical Interview for the DSM-IV Axis I Disorders: Research Version (SCID-I:
I/NP; First et al., 2002) to the 143 participants who scored above 15 on the pre-study CESD-R in
order to determine these participants’ diagnostic group (non-MDD versus MDD). The PI
administered the SCID-I to 104 of the 143 participants. Thirty-nine participants were not
interviewed because they did not respond to the PI’s attempts to reach them. These participants
were placed in the non-MDD group. Based on the SCID-I results, the PI determined that 32
(30.8%) of the 104 interviewed participants (or 12.1% of the entire study sample of 265), met
criteria for a current major depressive episode. These participants were placed in the MDD
group. The 72 participants who did not meet criteria for a current major depressive episode
according to the SCID-I were placed in the non-MDD group.
Non-MDD participants did not differ from MDD participants on gender, χ2(1, N = 265) =
.91, p = .34, phi = .059. Because age, pre-study CESD-R, and post-study CESD-R data were not
normally distributed and did not improve following transformations, we conducted Mann-
Whitney U tests, which compare the medians of two independent groups with the same
distributions. Although this test typically involves comparing the medians of two independent
groups with similar distributions, when the two groups being compared have different
distributions, it is necessary to compare the mean ranks instead. The mean ranks for each group
are computed by ranking data scores from both groups together from lowest to highest, and then
determining the mean rank for each group. The group with the higher mean rank has the higher
scores. Distributions for the non-MDD and MDD participants on age and pre- and post-study
CESD-R total scores were different. Non-MDD participants did not differ from MDD
participants on age, Mann Whitney U = 2989.50, n1 = 233, n2 = 32, p = .069, r = -.112. However,
the two diagnostic groups did differ on their pre- and post-study CESD-R total scores. More
specifically, non-MDD participants scored significantly lower on their pre-study CESD-R total
scores (mean rank = 122.01) than MDD participants (mean rank = 213.00), Mann Whitney U =
1168.00, n1 = 233, n2 = 32, p < .01, r = -.387; non-MDD participants also scored significantly
lower on their post-study CESD-R total scores (mean rank = 79.67) than MDD participants
(mean rank = 138.00), Mann Whitney U = 625.00, n1 = 150, n2 = 25, p < .01, r = -.403.
Participants’ diagnostic group (non-MDD coded 0 and MDD coded 1) was positively correlated
with their pre-study CESD-R total scores, Pearson’s r(265) = .42, p < .00, and post-study CESD-
R total scores, Pearson’s r(175) = .43, p < .001.
Adverse Life Events Measure. We calculated descriptive statistics for our adverse life
events measure (ALEM) both by collapsing across all days for a total (i.e., overall) analysis, and
by examining each day and make-up day separately. As mentioned previously, the six ALEM
scales included failure, death, romantic loss, chronic stress, social isolation, and winter. ALEs
were measured on a 5-point Likert scale (1 = not at all or N/A, 2 = a little bit, 3 = moderately, 4
= quite a bit, and 5 = entirely). Frequencies/percentages and descriptive statistics for ALEs are
presented in Tables 6 through 17 in the following order: failure (Tables 6 and 7), death (Tables 8
and 9), romantic loss (Tables 10 and 11), chronic stress (Tables 12 and 13), social isolation
(Tables 14 and 15), and winter (Tables 16 and 17). Sample sizes for make-up days were
relatively small (i.e., n < 30), making it difficult to interpret descriptive statistics and raising
concerns about the representativeness of the sample. For this reason, we will focus this
discussion on days rather than make-up days.
Mean and median levels of ALEs ranged from low to moderate across days. The most
frequent response for each ALE was 1 (i.e., not at all or N/A) while the least frequent response
was 5 (i.e., entirely). We observed a number of trends in the data across days. Sample size
decreased across days, going from 239 on Day 1 to 73 on Day 9. Mean and median levels of
ALEs were highest on Day 1. Positive skewness increased over days for all ALEs except winter.
Finally, distributions ranged from approximately symmetrical to highly, positively skewed.
Frequencies of the different response types (i.e., 1, 2, 3, 4, and 5 on a 5-point Likert
scale) were relatively small for all ALEs except chronic stress on Day 1. This trend became
increasingly apparent when we examined responses greater than 1 (i.e., 2, 3, 4, and 5). For
example, Table 18 shows the frequencies and percentages of each response level for all ALEs on
Day 1, the day with the largest sample size (i.e., N = 239). As can be seen, numerous frequencies
were less than ten. Furthermore, all ALEs except chronic stress had at least one response level
with a frequency smaller than 30.

Table 6
Frequencies and Percentages (in Parentheses) of Responses to Failure, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
R (n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
1 915 (50.8) 92 (38.5) 100 (48.1) 94 (50.3) 100 (54.6) 91 (52.9) 93 (56.4) 87 (54.0) 85 (53.5) 31 (42.5)
2 341 (18.9) 56 (23.4) 49 (23.6) 27 (14.4) 26 (14.2) 31 (18.0) 33 (20.0) 21 (13.0) 30 (18.9) 21 (28.8)
3 206 (11.4) 33 (13.8) 19 (9.1) 32 (17.1) 21 (11.5) 22 (12.8) 12 (7.3) 17 (10.6) 17 (10.7) 8 (11.0)
4 183 (10.2) 23 (9.6) 18 (8.7) 19 (10.2) 22 (12.0) 17 (9.9) 17 (10.3) 19 (11.8) 17 (10.7) 4 (5.5)
5 156 (8.7) 35 (14.6) 22 (10.6)) 15 (8.0) 14 (7.7) 11 (6.4) 10 (6.1) 17 (10.6) 10 (6.3) 9 (12.3)
Make-up Day
1 2 3 4 5 6 7 8 9
R (n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
1 6 (54.5) 7 (70.0) 8 (50.0) 8 (47.1) 16 (66.7) 15 (60.0) 13 (50.0) 13 (54.2) 56 (55.4)

2 2 (18.2) 1 (10.0) 3 (18.8) 3 (17.6) 3 (12.5) 2 (8.0) 5 (19.2) 5 (20.8) 23 (22.8)
3 1 (9.1) 1 (10.0) 0 (0.0) 2 (11.8) 1 (4.2) 6 (24.0) 4 (15.4) 3 (12.5) 7 (6.9)
4 2 (18.2) 1 (10.0) 4 (25.0) 2 (11.8) 3 (12.5) 1 (4.0) 3 (11.5) 2 (8.3) 9 (8.9)
5 0 (0.0) 0 (0.0) 1 (6.3) 2 (11.8) 1 (4.2) 1 (4.0) 1 (3.8) 1 (4.2) 6 (5.9)
Note. R = Response; Responses were on a 5-point Likert scale: 1 = Not at all or N/A; 2 = A little bit; 3 = Moderately; 4 = Quite a bit;
5 = Entirely.
78
Table 7
Descriptive Statistics of Responses to Failure, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
(n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
Mean 2.07 2.38 2.10 2.11 2.04 1.99 1.90 2.12 1.97 2.16
Median 1.00 2.00 2.00 1.00 1.00 1.00 1.00 1.00 1.00 2.00
SD 1.34 1.44 1.37 1.34 1.36 1.28 1.26 1.44 1.28 1.36
Skewness 0.98 0.68 1.03 0.86 0.97 1.06 1.25 0.90 1.09 1.04
Kurtosis -0.37 -0.92 -0.27 -0.57 -0.47 -0.13 0.28 -0.69 -0.10 -0.13
Make-up Day
1 2 3 4 5 6 7 8 9
(n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
Mean 1.91 1.60 2.19 2.24 1.75 1.84 2.00 1.88 1.87
Median 1.00 1.00 1.50 2.00 1.00 1.00 1.50 1.00 1.00
SD 1.22 1.08 1.47 1.48 1.26 1.18 1.23 1.19 1.23
Skewness 1.01 1.69 0.78 0.85 1.51 1.16 0.97 1.27 1.34
Kurtosis -0.56 1.86 -1.12 -0.71 0.96 0.46 -0.18 0.73 0.63
Note. Total = all days combined. Responses were on a 5-point Likert scale: 1 = Not at all or N/A; 2 = A little bit; 3 = Moderately; 4 =
Quite a bit; 5 = Entirely.
79
Table 8
Frequencies and Percentages (in Parentheses) of Responses to Death of a Loved One, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
R (n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
1 1621 (90.0) 211 (88.3) 192 (92.3) 170 (90.9) 166 (90.7) 151 (87.8) 149 (90.3) 146 (90.7) 146 (91.8) 67 (91.8)
2 60 (3.3) 9 (3.8) 8 (3.8) 3 (1.6) 8 (4.4) 9 (5.2) 6 (3.6) 4 (2.5) 6 (3.8) 0 (0.0)
3 35 (1.9) 5 (2.1) 2 (1.0) 3 (1.6) 1 (0.5) 7 (4.1) 4 (2.4) 4 (2.5) 2 (1.3) 1 (1.4)
4 36 (2.0) 5 (2.1) 3 (1.4) 3 (1.6) 4 (2.2) 1 (0.6) 2 (1.2) 2 (1.2) 3 (1.9) 2 (2.7)
5 49 (2.7) 9 (3.8) 3 (1.4) 8 (4.3) 4 (2.2) 4 (2.3) 4 (2.4) 5 (3.1) 2 (1.3) 3 (4.1)
Make-up Day
1 2 3 4 5 6 7 8 9
R (n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
1 9 (81.8) 8 (80.0) 14 (87.5) 15 (88.2) 20 (83.3) 23 (92.0) 23 (88.5) 22 (91.7) 89 (88.1)

2 0 (0.0) 0 (0.0) 1 (6.3) 0 (0.0) 3 (12.5) 0 (0.0) 1 (3.8) 0 (0.0) 2 (2.0)
3 0 (0.0) 1 (10.0) 0 (0.0) 0 (0.0) 0 (0.0) 1 (4.0) 0 (0.0) 0 (0.0) 4 (4.0)
4 2 (18.2) 1 (10.0) 0 (0.0) 1 (5.9) 0 (0.0) 0 (0.0) 1 (3.8) 2 (8.3) 4 (4.0)
5 0 (0.0) 0 (0.0) 1 (6.3) 1 (5.9) 1 (4.2) 1 (4.0) 1 (3.8) 0 (0.0) 2 (2.0)
5 = Entirely.
80
Table 9
Descriptive Statistics of Responses to Death of a Loved One, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
(n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
Mean 1.24 1.29 1.16 1.27 1.21 1.24 1.22 1.24 1.17 1.27
Median 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00
SD 0.82 0.91 0.64 0.92 0.76 0.76 0.77 0.83 0.66 0.95
Skewness 3.62 3.25 4.67 3.45 4.03 3.62 3.90 3.72 4.39 3.36
Kurtosis 12.25 9.57 22.33 10.65 15.77 13.39 14.99 13.16 19.67 9.99
Make-up Day
1 2 3 4 5 6 7 8 9
(n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
Mean 1.55 1.50 1.31 1.41 1.29 1.24 1.31 1.25 1.30
Median 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00
SD 1.21 1.08 1.01 1.18 0.86 0.88 0.97 0.85 0.88
Skewness 1.92 1.98 3.65 2.72 3.86 3.88 3.30 3.22 2.99
Kurtosis 2.04 2.82 13.72 6.40 16.30 15.34 10.31 9.12 8.06
81
Table 10
Frequencies and Percentages (in Parentheses) of Responses to Romantic Loss, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
R (n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
1 1409 (78.2) 172 (72.0) 163 (78.4) 149 (79.7) 151 (82.5) 133 (77.3) 136 (82.4) 125 (77.6) 131 (82.4) 59 (80.8)
2 141 (7.8) 26 (10.9) 14 (6.7) 10 (5.3) 11 (6.0) 13 (7.6) 11 (6.7) 11 (6.8) 9 (5.7) 5 (6.8)
3 69 (3.8) 6 (2.5) 8 (3.8) 8 (4.3) 6 (3.3) 6 (3.5) 6 (3.6) 7 (4.3) 6 (3.8) 3 (4.1)
4 77 (4.3) 14 (5.9) 12 (5.8) 7 (3.7) 7 (3.8) 8 (4.7) 5 (3.0) 8 (5.0) 5 (3.1) 1 (1.4)
5 105 (5.8) 21 (8.8) 11 (5.3) 13 (7.0) 8 (4.4) 12 (7.0) 7 (4.2) 10 (6.2) 8 (5.0) 5 (6.8)
Make-up Day
1 2 3 4 5 6 7 8 9
R (n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
1 8 (72.7) 6 (60.0) 13 (81.3) 8 (47.1) 18 (75.0) 19 (76.0) 20 (76.9) 18 (75) 80 (79.2)

2 1 (9.1) 0 (0.0) 1 (6.3) 7 (41.2) 2 (8.3) 4 (16.0) 3 (11.5) 1 (4.2) 12 (11.9)
3 0 (0.0) 1 (10.0) 1 (6.3) 0 (0.0) 3 (12.5) 2 (8.0) 1 (3.8) 3 (12.5) 2 (2.0)
4 2 (18.2) 1 (10.0) 0 (0.0) 0 (0.0) 1 (4.2) 0 (0.0) 1 (3.8) 0 (0.0) 5 (5.0)
5 0 (0.0) 2 (20.0) 1 (6.3) 2 (11.8) 0 (0.0) 0 (0.0) 1 (3.8) 2 (8.3) 2 (2.0)
5 = Entirely.
82
Table 11
Descriptive Statistics of Responses to Romantic Loss, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
(n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
Mean 1.52 1.69 1.53 1.53 1.42 1.56 1.40 1.55 1.43 1.47
Median 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00
SD 1.13 1.30 1.15 1.18 1.03 1.20 1.00 1.18 1.06 1.12
Skewness 2.17 1.75 2.09 2.14 2.54 2.04 2.63 2.05 2.51 2.47
Kurtosis 3.37 1.54 3.00 3.16 5.29 2.77 5.93 2.82 5.14 4.97
Make-up Day
1 2 3 4 5 6 7 8 9
(n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
Mean 1.64 2.30 1.44 1.88 1.46 1.32 1.46 1.63 1.39
Median 1.00 1.00 1.00 2.00 1.00 1.00 1.00 1.00 1.00
SD 1.21 1.77 1.09 1.27 0.88 0.63 1.03 1.24 0.91
Skewness 1.70 0.79 2.80 1.91 1.79 1.86 2.50 1.98 2.62
Kurtosis 1.36 -1.38 7.97 3.15 2.09 2.46 5.91 2.99 6.26
83
Table 12
Frequencies and Percentages (in Parentheses) of Responses to Chronic Stress, Totals and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
R (n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
1 644 (35.7) 53 (22.2) 64 (30.8) 64 (34.2) 76 (41.5) 77 (44.8) 62 (37.6) 71 (44.1) 63 (39.6) 26 (35.6)
2 298 (16.5) 40 (16.7) 35 (16.8) 27 (14.4) 23 (12.6) 28 (16.3) 29 (17.6) 22 (13.7) 27 (17.0) 18 (24.7)
3 282 (15.6) 45 (18.8) 31 (14.9) 25 (13.4) 29 (15.8) 22 (12.8) 30 (18.2) 19 (11.8) 28 (17.6) 11 (15.1)
4 279 (15.5) 42 (17.6) 39 (18.8) 34 (18.2) 27 (14.8) 23 (13.4) 22 (13.3) 24 (14.9) 23 (14.5) 10 (13.7)
5 298 (16.5) 59 (24.7) 39 (18.8) 37 (19.8) 28 (15.3) 22 (12.8) 22 (13.3) 25 (15.5) 18 (11.3) 8 (11.0)
Make-up Day
1 2 3 4 5 6 7 8 9
R (n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
1 5 (45.5) 4 (40.0) 5 (31.3) 7 (41.2) 5 (20.8) 12 (48.0) 9 (34.6) 7 (29.2) 34 (33.7)

2 3 (27.3) 2 (20.0) 4 (25.0) 1 (5.9) 7 (29.2) 3 (12.0) 3 (11.5) 6 (25.0) 20 (19.8)
3 0 (0.0) 0 (0.0) 3 (18.8) 2 (11.8) 4 (16.7) 4 (16.0) 5 (19.2) 0 (0.0) 24 (23.8)
4 3 (27.3) 2 (20.0) 1 (6.3) 3 (17.6) 2 (8.3) 3 (12.0) 3 (11.5) 7 (29.2) 11 (10.9)
5 0 (0.0) 2 (20.0) 3 (18.8) 4 (23.5) 6 (25.0) 3 (12.0) 6 (23.1) 4 (16.7) 12 (11.9)
5 = Entirely.
84
Table 13
Descriptive Statistics of Responses to Chronic Stress, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
(n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
Mean 2.61 3.06 2.78 2.75 2.50 2.33 2.47 2.44 2.41 2.40
Median 2.00 3.00 3.00 3.00 2.00 2.00 2.00 2.00 2.00 2.00
SD 1.50 1.49 1.52 1.56 1.52 1.47 1.44 1.54 1.42 1.38
Skewness 0.35 -0.06 0.17 0.19 0.44 0.65 0.49 0.52 0.52 0.61
Kurtosis -1.35 -1.41 -1.45 -1.51 -1.32 -1.06 -1.14 -1.30 -1.10 -0.92
Make-up Day
1 2 3 4 5 6 7 8 9
(n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
Mean 2.09 2.60 2.56 2.76 2.88 2.28 2.77 2.79 2.48
Median 2.00 2.00 2.00 3.00 2.50 2.00 3.00 2.00 2.00
SD 1.30 1.71 1.50 1.71 1.51 1.49 1.61 1.56 1.37
Skewness 0.80 0.45 0.60 0.16 0.31 0.72 0.22 0.15 0.50
Kurtosis -1.16 -1.79 -0.97 -1.81 -1.37 -0.96 -1.53 -1.67 -0.94
85
Table 14
Frequencies and Percentages (in Parentheses) of Responses to Social Isolation, Totals and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
R (n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
1 864 (47.9) 82 (34.3) 98 (47.1) 85 (45.5) 90 (49.2) 101 (58.7) 82 (49.7) 82 (50.9) 79 (49.7) 38 (52.1)
2 352 (19.5) 51 (21.3) 33 (15.9) 45 (24.1) 32 (17.5) 30 (17.4) 31 (18.8) 30 (18.6) 33 (20.8) 16 (21.9)
3 223 (12.4) 28 (11.7) 28 (13.5) 23 (12.3) 29 (15.8) 16 (9.3) 25 (15.2) 21 (13.0) 19 (11.9) 8 (11)
4 227 (12.6) 47 (19.7) 25 (12.0) 23 (12.3) 25 (13.7) 15 (8.7) 13 (7.9) 13 (8.1) 20 (12.6) 8 (11)
5 135 (7.5) 31 (13.0) 24 (11.5) 11 (5.9) 7 (3.8) 10 (5.8) 14 (8.5) 15 (9.3) 8 (5.0) 3 (4.1)
Make-up Day
1 2 3 4 5 6 7 8 9
R (n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
1 5 (45.5) 4 (40.0) 8 (50.0) 9 (52.9) 7 (29.2) 13 (52.0) 11 (42.3) 10 (41.7) 60 (59.4)

2 3 (27.3) 1 (10.0) 4 (25.0) 2 (11.8) 6 (25.0) 5 (20.0) 8 (30.8) 9 (37.5) 13 (12.9)
3 0 (0.0) 1 (10.0) 1 (6.3) 2 (11.8) 3 (12.5) 2 (8.0) 1 (3.8) 2 (8.3) 14 (13.9)
4 3 (27.3) 3 (30.0) 3 (18.8) 1 (5.9) 8 (33.3) 3 (12.0) 5 (19.2) 1 (4.2) 11 (10.9)
5 0 (0.0) 1 (10.0) 0 (0.0) 3 (17.6) 0 (0.0) 2 (8.0) 1 (3.8) 2 (8.3) 3 (3.0)
5 = Entirely.
86
Table 15 Descriptive Statistics of Responses to Social Isolation, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
(n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
Mean 2.12 2.56 2.25 2.09 2.05 1.85 2.07 2.06 2.03 1.93
Median 2.00 2.00 2.00 2.00 2.00 1.00 2.00 1.00 2.00 1.00
SD 1.33 1.45 1.44 1.26 1.24 1.24 1.32 1.34 1.26 1.21
Skewness 0.87 0.38 0.74 0.91 0.81 1.30 1.00 1.03 0.96 1.11
Kurtosis -0.58 -1.31 -0.90 -0.38 -0.63 0.47 -0.23 -0.24 -0.34 0.10
Make-up Day
1 2 3 4 5 6 7 8 9
(n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
Mean 2.09 2.60 1.94 2.24 2.50 2.04 2.12 2.00 1.85
Median 2.00 2.50 1.50 1.00 2.00 1.00 2.00 2.00 1.00
SD 1.30 1.58 1.18 1.60 1.25 1.37 1.28 1.22 1.19
Skewness 0.80 0.20 0.97 0.91 0.07 1.09 0.90 1.43 1.12
Kurtosis -1.16 -1.84 -0.55 -0.80 -1.67 -0.14 -0.51 1.47 -0.04
87
Table 16 Frequencies and Percentages (in Parentheses) of Responses to Winter, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
R (n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
1 1552 (86.1) 194 (81.2) 175 (84.1) 163 (87.2) 165 (90.2) 150 (87.2) 143 (86.7) 137 (85.1) 134 (84.3) 63 (86.3)
2 141 (7.8) 19 (7.9) 18 (8.7) 13 (7.0) 11 (6.0) 15 (8.7) 17 (10.3) 14 (8.7) 15 (9.4) 3 (4.1)
3 50 (2.8) 12 (5.0) 7 (3.4 4 (2.1) 3 (1.6) 3 (1.7) 2 (1.2) 5 (3.1) 5 (3.1) 4 (5.5)
4 32 (1.8) 9 (3.8) 4 (1.9) 3 (1.6) 3 (1.6) 1 (0.6) 2 (1.2) 3 (1.9) 2 (1.3) 2 (2.7)
5 26 (1.4) 5 (2.1) 4 (1.9) 4 (2.1) 1 (0.5) 3 (1.7) 1 (0.6) 2 (1.2) 3 (1.9) 1 (1.4)
Make-up Day
1 2 3 4 5 6 7 8 9
R (n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
1 9 (81.8) 9 (90.0) 13 (81.3) 16 (94.1) 20 (83.3) 23 (92) 23 (88.5) 23 (95.8) 92 (91.1)

2 1 (9.1) 1 (10.0) 3 (18.8) 1 (5.9) 3 (12.5) 1 (4.0) 2 (7.7) 0 (0.0) 4 (4.0)
3 1 (9.1) 0 (0.0) 0 (0.0) 0 (0.0) 1 (4.2) 1 (4.0) 1 (3.8) 0 (0.0) 1 (1.0)
4 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (3.0)
5 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 1 (4.2) 1 (1.0)
5 = Entirely.
88
Table 17
Descriptive Statistics of Responses to Winter, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
(n = 1801) (n = 239) (n = 208) (n = 187) (n = 183) (n = 172) (n = 165) (n = 161) (n = 159) (n = 73)
Mean 1.24 1.38 1.29 1.25 1.16 1.21 1.19 1.25 1.27 1.29
Median 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00
SD 0.72 0.90 0.79 0.76 0.58 0.67 0.57 0.72 0.75 0.81
Skewness 3.49 2.57 3.20 3.64 4.26 4.12 4.01 3.37 3.40 3.00
Kurtosis 12.50 5.89 10.35 13.37 19.65 18.67 18.93 11.94 12.17 8.72
Make-up Day
1 2 3 4 5 6 7 8 9
(n = 11) (n = 10) (n = 16) (n = 17) (n = 24) (n = 25) (n = 26) (n = 24) (n = 101)
Mean 1.27 1.10 1.19 1.06 1.21 1.12 1.15 1.17 1.19
Median 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00 1.00
SD 0.65 0.32 0.40 0.24 0.51 0.44 0.46 0.82 0.69
Skewness 2.42 3.16 1.77 4.12 2.54 3.88 3.22 4.90 4.05
Kurtosis 5.51 10.00 1.28 17.00 6.26 15.34 10.48 24.00 16.33
89
Table 18
Frequencies and Percentages (in Parentheses) of Responses to Adverse Life Events on

Day 1
Adverse Life Event
Response Failure Death Romantic Chronic Social Winter

Loss Stress Isolation
1 92 (38.5) 211 (88.3) 172 (72) 53 (22.2) 82 (34.3) 194 (81.2)
2 56 (23.4) 9 (3.8) 26 (10.9) 40 (16.7) 51 (21.3) 19 (7.9)
3 33 (13.8) 5 (2.1) 6 (2.5) 45 (18.8) 28 (11.7) 12 (5)
4 23 (9.6) 5 (2.1) 14 (5.9) 42 (17.6) 47 (19.7) 9 (3.8)
5 35 (14.6) 9 (3.8) 21 (8.8) 59 (24.7) 31 (13) 5 (2.1)
Note. Responses were on a 5-point Likert scale: 1 = Not at all or N/A; 2 = A little bit; 3
= Moderately; 4 = Quite a bit; 5 = Entirely.
We analyzed whether levels of ALEs differed by diagnostic group (non-MDD versus
MDD). In order to avoid violating the assumption of independent observations, we examined
data from Day 1, which had the largest number of observations (N = 239). Because ALEs were
based on an ordinal scale and the distributions of ALE scores were highly skewed (i.e., violated
the normality assumption), we conducted Mann-Whitney U tests. As mentioned previously, this
test typically involves comparing the medians of two independent groups with the same
distributions. However, when the two groups being compared have different distributions, the
Mann-Whitney U test compares mean ranks instead. Distributions for non-MDD and MDD
groups were different for all ALEs except winter. Results indicated that levels of ALEs differed
by diagnostic group for failure, death, romantic loss, chronic stress, and social isolation (see
Table 19), with non-MDD participants reporting lower levels of ALEs than MDD participants.
However, levels of winter did not differ by diagnostic group.

Table 19
Results of Analyses Comparing Participants With and Without Major Depressive

Disorder on Levels of Adverse Life Events for Day 1
Non-MDD MDD
(n = 30) (n = 209)
ALE Mean rank Mean rank Mann-Whitney U p*
Failure 116.75 142.67 2455.00 .046

Death 118.05 133.57 2728.00 .040
Romantic Loss 115.96 148.12 2291.50 .003
Chronic Stress 114.71 156.83 2030.00 .001
Social Isolation 114.48 158.45 1981.50 .001
Winter 120.97 113.25 2932.50 .401
Median Median
1 1
Note. ALE = adverse life event. MDD = major depressive disorder. IQR = interquartile rank.
Medians are reported for winter because non-MDD and MDD groups had the same distributions.
* two-tailed
Adaptive symptom cluster and nonadaptive symptom cluster scores. We calculated
descriptive statistics for each adaptive symptom cluster (ASC) and nonadaptive symptom cluster
(NSC) by day and make-up day. As mentioned previously, there were two symptom cluster
scores for each ALE, including one ASC and one NSC score. ASC and NSC scores were
calculated by averaging the Depressive Symptoms Scale (DSS) scale scores that the situation-
symptom congruence hypothesis (SSCH) predicted to be prominent and not be prominent,
respectively, following their corresponding ALEs. DSS scale scores were calculated by
averaging the responses of all DSS items comprising a particular DSS scale. DSS item responses
were based on a 5-point Likert scale (1 = not at all or N/A, 2 = a little bit, 3 = moderately, 4 =
quite a bit, and 5 = entirely).

For example, the symptom cluster scores for failure were failure-ASC and failure-NSC.
Because the SSCH predicts that emotional pain, pessimism, fatigue, anhedonia, rumination, and
guilt will be prominent following failure, a participant’s failure-ASC score was calculated by
averaging his or her scores on those particular DSS scales. Similarly, a participant’s failure-NSC
score was calculated by averaging his or her scores on those scales that the SSCH does not
predict to be prominent following failure, including crying, increased sleep, and desire for social
support.
Descriptive statistics for ASCs and NSCs for all ALEs examined by day and make-up
day are presented in Tables 20 through 31 in the following order: failure-ASC/NSC (Tables 20
and 21), death-ASC/NSC (Tables 22 and 23), romantic loss-ASC/NSC (Tables 24 and 25),
chronic stress-ASC/NSC (Tables 26 and 27), social isolation-ASC/NSC (Tables 28 and 29), and
winter-ASC/NSC (Tables 30 and 31). Sample sizes for make-up days were relatively small (i.e.,
n < 30), making it difficult to describe the data and raising concerns about the representativeness
of the sample. For this reason, we will focus this discussion on days rather than make-up days.
Participants endorsed low to moderate levels of all ASCs and NSCs across days. Mean
and median levels of ASCs were typically greater than mean and median levels of NSCs for
failure, chronic stress, and winter while mean and median levels of ASCs were typically lower
than mean and median levels of NSCs for death, romantic loss, and social isolation. Distributions
for ASCs and NSC varied, ranging from approximately symmetrical to highly, positively
skewed. We observed a number of trends in the data across days. Sample size decreased across
days, going from 239 on Day 1 to 73 on Day 9. Mean and median levels of ASCs and NSCs
were consistently highest on Day 1 and lowest on Day 9. Levels of both ASCs and NSCs
decreased over days. Positive skewness increased over days for ASCs and NSCs.
Adverse Life Events and Depressive Symptoms Patterns
Table 20
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Failure, Total and by Day
Day
Total 1 2 3 4
ASC NSC ASC NSC ASC NSC ASC NSC ASC NSC
(n = 1801) (n = 1801) (n = 239) (n = 239) (n = 208) (n = 208) (n = 187) (n = 187) (n = 183) (n = 183)
Mean 2.48 2.05 2.74 2.40 2.55 2.12 2.43 2.02 2.36 1.89
Median 2.42 1.89 2.75 2.22 2.49 1.89 2.34 1.86 2.23 1.78
SD 0.89 0.80 0.88 0.86 0.90 0.83 0.85 0.78 0.87 0.77
Skewness 0.35 1.03 0.06 0.65 0.34 0.99 0.35 1.04 0.42 1.47
Kurtosis -0.71 0.83 -1.03 -0.18 -0.86 0.64 -0.72 1.09 -0.75 2.37
Day
5 6 7 8 9
(n = 172) (n = 172) (n = 165) (n = 165) (n = 161) (n = 161) (n = 159) (n = 159) (n = 73) (n = 73)
Mean 2.32 2.01 2.46 2.01 2.45 1.95 2.35 1.93 2.22 1.85
Median 2.24 1.78 2.47 1.89 2.37 1.78 2.25 1.86 2.08 1.67
SD 0.90 0.77 0.89 0.75 0.94 0.75 0.83 0.75 0.78 0.74
Skewness 0.70 1.23 0.18 0.80 0.48 1.01 0.42 1.15 0.57 1.24
Kurtosis -0.13 1.74 -0.82 0.26 -0.55 0.49 -0.38 1.35 -0.22 1.51
Note. Total = all days and make-up days combined. ASC = adaptive symptom cluster; NSC = nonadaptive symptom cluster. The ASC
and NSC scores were calculated by averaging the Depressive Symptoms Scale (DSS) scores that were hypothesized to be prominent
and not prominent, respectively, following failure. DSS scores were calculated by averaging the responses of all items comprising a
particular scale. DSS item responses were based on a 5-point Likert scale: 1 = Not at all or N/A; 2 = A little bit; 3 = Moderately; 4 =
93
Table 21
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Failure by Make-Up Day
Make-up Day
2 3 4 5 6
(n = 11) (n = 11) (n = 10) (n = 10) (n = 16) (n = 16) (n = 17) (n = 17) (n = 24) (n = 24)
Mean 2.64 2.18 2.49 1.98 2.68 2.12 2.92 2.24 2.78 2.14
Median 2.88 2.25 2.10 1.79 2.73 1.89 2.65 2.08 2.69 2.04
SD 0.81 0.57 1.05 1.01 0.73 0.81 1.22 0.86 0.98 0.62
Skewness -0.40 -0.42 0.35 1.77 -0.18 1.51 0.18 0.93 -0.05 0.46
Kurtosis -1.60 -0.58 -1.59 3.78 -0.20 2.66 -1.42 0.32 -1.15 -0.11
Make-up Day
7 8 9 10
ASC NSC ASC NSC ASC NSC ASC NSC
(n = 25) (n = 25) (n = 26) (n = 26) (n = 24) (n = 24) (n = 101) (n = 101)
Mean 2.56 1.96 2.57 1.92 2.65 2.16 2.39 1.99

Median 2.39 1.89 2.50 1.81 2.69 2.04 2.38 1.78
SD 0.79 0.66 1.00 0.63 1.04 0.90 0.78 0.78
Skewness 0.31 0.32 0.63 0.28 0.01 1.32 0.11 1.23
Kurtosis -0.03 -0.75 0.02 -1.41 -0.93 2.36 -0.78 1.61
Note. ASC = adaptive symptom cluster; NSC = nonadaptive symptom cluster. The ASC and NSC scores were calculated by averaging
the Depressive Symptoms Scale (DSS) scores that were hypothesized to be prominent and not prominent, respectively, following
failure. DSS scores were calculated by averaging the responses of all items comprising a particular scale. DSS item responses were
based on a 5-point Likert scale: 1 = Not at all or N/A; 2 = A little bit; 3 = Moderately; 4 = Quite a bit; 5 = Entirely.
94
Table 22
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Death of a Loved One, Total and by Day
Day
Total 1 2 3 4
(n = 1801) (n = 1801) (n = 239) (n = 239) (n = 208) (n = 208) (n = 187) (n = 187) (n = 183) (n = 183)
Mean 2.08 2.46 2.44 2.72 2.18 2.52 2.06 2.42 1.93 2.34
Median 1.90 2.40 2.28 2.74 1.99 2.41 1.86 2.30 1.70 2.25
SD 0.84 0.86 0.93 0.84 0.89 0.86 0.81 0.81 0.81 0.85
Skewness 1.02 0.34 0.56 0.07 0.89 0.38 0.93 0.32 1.53 0.41
Kurtosis 0.70 -0.63 -0.55 -0.88 0.28 -0.72 0.60 -0.74 2.44 -0.62
Day
5 6 7 8 9
(n = 172) (n = 172) (n = 165) (n = 165) (n = 161) (n = 161) (n = 159) (n = 159) (n = 73) (n = 73)
Mean 1.99 2.33 2.02 2.46 1.99 2.43 1.92 2.35 1.85 2.22
Median 1.85 2.19 1.93 2.38 1.80 2.34 1.78 2.36 1.62 2.09
SD 0.81 0.86 0.78 0.86 0.81 0.90 0.76 0.83 0.77 0.77
Skewness 1.11 0.71 0.87 0.23 1.23 0.39 1.34 0.40 1.27 0.64
Kurtosis 1.10 0.05 0.56 -0.70 1.45 -0.68 2.47 -0.48 1.56 0.20
95
Table 23
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Death of a Loved One by Make-Up Day
Make-up Day
1 2 3 4 5
(n = 11) (n = 11) (n = 10) (n = 10) (n = 16) (n = 16) (n = 17) (n = 17) (n = 24) (n = 24)
Mean 2.31 2.57 2.08 2.44 2.25 2.61 2.28 2.90 2.18 2.77
Median 2.19 2.65 1.96 2.11 2.07 2.66 2.03 2.74 2.13 2.83
SD 0.64 0.80 1.13 1.05 0.92 0.70 0.99 1.14 0.76 0.91
Skewness -0.05 -0.23 2.18 0.50 1.20 -0.41 0.68 0.14 1.02 -0.20
Kurtosis 0.00 -1.36 5.85 -1.09 1.91 -0.53 -0.40 -1.24 1.44 -0.93
Make-up Day
6 7 8 9
(n = 25) (n = 25) (n = 26) (n = 26) (n = 24) (n = 24) (n = 101) (n = 101)
Mean 2.01 2.54 1.91 2.58 2.11 2.68 2.01 2.38

Median 1.87 2.39 1.74 2.44 1.71 2.89 1.84 2.44
SD 0.71 0.73 0.68 1.00 0.90 1.01 0.82 0.74
Skewness 0.86 0.48 0.57 0.62 1.05 -0.26 1.12 0.06
Kurtosis 0.26 0.58 -1.01 -0.11 0.61 -0.90 1.02 -0.65
96
Table 24
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Romantic Loss, Total and by Day
Day
Total 1 2 3 4
(n = 1801) (n = 1801) (n = 239) (n = 239) (n = 208) (n = 208) (n = 187) (n = 187) (n = 183) (n = 183)
Mean 2.27 2.42 2.64 2.61 2.38 2.44 2.25 2.35 2.13 2.30
Median 2.12 2.37 2.59 2.58 2.23 2.32 2.14 2.27 2.00 2.22
SD 0.84 0.86 0.89 0.83 0.88 0.86 0.80 0.81 0.79 0.86
Skewness 0.69 0.38 0.36 0.15 0.61 0.49 0.63 0.38 1.04 0.48
Kurtosis -0.12 -0.51 -0.76 -0.73 -0.33 -0.41 -0.16 -0.57 0.95 -0.44
Day
5 6 7 8 9
(n = 172) (n = 172) (n = 165) (n = 165) (n = 161) (n = 161) (n = 159) (n = 159) (n = 73) (n = 73)
Mean 2.15 2.30 2.21 2.44 2.17 2.42 2.12 2.33 1.99 2.23
Median 1.96 2.19 2.24 2.35 2.11 2.37 2.02 2.27 1.78 2.18
SD 0.85 0.84 0.81 0.86 0.83 0.92 0.78 0.84 0.74 0.81
Skewness 0.90 0.68 0.53 0.30 0.81 0.36 0.87 0.43 1.04 0.69
Kurtosis 0.25 0.13 -0.23 -0.54 0.18 -0.77 0.73 -0.38 0.83 0.63
97
Table 25
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Romantic Loss by Make-Up Day
Make-up Day
1 2 3 4 5
(n = 11) (n = 11) (n = 10) (n = 10) (n = 16) (n = 16) (n = 17) (n = 17) (n = 24) (n = 24)
Mean 2.42 2.56 2.21 2.46 2.42 2.59 2.49 2.95 2.41 2.77
Median 2.70 2.67 2.00 2.04 2.21 2.71 2.26 3.03 2.41 2.70
SD 0.70 0.80 0.90 1.22 0.77 0.69 1.09 1.10 0.80 0.89
Skewness -0.49 0.12 1.19 0.69 0.35 -0.33 0.54 0.01 0.38 -0.18
Kurtosis -0.16 -0.84 2.26 -0.65 -0.53 -0.96 -0.99 -0.94 -0.53 -1.11
Make-up Day
6 7 8 9
(n = 25) (n = 25) (n = 26) (n = 26) (n = 24) (n = 24) (n = 101) (n = 101)
Mean 2.21 2.55 2.26 2.47 2.32 2.70 2.19 2.34

Median 2.03 2.65 2.18 2.18 2.06 2.85 2.01 2.40
SD 0.76 0.74 0.77 1.01 0.89 1.03 0.78 0.74
Skewness 0.69 -0.02 0.53 0.69 0.48 -0.25 0.70 0.03
Kurtosis 0.00 -0.55 -0.84 0.00 -0.81 -0.80 0.14 -0.69
98
Table 26
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Chronic Stress, Total and by Day
Day
Total 1 2 3 4
(n = 1801) (n = 1801) (n = 239) (n = 239) (n = 208) (n = 208) (n = 187) (n = 187) (n = 183) (n = 183)
Mean 2.52 2.11 2.77 2.45 2.58 2.19 2.47 2.08 2.40 1.96
Median 2.47 1.94 2.77 2.27 2.50 2.01 2.42 1.94 2.29 1.77
SD 0.89 0.79 0.86 0.85 0.89 0.83 0.84 0.77 0.88 0.76
Skewness 0.29 0.95 0.01 0.59 0.30 0.86 0.30 0.95 0.33 1.38
Kurtosis -0.74 0.56 -0.98 -0.36 -0.85 0.23 -0.77 0.83 -0.85 1.96
Day
5 6 7 8 9
(n = 172) (n = 172) (n = 165) (n = 165) (n = 161) (n = 161) (n = 159) (n = 159) (n = 73) (n = 73)
Mean 2.35 2.04 2.51 2.06 2.49 2.02 2.39 1.98 2.27 1.88
Median 2.28 1.86 2.49 1.93 2.42 1.93 2.32 1.85 2.17 1.70
SD 0.89 0.78 0.89 0.75 0.94 0.76 0.84 0.72 0.79 0.72
Skewness 0.65 1.21 0.14 0.76 0.41 0.97 0.36 1.13 0.52 1.25
Kurtosis -0.14 1.46 -0.83 0.12 -0.61 0.53 -0.52 1.48 -0.25 1.71
99
Table 27
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Chronic Stress by Make-Up Day
Make-up Day
1 2 3 4 5
(n = 11) (n = 11) (n = 10) (n = 10) (n = 16) (n = 16) (n = 17) (n = 17) (n = 24) (n = 24)
Mean 2.66 2.26 2.52 2.06 2.70 2.23 2.95 2.37 2.83 2.25
Median 2.85 2.48 2.20 1.85 2.80 2.01 2.82 2.22 2.81 2.21
SD 0.84 0.57 1.03 1.06 0.71 0.80 1.20 0.95 0.98 0.65
Skewness -0.44 -0.32 0.29 1.64 -0.29 1.08 0.10 0.72 -0.14 0.59
Kurtosis -1.37 -1.00 -1.56 3.18 -0.02 1.20 -1.43 -0.25 -1.10 0.12
Make-up Day
6 7 8 9
(n = 25) (n = 25) (n = 26) (n = 26) (n = 24) (n = 24) (n = 101) (n = 101)
Mean 2.61 2.05 2.64 1.99 2.71 2.22 2.44 2.04

Median 2.47 1.92 2.54 1.78 2.82 2.00 2.45 1.87
SD 0.79 0.63 1.01 0.70 1.02 0.90 0.79 0.72
Skewness 0.28 0.33 0.53 0.56 -0.16 0.93 0.07 1.01
Kurtosis 0.07 -0.91 -0.24 -0.94 -0.87 0.75 -0.83 0.76
100
Table 28
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Social Isolation, Total and by Day
Day
Total 1 2 3 4
(n = 1801) (n = 1801) (n = 239) (n = 239) (n = 208) (n = 208) (n = 187) (n = 187) (n = 183) (n = 183)
Mean 2.08 2.46 2.44 2.72 2.18 2.52 2.06 2.42 1.93 2.34
Median 1.90 2.40 2.28 2.74 1.99 2.41 1.86 2.30 1.70 2.25
SD 0.84 0.86 0.93 0.84 0.89 0.86 0.81 0.81 0.81 0.85
Skewness 1.02 0.34 0.56 0.07 0.89 0.38 0.93 0.32 1.53 0.41
Kurtosis 0.70 -0.63 -0.55 -0.88 0.28 -0.72 0.60 -0.74 2.44 -0.62
Day
5 6 7 8 9
(n = 172) (n = 172) (n = 165) (n = 165) (n = 161) (n = 161) (n = 159) (n = 159) (n = 73) (n = 73)
Mean 1.99 2.33 2.02 2.46 1.99 2.43 1.92 2.35 1.85 2.22
Median 1.85 2.19 1.93 2.38 1.80 2.34 1.78 2.36 1.62 2.09
SD 0.81 0.86 0.78 0.86 0.81 0.90 0.76 0.83 0.77 0.77
Skewness 1.11 0.71 0.87 0.23 1.23 0.39 1.34 0.40 1.27 0.64
Kurtosis 1.10 0.05 0.56 -0.70 1.45 -0.68 2.47 -0.48 1.56 0.20
101
Table 29
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Social Isolation by Make-Up Day
Make-up Day
1 2 3 4 5
(n = 11) (n = 11) (n = 10) (n = 10) (n = 16) (n = 16) (n = 17) (n = 17) (n = 24) (n = 24)
Mean 2.31 2.57 2.08 2.44 2.25 2.61 2.28 2.90 2.18 2.77
Median 2.19 2.65 1.96 2.11 2.07 2.66 2.03 2.74 2.13 2.83
SD 0.64 0.80 1.13 1.05 0.92 0.70 0.99 1.14 0.76 0.91
Skewness -0.05 -0.23 2.18 0.50 1.20 -0.41 0.68 0.14 1.02 -0.20
Kurtosis 0.00 -1.36 5.85 -1.09 1.91 -0.53 -0.40 -1.24 1.44 -0.93
Make-up Day
6 7 8 9
(n = 25) (n = 25) (n = 26) (n = 26) (n = 24) (n = 24) (n = 101) (n = 101)
Mean 2.01 2.54 1.91 2.58 2.11 2.68 2.01 2.38

Median 1.87 2.39 1.74 2.44 1.71 2.89 1.84 2.44
SD 0.71 0.73 0.68 1.00 0.90 1.01 0.82 0.74
Skewness 0.86 0.48 0.57 0.62 1.05 -0.26 1.12 0.06
Kurtosis 0.26 0.58 -1.01 -0.11 0.61 -0.90 1.02 -0.65
102
Table 30
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Winter, Total and by Day
Day
Total 1 2 3 4
(n = 1801) (n = 1801) (n = 239) (n = 239) (n = 208) (n = 208) (n = 187) (n = 187) (n = 183) (n = 183)
Mean 2.41 2.30 2.59 2.65 2.41 2.41 2.34 2.27 2.29 2.16
Median 2.33 2.17 2.53 2.59 2.24 2.27 2.24 2.16 2.20 2.05
SD 0.87 0.84 0.85 0.87 0.85 0.87 0.83 0.79 0.87 0.79
Skewness 0.41 0.63 0.21 0.29 0.58 0.55 0.40 0.59 0.51 0.91
Kurtosis -0.50 -0.27 -0.64 -0.88 -0.23 -0.49 -0.61 -0.25 -0.34 0.50
Day
5 6 7 8 9
(n = 172) (n = 172) (n = 165) (n = 165) (n = 161) (n = 161) (n = 159) (n = 159) (n = 73) (n = 73)
Mean 2.30 2.17 2.45 2.24 2.41 2.22 2.32 2.15 2.22 2.03
Median 2.18 2.01 2.36 2.22 2.31 2.12 2.29 2.03 2.18 1.90
SD 0.85 0.84 0.87 0.81 0.92 0.84 0.87 0.76 0.83 0.73
Skewness 0.66 0.87 0.35 0.47 0.36 0.73 0.47 0.80 0.69 0.95
Kurtosis -0.08 0.14 -0.51 -0.34 -0.78 0.03 -0.45 0.70 0.46 0.67
103
Table 31
Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster Scores for Winter by Make-Up Day
Make-up Day
1 2 3 4 5
(n = 11) (n = 11) (n = 10) (n = 10) (n = 16) (n = 16) (n = 17) (n = 17) (n = 24) (n = 24)
Mean 2.56 2.45 2.42 2.26 2.55 2.46 2.98 2.55 2.78 2.47
Median 2.69 2.81 1.96 1.99 2.72 2.22 2.98 2.32 2.77 2.38
SD 0.78 0.70 1.19 0.95 0.63 0.78 1.04 1.11 0.86 0.82
Skewness 0.23 -0.56 0.84 0.88 -0.25 0.25 -0.02 0.44 -0.19 0.35
Kurtosis -0.78 -0.95 -0.21 0.83 -1.24 -0.59 -0.60 -1.24 -0.78 -0.66
Make-up Day
6 7 8 9
(n = 25) (n = 25) (n = 26) (n = 26) (n = 24) (n = 24) (n = 101) (n = 101)
Mean 2.57 2.26 2.47 2.29 2.73 2.37 2.34 2.22

Median 2.71 2.09 2.30 2.21 2.81 2.18 2.29 2.06
SD 0.76 0.72 1.04 0.79 1.07 0.89 0.76 0.76
Skewness -0.28 0.53 0.61 0.55 -0.21 0.38 0.13 0.59
Kurtosis -0.51 -0.39 -0.24 -0.65 -1.01 -0.94 -0.61 -0.14
winter. DSS scores were calculated by averaging the responses of all items comprising a particular scale. DSS item responses were
104
Depressive Symptoms Scale scores. We calculated descriptive statistics for each
Depressive Symptoms Scale (DSS) scale score by day and make-up day. As mentioned
previously, we examined the following nine DSS scales: emotional pain, pessimism, fatigue,
anhedonia, rumination, crying, guilt, increased sleep, and desire for social support. DSS scale
scores were calculated by averaging the responses of all items comprising their respective scale.
DSS item responses were based on a 5-point Likert scale (1 = not at all or N/A, 2 = a little bit, 3
= moderately, 4 = quite a bit, and 5 = entirely).
Descriptive statistics for DSS scales examined by day are presented in Tables 32 through
40 in the following order: emotional pain (Table 32), pessimism (Table 33), fatigue (Table 34),
anhedonia (Table 35), rumination (Table 36), crying (Table 37), guilt (Table 38), increased sleep
(Table 39), and desire for social support (Table 40). Sample sizes for make-up days were
relatively small (i.e., n < 30), making it difficult to interpret descriptive statistics and raising
concerns about the representativeness of the sample. For this reason, we will focus this
discussion on days rather than make-up days.
Participants endorsed low to moderate levels of all DSS scale scores across days.
Distributions for fatigue were approximately symmetrical while those for pessimism, anhedonia,
and rumination ranged from approximately symmetrical to moderately, positively skewed.
Distributions ranged from approximately symmetrical to highly, positively skewed. We observed
a number of trends in the data across days. Sample size decreased across days, going from 239
on Day 1 to 73 on Day 9. Mean and median levels of all DSS scales were typically highest on
Day 1. The days on which mean and median levels of DSS scales were lowest varied. Levels of
DSS scales mostly decreased over days. Positive skewness typically increased across days for all
DSS scales except fatigue.

Table 32

Descriptive Statistics for Emotional Pain, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.27 2.59 2.38 2.24 2.15 2.15 2.22 2.24 2.11 1.98
Median 2.20 2.40 2.20 2.00 2.00 2.00 2.20 2.00 2.00 1.80
SD 1.01 1.06 1.06 .99 .95 1.03 .99 1.05 .90 .88
Skewness 0.64 .24 .46 .61 .85 .87 .52 .80 .85 1.22
Kurtosis -0.44 -1.08 -.85 -.45 .08 .01 -.61 -.16 .43 1.43
Make-up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 2.51 2.30 2.55 2.75 2.56 2.30 2.22 2.40 2.18
Median 3.00 1.80 2.50 2.20 2.40 2.20 1.90 2.10 2.20
SD .76 1.29 1.00 1.39 1.08 .84 1.06 1.22 .86
Skewness -.64 1.08 .28 .43 .35 .51 .94 .66 .42
Kurtosis -1.56 .68 -1.01 -1.32 -.96 .03 .24 -.72 -.58
106
Table 33

Descriptive Statistics for Pessimism, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.45 2.69 2.54 2.39 2.35 2.30 2.41 2.45 2.34 2.25
Median 2.40 2.60 2.60 2.40 2.20 2.20 2.40 2.40 2.20 2.20
SD 0.99 .96 1.02 .94 .99 .99 .99 1.06 .91 .90
Skewness 0.44 .16 .39 .49 .56 .70 .43 .46 .54 .51
Kurtosis -0.50 -.70 -.64 -.34 -.54 .02 -.30 -.61 -.12 -.24
Make up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 2.58 2.56 2.70 2.86 2.75 2.48 2.48 2.63 2.35
Median 2.60 2.30 2.80 2.80 2.70 2.40 2.30 2.70 2.40
SD .93 1.33 1.10 1.38 1.08 .89 1.03 1.02 .86
Skewness -.26 .34 .37 .23 .27 .14 .72 .04 .21
Kurtosis -1.14 -1.50 -.25 -1.28 -.96 -.78 .15 -.74 -.82
107
Table 34

Descriptive Statistics for Fatigue, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.86 3.05 2.86 2.78 2.75 2.68 2.98 2.91 2.74 2.66
Median 2.80 3.20 2.80 2.80 2.80 2.60 3.00 2.80 2.80 2.80
SD 1.03 .97 .96 .98 1.06 1.03 1.05 1.13 1.02 .99
Skewness 0.08 -.16 .16 .17 .13 .33 -.09 .14 .24 .06
Kurtosis -0.78 -.76 -.70 -.80 -.72 -.52 -.84 -.96 -.57 -.57
Make-up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 3.04 2.94 3.11 3.66 3.20 3.03 2.92 3.22 2.77
Median 3.20 2.50 3.10 3.80 3.30 3.20 2.80 3.70 2.80
SD .85 1.29 .72 1.17 .98 .91 1.13 1.24 .96
Skewness .08 .47 .33 -.46 -.22 -.75 .17 -.61 -.05
Kurtosis -.15 -1.17 -1.00 -1.03 -.65 -.21 -.78 -.85 -.69
108
Table 35

Descriptive Statistics for Anhedonia, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.16 2.24 2.17 2.10 2.08 2.00 2.17 2.20 2.09 2.04
Median 2.00 2.20 2.00 2.00 2.00 1.80 2.20 2.00 2.00 1.80
SD 0.90 .88 .89 .88 .91 .85 .86 .97 .87 .88
Skewness 0.56 .39 .66 .52 .56 .79 .42 .62 .59 .99
Kurtosis -0.41 -.72 -.10 -.53 -.74 .13 -.62 -.18 -.30 .73
Make-up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 2.51 2.32 2.36 2.66 2.67 2.50 2.24 2.42 2.14
Median 3.00 2.10 2.30 2.40 2.70 2.60 2.00 2.10 2.00
SD .90 1.13 .63 1.26 1.04 .93 .97 1.08 .83
Skewness -.42 .34 -.29 .35 -.02 -.07 .97 .34 .42
Kurtosis -1.20 -1.19 .07 -.80 -1.17 -1.11 1.09 -1.15 -.62
109
Table 36

Descriptive Statistics for Rumination, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.83 2.96 2.72 2.60 2.45 2.45 2.53 2.50 2.48 2.27
Median 2.75 2.80 2.60 2.60 2.40 2.30 2.40 2.40 2.40 2.20
SD 1.07 .97 .94 .92 .94 .99 1.01 .97 .99 .85
Skewness 0.18 .17 .24 .21 .40 .58 .30 .35 .47 .77
Kurtosis -0.82 -.89 -.79 -.72 -.71 -.34 -.76 -.74 -.40 .47
Make-up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 2.69 2.56 2.78 2.86 2.74 2.54 2.75 2.71 2.54
Median 2.60 2.60 2.60 3.00 2.70 2.40 2.40 2.60 2.40
SD .97 .96 .87 1.28 1.09 1.06 1.11 1.01 .91
Skewness -.20 -.03 .02 .25 .37 .89 .54 .09 .27
Kurtosis -.72 -.29 -.13 -1.53 -.57 .66 -.73 -1.05 -.53
110
Table 37

Descriptive Statistics for Crying, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 1.58 1.90 1.65 1.49 1.44 1.49 1.51 1.53 1.45 1.45
Median 1.00 1.50 1.13 1.00 1.00 1.00 1.00 1.00 1.00 1.00
SD 0.96 1.12 1.02 0.84 0.86 0.83 0.83 0.92 0.89 0.91
Skewness 1.97 1.25 1.80 2.19 2.42 2.07 2.14 2.13 2.58 2.53
Kurtosis 3.17 0.40 2.38 4.68 5.46 3.92 4.62 4.15 6.46 6.21
Make-up day
1 2 3 4 5 6 7 8 9
N 11 10 16 17 24 25 26 24 101
Mean 1.73 1.53 1.58 2.01 1.66 1.49 1.42 1.82 1.56
Median 1.75 1.00 1.13 1.75 1.00 1.00 1.00 1.13 1.00
SD 0.81 1.24 1.06 1.30 1.13 0.99 0.77 1.20 1.02
Skewness 1.63 3.00 2.68 1.31 1.62 1.94 2.29 1.31 2.15
Kurtosis 3.41 9.23 7.69 0.97 1.22 2.10 4.96 0.65 3.75
111
Table 38

Descriptive Statistics for Guilt, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.27 2.67 2.39 2.24 2.15 2.10 2.24 2.21 2.11 1.92
Median 2.00 2.75 2.25 2.00 2.00 1.75 2.25 2.00 1.75 1.75
SD 1.08 1.09 1.12 1.07 1.01 1.12 1.05 1.12 1.03 .87
Skewness 0.69 .19 .62 .73 .85 .97 .66 .79 .82 1.00
Kurtosis -0.42 -.94 -.64 -.38 .01 -.01 -.25 -.32 -.14 .27
Make-up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 2.32 2.00 2.27 2.50 2.59 2.25 2.50 2.35 2.14
Median 2.50 2.00 2.50 2.25 2.50 2.00 2.50 2.13 2.00
SD .94 .75 .82 1.43 1.14 .98 1.17 1.09 .93
Skewness -.51 .16 -.19 .76 .26 1.30 .63 .28 1.00
Kurtosis -1.24 -1.50 -.90 -.87 -1.07 1.79 -.26 -1.11 .87
112
Table 39

Descriptive Statistics for Increased Sleep, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.19 2.47 2.19 2.15 2.04 2.21 2.18 2.12 2.13 1.95
Median 2.00 2.33 2.00 2.00 1.67 2.00 2.00 2.00 2.00 1.67
SD 1.11 1.12 1.11 1.08 1.08 1.10 1.12 1.15 1.13 0.98
Skewness 0.87 0.59 0.93 0.85 1.16 0.90 0.99 1.02 0.91 1.21
Kurtosis -0.11 -0.48 -0.07 -0.21 0.73 -0.01 0.22 0.13 -0.20 1.27
Make-up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 2.12 2.00 2.17 2.63 2.46 2.17 2.26 2.56 2.11
Median 2.00 1.67 2.17 2.33 2.50 2.00 1.67 2.67 1.67
SD 0.85 1.31 0.96 1.07 1.08 1.08 1.30 1.36 1.04
Skewness 0.80 1.57 0.38 0.87 0.34 0.81 0.72 0.25 0.94
Kurtosis -0.40 2.31 -0.82 0.58 -0.64 -0.28 -0.90 -1.16 0.13
113
Table 40

Descriptive Statistics for Desire for Social Support, Total and by Day and Make-Up Day
Day
Total 1 2 3 4 5 6 7 8 9
n 1801 239 208 187 183 172 165 161 159 73
Mean 2.38 2.83 2.52 2.43 2.20 2.33 2.33 2.19 2.22 2.14
Median 2.00 2.67 2.33 2.00 2.00 2.00 2.00 2.00 2.00 2.00
SD 1.17 1.18 1.15 1.23 1.14 1.17 1.17 1.11 1.15 1.07
Skewness 0.63 0.14 0.47 0.59 1.01 0.68 0.62 0.84 0.90 0.86
Kurtosis -0.64 -1.04 -0.77 -0.81 0.19 -0.55 -0.59 -0.24 -0.06 -0.11
Make-up day
1 2 3 4 5 6 7 8 9
n 11 10 16 17 24 25 26 24 101
Mean 2.70 2.40 2.63 2.08 2.32 2.23 2.08 2.11 2.30
Median 3.00 2.00 2.67 2.33 2.00 2.00 2.00 2.00 2.00
SD 0.95 1.19 1.12 0.90 1.12 1.17 1.07 1.09 1.22
Skewness -0.59 1.14 0.32 0.49 0.97 0.86 0.77 0.83 0.72
Kurtosis -0.51 1.28 -0.24 -0.43 -0.07 -0.08 -0.53 -0.25 -0.67
114
Correlations. We examined correlations for all predictor and outcome variables. To
avoid violating the assumption of independence of observations, we limited our examination to
correlations for Day 1. Table 41 presents a correlation matrix for ALEs, ASC/NSC scales, and
diagnostic group on Day 1. Cohen’s (1988) guidelines for interpreting correlations suggest that a
correlation equal to or greater than .10 is small, equal to or greater than .30 is medium, and equal
to or greater than .50 is large.
Based on these guidelines, correlations between ALEs ranged from small to medium and
were positive in direction. For the most part, correlations between ALEs and ASC/NSC ranged
from small to medium and were positive in direction. One exception involved the correlations
between social isolation and ASC/NSCs, which were mostly large and positive in direction.
Another exception involved the correlations between winter and ASC/NSCs, which were mostly
less than small (i.e., less than .10) and positive in direction. Correlations between ALEs and
diagnostic group were mostly small and positive in direction. Correlations between ASCs and
NSCs were large and positive in direction. Correlations between the ASC/NSCs and diagnostic
group were mostly medium and positive in direction.

Table 41
Correlations for Adaptive and Nonadaptive Symptom Clusters, ALEs, and Diagnostic Group on Day 1 (N
= 239)
1 2 3 4 5 6 7 8 9
1
1. Failure
2. Death .19** 1
3. Rm. Loss .36** .15* 1
4. Stress .28** .10 .31** 1
5. Isolation .27** .20** .37** .43** 1
6. Winter .13 .31** .20** .11 .10 1
7. Fail-ASC .42** .24** .33** .51** .55** .08 1
8. Fail-NSC .39** .23** .27** .40** .52** .12 .69** 1
9. Dth-ASC .39** .29** .34** .42** .56** .10 .77** .91** 1
10. Dth-NSC .42** .21** .29** .51** .54** .09 .98** .74** .73**
11. RL-ASC .44** .28** .35** .48** .59** .11 .90** .87** .96**
12. RL-NSC .38** .18** .26** .48** .49** .08 .92** .71** .65**
13. Strss-ASC .41** .22** .31** .51** .54** .07 .99** .67** .73**
14. Strss-NSC .42** .26** .32** .45** .56** .13 .81** .97** .96**
15. Isol-ASC .39** .29** .34** .42** .56** .10 .77** .91** 1.00**
16. Isol-NSC .42** .21** .29** .51** .54** .09 .98** .74** .73**
17. Wint-ASC .35** .18** .24** .44** .46** .10 .86** .70** .60**
18. Wint-NSC .44** .27** .34** .50** .59** .09 .93** .85** .94**
19. Diag. Grp. .11 .10 .20** .21** .22** -.06 .39** .29** .32**
Note. Dth = Death; RL = Romantic loss; Strss = Chronic stress; Isol = Social isolation; Wint = Winter;
Diag. Grp. = Diagnostic group.
* Correlation is significant at the .05 level (2-tailed).
** Correlation is significant at the .01 level (2-tailed).
10 11 12 13 14 15 16 17 18
1. Failure
2. Death
3. Rm. Loss
4. Stress
5. Isolation
6. Winter
7. Fail-ASC
8. Fail-NSC
9. Dth-ASC
10. Dth-NSC 1
11. RL-ASC .86** 1
12. RL-NSC .97** .75** 1
13. Strss-ASC .98** .87** .93** 1
14. Strss-NSC .82** .94** .78** .78** 1
15. Isol-ASC .73** .96** .65** .73** .96** 1
16. Isol-NSC 1.00** .86** .97** .98** .82** .73** 1
17. Wint-ASC .93** .69** .98** .87** .76** .60** .93** 1
18. Wint-NSC .89** .99** .80** .91** .93** .94** .89** .73** 1
19. Diag. Grp. .38** .34** .37** .38** .33** .32** .38** .36** .35**
Note. Dth = Death; RL = Romantic loss; Strss = Chronic stress; Isol = Social isolation; Wint = Winter;
Diag. Grp. = Diagnostic group.
Table 42 presents a correlation matrix for ALEs, DSS scales, and diagnostic group for
Day 1. Based on Cohen’s (1988) guidelines, most correlations between ALEs and the DSS scales
ranged from small to medium, and were positive in direction. One exception involved
correlations between winter and DSS scales, which ranged from less than small (i.e., less than
.10) to medium, and were positive in direction. For the most part, correlations between DSS
scales ranged from medium to large, and were positive in direction. Exceptions included the
small, positive correlations between desire for social support and the following DSS scales:
fatigue, anhedonia, and increased sleep. For the most part, correlations between DSS scales and
diagnostic group were medium and positive in direction. Exceptions included the small, positive
correlations between diagnostic group and the following DSS scales: increased sleep and desire
for social support.

Table 42

Correlations for scores on Adverse Life Events, Depressive Symptoms Scale Scales, and Diagnostic Group on Day 1 (N = 239)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
1. Failure 1
2. Death .19** 1
3. Rom. Loss .36** .15* 1
4. Stress .28** .10 .31** 1
5. Isolation .27** .20** .37** .43** 1
6. Winter .13 .31** .20** .11 .10 1
7. Emot. Pain .41** .30** .36** .44** .54** .12 1
8. Pessimism .38** .17** .25** .49** .49** .00 .78** 1
9. Fatigue .29** .17** .23** .44** .41** .04 .68** .74** 1
10. Anhedonia .30** .20** .29** .41** .46** .09 .76** .76** .77** 1
11. Rumination .39** .23** .28** .49** .54** .11 .78** .77** .65** .67** 1
12. Crying .31** .27** .29** .33** .45** .12 .72** .55** .47** .48** .57** 1
13. Guilt .45** .22** .32** .44** .49** .06 .82** .79** .64** .68** .77** .60** 1
14. Incr. Sleep .31** .10 .13 .31** .33** .13* .44** .48** .62** .42** .46** .40** .47** 1
15. Soc. Supp. .26** .15* .20** .28** .41** .03 .43** .32** .22** .23** .48** .44** .38** .25** 1
16. Diag. Grp. .11 .10 .20** .21** .22** -.06 .36** .34** .34** .40** .30** .30** .32** .21** .14* 1
Note. Rom. Loss = Romantic loss; Stress = Chronic stress; Isolation = Social isolation; Emot. Pain = Emotional pain; Incr. Sleep = Increased
sleep; Soc. Supp. = Desire for social support; Diag. Grp. = Diagnostic group.
119
Data Screening
We screened data by examining missing data, outliers, and assumptions for multilevel
modeling. Assumptions for multilevel modeling include linear relationships, homoscedasticity,
and normal distribution of residuals (Maas & Hox, 2003).
Missing data. As mentioned previously, our study asked participants to complete
repeated measures over nine consecutive days (i.e., Days 1 through 9). However, participants
who missed days were given the opportunity to complete make-up days (i.e., Make-up Days 1
through 9). Rather than combining data from Days 1 through 9 with data from Make-up Days 1
through 9 (e.g., treating Make-up Day 1 data as if it took place on Day 1), we treated Days 1
through 9 and Make-up Days 1 through 9 as separate data points. As a result, a participant’s
repeated measures were distributed over 18 possible time points or observations. Coupled with
the fact that participants completed between one and nine repeated measures, our data was
characterized by varying numbers of observations across days and participants, and a large
amount of missing data.
Multilevel modeling can accommodate a large amount of missing data (Singer & Willett,
2003) if the data is missing at random (MAR; Little & Rubin, 1987). More specifically, a
participant’s missingness should not be related to the value of their unobserved data. For
example, a participant’s missingness on chronic stress at a particular time point should not be
related to their level of chronic stress. Although this can be difficult to determine, one technique
for addressing the MAR assumption is to examine whether missingness on a particular variable
is predicted by a participant’s preceding values on that variable. There is evidence that the data
for a variable is MAR if the variable does not predict subsequent missingness on the variable.
We completed five binary logistic regressions to determine whether missingness on a
particular variable on Day 2 was predicted by a participants’ values on that variable on Day 1.
We selected a sample of key predictor and response variables for these analyses, including two
ALEs (i.e., failure and chronic stress), and three DSS scale scores (i.e., emotional pain, fatigue,
and desire for social support). Each regression included one of these variables as the predictor
and a missing data indicator for that variable as an outcome. For each regression, 45 participants
had completed Day 1 but missed Day 2 while 194 participants had completed both Days 1 and 2.
The results of each regression indicated that participants’ values on the predictor variable did not
predict missingness on that variable. These results provide some evidence that our data met the
MAR assumption.
Leverage and influence. Mplus does not provide measures of leverage or influence for
2-level random models. However, we used the Cook’s Distance function in the Statistical
Package for the Social Sciences Version 21 (SPSS v21) to examine influential observations. We
focused this examination on our Hypothesis 2 models and participants’ first observation. Our
Hypothesis 2 models examined the relationship between ALEs and DSS scale scores. Cook and
Weisberg (1982) suggest that Ds that are greater than one may be influential. Among the six
models, we identified between nine and thirteen observations that could be influential. For two of
the six models, namely failure and romantic loss, we examined whether the observations were
influential by examining model fit before and after removing the observations. The Bayesian
information criterion (BIC) is a statistic that provides an estimate of model performance, with
lower BICs indicating increased model fit (Raftery, 1995; Schwarz, 1978). Using the BIC, we
determined that model fit worsened after removing the observations, suggesting that the
observations were not influential. As a result, we elected to retain all observations in our
Hypothesis 1 and 2 models.
Assumptions
Mplus does not provide graphical representations of linearity. As a result, we examined
linearity by creating scatterplots in SPSS. In order to avoid violating the assumption of
independent observations, we included data from all participants’ first observations. Visual
examination of scatterplots indicated that the relationships between our predictor and outcome
variables were not linear. In order to capture the nonlinear relationship, we conducted
polynomial analysis and examined Loess and quadratic fit lines.
Based on visual comparisons of linear, Loess, and quadratic fit lines coupled with
examinations of changes in R2s after adding a polynomial, we determined that the polynomial
resulted in little to no improvement in linearity. Chronic stress and winter (to a lesser degree)
showed the largest improvement in linearity after adding a polynomial. For example, in the case
of chronic stress, we saw improvement in linearity for the relationship between chronic stress
and rumination as evidenced by a trendline that more closely fit the data coupled with a 2%
increase in R2 (.24 to .26) after adding a polynomial. We also saw improvement in linearity for
the relationship between chronic stress and crying as evidenced by a trendline that more closely
fit the data coupled with a 3% increase in R2 (.11 to .14) after adding a polynomial. Finally, in
the case of winter, we saw improvement in linearity for the relationship between winter and
rumination as evidenced by a trendline that more closely fit the data coupled with a 2% increase
in R2 (.02 to .04) after adding a polynomial.
Based on these minor improvements in linearity for chronic stress and winter after adding
polynomials, we elected to compare model fit for linear and quadratic multilevel models in
Mplus. Because multilevel modeling can accommodate dependent observations, we included all
observations in these analyses. We estimated separate linear models for chronic stress and winter
by including linear effects for each model’s predictor onto all of its outcomes. We estimated
quadratic models for chronic stress and winter by including quadratic effects for each model’s
predictor onto all of its outcomes.
As mentioned previously, the Bayesian Information Criterion (BIC) is a statistics that
provides an estimate of model performance, with lower BICs indicating superior model fit
(Schwarz, 1978; Raftery, 1995). In the case of chronic stress, the BIC increased from 28426.35
for the linear model to 28466.26 for the quadratic model, indicating a decrease in model fit after
adding the polynomial. In the case of winter, the BIC increased from 28770.30 for the linear
model to 28824.68 for the quadratic model, again indicating a decrease in model fit after adding
a polynomial. In summary, adding polynomials to capture nonlinearity resulted in decreased
model fit for both chronic stress and winter. Based on these results coupled with the minor
improvements in linearity observed after adding polynomials to our models, we elected to retain
the linear models.
Because Mplus does not provide information about homoscedasticity or normal
distribution of residuals, we were unable to determine whether our data violated these
assumptions. However, we estimated all of our models using MLR, the Mplus option for
maximum likelihood estimation with robust standard errors (Muthén & Muthén, 2008-2012).
Estimators with robust standard errors are also referred to as heteroscedastic-consistent standard
error estimators, sandwich estimators, empirical covariance matrix estimators (Zorn, 2006), and
Huber/White estimators (Maas & Hox, 2004). Using an estimator with robust standard errors can
correct for the inefficiency of variance-covariance estimates in the presence of heteroscedasticity
(Zorn, 2006; Savalei, 2014, Hayes & Cai, 2007; White, 1980) and non-normal residuals (Huber,
1967; White, 1982; Maas & Hox, 2004).
Hypothesis Testing
Hypothesis 1. Hypothesis 1 stated that the relationship between a particular ALE and its
adaptive symptom cluster (ASC) score would be positive in direction, and would be significantly
stronger than the relationship between that ALE and its nonadaptive symptom cluster (NSC)
score. As mentioned previously, an ASC score was calculated by taking the average of the DSS
scale scores that the situation-symptom congruence hypothesis (SSCH) predicted to be
prominent following a particular ALE. Similarly, an NSC score was calculated by taking the
average of the DSS scale scores that the SSCH did not predict to be prominent following a
particular ALE.
We tested Hypothesis 1 by estimating six different Hypothesis 1 models, one for each
ALE and its corresponding ASC and NSC scores. At level one, each model included one
predictor variable (i.e, ALE), and two outcome variables (i.e., ASC and NSC scores specific to
the ALE). We controlled for gender and age at Level 2. By estimating each model, we were able
to do the following: (1) determine the direction of the relationship between each ALE and its
ASC score by examining the direction of the slope relationship between the ALE and the ASC
score; and (2) determine whether the relationship between the ALE and its ASC score was
significantly stronger than the relationship between the ALE and its NSC score by computing the
respective correlations, and comparing them using Fisher’s r-to-z transformation (Fisher, 1921)
and Steiger’s Z test (Steiger, 1980) for comparing dependent correlations.
Hypothesis 1a. Hypothesis 1a stated that the relationship between failure and the failure-
ASC score would be positive in direction, and would be significantly stronger than the
relationship between failure and the failure-NSC score. Results of the Hypothesis 1a multilevel
model are displayed in Table 43. Results of the Hypothesis 1a correlation analyses and Steiger’s
Z tests are displayed in Table 44, and visually presented in Figure 1. Results indicated that
failure was positively associated with the failure-ASC score (b SE = 0.015, p < .001),
and failure was positively associated with failure-NSC (b SE = 0.015, p < .001). The
results of a Steiger’s Z test showed that the correlation between failure and the failure-ASC score
(r = .38) was significantly stronger than the correlation between failure and the failure-NSC
score (r = .27; z = 2.95, p = .002). These results support Hypothesis 1a.

Table 43
Hypothesis 1 Multilevel Models: Adverse Life Events, Gender, and Age Predicting Adaptive and Nonadaptive Symptom Cluster Scores
(N = 1801)
Unstandardized Standardized
coefficients coefficients
Response variables Level Predictor variables Estimate SE p Estimate r2 R2
Failure-ASC score 1 Failure 0.14 0.02 <.001 0.38 .14***

Gender -0.06 0.11 .58 -0.04
2 .01
Age 0.01 0.01 .26 0.08
Failure-NSC score 1 Failure 0.10 0.02 <.001 0.27 .07***

Gender 0.11 0.90 .22 0.08
2 .01
Age -0.001 0.004 .85 -0.01
Death-ASC score 1 Death of a loved one 0.13 0.04 <.001 0.19 .04
Gender 0.07 0.10 .46 0.05
2 .01
Age 0.01 0.01 .18 0.10
Death-NSC score 1 Death of a loved one 0.07 0.03 .011 0.13 .02
Gender -0.05 0.11 0.62 -0.03
2 Age 0.002 0.01 0.64 0.03 .002
126
Romantic loss-ASC score 1 Romantic Loss 0.15 0.02 <.001 0.33 .12***
Gender -0.03 0.10 .75 -0.02
2 .005
Age 0.01 0.01 .33 0.07
Romantic loss-NSC score 1 Romantic Loss 0.10 0.02 <.001 0.24 .06**
Gender 0.01 0.11 .89 0.01
2 .001
Age 0.002 0.01 .64 0.03
Chronic stress-ASC score 1 Chronic stress 0.17 0.01 <.001 0.51 .26***
Gender -0.09 0.10 .37 -0.06
2 .007
Age 0.004 0.01 .42 0.06
Chronic stress-NSC score 1 Chronic Stress 0.14 0.01 <.001 0.44 .19***
Gender 0.07 0.08 .39 0.05
2 Age 0.002 0.004 .68 0.03 .004
127
Social isolation-ASC score 1 Social Isolation 0.21 0.02 <.001 0.48 .23***
Gender 0.07 0.08 .38 0.06
2 .008
Age 0.004 0.004 .34 0.07
Social isolation-NSC score 1 Social isolation 0.17 0.01 <.001 0.46 .21***
Gender -0.06 0.10 .56 -0.04
2 .001
Age 0.00 0.01 .99 0.001
Winter-ASC score 1 Winter 0.11 0.03 <.001 0.16 .03*

Gender 0.02 0.11 .83 0.01
2 .001
Age 0.002 0.01 .69 0.03
Winter-NSC score 1 Winter 0.08 0.02 <.001 0.12 .01

Gender -0.02 0.10 .85 -0.01
2 Age 0.01 0.01 .22 0.08 .007
Note. ASC = adaptive symptom cluster; NSC = nonadaptive symptom cluster; Death = death of a loved one; Level 1 = within level;
Level 2 = between level.
* p < .05 ** p < .01 *** p < .000
128
Table 44
Correlation Matrix and Steiger’s Z Test Results for Adverse Life Events and Adaptive/Nonadaptive Symptom Cluster Scores (N = 265)
Correlations
Number of Steiger’s
ALE Variables 1 2 3 observations Z p (2-tails) p (1-tail)
Failure 1. Failure --- .39 .27 1801 2.95 .003 .002
2. Failure-ASC Score --- .81
3. Failure-NSC Score ---
Death 1. Death --- .19 .13 1801 1.62 .106 .053
2. Death-ASC Score --- .80
3. Death-NSC Score ---
Romantic loss 1. Romantic loss --- .33 .24 1801 2.68 .007 .004
2. Romantic loss-ASC Score --- .83
3. Romantic loss-NSC Score ---
Chronic stress 1. Chronic stress --- .51 .44 1801 2.76 .006 .003
2. Chronic stress-ASC Score --- .87
3. Chronic stress-NSC Score ---
Social isolation 1. Social isolation --- .48 .46 1801 0.55 .584 .292
2. Social isolation-ASC Score --- .81
3. Social isolation-NSC Score ---
Winter 1. Winter --- .16 .11 1801 1.40 .163 .082
2. Winter-ASC Score --- .83
3. Winter-NSC Score ---
Note. ALE = adverse life event; ASC = adaptive symptom cluster; NSC = nonadaptive symptom cluster. Correlations between the two
dependent variables for each ALE category (i.e., ALE-ASC and ALE-NSC) are included because they are required for the formula
used to conduct Steiger’s Z test.
129
Figure 1. Results of correlational analyses and Steiger’s Z tests by adverse life event (ALE).
Black diamonds represent correlations between each ALE and its adaptive symptom cluster
(ASC) score. Grey circles represent correlations between each ALE and its nonadaptive
symptom cluster (NSC) score. Significance tests (using Steiger’s Z test, which incorporates
Fisher’s r-to-Z transformation) compared each ALE-ASC correlation to its corresponding ALE-
NSC correlation.
Hypothesis 1b. Hypothesis 1b stated that the relationship between death of a loved one
(death) and the death-ASC score would be positive in direction, and would be significantly
stronger than the relationship between death and the death-NSC score. Results of the Hypothesis
1b multilevel model are displayed in Table 43 Results of the Hypothesis 1b correlation analyses
and Steiger’s Z tests are displayed in Table 44, and visually presented in Figure 1. Results
indicated that death was positively associated with the death-ASC score (b SE = 0.036,
p < .000) and the death-NSC score (b SE = 0.028, p = .011). In addition, the results of a
Steiger’s Z test showed that the correlation between death and the death-ASC score (r = .19) was
not significantly stronger than the correlation between death and the death-NSC score (r = .13; z
= 1.62, p = .053). These results do not support Hypothesis 1b.
Hypothesis 1c. Hypothesis 1c stated that the relationship between romantic loss and the
romantic loss-ASC score would be positive in direction, and would be significantly stronger than
the relationship between romantic loss and the romantic loss-NSC score. Results of the
Hypothesis 1c multilevel model are displayed in Table 43. Results of the Hypothesis 1c
correlation analyses and Steiger’s Z tests are displayed in Table 44, and visually presented in
Figure 1. Results indicated that romantic loss was positively associated with the romantic loss-
ASC score (b SE = 0.018, p < .001) and the romantic loss-NSC score (b SE =
0.016, p < .001). In addition, the results of a Steiger’s Z test showed that the correlation between
romantic loss and the romantic loss-ASC score (r = .33) was significantly stronger than the
correlation between romantic loss and the romantic loss-NSC score (r = .24; z = 2.68, p = .004).
These results support Hypothesis 1c.
Hypothesis 1d. Hypothesis 1d stated that the relationship between chronic stress and the
chronic stress-ASC score would be positive in direction, and would be significantly stronger than
the relationship between chronic stress and the chronic stress-NSC score. Results of the
Hypothesis 1d multilevel model are displayed in Table 43 Results of the Hypothesis 1d
Figure 1. Results indicated that chronic stress was positively associated with the chronic stress-
ASC score (b SE = 0.013, p = < .001) and the chronic stress-NSC score (b SE =
0.013, p < .001). In addition, the results of a Steiger’s Z test showed that the correlation between
chronic stress and the chronic stress-ASC score (r = .51) was significantly stronger than the
correlation between chronic stress and the chronic stress-NSC score (r = .44; z = 2.76, p = .003).
These results support Hypothesis 1d.
Hypothesis 1e. Hypothesis 1e stated that the relationship between social isolation and the
social isolation-ASC score would be positive in direction, and would be significantly stronger
than the relationship between social isolation and the social isolation-NSC score. Results of the
Hypothesis 1a multilevel model are displayed in Table 43 Results of the Hypothesis 1e
Figure 1. Results indicated that social isolation was positively associated with the social
isolation-ASC score (b SE = 0.018, p < .001) and the social isolation-NSC score (b
SE = 0.014, p < .001). However, results of the Steiger’s Z test showed that the
correlation between social isolation and the social isolation-ASC score (r = .48) was not
significantly stronger than the correlation between social isolation and the social isolation-NSC
score (r = .46; z = 0.55, p = .292). These results do not support Hypothesis 1e.
Hypothesis 1f. Hypothesis 1f stated that the relationship between winter and the winter-
ASC score would be positive in direction, and would be significantly stronger than the
relationship between winter and the winter-NSC score. Results of the Hypothesis 1f multilevel
model are displayed in Table 43 Results of the Hypothesis 1f correlation analyses and Steiger’s
Z tests are displayed in Table 44, and visually presented in Figure 1. Results indicated that
winter was positively associated with the winter-ASC score (b SE = 0.026, p < .001)
and the winter-NSC score (b SE = 0.022, p < .001). In addition, results of the Steiger’s Z
test showed that the correlation between winter and the winter-ASC score (r = .16) was not
significantly stronger than the correlation between winter and the winter-NSC score (r = .11; z =
1.40, p = .082). However, the coefficient of determination, r2, was significant for winter and
winter-ASC (r2 = .027, p = .034) but not for winter and winter-NSC (r2 = .013, p = .075). The
coefficient of determination is a measure of the strength of relationship between two variables.
These results suggest that there was a significant relationship between winter and winter-ASC
but not between winter and winter-NSC. Taken together, these results provide partial support for
Hypothesis 1f.
Hypothesis 2. Hypothesis 2 stated that the depressive symptom patterns of participants
without major depressive disorder (non-MDD) would be consistent with the depressive symptom
patterns of participants with major depressive disorder (MDD) for each ALE. We tested this
hypothesis by estimating a multivariate multilevel model. At level 1, the model contained ALE
and time as predictor variables of the nine depressive symptoms. ALEs included failure, death of
a loved one, romantic loss, chronic stress, social isolation, and winter. The nine depressive
symptoms included emotional pain, pessimism, fatigue, anhedonia, rumination, crying, guilt,
increased sleep, and desire for social support. At level 2, we added an ALE * Diagnostic Group
cross-level interaction term to examine whether the relationship between ALE and pattern of
depressive symptoms varied by diagnostic group (non-MDD versus MDD).
Hypothesis 2a. Hypothesis 2a stated that the relationship between failure and each
depressive symptom would be consistent for non-MDD participants and MDD participants. The
results of the analysis testing the failure by diagnostic group interaction term were not significant
for any of the depressive symptoms (see Table 46), suggesting that the depressive symptom
patterns associated with failure did not differ by diagnostic group. These results support
Hypothesis 2a.
Table 45

Hypothesis 2a Multilevel Model Results for Failure
Unstandardized Coefficients Standardized

Coefficients
Predictor Variables, Cross-
Outcome Level Interaction Term, and
Variables Level Control Variables Estimate SE p Estimate R2
Emotional Pain Failure 0.130 0.022 <.001 0.258

Time -0.018 0.004 <.001 -0.122
1 .248***
Diagnostic Group 0.574 0.187 .002 0.290
Failure * Diagnostic Group 0.056 0.055 .308 0.083
Gender -0.021 0.108 .843 -0.013

2 .018
Age 0.010 0.005 .064 0.133
Pessimism Failure 0.132 0.020 <.001 0.285

Time -0.011 0.004 .007 -0.079
1 .248***
Diagnostic Group 0.640 0.174 <.001 0.351
Gender -0.028 0.105 .790 -0.017

2 .002
Age 0.003 0.005 .558 0.041
135
Coefficients
Fatigue Failure 0.092 0.018 <.001 0.183

Time -0.004 0.004 .283 -0.030
1 .238
Gender -0.025 0.118 .832 -0.015

2 .000
Age 0.000 0.006 .991 0.001
Anhedonia Failure 0.082 0.016 <.001 0.188

Time -0.001 0.004 .691 -0.011
1 .266***
Gender -0.041 0.103 .691 -0.027

2 .029
Age 0.011 0.005 .022 0.169
Rumination Failure 0.168 0.021 <.001 0.310

Time -0.016 0.004 <.001 -0.104
1 .219***
Failure * Diagnostic Group -0.010 0.052 .845 -0.014
Gender -0.129 0.111 .247 -0.077

2 .006
Age -0.001 0.005 .920 -0.007
136
Coefficients
Crying Failure 0.125 0.027 <.001 0.260

Time -0.011 0.004 .012 -0.069
1 .163***
Gender 0.257 0.089 .004 0.185

2 .034
Age 0.001 0.005 .801 0.020
Guilt Failure 0.175 0.021 <.001 0.339

Time -0.021 0.004 <.001 -0.139
1 .257***
Gender -0.280 0.122 .002 -0.154

2 .024
Age 0.001 0.005 .885 0.010
Increased Sleep Failure 0.043 0.020 .029 0.083

Time -0.008 0.005 .072 -0.056
1 .102*
Gender 0.062 0.128 .627 0.013

2 .018
Age -0.001 0.006 .059 -0.129
137
Coefficients
Desire for Social Failure 0.095 0.021 <.001 0.169

Support Time -0.030 0.005 <.001 -0.186
1 .085**
Gender 0.062 0.128 .627 -0.013

2 .003
Age -0.011 0.006 .059 0.057
Note. DSS = Depressive Symptoms Scale
138
Hypothesis 2b. Hypothesis 2b stated that the relationship between death of a loved one
and each depressive symptom would be consistent for non-MDD and MDD participants. The
results of the analysis testing the death by diagnostic group interaction term were not significant
for any of the depressive symptoms (see Table 47), suggesting that the depressive symptom
patterns associated with death of a loved one did not differ by diagnostic group. These results
support Hypothesis 2b.

Table 46
Hypothesis 2b Multilevel Model Results for Death of a Loved One
Coefficients Coefficients
Emotional Pain Death 0.139 0.041 .001 0.169

Time -0.021 0.004 <.001 -0.148
1 .199***
Death * Diagnostic Group -0.045 0.094 .633 -0.044
Gender -0.043 0.114 .709 -0.024

2 .016
Age 0.010 0.006 .083 0.124
Pessimism Death 0.065 0.041 .113 0.087

Time -0.014 0.004 .001 -0.108
1 .178***
Gender -0.038 0.112 .731 -0.022

2 .003
Age 0.004 0.006 .512 0.047
140
Fatigue Death 0.071 0.038 .066 0.085

Time -0.007 0.004 .106 -0.046
1 .209***
Gender -0.038 0.122 .756 -0.021

2 .000
Age 0.000 0.006 .966 0.003
Anhedonia Death 0.055 0.031 .078 0.078

Time -0.004 0.004 .326 -0.029
1 .230***
Gender -0.050 0.106 .635 -0.032

2 .029
Age 0.012 0.005 .023 0.167
Rumination Death 0.157 0.049 .001 0.178

Time -0.021 0.005 <.001 -0.133
1 .154***
Gender -0.158 0.120 .187 -0.087

2 .008
Age -0.001 0.005 .893 -0.009
141
Crying Death 0.110 0.046 .018 0.124

Time -0.015 0.004 .001 -0.094
1 .123**
Death * Diagnostic Group 0.069 0.106 .515 0.063
Gender 0.245 0.091 .007 0.169

2 .029
Age 0.001 0.005 .784 0.022
Guilt Death 0.117 0.041 .004 0.142

Time -0.021 0.004 <.001 -0.173
1 .176***
Gender -0.300 0.129 .020 -0.152

2 .023
Age 0.001 0.006 .857 0.012
Increased Death 0.046 0.035 .186 0.054

Sleep Time -0.009 0.005 .043 -0.062
1 .099*
Gender 0.051 0.129 .692 0.025

2 .017
Age -0.012 0.006 .059 -0.129
142
Desire for Death 0.158 0.051 .002 0.171

Social Support Time -0.033 0.005 <.001 -0.200
1 .082**
Gender -0.055 0.146 .708 -0.026

2 .003
Age 0.004 0.006 .515 0.045
Note. DSS = Depressive Symptoms Scale.
143
Hypothesis 2c. Hypothesis 2c stated that the relationship between romantic loss and each
depressive symptom would be consistent for non-MDD and MDD participants. The results of the
analysis testing the romantic loss by diagnostic group interaction term were not significant for
any of the depressive symptoms (see Table 48), suggesting that the depressive symptom patterns
associated with romantic loss did not differ by diagnostic group. These results support
Hypothesis 2c.
Table 47

Hypothesis 2c Multilevel Model Results for Romantic Loss
Predictor Variables, Cross-Level
Outcome Interaction Term, and Control
Variables Level Variables Estimate SE p Estimate R2
Emotional Pain Romantic Loss 0.168 0.027 <.001 0.280

Time -0.019 0.004 <.001 -0.128
1 .246***
Romantic Loss * Diagnostic Group -0.011 0.051 .830 -0.013
Gender -0.035 0.109 .751 -0.020

2 .017
Age 0.010 0.006 .007 0.130
Pessimism Romantic Loss 0.109 0.023 <.001 0.200

Time -0.012 0.004 .003 -0.093
1 .209***
Romantic Loss * Diagnostic Group 0.012 0.053 .819 0.015
Gender -0.038 0.109 .730 -0.022

2 .002
Age 0.003 0.005 .535 0.044
145
Fatigue Romantic Loss 0.093 0.021 <.001 0.156

Time -0.006 0.004 .187 -0.038
1 .223***
Gender -0.033 0.119 .782 -0.019

2 .000
Age 0.000 0.006 .962 0.004
Anhedonia Romantic Loss 0.114 0.025 <.001 0.221

Time -0.002 0.004 .639 -0.013
1 .272***
Gender -0.050 0.103 .630 -0.032

2 .028
Age 0.011 0.005 .026 0.165
Rumination Romantic Loss 0.165 0.022 <.001 0.258

Time -0.019 0.005 <.001 -0.121
1 .184
Gender -0.143 0.115 .215 -0.081

2 .007
Age 0.000 0.005 .968 -0.003
146
Crying Romantic Loss 0.154 0.029 <.001 0.240

Time -0.012 0.005 .010 -0.074
1 .158
Gender 0.244 0.090 .007 0.172

2 .030
Age 0.001 0.005 .825 0.018
Guilt Romantic Loss 0.149 0.024 <.001 0.247

Time -0.023 0.004 <.001 -0.159
1 .209***
Gender -0.293 0.126 0.020 -0.153

2 .024
Age 0.001 0.006 0.841 0.014
Increased Romantic Loss 0.041 0.022 .063 0.066

Sleep Time -0.008 0.005 .068 -0.056
1 .103*
Gender 0.059 0.129 .648 0.029

2 .017
Age -0.011 0.006 .064 -0.128
147
Desire for Romantic Loss 0.098 0.029 .001 0.148

1 .079**
Gender -0.034 0.144 .811 -0.016

2 .004
Age 0.005 0.006 .408 0.057
148
Hypothesis 2d. Hypothesis 2d stated that the relationship between chronic stress and each
depressive symptom would be would be consistent for non-MDD and MDD participants. The
results of the analysis testing the social isolation by diagnostic group interaction term were not
significant for any of the depressive symptoms (see Table 49), suggesting that the depressive
symptom patterns associated with social isolation did not differ by diagnostic group. These
results support Hypothesis 2d.

Table 48

Hypothesis 2d Multilevel Model Results for Chronic Stress
Predictor Variables, Control
Outcome Variables, and Cross-Level
Variables Level Interaction Term Estimate SE p Estimate R2
Emotional Pain Chronic Stress 0.168 0.017 <.001 0.366

Time -0.016 0.004 <.001 -0.108
1 .299***
Chronic Stress * Diagnostic Group 0.024 0.044 .582 0.045
Gender -0.036 0.104 .727 -0.022

2 .019
Age 0.010 0.005 .065 0.135
Pessimism Chronic Stress 0.178 0.016 <.001 0.419

Time -0.009 0.004 .022 -0.063
1 .328***
Gender -0.043 0.098 .661 -0.028

2 .002
Age 0.003 0.005 .604 0.037
150
Fatigue Chronic Stress 0.136 0.016 <.001 0.295

Time -0.003 0.004 .492 -0.018
1 .281***
Chronic Stress * Diagnostic Group 0.000 0.037 .993 -0.001
Gender -0.035 0.112 .754 -0.021

2 .000
Age 0.000 0.005 .949 -0.005
Anhedonia Chronic Stress 0.098 0.015 <.001 0.251

Time 0.000 0.003 .898 -0.004
1 .289***
Gender -0.051 0.100 .612 -0.034

2 .031
Age 0.011 0.005 .019 0.172
Rumination Chronic Stress 0.254 0.017 <.001 0.501

Time -0.013 0.004 .001 -0.082
1 .344***
Chronic Stress * Diagnostic Group -0.066 0.053 .208 -0.111
Gender -0.145 0.100 .147 -0.097

2 .010
Age -0.002 0.005 .732 -0.025
151
Crying Chronic Stress 0.143 0.019 <.001 0.292

Time -0.010 0.004 .021 -0.062
1 .184***
Gender 0.243 0.089 .007 0.177

2 .032
Age 0.001 0.005 .812 0.020
Guilt Chronic Stress 0.191 0.019 <.001 0.408

Time -0.020 0.004 <.001 -0.131
1 .297***
Gender -0.290 0.115 .012 -0.165

2 .027
Age 0.000 0.005 .950 0.004
Increased Sleep Chronic Stress 0.094 0.017 <.001 0.202

Time -0.007 0.004 .140 -0.043
1 .137**
Gender 0.055 0.126 .659 0.028

2 .020
Age -0.012 0.006 .045 -0.137
152
Desire for Chronic Stress 0.134 0.024 <.001 0.263

1 .118***
Gender -0.030 0.140 .831 -0.015

2 .003
Age 0.005 0.006 .471 0.051
153
Hypothesis 2e. Hypothesis 2e stated that the relationship between social isolation and
each depressive symptom would be consistent for non-MDD and MDD participants. The results
of the analysis testing the social isolation by diagnostic group interaction term were significant
for anhedonia (b SE=0.036, p=.009) and desire for social support (b SE=0.065,
p=.021). The social isolation by diagnostic group interaction terms were not significant for any
of the remaining symptoms (see Table 50). These results largely support Hypothesis 2e.
Table 49

Hypothesis 2e Multilevel Model Results for Social Isolation
Emotional Pain Social Isolation 0.207 0.023 <.001 0.396

Time -0.013 0.004 .001 -0.090
1 .328***
Social Isolation * Diagnostic Group 0.059 0.052 .253 0.089
Gender -0.034 0.101 .736 -0.022

2 .013
Age 0.008 0.005 .134 0.110
Pessimism Social Isolation 0.162 0.020 <.001 0.340

Time -0.008 0.004 .043 -0.059
1 .285***
Gender -0.039 0.102 .705 -0.024

2 .001
Age 0.001 0.005 .771 0.020
155
Fatigue Social Isolation 0.136 0.019 <.001 0.264

Time -0.002 0.004 .647 -0.013
1 .268***
Gender -0.034 0.114 .763 -0.021

2 .001
Age -0.001 0.005 .794 -0.019
Anhedonia Social Isolation 0.121 0.019 <.001 0.270

Time 0.001 0.004 .682 0.011
1 .310***
Gender -0.048 0.098 .629 -0.033

2 .026
Age 0.010 0.005 .032 0.158
Rumination Social Isolation 0.233 0.020 <.001 0.416

Time -0.013 0.005 .004 -0.082
1 .278***
Social Isolation * Diagnostic Group -0.066 0.054 .231 -0.090
Gender -0.146 0.106 .170 -0.091

2 .010
Age -0.003 0.005 .533 -0.043
156
Crying Social Isolation 0.191 0.026 <.001 0.342

Time -0.007 0.004 .103 -0.044
1 .223***
Gender 0.246 0.086 .004 0.185

2 .035
Age -0.001 0.005 .866 -0.014
Guilt Social Isolation 0.196 0.023 <.001 0.373

Time -0.018 0.004 <.001 -0.122
1 .286***
Gender -0.294 0.121 .015 -0.162

2 .026
Age -0.001 0.005 .827 -0.015
Increased Sleep Social Isolation 0.083 0.022 <.001 0.158

Time -0.006 0.005 204 -0.039
1 .129**
Gender 0.058 0.127 .650 0.029

2 .022
Age -0.013 0.006 .036 -0.144
157
Desire for Social Social Isolation 0.183 0.026 <.001 0.316

Support Time -0.028 0.005 <.001 -0.167
1 .141***
Social Isolation * Diagnostic Group -0.150 0.065 .021 -0.203
Gender -0.040 0.135 .766 -0.021

2 .002
Age 0.003 0.006 .649 0.033
158
We conducted simple effects analyses to examine the social isolation-anhedonia
relationship and the social isolation-desire for social support relationship for each diagnostic
group. Results of the simple effects analysis demonstrated that social isolation was positively
related to anhedonia for both the MDD group (b SE=0.028, p=.000) and the non-MDD
group (b SE=0.019, p=.000). However, across all levels of social isolation, levels of
anhedonia were higher for MDD participants than non-MDD participants. Furthermore, as social
isolation increased, levels of anhedonia increased at a higher rate for MDD participants than non-
MDD participants. These results suggest that as levels of social isolation increased, levels of
anhedonia increased at a higher rate for MDD participants than non-MDD participants. A visual
depiction of these results is presented in Figure 2.
The simple effects analysis for the social isolation-desire for social support relationship
showed that social isolation was positively related to desire for social support for the non-MDD
group (b SE=0.026, p=.000). However, the relationship between social isolation and
desire for social support was not significant for the MDD group (b SE=0.062, p=.776).
These results suggest that as the level of social isolation increased, the level of desire for social
support increased for the non-MDD group but not for the MDD group (see Figure 2).
Figure 2. The relationships between social isolation and DSS scales (i.e., anhedonia and desire
for social support) for non-MDD and MDD participants. Lines represent non-MDD participants
while dashes represent MDD participants. The relationship between social isolation and
anhedonia was significant for both non-MDD participants and MDD participants. The
relationship between social isolation and desire for social support was significant for non-MDD
participants but not for MDD participants.
Hypothesis 2f. Hypothesis 2f stated that the relationship between winter and each
depressive symptom would be consistent for non-MDD and MDD participants. As shown in
Table 51, the results of the analysis testing the winter by diagnostic group interaction term were
significant for anhedonia (b SE=0.086, p=.020), rumination (b SE=0.062,
p=.007), and crying (b SE=0.076, p=.046). The winter by diagnostic group interaction
terms were not significant for any of the remaining symptoms. These results largely support
Hypothesis 2f.
Table 50
Hypothesis 2f Multilevel Model Results for Winter
Variables Control Variables Estimate SE p Estimate R2
Emotional Pain Winter 0.071 0.031 .022 0.077

Time -0.021 0.004 <.001 -0.145
1 .183***
Winter * Diagnostic Group 0.060 0.077 .431 0.041
Gender -0.028 0.115 .809 -0.015

2 .020
Age 0.011 0.006 .048 0.141
Pessimism Winter 0.052 0.026 .049 0.061

Time -0.014 0.004 .001 -0.105
1 .176***
Gender -0.033 0.112 .766 -0.019

2 .003
Age 0.004 0.006 .437 0.054
162
Fatigue Winter 0.104 0.035 .003 0.112

Time -0.006 0.004 .145 -0.042
1 .218***
Gender -0.033 0.121 .787 -0.018

2 .000
Age 0.011 0.006 .896 0.010
Anhedonia Winter 0.049 0.025 .050 0.061

Time -0.003 0.004 .380 -0.026
1 .237***
Gender -0.046 0.106 .664 -0.029

2 .031
Age 0.012 0.005 .018 0.173
Rumination Winter 0.085 0.029 .004 0.085

Time -0.020 0.005 <.001 -0.131
1 .138***
Winter * Diagnostic Group -0.167 0.062 .007 -0.105
Gender -0.135 0.121 .262 -0.074

2 .006
Age 0.001 0.006 .851 0.013
163
Crying Winter 0.055 0.031 .078 0.055

Time -0.014 0.005 .002 -0.089
1 .108*
Gender 0.250 0.095 .008 0.168

2 .029
Age 0.003 0.005 .625 0.038
Guilt Winter 0.097 0.027 <.001 0.104

Time -0.025 0.005 <.001 -0.169
1 .172***
Gender -0.288 0.130 .027 -0.145

2 .022
Age 0.002 0.006 .711 0.025
Increased Winter 0.154 0.037 <.001 0.159

Sleep Time -0.009 0.005 .061 -0.057
1 .121*
Gender 0.054 0.129 .678 0.027

2 .017
Age -0.011 0.006 .053 -0.129
164
Desire for Winter 0.056 0.040 .159 0.053

1 .064*
Gender -0.030 0.145 .836 -0.014

2 .004
Age 0.006 0.006 .337 0.065
165
We conducted simple effects analyses to examine the winter-anhedonia relationship,
winter-rumination relationship, and winter-crying relationship for each diagnostic group. Results
of the simple effects analysis for the winter-anhedonia relationship demonstrated that winter was
positively related to anhedonia for the MDD group (b SE=0.084, p=.008). However, the
relationship between winter and anhedonia was not significant for the non-MDD group
(b SE=0.025, p=.055). These results suggest as level of winter increased, level of
anhedonia increased for the MDD group but not the non-MDD group. A visual depiction of these
results is presented in Figure 3.
Results of the simple effects analysis for the winter-rumination relationship showed that
winter was negatively related to rumination for the MDD group (b SE=0.050, p=.021)
and positively related to rumination for the non-MDD group (b SE=0.084, p=.008).
These results suggest that as the level of winter increased, the level of rumination increased for
the non-MDD group and decreased for the MDD group (see Figure 3). Finally, the results of the
simple effects analysis for the winter-crying relationship demonstrated that winter was positively
related to crying for the MDD group (b SE=0.070, p=.006). However, the relationship
between winter and crying was not significant for the non-MDD group (b SE=0.031,
p=.083). These results suggest that as the level of winter increased, the level of crying increased
for the MDD group but not for the non-MDD group (see Figure 3).
Figure 3. The relationships between winter and DSS scales (i.e., anhedonia, rumination, and
crying) for non-MDD and MDD participants. Lines represent non-MDD participants while
dashes represent MDD participants. The relationship between winter and anhedonia was
significant for MDD participants but not for non-MDD participants. The relationship between
winter and rumination was significant for both non-MDD participants and MDD participants.
The relaitonship between winter and crying was signficant for MDD participants but not for non-
MDD participants.
Chapter V: Discussion
The aim of our study was to increase understanding of the relationship between adverse
life events (ALEs) and depressive symptom patterns by testing the situation-symptom
congruence hypothesis (SSCH), and examining ALE-depressive symptom pattern relationships
in individuals with major depressive disorder (MDD) and without major depressive disorder
(non-MDD). The SSCH is grounded in evolutionary theory, and argues that different adverse
situations should lead to distinct depressive symptom patterns that help the individual solve the
adaptive challenges characteristics of the adverse situations. We sought to answer two main
research questions in our investigation: (1) are different ALEs associated with depressive
symptom patterns in a manner that is consistent with SSCH predictions? And (2) are the ALE-
symptom relationships observed for non-MDD individuals consistent with those observed for
MDD?
While a handful of past studies have addressed these questions, they had numerous
limitations. We tested the SSCH using a methodology that addressed some of the limitations of
these investigations. First, we collected self-report information about events/issues and
depressive symptoms that occurred over the past day rather than the past year, thereby increasing
reliability and validity by decreasing the impact of self-enhancement, faulty memory, and
anchoring bias. Second, by using a repeated measure design in which each participant had one or
more observations, we were able to focus on between- as well as within- person variation.
Because past research investigations of the SSCH have not utilized within-person samples, this
was an important next step.
Third, our study included a sample of participants with a diagnosis of MDD, allowing for
an investigation of whether the relationships between ALEs and patterns of depressive symptoms
for non-MDD participants is consistent with those for MDD participants. While Keller et al.
(2007) also included a sample of participants with a diagnosis of MDD when they examined
ALE-depressive symptom pattern relationships, they did not test the SSCH and did not examine
some ALEs (i.e., social isolation and winter) and depressive symptoms (crying, desire for social
support, pessimism, and rumination) about which the SSCH makes predictions.
Fourth, we investigated ALEs and depressive symptoms that occurred naturally and were
not the result of mood induction procedures. In doing so, we were able to avoid the validity and
demand effect issues that may have limited Keller and Nesse’s (2006) analogue study. Fifth, our
study involved a community sample while past investigations involved samples limited to
college students (Keller & Ness, 2005, 2006) or Caucasian twin pairs (Keller et al., 2007), or
participants recruited through professional mailing lists. As such, our participants covered a
wider range of ages, ethnicities, occupations, and socioeconomic backgrounds, thereby
increasing generalizability and external validity.
Sixth, participants in our study could endorse multiple ALE categories, and indicate the
degree to which their self-identified ALE involved each ALE category. As a result, we were able
to examine the association between a participant’s level or degree of ALE and level of different
symptoms. It is possible that finer quantitative distinctions allowed us to measure ALEs more
accurately than past researchers, who asked participants to choose a single ALE category to
indicate which ALE they believed led to their dysphoric episode. By making finer quantitative
distinctions in the measurement of ALEs, we may have increased the internal validity of the
predictor variables in our study. Seventh, we utilized multilevel modeling (MLM) to test our
hypotheses, which can accommodate data in which observations are nested within individuals.
MLM can also flexibly handle data in which the number of observations varies across
participants, thereby preventing the loss of data that might have influenced the results.
Taken together, these methodological attributes extend past research and add weight to
our findings. In this chapter, we will begin by summarizing and integrating our results. Next, we
will explain our findings. We will then discuss our findings in the context of past literature while
addressing the implications of convergent and divergent findings. Finally, we will discuss
additional implications of our findings, the limitations of our research, directions for future
research, and conclusions.
Summary of Findings
Our findings largely support our hypotheses. Failure, romantic loss, chronic stress, and
winter (to a lesser extent), were associated with distinct patterns of depressive symptoms that
were consistent with the evolutionary predictions of the SSCH while death of a loved one and
social isolation were not. Gender and age did not have a significant impact on these depressive
symptom patterns.
Non-MDD and MDD participants experienced consistent depressive symptom patterns
across all ALEs. The only variation across these diagnostic groups involved social isolation and
winter. As levels of social isolation increased, levels of anhedonia increased significantly for
both MDD and non-MMD participants although at a higher rate for MDD participants; and levels
of desire for social support increased significantly for non-MDD participants but not for MDD
participants. As levels of winter increased, levels of anhedonia increased significantly for MDD
participants but not for non-MDD participants; levels of rumination increased significantly for
non-MDD participants but decreased significantly for MDD participants; and levels of crying
increased significantly for MDD participants but not for non-MDD participants.
As days of participation increased, levels of most depressive symptoms decreased
significantly for all ALEs. Levels of the following depressive symptoms did not significantly
decrease with time: fatigue, anhedonia, and increased sleep for failure, romantic loss, chronic
stress, and winter; fatigue and anhedonia for death of a loved one; and fatigue, anhedonia,
crying, and increased sleep for social isolation. Gender and age consistently impacted two or
three depressive symptoms for all ALEs. Females reported more crying for all ALEs while males
reported more guilt for all ALEs except winter. Older participants experienced more emotional
pain for all ALEs except social isolation, and more anhedonia for all ALEs.
Hypothesis 1: Findings, Explanations, and Implications
Hypothesis 1 was based on the SSCH, which predicts that specific depressive symptoms
are likely to be more pronounced following certain adverse situations because they serve to solve
the adaptive challenges characteristic of the adverse situation. Specific ALE-symptom
predictions are based on the proposed evolutionary function of the symptoms. Hypothesis 1
stated that the relationship between a particular ALE and its adaptive symptom cluster (ASC)
would be significant and positive in direction. Furthermore, it was hypothesized that the ALE-
ASC relationship would be significantly stronger than the relationship between that ALE and its
corresponding nonadaptive symptom cluster (NSC). An ASC was composed of the group of
symptoms that the SSCH predicted to be prominent following a particular ALE. An NSC was
composed of the group of symptoms that the SSCH predicted would not be prominent following
a particular ALE.
For example, Hypothesis 1a stated that the relationship between failure and the failure-
ASC would be significant and positive in direction. Furthermore, the relationship between failure
and failure-ASC would be significantly stronger than the relationship between failure and
failure-NSC. Hypotheses 1b – 1f were the same as Hypothesis 1a except that each one involved a
different ALE and corresponding ASC and NSC.
Failure. According to the SSCH, failure at an important goal is an adverse situation in
which an individual has likely invested a large amount of fitness-relevant resources but has failed
to achieve a return on his or her investment. As a result, depressive symptoms that help the
individual solve these adaptive challenges should be more pronounced in failure situations.
Hypothesis 1a stated that failure should be more strongly associated with depressive symptoms
that make situations in which there is a loss of fitness-relevant resources painful (i.e., emotional
pain); stop continued investment in failing pursuits (i.e., pessimism); decrease effortful behavior
in unpropitious situations (i.e., fatigue), decrease approach and risk-taking behaviors in
unpropitious situations (i.e., anhedonia); help the individual analyze/learn from the current
situation in order to avoid similar situations in the future (i.e., rumination); and assist the
individual in gaining insight into one’s role in the problematic situation (i.e., guilt). Our findings
were consistent with the evolutionary predictions of the SSCH regarding failure, and therefore,
support Hypothesis 1a. Gender and age did not have a significant impact on depressive symptom
patterns for failure.
Death of a loved one. According to the SSCH, death of a loved one is an adverse
situation which involves the permanent loss of a fitness-relevant resource in the form of an
important social bond. As a result, depressive symptoms that help the individual solve these
adaptive challenges should be more pronounced in situations that involve death of a loved one.
Hypothesis 1b stated that situations that involve death of a loved one should be more strongly
associated with symptoms that make situations in which there is a loss of fitness-relevant
resources painful (i.e., emotional pain); strengthen social bonds (i.e., crying); and create new
social bonds or strengthen deficient social bonds (i.e., desire for social support). Our findings
were not consistent with SSCH predictions regarding death of a loved one, and therefore, did not
support Hypothesis 1b. Gender and age did not have a significant impact on depressive symptom
patterns for death of a loved one.

Romantic loss. According to the SSCH, romantic loss is an adverse situation that
involves the loss of a fitness-relevant resource in the form of an important romantic relationship.
As a result, depressive symptoms that help the individual solve these adaptive challenges should
be more pronounced in situations of romantic loss. Hypothesis 1c stated that romantic loss
should be more strongly associated with symptoms that make situations in which there is a loss
of fitness-relevant resources painful (i.e., emotional pain); help the individual analyze/learn from
the current situation in order to avoid similar situations in the future (i.e., rumination); strengthen
social bonds (i.e., crying); assist the individual in gaining insight into one’s role in the
problematic situation (i.e., guilt), and create new social bonds or strengthen deficient social
bonds (i.e., desire for social support). Our findings were consistent with SSCH predictions
regarding romantic loss, and therefore, support Hypothesis 1c. Gender and age did not have a
significant impact on depressive symptom patterns for romantic loss.
Chronic stress. According to the SSCH, chronic stress is an adverse situation in which
an individual is having a difficult time coping with all that is going on, and may be anxious about
their present or future. As a result, depressive symptoms that help the individual solve these
adaptive challenges should be more pronounced in situations of chronic stress. Hypothesis 1d
stated that chronic stress should be more strongly associated with symptoms that stop continued
investment in failing pursuits (i.e., pessimism), decrease effortful behavior in unpropitious
situations (i.e., fatigue), decrease approach and risk-taking behaviors in unpropitious situations
(i.e., anhedonia), help the individual analyze/learn from the current situation in order to avoid
similar situations in the future (i.e., rumination); and assist the individual in gaining insight into
one’s role in the problematic situation (i.e., guilt). Our findings were consistent with SSCH
predictions regarding chronic stress, and therefore, support Hypothesis 1d. Gender and age did
not have a significant impact on depressive symptom patterns for chronic stress.
Social isolation. According to the SSCH, social isolation is an adverse situation which
involves a real or perceived lack of social bonds or resources. As a result, depressive symptoms
that help the individual solve these adaptive challenges should be more pronounced in situations
of social isolation. Hypothesis 1e stated that social isolation should be more strongly associated
with symptoms that make situations in which there is a loss of fitness-relevant resources painful
(i.e., emotional pain); strengthen social bonds (i.e., crying); and create new social bonds or
strengthen deficient social bonds (i.e., desire for social support). Our findings were not consistent
with SSCH predictions regarding social isolation, and therefore, did not support Hypothesis 1e.
Gender and age did not have a significant impact on depressive symptom patterns for social
isolation.
Winter. According to the SSCH, winter (i.e., ancestral winter) is an adverse situation in
which fitness-relevant resources such as food are scarce and chances of success are less
favorable. As a result, depressive symptoms that help the individual solve these adaptive
challenges should be more pronounced in situations that involve winter. Hypothesis 1f stated that
winter should be more strongly associated with symptoms that decrease effortful behavior in
unpropitious situations (i.e., fatigue), decrease approach- and risk-taking behaviors in
unpropitious situations (i.e., anhedonia), and conserve energy in unpropitious situations (i.e.,
increased sleep).Our findings were partially consistent with SSCH predictions regarding winter,
and therefore, partially support Hypothesis 1f. Gender and age did not have a significant impact
on depressive symptom patterns for winter.
Hypothesis 1: Integration of Findings with Past Literature
Hypothesis 1: Convergent findings. Our findings for failure, romantic loss, and winter
(Hypothesis 1a, 1c, and 1f, respectively) support our hypotheses and the SSCH, and are largely
consistent with past research investigations of the SSCH. Keller and Nesse (2005, 2006) found
the same results when they examined the same associations in non-MDD (non-major depressive
disorder) college students who had experienced a depressive episode precipitated by an ALE
over the previous year.
Hypothesis 1: Explanations and implications of convergent findings. There are
numerous explanations for and implications of the consistencies between our findings and those
of past research regarding failure, romantic loss, and winter. We examined the association
between ALEs and depressive symptom patterns in a community sample of non-MDD and MDD
participants who had experienced one or more depressive episodes and ALEs over up to nine
consecutive or nonconsecutive days while Keller and Nesse (2005, 2006) examined the same
associations in non-MDD college students who had experienced a depressive episode
precipitated by an ALE over the previous year. Both college students and individuals from the
general population who experienced failure, romantic loss, and winter also experienced SSCH
predicted symptom patterns that may have helped them cope with their situations. Consistent
findings despite sample differences suggest that the SSCH predicted symptom patterns
associated with failure, romantic loss, and winter are not limited to a homogenous population
such as college students. Additionally, these ALE-symptom pattern relationships were observed
when participants reported depressive episodes and ALEs experienced over the past year as well
as over the past day. While this does not provide evidence that these ALEs caused their
corresponding adaptive symptom patterns, collecting self-report information closer in time to
when the ALEs and depressive symptoms were actually experienced increases confidence that
these relationships were not the result of third variables.
Hypothesis 1: Divergent findings. Our findings for death of a loved one (Hypothesis 1b)
are inconsistent with our hypothesis and past research. Keller and Nesse (2005) conducted a
cross-sectional, between-person study, and found that all relevant symptoms were consistent
with SSCH predictions. Keller and Nesse (2006) conducted two cross-sectional, between-person
studies, the second of which was an analogue study that involved a mood induction procedure
and asked participants to imagine experiencing death of a loved one. In both studies, they found
that all relevant symptoms were consistent with SSC predictions.
Although our findings for chronic stress (Hypothesis 1d) are consistent with our
hypothesis, they are inconsistent with past research. Keller and Nesse (2005, 2006) conducted
two cross-sectional studies. Inconsistent with our findings and the SSCH, they found that levels
of adaptive and nonadaptive depressive symptoms did not vary significantly for chronic stress.
Our findings for social isolation (Hypothesis 1e) are inconsistent with both our hypothesis and
past research. Keller and Nesse (2005, 2006) conducted two cross-sectional studies and found
that social isolation was associated with depressive symptom patterns that were consistent with
SSCH predictions.
Hypothesis 1: Explanations and implications of divergent findings. The
inconsistencies between our findings and those of past research suggest that some of the ALE-
symptom relationships (i.e., those that involve death of a loved one, chronic stress, and social
isolation) observed in past research (Keller & Nesse, 2005, 2006) may not hold in research
characterized by various methodological differences (e.g., sample, design). These inconsistencies
have a number of plausible explanations and corresponding implications, some of which may
refine the SSCH and its theoretical precision, and inform future research.
Death of a loved one, chronic stress, and social isolation. One explanation for the
inconsistencies between our findings and those of past research (Keller & Nesse, 2005, 2006)
regarding death of a loved one, chronic stress, and social isolation involves the different
combinations of symptoms examined across studies. For example, Keller and Nesse (2005)
examined five of the nine symptoms we examined in addition to two other symptoms. Keller and
Nesse (2006, Study 1) examined all of the symptoms we examined in addition to one other
symptom. Keller and Nesse (2006, Study 2) examined seven of the nine symptoms we examined,
in addition to one other symptom. As a result, a specific symptom may be more pronounced
relative to the other symptoms in one study but less pronounced relative to the other symptoms in
another study that examined a different combination of symptoms. Support for this explanation
comes from the fact that our results are most consistent with the past study that examined the
combination of symptoms most similar to those examined in our study (i.e., Keller and Nesse,
2006, Study 1). This explanation implies that methodological differences should be considered
when comparing findings of different studies. Also, researchers should build on past research
investigations of the SSCH by using similar methodologies while systematically varying certain
dimensions in order to isolate the influence of a particular variable.
Death of a loved one and social isolation. One explanation for the inconsistencies
between our findings and those of past research (Keller & Nesse, 2005, 2006) regarding death of
a loved one and social isolation involves differences in how ALEs were operationalized. Keller
and Nesse (2005, 2006) operationalized an ALE as an event the participant identified as causing
the worst period of low mood they had experienced during the previous year. Our study
operationalized an ALE as the most stressful event or issue the participant reported they had
experienced or focused on during the assessment period (i.e., since they last completed daily
measures, or in the past 24 hours if they had not completed daily measures in the last 24 hours).
According to our operationalization, an ALE could involve actually experiencing an
event/issue, thinking about an event/issue that actually happened in the past, or thinking about or
imagining an event/issue that never happened. Regarding death of a loved one, Keller and Nesse
found the SSC predicted symptom pattern when they operationalized death of a loved one as an
event that actually happened over the past year (2006, Study 1; 2005), and when they
operationalized death of a loved one as imagining the experience (2006, Study 2). It is possible
that the SSCH predicted symptom pattern for death of a loved one is associated with actually
experiencing and imagining death of a loved one but not with merely thinking about a loved
one’s death that occurred in the more distant past. Again, finer distinctions in this ALE category
may increase the theoretical precision and accuracy of the SSCH, and may be necessary for
detecting relationships.
Regarding social isolation, Keller and Nesse (2005, 2006), found the SSCH predicted
symptom pattern when they operationalized social isolation as an event that actually happened
over the past year. It is possible that the SSCH predicted symptom pattern is associated with
actually experiencing social isolation but not with imagining it and/or thinking about it
happening in the past. Again, our operationalization of ALEs may have been too broad, and finer
distinctions may allow for detection of the relationship between these ALEs and depressive
symptom patterns.
Additionally, our operationalization may have involved social isolation that was short-
term and less severe. As such, it is possible that our operationalization of social isolation
involved a different construct, short-term social isolation, which may be less severe, and may or
may not be related to the same depressive symptom pattern as long-term social isolation. This
explanation highlights the importance of specifying a minimum or maximum duration when
measuring certain ALEs in order to ensure construct validity. It is also possible that our
operationalization of social isolation involved both short- and long-term social isolation, and that
finer distinctions are necessary for detecting relationships. Perhaps short-term social isolation
and long-term social isolation involve different adaptive challenges, and therefore, different
depressive symptom patterns.

A second explanation for the inconsistency between our findings and those of past
research (Keller & Nesse, 2005, 2006) regarding death of a loved one and social isolation
involves the influence of time. Our study involved a daily diary design in which participants
completed the same daily measure over up to nine consecutive or nonconsecutive days. Results
indicated that time was significantly and negatively associated with ASCs and NSCs for all
ALEs except winter—time was significantly and negatively associated with winter-NSC but not
winter-ASC. With the exception of winter-ASC, as time increased, levels of all ASCs and NSCs
decreased.
We would have preferred to account for the influence of time by including it as a Level 1
predictor in our Hypothesis 1 multilevel models. However, doing so would not allow us to test
our hypotheses because multiple predictors (i.e., ALE and time) result in a multiple correlation
(R) rather than a correlation (r). A multiple correlation is the correlation between multiple
predictor variables and a single outcome variable. Our hypotheses involved examining the
correlations between a single ALE and outcome variable. As a result, we elected not to include
time as a predictor in our Hypothesis 1 models. It is possible that time’s influence on the
outcome variables (i.e., ASC and NSC) for certain ALEs (i.e., death of a loved one and social
isolation) masked the relationships between those ALEs and their corresponding ASCs and
NSCs.
As an example, without the influence of time, the relationship between social isolation
and social isolation-ASC may be significantly larger than the relationship between social
isolation and social isolation-NSC. This would be consistent with our hypothesis and the SSCH.
However, because we were unable to remove the influence of time, it may have differentially
influenced social isolation-ASC and social isolation-NSC in such a way that the correlation
between social isolation and social isolation-ASC became substantially smaller while the
correlation between social isolation and social isolation-NSC became minimally smaller. This
would cause the two correlations to be closer together, and possibly cause the correlation
between social isolation and social isolation-ASC to no longer be significantly larger than the
correlation between social isolation and social isolation-NSC. Time may have had the same
effect on our results for death of a loved one.
Support for this explanation comes from the results of a follow-up analysis in which we
included time in our Hypothesis 1 models. For those ALEs which did not support Hypothesis 1
(i.e., death of a loved one and social isolation), the associations between time and ASC appeared
to be larger than the corresponding associations between time and NSCs. The association
between time and death-ASC (b = -0.023, SE = 0.004, p < .001) appeared to be larger than the
association between time and death-NSCs (b = -0.013, SE = 0.003, p < .001). Similarly, the
association between time and social isolation-ASC (b = -0.016, SE = 0.003, p < .001) appeared to
be larger than the association between time and social isolation-NSCs (b = -0.007, SE = 0.003, p
< .05).
On the other hand, for those ALEs which largely supported Hypothesis 1 (i.e., failure,
romantic loss, chronic stress, and winter), the associations between time and ASC did not appear
to be substantially larger than the corresponding associations between time and NSCs. For
example, the association between time and failure-ASC (b = -0.011, SE = 0.003, p < .01) did not
appear to be larger than the association between time and failure-NSCs (b = -0.016, SE = 0.003,
p < .001). This explanation implies that time should be accounted for when examining the ALE-
symptom relationships using longitudinal or repeated measure designs. Additionally, potential
conflict between design and analytic approach should be carefully considered in research that is
longitudinal or involves repeated measures.

Death of a loved one. One explanation for the inconsistencies between our findings and
those of past research (Keller & Nesse, 2005, 2006) regarding death of a loved one involves
differences in how death of a loved one was operationalized coupled with different sampling
procedures. Keller and Nesse operationalized an ALE as an event the participant identified as
causing the worst period of low mood they experienced during the previous year. Additionally,
Keller and Nesse preselected participants who reported experiencing a period of low mood
during the previous year and oversampled participants who had experienced less common ALEs
such as death of a loved one and winter. Our study operationalized an ALE as the most stressful
event or issue the participant reported they had experienced or focused on during the assessment
period (i.e., since they last completed daily measures, or in the past 24 hours if they had not
completed daily measures in the last 24 hours). Additionally, our sampling procedures did not
involve preselecting participants who were more likely to experience periods of low mood or
oversampling participants who were more likely to experience less common ALEs.
The relatively brief time period during which an event/issue could occur or be focused on
in our study (i.e., approximately 24 hours) likely resulted in less severe ratings of uncommon
ALEs such as death of a loved one. The likelihood of experiencing or focusing on the death of a
loved one over a 24-hour period is low. Furthermore, we did not compensate for this issue by
preselecting participants for dysphoric episodes or oversampling for uncommon ALEs. These
methodological features may have resulted in less variability in our data for death of a loved one
and winter, making it more difficult than it was in past studies to detect an effect. In support of
this explanation, our participants’ average level of death of a loved one and winter across days
was low and highly negatively skewed. This explanation implies that our methodology may not
have been appropriate for examining less common ALEs such as death of a loved one. This issue
may be addressed by employing sampling procedures that involve preselection and
oversampling.
Chronic stress. One explanation for the inconsistencies between our findings and those
of past studies (Keller & Nesse, 2005, 2006) regarding chronic stress involves retrospective bias.
Research indicates that retrospective reports about experiences that occurred a week or more in
the past are less valid and reliable, and more biased when compared to concurrent reports (Henry
et al., 1985; Schwarz & Sudman, 1994; Smith et al., 1999). An individual’s report about a period
of low mood and what they believe may have led to it may change over time and become
contaminated for a number of reasons, including but not limited to reduced recollection of
details, or the tendency to distort the past in a way that reflects better on the self.
In past studies (Keller and Nesse, 2005, 2006), participants reported on ALEs that
occurred in the past year while those in our study reported on ALEs much closer in time to when
they occurred. As such, past studies were subject to a higher degree of retrospective bias than our
study. It is possible that one or more forms of retrospective bias contributed to Keller and
Nesse’s (2005, 2006) findings regarding the relationship between chronic stress and depressive
symptom patterns. For example, as time passes, participants may be more likely to falsely
attribute a socially undesirable ALE such as failure to a less socially undesirable ALE such as
chronic stress. As another example, as time passes, the accuracy of a participant’s memory of a
specific ALE (i.e., failure) may decrease, making it more likely that the participant will report a
more heterogeneous, catchall ALE category such as chronic stress. This explanation implies that
ALE categories that are less socially undesirable and/or more heterogeneous (i.e., chronic stress)
may be more vulnerable to certain forms of retrospective bias. This vulnerability may be
addressed by examining these ALEs prospectively or reducing the period of time between when
these ALEs occur and when they are reported.

A second explanation for the inconsistencies between our findings and those of past
research (Keller & Nesse, 2005, 2006) regarding chronic stress involves differences in how
ALEs were measured. In Keller and Nesse’s (2005, 2006) studies, participants could only
endorse a single ALE category to indicate the ALE they believed led to their dysphoric episode.
As a result, a participant who believed two or more different ALEs contributed equally to their
dysphoric episode was forced to leave important information out. In order to avoid this, some
participants in their studies may have endorsed chronic stress because it is a heterogeneous
category that can involve ongoing difficulties in more than one area of one’s life.
In our study, participants could endorse multiple ALE categories, and indicate the degree
to which their self-identified ALE involved each ALE category. As a result, we were able to
examine the association between a participant’s level or degree of ALE and level of different
symptoms. It is possible that finer quantitative distinctions allowed us to measure ALEs more
accurately than Keller and Nesse (2006, 2005). This may have increased our internal validity and
led to different results. This explanation implies that the heterogeneous nature of chronic stress
may make it vulnerable to contamination when participants are forced to endorse a single ALE
category as present or absent. This vulnerability might be addressed by allowing participants to
indicate the degree to which their self-identified stressful event involved an ALE category,
and/or by allowing participants to endorse multiple ALE categories.
Social isolation. One explanation for the inconsistencies between our findings and those
of past research (Keller & Nesse, 2005, 2006) regarding social isolation involves sample
differences. We included a group of participants with major depressive disorder (MDD) while
Keller and Nesse (2005, 2006) did not. Our results indicated that the association between social
isolation and two depressive symptoms (i.e., anhedonia and desire for social support) varied for
participants with and without MDD. Although social isolation was positively related to
anhedonia for both groups, levels of anhedonia were higher and increased at a higher rate for
participants with MDD. Social isolation was positively related to desire for social support for
non-MDD but not MDD participants.
The SSCH predicts that anhedonia will be less pronounced in association with social
isolation while desire for social support will be more pronounced. One possibility is that the
hypothesized relationship between social isolation and depressive symptom pattern exists for
non-MDD participants but varies across non-MDD and MDD groups in such a way that the
effects cancel one another out. Another possibility is that the association between social isolation
and depressive symptom pattern for non-MDD and MDD participants follows a similar but not
identical pattern, with the difference being in desire for social support. Non-MDD participants
may desire social support while MDD participants may not. One or both of these possibilities
may explain why we did not find a significant difference between the social isolation-ASC
relationship and the social isolation-NSC relationship. This implies that some ALE-symptom
relationships should be examined separately for non-MDD and MDD participants.
Hypothesis 2: Findings, Explanations, and Implications
Hypothesis 2 stated that the depressive symptom patterns of non-MDD participants
would be consistent with the depressive symptom patterns of MDD participants for each ALE.
For example, Hypothesis 2a stated that the depressive symptom pattern of non-MDD participants
would be consistent with the depressive symptom pattern of MDD participants for failure.
Hypothesis 2b – 2f were the same as Hypothesis 2a except that each one involved a different
ALE.
The SSCH assumes that MDD can, at times, be an adaptive response to an adverse
situation, and can, at other times, be a maladaptive response that results from an inability to
remove oneself from an adverse situation or from a biological defect. The SSCH does not make
specific predictions about whether ALE-symptom relationships should vary for MDD and non-
MDD individuals. However, Keller and Nesse (2005, 2006) examined ALE-symptom
relationships in non-MDD participants and found depressive symptom patterns that are similar to
several previously established MDD subtypes (i.e., bereavement, melancholia, and hopelessness
depression). Therefore, we hypothesized that ALE-depressive symptom pattern relationships
would be consistent across diagnostic groups (i.e., non-MDD versus MDD) for all ALE
categories.
Our findings fully supported Hypotheses 2a – 2d, and largely supported Hypotheses 2e
and 2f. Participants with and without MDD experienced similar depressive symptom patterns for
failure, death of a loved one, romantic loss, and chronic stress. Participants with and without
MDD experienced similar depressive symptom patterns with two exceptions in the case of social
isolation (i.e., anhedonia and desire for social support) and three exceptions in the case of winter
(i.e., anhedonia, rumination, and crying). More specifically, as social isolation increased,
anhedonia increased significantly for both non-MDD and MDD participants, though at a higher
rate for MDD participants. Additionally, as social isolation increased, desire for social support
increased significantly for non-MDD but not MDD participants. As winter increased, anhedonia
increased significantly for MDD but not non-MDD participants. Additionally, as winter
increased, rumination increased significantly for non-MDD participants but decreased
significantly for MDD participants. Finally, as winter increased, crying increased significantly
for MDD but not non-MDD participants.
Our findings suggest that individuals with and without MDD experience largely
consistent depressive symptom patterns when they are confronted with adverse situations. More
specifically, in situations of failure, death of a loved one, romantic loss, and chronic stress, MDD
and non-MDD individuals experience similar depressive symptom patterns. In situations of

social isolation and winter, MDD and non-MDD participants only vary on two and three
symptoms, respectively. As levels of social isolation increased, levels of anhedonia increased
significantly for both MDD and non-MMD participants although at a higher rate for MDD
participants; and levels of desire for social support increased significantly for non-MDD
individuals but not for MDD participants. As levels of winter increased, levels of anhedonia
increased significantly for MDD participants but not for non-MDD participants; levels of
rumination increased significantly for non-MDD participants but decreased significantly for
MDD participants; and levels of crying increased significantly for MDD participants but not for
non-MDD participants.
One explanation for this variation in ALE-depressive symptom pattern relationships
across diagnostic groups for social isolation and winter is that certain symptoms may be adaptive
in subthreshold depression but maladaptive in clinical depression. As an example, Allen and
Badcock’s (2003) social risk hypothesis (SRH) of depressed mood may help explain why social
isolation is positively associated with desire for social support in individuals without MDD but
not in individuals with MDD. The SRH argues that depressed mood “evolved to minimize risk in
social interactions in which individuals perceive that the ratio of their social value to others, and
their social burden on others, is at a critically low level” (p. 887).
The SRH is based on the assumption that each member of a social group has a certain
level of social value and social burden to the group. When these values are nearly equivalent for
an individual, he or she is more likely to be excluded from the group, which provides many
fitness-relevant resources (e.g., reproductive opportunities) that have provided an adaptive
advantage over the evolutionary course. Allen and Badcock (2003) argue that certain features of
depressed mood states are mechanisms that reduce social risk for an individual who is at risk for
social exclusion. It is possible that desire for social support may be adaptive when an
individual’s ratio of social value to social burden is within a certain range but become
maladaptive when it falls below that range. When it reaches this critically low level, it may be
adaptive to not want or seek social support, thereby decreasing the individual’s social burden,
increasing their ratio of social value to social burden, and reducing their risk of social exclusion.
This explanation has implications for practice because a symptom that was maladaptive
in certain situations over evolutionary time is not necessarily adaptive in modern times. For
example, wanting or seeking social support may benefit clinically depressed individuals
experiencing social isolation today. There are many sources of social support that are unrelated
to one’s friends and loved one, and therefore, would not put the depressed individual at risk for
burdening their support group and being socially excluded. Two examples of these alternative
sources of social support including mental health support groups and mental health providers.
We accounted for time by including time as a predictor in our Hypothesis 2 models. Our
results indicated that time was negatively associated with most depressive symptoms for all
ALEs. Exceptions include the following: fatigue, anhedonia, and sleep for failure, romantic loss,
chronic stress, and winter; fatigue and anhedonia for death of a loved one; and fatigue,
anhedonia, crying, and sleep for social isolation. This effect likely resulted from repeated testing,
and demonstrates that time was a threat to internal validity. These findings imply that time
should be accounted for in research that is longitudinal or involves repeated measures.
Gender and age consistently influenced one or two of the same depressive symptoms
across all ALEs. Females reported more crying for all ALEs, and males reported more guilt for
all ALEs except winter. Older individuals experienced more emotional pain for all ALEs except
social isolation, and more anhedonia for all ALEs. These findings suggest that gender and age
impact certain depressive symptoms in a consistent manner for most ALEs. The influence of
gender and age should be considered in research examining depressive symptoms.

One explanation for the association between gender and depressive symptoms involves
agency and communion. Agency involves an orientation toward the self in the service of
accomplishing a goal, increasing power, or exerting influence while communion involves an
orientation toward other people in the service of connecting and congregating. Research
indicates that males typically report more agency attributes than females while females report
more communion attributes than males (Helgeson & Fritz, 1999). From an evolutionary
perspective, guilt and crying may be adaptations that provided a selective advantage for males
and females, respectively, in adverse situations. As the more agentic sex, males who experienced
more guilt in association with adverse situations may have been able to focus more on their roles
in those situations, and learn how to avoid or decrease the likelihood of experiencing such
situations in the future. As the more communal sex, females who exhibited more crying in
adverse situations may have been able to elicit more support from their social group. It is also
possible that guilt and crying are concomitants of adaptations (i.e., agency and communion,
respectively).
Gender and age should be considered when using the SSCH to conceptualize a depressive
episode and design a treatment plan. Males may be higher on guilt and females may be higher on
crying regardless of the ALE they are experiencing. Furthermore, older individuals may be
higher on emotional pain and anhedonia than younger individuals for most ALEs. Finally, if it is
true that gender differences on agency and communion result in higher levels of guilt for males
and higher levels of crying for females, clinicians should consider whether males high on guilt
and females high on crying have a healthy balance of agency and communion. Research suggests
that a balance of agentic and communal traits is associated with increased well-being (Helgeson
& Fritz, 1999). Helping a client develop a healthy balance of agency and communion may help
him or her gain a more realistic perspective on their role in creating a particular adverse
situation, and/or develop skills for increasing or accessing social support. This may, in turn, lead
to appropriate levels of guilt and decreased crying.
Hypothesis 2: Integration of Findings with Past Literature
Hypothesis 2: Convergent findings. The only past study that examined whether non-
MDD and MDD participants have similar ALE-depressive symptom patterns was conducted by
Keller et al. (2007).They examined the association between ALEs and depressive symptom
patterns in separate between-person, within-person, and MDD samples. They looked at the
consistency of depressive symptom patterns across samples for each ALE category. Their study
involved four of the six ALEs examined in our study, in addition to five other ALEs. More
specifically, they examined death, romantic loss, failure, chronic stress, health, interpersonal
conflict, scare, other, and nothing. They did not examine social isolation or winter. They looked
at five of the nine symptoms we examined in addition to seven other symptoms. More
specifically, they examined emotional pain, fatigue, anhedonia, guilt, increased sleep, appetite
loss, poor concentration, appetite gain, insomnia, self-harm, psychomotor retardation, and
restlessness. They did not examine pessimism, rumination, crying, or desire for social support.
Comparisons between our Hypothesis 2 findings and those of Keller et al. (2007) are
difficult for numerous reasons, and should be interpreted with caution. To begin with, we
examined whether the relationship between each ALE and each depressive symptom varied by
diagnostic group (non-MDD versus MDD) while they examined higher and lower than average
symptom levels separately for non-MDD and MDD participants and then compared the
consistency of these results across samples. As a result, their findings regarding a particular
ALE-depressive symptom relationship depend on the other symptoms included in their analyses
while our Hypothesis 2 findings do not. Additionally, they only looked at four of the six ALEs
examined in our study, and five of the nine symptoms examined in our study.
Nonetheless, our Hypothesis 2 findings for failure, death of a loved one, romantic loss,
and chronic stress are largely consistent with those of Keller et al. (2007). They found highly
consistent results for these ALEs across their between-, within-, and MDD samples. Past
research has not examined whether non-MDD and MDD participants have similar ALE-
depressive symptom patterns for social isolation and winter. Therefore, we cannot consider our
Hypothesis 2 findings for social isolation and winter in the context of past research.
Hypothesis 2: Explanations and implications of convergent findings. There are a
number of explanations and implications for the consistencies between our findings and those of
Keller et al. (2007) regarding failure, death of a loved one, romantic loss, and chronic stress.
First, Keller et al. (2007) were the first to examine whether ALE-depressive symptom pattern
relationships were consistent across diagnostic groups (i.e., non-MDD and MDD). Therefore,
replicating their study was an important next step. Additionally, consistencies across diagnostic
groups extend beyond the symptoms examined in their study to those examined in our study.
Second, consistencies across diagnostic groups extend beyond Caucasian twin pairs to
individuals from the general population. Third, consistencies across diagnostic groups were
observed when participants reported depressive episodes and ALEs experienced over the past
year as well as over the past day. Collecting self-report information closer in time to when it
actually occurred increases reliability and validity by decreasing the impact of self-enhancement,
faulty memory, and anchoring bias.
Additional Implications of Findings for Theory, Research, and Practice
At present, researchers, theorists, and clinicians vary in their approaches to subtyping
depression. For example, some use the method adopted by the DSM-IV-TR (APA, 2000) and
DSM-V (APA, 2013), which subtype depression based on symptom profiles. Other researchers
and clinicians subtype depression based on the type of precipitating event that leads to the
depressive episode. Still others subtype depression based on the diathesis-stress model, which
asserts that depressive episodes arise from an interaction between unfavorable situations and
stable dispositional factors. While these approaches to subtyping depression have increased our
understanding of how depressive reactions vary, they are limited in their explanatory power for
the following reasons: they lack a unifying framework, and they typically focus on clinical
depression. The SSCH provides an alternative method for subtyping depression that provides a
unified framework based on why certain symptom profiles are expressed during a particular
depressive episode, and can be applied to both clinical and subthreshold depression.
Our findings for failure, romantic loss, chronic stress, and winter also have implications
for evolutionary models of depression. Consistent with evolutionary models of depression, our
findings suggest that depressive symptoms may have evolved because they have helped human
beings cope more effectively with fitness-relevant situations that recurred over evolutionary
time. Because empirical investigations of evolutionary models remains limited (Kennair, 2003),
our findings bolster support for the evolutionary approach to depression, which is based largely
on theoretical research.
Our findings also support the idea that depressive symptoms are domain-independent or
can be adaptive in unfavorable situations in many domains (Klinger, 1975; Nesse, 2000). This
bolsters support for evolutionary models of depression that are domain independent and
challenges evolutionary models that are domain-specific, which limit the functionality of
depressive symptoms to particular domains. As discussed in the Evolutionary Models of
Depression section of Chapter I, one dimension on which evolutionary models vary is the
domain in which the depressive state is hypothesized to function. Domain-specific models limit
the functionality of depressive symptoms to particular types of situations such as those that
involve social interactions (Allen & Badcock, 2003), social competition (Price, Sloman, Gardner,
Gilbert, & Rohde, 1994), or social problem-solving (Watson & Andrews, 2002) while domain-
independent models argue that symptoms of depression can be adaptive in various types of
situations that involve fitness challenges (Nesse, 2000). Some evolutionary models that are
domain-independent include the SSCH (Keller & Nesse, 2006, 2005) and Nesse’s domain-
independent approach to low mood (Nesse, 2000, 2009a); and some domain-specific models
include the social navigation hypothesis (Watson & Andrews, 2002), analytical rumination
hypothesis (Andrews & Thompson, 2009), social risk hypothesis (Allen & Backcock, 2003), and
social competition hypothesis (Price et al., 1994).
Other evolutionary models cannot explain our finding that different ALEs were
associated with distinct depressive symptom patterns. Two examples of models that cannot
explain this finding include Watson and Andrew’s (2002) social navigation hypothesis (SNH)
and Andrews and Thomson’s (2009) analytical rumination hypothesis (ARH). The SNH argues
that clinical depression functions in the domain of social problem-solving to (a) increase the
individual’s capacity to analyze and resolve fitness-relevant social problems, and (b) produce
symptoms such as anhedonia and psychomotor perturbation to motivate social partners to
provide support and make concessions that may improve the individual’s situation. Similarly, the
ARH asserts that clinical depression is an evolved response that functions in the domain of
complex problem-solving to minimize distraction from and sustain analysis of complex problems
by (a) allowing the problem to have prioritized access to processing resources, (b) producing an
anhedonic state which reduces the desire to participate in other activities, and (c) eliciting
physical changes that limit exposure to other stimuli.
While the proponents of the SNH and ARH may view some or all of the ALEs we
examined as belonging to the domain of social or complex problem solving, respectively, they
cannot explain why depressive symptom patterns would vary in different situations of complex
problem solving. Instead, they would seem to suggest that symptoms such as rumination,
anhedonia, and fatigue would be elevated regardless of the situation because: (1) in the case of
the SNH, they would increase the individual’s ability to analyze and resolve fitness-relevant
social problems and motivate social partners to provide support and make concession to improve
the depressed individual’s situation; and (2) in the case of the ARH, they would function to
minimize distraction and sustain analysis of problems.
Our findings for failure, romantic loss, chronic stress, and winter also have implications
for biopsychosocial approaches to depression. Similar to past investigations of the ALE-
depressive symptom pattern relationships based on biopsychosocial approaches (Keller, Neale, &
Kendler, 2007), we found that different ALEs were associated with distinct depressive symptom
patterns in a combined between- and within-person sample. As a result, our findings bolster
support for the role of ALEs in the clinical presentation of depression.
Our findings offer an ultimate or evolutionary understanding of ALE-depressive
symptom pattern relationships that compliments the proximate understanding of biopsychosocial
approaches. Researchers and theorists increasingly recognize that a comprehensive
understanding of any psychological phenomenon requires examination at both a proximate and
ultimate level of analysis (Gilbert, 2013; Brune et al., 2012; Confer et al., 2010; Sterelny, 2003).
While biopsychosocial approaches attempt to explain what and/or how biological/genetic,
psychological, and/or social/environmental factors interact to shape the clinical presentation of
depression, evolutionary approaches such as the SSCH explain that these depressive symptom
patterns may be evolved responses that are triggered in different types of adverse situations
because they help individuals cope with the adaptive challenges of different situations. This level
of understanding may inform biopsychosocial approaches by providing clues about the types of
adverse situations that are associated with depression, and the types of symptoms that are likely
to be elevated in different adverse situations.
Our findings also have numerous implications for the practice of psychology. There is
strong evidence for a genetic role in MDD—twin studies attribute 40% to 50% of MDD
heritability to genetics (reviewed in Levinson, 2005). Other important factors may include
neurobiology (Thase, 2009), early adverse experiences (Goodman & Brand, 2009), parental
depression (Hammen, 2009), cognition (Joorman, 2009), interpersonal-behavioral characteristics
(Joiner & Timmons, 2009), and social environment and life stress (Monroe, Slavich, &
Georgiades, 2009). Clinicians should consider all of these proximate factors when
conceptualizing and treating depression. However, they may complement a proximate level of
understanding with an evolutionary or ultimate level of understanding.
Clinicians can examine the pattern of symptoms for clues about the type(s) of adverse
situations that may be contributing to the depressive episode. Helping the client work through or
resolve the challenging situation(s) can be incorporated into the treatment plan. For example, a
client who presents with more pronounced emotional pain, fatigue, pessimism, guilt, rumination,
and anhedonia may be experiencing some type of failure. The clinician can work with the client
to identify, work through, and resolve their perceived failure. A number of evolutionary
psychologists have designed and utilized evolutionary interventions or therapies for depression
that involve identifying and resolving adverse life situations as part of conceptualization and
treatment (Nesse, 2009b; Giosan, Muresan, & Moldovan, 2014; Giosan, et al., 2014).
Additionally, because specific symptoms may serve particular adaptive functions, they can
provide information about the needs of the client, which can be incorporated into the treatment
plan. For example, an individual who presents with more crying and desire for social support
may lack sufficient social support. To address this, the clinician can design a treatment plan that
involves increasing the client’s levels of perceived or actual social support.
While it is important to consider the possibility that a depressive episode is a normal and
adaptive response to an adverse situation, clinicians should also entertain the possibility that
depressive episodes may be evolved responses that were adaptive in ancestral environments but
are maladaptive in modern environments. It may also be helpful to engage in a discussion with
the client about evolutionary perspectives of depression and depressive symptoms. Doing so may
improve the client’s understanding of what adaptive challenges he or she may be facing, why he
or she may be experiencing certain symptoms, and what these symptoms suggest about resources
or changes that may help him or her resolve these adaptive challenges.
Our Hypothesis 1 findings indicated that a combined sample of participants with and
without MDD experienced ALE-depressive symptom pattern relationships that were largely
consistent with the SSCH. Our Hypothesis 2 findings demonstrated that these ALE-symptom
relationships are highly consistent across non-MDD and MDD participants. Together, our
Hypothesis 1 and Hypothesis 2 findings imply that both non-MDD and MDD individuals who
confront ALEs may experience depressive symptom patterns that may have evolved to help them
effectively cope with the adaptive challenges characteristic of their adverse situations.
This has implication for evolutionary models of depression. Adaptationist models view
clinical depression as an adaptation. Some adaptation models include the social navigation
hypothesis (Watson & Andrews, 2002), defection hypothesis (Hagen, 1999), and analytical
rumination hypothesis (Andrews & Thomson, 2009). Dysregulation models view depressed
mood as an adaptation and may assume clinical depression is the product of an adaptive
mechanism (i.e., the capacity for depressed mood) that has stopped functioning properly. Some
dysregulation models include the social risk hypothesis (Allen & Badcock, 2003), social
competition hypothesis (Price et al., 1994), and Nesse’s generic theory of low mood (Nesse,
2000, 2009a). Both adaptation and dysregulation models should consider the possibility that both
subthreshold and clinical depressive episodes may at times be adaptive responses that evolved
because they helped individuals cope with the fitness-challenges of adverse situations over
evolutionary time.
Limitations and Future Directions for Research
Our study had a number of limitations. Future researchers can improve and build on our
study by addressing these limitations and taking new directions. First, because our data were
collected retrospectively, we cannot assume that depressive symptom patterns were caused by
ALEs. We were only able to establish associations between perceived ALEs and depressive
symptom patterns. However, by assessing ALEs and depressive symptoms close in time to when
they were experienced (i.e., within the past day), we were able to reduce the likelihood that our
data were unreliable or invalid due to contamination caused by the tendency to recall the past in
a way that reflects better on the self, faulty memory, and the inclination to give excessive weight
to a particular aspect of one’s experience and. Future researchers may further reduce the
likelihood of retrospective biases by conducting prospective research in which ALEs and
depressive symptoms are measured regularly over a longer duration. Participants who end up
experiencing ALEs could be selected for analyses that examine depressive symptom patterns
following different ALEs.
Second, we utilized self-report measures to collect our data, which can lead to unreliable
and biased data. For example, the experience of being fired from a job while still financially
dependent on one’s parents is likely to be very different than being fired from a job while
financially independent and providing for a family of five. In other words, the significance and
level of negative impact of a particular event varies considerably from one person to another, and
is more difficult to capture with self-report measures. However, interview-based measures can
control for many sources of bias that plague self-report measures (Paykel, 2003; Tennant, 2002).
Unfortunately, utilizing interview-based measures in our study was impractical due to the
amount of time, effort, and resources they require. Researchers with adequate resources may
reduce the likelihood of unreliable and biased data by using interview-based rather than self-
report measures to assess ALEs.
Third, our sample was largely composed of young, Caucasian females. However, our
sample did represent a more heterogeneous group than those utilized in most previous
investigations, which were limited to college students (Keller & Nesse, 2005, 2006) and
Caucasian twin pairs (Keller et al., 2007). Nonetheless, a more diverse sample could examine
whether the relationships under investigations generalize across different populations. For
example, examining the consistency of ALE-symptom relationships across cultures would help
determine whether these relationships are universal and likely to have evolutionary origins.
Cross-cultural research is particularly important in evolutionary research because it can
determine whether traits or behaviors are universal or specific to certain cultures. Traits and
behaviors that are universal provide evidence of biological or evolutionary origins. Future
researchers should test the SSCH and/or examine ALE-symptom relationships in different
populations. Oversampling or selecting for certain sample characteristics may be necessary for
attaining a more diverse sample.
Fourth, we did not account for time in some of our Hypothesis 1 models. Although a
follow-up analysis revealed that time had a significant, negative relationship with our Hypothesis
1 outcome variables (i.e., ASCs and NSC for all ALEs), we elected not to include time in our
Hypothesis 1 models because doing so would have prevented us from testing Hypothesis 1a – 1f.
As a result, time may have influenced our results via Type I or Type II error. Future researchers
who employ longitudinal or repeated measure designs to examine the relationship between ALEs
and depressive symptoms should account for the influence of time. This may require careful
consideration regarding design features and/or analytic approaches that may come into conflict
and prevent hypothesis testing.
Fifth, we conducted separate analyses for each ALE category despite the fact that more
than one ALE may have been associated with a participant’s depressive symptoms on a
particular day. As a result, we did not explore the relationship between multiple ALEs and
depressive symptom patterns. For example, a participant may simultaneously experience failure
and death of a loved one in association with a depressive episode; or they may experience the
end of a relationship as both a romantic loss and failure. One way that we attempted to address
this was by asking participants to endorse ALEs on a 5-point Likert scale, indicating the extent to
which their self-identified stressful event involved each ALE category. Therefore, each analysis
examined the relationship between a specified level of ALE and depressive symptom pattern.
Nonetheless, examining the relationship between multiple ALEs and depressive symptom
patterns would provide relevant information about the relationships under investigation.
Sixth, we did not conduct separate analyses on our between- and within-person samples.
As a result, we were unable to determine whether results for between- and within-person samples
were consistent, which would have allowed us to rule out the possibility that depressive
symptoms patterns were caused by stable interpersonal differences results rather than ALEs.
Future researchers should conduct separate analyses for between- and within-person samples,
and control for stable interpersonal differences (Keller et al., 2007).
Seventh, we did not conduct separate tests of the SSCH on each of our diagnostic groups
(non-MDD and MDD). Instead, for Hypothesis 1, we tested the SSCH on a combined non-MDD
and MDD sample by statistically comparing the ALE-ASC relationship to the ALE-NSC
relationship. For Hypothesis 2, we conducted a separate analysis to examine whether or not there
was a significant ALE x Diagnostic Group interaction for each of the outcome variables (i.e.,
individual depressive symptoms). If there were significant ALE x Diagnostic Group interactions
for any of the outcomes, simple effects analyses were completed to look at the difference in the
ALE-symptom relationships for each diagnostic group (i.e., non-MDD and MDD). In other
words, we did not conduct separate analyses for our non-MDD and MDD groups so that we
could statistically compare the ALE-ASC relationship to the ALE-NSC relationship. As a result,
we were unable to directly separately examine whether each diagnostic group experiences ALE-
depressive symptom pattern relationships that are consistent with the evolutionary predictions of
the SSCH. While our results suggest that this is the case, findings based on separate analyses
would bolster support by providing more robust evidence.
Eighth, data for all ALEs (i.e., our predictor variables) except chronic stress was
positively skewed. Most participants endorsed low levels of these ALEs. This was especially true
for rare ALEs such as death of a loved one and winter. This limited variability may have made it
more difficult to detect effects. Nonetheless, we were able to find an effect for most of our
hypotheses despite this limited variability. Future researchers may attain more variability in their
data by preselecting participants who are likely to experience or have experienced more
depressive episodes and/or oversampling participants who are likely to experience or have
experienced rare ALEs such as death of a loved one.
Ninth, participants in our study did not exclusively report ALEs they had experienced.
Instead, ALEs were operationalized as events/issues that were either experienced or focused on
within the past 24 hours. As such, we cannot determine whether our results involved the
relationships between experiencing ALEs and depressive symptom patterns or focusing on ALEs
and depressive symptom patterns. It is also possible that our operationalization was too broad or
involved more than one construct. Finer distinctions may be necessary for detecting an effect.
Future researchers may address this limitation by operationalizing ALEs in a more precise
manner (i.e., adverse events that were actually experienced during the observation period).
Tenth, we did not find support for some of our hypothesis (i.e., death of a loved one and
social isolation). Furthermore, some of the correlations between our predictor and response
variables were small (Cohen, 1988). Additionally, most ALEs were significantly associated with
both the adaptive and nonadaptive symptom clusters (although the latter assumptions were
typically significantly smaller). Together, these findings indicate that ALEs only explain a small
portion of the variance in depressive symptom patterns. It is possible that one or more of our
study limitations resulted in insignificant findings and/or small correlations, and that addressing
these limitations in future research may lead to different results. However, future researchers
should also consider the possibility that other variables lead to variation in depressive symptom
patterns. Eleventh, we did not examine some ALEs and depressive symptoms about which the
SSCH makes predictions. Future research should examine a wider range of ALEs (e.g., threat
and interpersonal conflict), and symptoms (e.g., increased appetite, decreased appetite, and
anxiety).
Twelfth, participants responded to items addressing depressive symptoms and ALEs they
experienced over the past day for nine consecutive or nonconsecutive days. As such, demand
characteristics may have impacted our results. After their first daily measure, participants may
have come to believe that we were expecting to determine that ALEs led to an increase in
depressive symptoms or an increase in certain types of depressive symptoms. This may have
caused participants to alter their responses in order to conform to what they believed we wanted.
Future research might address this by increasing the amount of time between observations or
including additional measures to better conceal the purpose of the study.

Thirteenth, the SSCH argues that certain depressive reactions evolved because they
served an adaptive function in the adverse situations in which they were elicited over
evolutionary time. In our study, we tested whether different ALEs were associated with SSC
predicted depressive symptom pattern. Future research should examine whether these depressive
reactions are indeed adaptive for the individual. One method proposed by Keller and Nesse
(2006) was to examine individuals who experience a depressive episode following the same
ALE, and compare those individuals who endorse the SSC predicted depressive symptom
patterns to those who experience other depressive symptom patterns that are equal in severity.
Do the individuals who experience the SSC predicted depressive symptom patterns have better
psychological outcomes than those who experience other depressive symptom patterns? Some
outcomes may include faster remission or resolution of the adverse situation. Other outcomes
may also be specific to the ALE category and SSC predicted symptoms for that ALE. For
example, in situations of romantic loss, do individuals who endorse higher levels of crying and
desire for social support experience healthier levels of social support? Likewise, in situations of
failure, do individuals who experience higher levels of pessimism, fatigue, and emotional pain
withdraw more quickly from unattainable goals compared to those who do not?
Conclusion
The impact of depression on individual lives, public health, society, and the economy is
harmful and far-reaching. In an effort to better understand depression and reduce these
destructive consequences, many depression researchers focus on explaining why symptom
profiles of depression vary across individuals and across episodes within the same individual.
Along with the findings of a handful of recent studies, our findings demonstrate that the
situation-symptom congruence hypothesis (SSCH) is an effective approach for examining this
question and has important implications for theory, research, and practice.
We have determined that depressive symptom patterns vary depending on the ALE that
precedes the depressive episode. In other words, the type of ALE that precedes a depressive
episode explains some of the variation in symptom profiles across individuals and across
episodes within the same individual. Furthermore, the different ALE-depressive symptom pattern
associations are consistent with the evolutionary predictions of the SSCH. Finally, the
association between ALEs and depressive symptom patterns exists not only in clinical forms of
depression (i.e., major depressive disorder) but also in subthreshold forms of depression and
normal depressed mood.
Taken together, our findings suggest that both subthreshold and clinical depressive
episodes or reactions may have evolved because they helped individuals deal with adaptive
challenges of different types of adverse situations over evolutionary time. This evolutionary
explanation achieves a more comprehensive understanding of depression by complementing our
largely proximate understanding (i.e., how depression works) with an ultimate understanding
(i.e., why depression exists in the first place). These findings bolster support for further research
investigations of the SSCH. Such research can continue to extend our understanding of
depression at an ultimate level and inform theory and research that focuses on a proximate level
of understanding by “generat[ing] novel hypotheses … , defin[ing] categories of behavior, and
set[ting] criteria that must be addressed” (MacDougall-Shackleton, 2011, p. 2076). Practical
applications of our findings may improve how clinicians conceptualize and treat cases of
depression, and lead to a more integrated framework for subtyping clinical as well as
subthreshold forms of depression.

References
Allen, N. B., & Badcock, P. B. T. (2003). The social risk hypothesis of depressed mood:
Evolutionary, psychosocial, and neuorobiological perspectives. Psychological Bulletin,
129(6), 887-913. doi: http://dx.doi.org/10.1037/0033-2909.129.6.887
Andrews, P. W., & Thomson, J. A. (2009). The bright side of being blue: Depression as an
adaptation for analyzing complex problems. Psychological Review, 116(3), 620-654. doi:
http://dx.doi.org/10.1037/a0016242
Arnold, M. B. (1960). Physiological aspects. Emotion and personality (Vol. 1). New York:
Columbia University Press.
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders
(4th ed., text rev.). Washington, D.C.: Author.
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders
(5th ed.). Washington, D.C.: Author.
Badcock, P. B. T., & Allen, N. B. (2003). Adaptive social reasoning in depressed mood and
depressive vulnerability. Cognition and Emotion, 17(4), 647-670. doi:
http://dx.doi.org/10.1080/02699930302299
Basco, M. R., Bostic, J. Q., Davies, D., Rush, A. J., Witte, B., Hendrickse, W., & Barnett, V.
(2000). Methods to improve diagnostic accuracy in a community mental health setting.
American Journal of Psychiatry, 157, 1599-1605. doi:
http://dx.doi.org/10.1176/appi.ajp.157.10.1599
Baumeister, H., & Parker, G. (2012). Meta-review of depressive subtyping models. Journal of
Affective Disorders, 139, 126-140. doi: http://dx.doi.org/10.1016/j.jad.2011.07.015
Bebbington, P., Brugha, T., MacCarthy, B., Potter, J., Sturt, E., Wykes, J., Katz, R., &
McGuffin, P. (1988). The Camberwell Collaborative Depression Study: I. Depressed

probands: Adversity and the form of depression. British Journal of Psychiatry, 152, 754-
765. doi: http://dx.doi.org/10.1192/bjp.152.6.754
Beck, A. T., Ward, C. H., Mendelson, M., Mach, J. E., & Erbaugh, J. (1961). An inventory for
measuring depression. Archives of General Psychiatry, 4, 561-571. doi:
http://dx.doi.org/10.1001/archpsyc.1961.01710120031004
Beck, A. T. (1967). Depression: Clinical, experimental, and theoretical aspects. New York:
Harper & Row.
Beck, A. T., Steer, R. A. (1993). Manual for the Beck Depression Inventory. San Antonio,
Texas: Psychological Corporation.
Beck, A. T., Steer, R. A; & Brown, G. K. (1996). Manual for the Beck Depression Inventory-II.
San Antonio, Texas: Psychological Corporation.
Beck, A. T., Steer, R. A., & Garbin, M. G. (1988). Psychometric properties of the Beck
Depression Inventory: twenty-five years of evaluation. Clinical Psychology Review, 8,
77-100. doi: http://dx.doi.org/10.1016/0272-7358(88)90050-5
Brown, G. W., & Harris, T. O. (1978). Social origins of depression: A study of psychiatric
disorder in women. New York: Free Press.
Brown, G. W., & Harris, T. O. (1989). Life events and illness. New York: Guilford Press.
Brown, G. W., Harris, T. O., & Hepworth, C. (1994). Life events and endogenous depression: A
puzzle reexamined. Archives of General Psychiatry, 51, 525-534. doi:
Brown, G. W., Ni Brolchain, M., & Harris, T. O. (1979). Psychotic and neurotic depression: Part
3. Aetiological and background factors. Journal of Affective Disorders, 1, 195-211. doi:
http://dx.doi.org/10.1016/0165-0327(79)90005-3
Brugha, T. S., & Conroy, R. (1985). Categories of depression: Reported life events in a
controlled design. British Journal of Psychiatry, 147, 641-646. doi:
http://dx.doi.org/10.1192/bjp.147.6.641
Brune, M., Belsky, J., Fabrrega, H., Feierman, H. R., Gilbert, P., Glantz, K., Polimeni, J., . . .
Wilson, D. R. (2012). The crisis of psychiatry – Insights and prospects from evolutionary
theory. World Psychiatry, 11(1), 55-57. doi:
http://dx.doi.org/10.1016/j.wpsyc.2012.01.009
Centers for Disease Control and Prevention, National Center for Injury Prevention and Control.
(2010). Web-based Injury Statistics Query and Reporting System (WISQARS). Retrieved
October 4, 2010, from www.cdc.gov/ncipc/wisqars
Cohen, J. (1992). A power primer. Quantitative Methods in Psychology, 112(1), 155-159. doi:
http://dx.doi.org/10.1037/0033-2909.112.1.155
Cohen, J. (1988). Statistical Power Analysis for the Behavioral Sciences (2nd ed.). Hillsdale, New
Jersey: Erlbaum.
Confer, J. C., Easton, J. A., Fleischman, D. S., Goetz, D., Lewis, M. G., Perilloux, C., & Buss, D.
M. (2010). Evolutionary psychology: Controversies, questions, prospects, and limitation.
American Psychologist, 65(2), 110-126. doi: http://dx.doi.org/10.1037/a0018413
Cook, R. D., & Weisberg, S. (1982). Residuals and influence in regression. New York, NY:
Chapman and Hall.
Cooke, D. J., & Hole, D. J. (1983). The aetiological importance of stressful life events. British
Journal of Psychiatry, 143, 397-400. doi: http://dx.doi.org/10.1192/bjp.143.4.397
Cornelius, R. R. (1997). Toward a new understanding of weeping and catharsis? In F. J. Van
Bussel & A. J. W. Boelhouwer (Eds.), The (Non)Expression of Emotions in Health and
Disease (pp. 303-321). Tilberg, the Netherlands: Tilberg University Press.

Cornell, D. G., Milden, R. S., & Shrimp, S. (1985). Stressful life events associated with
endogenous depression. Journal of Nervous and Mental Disease, 173, 470-476. doi:
http://dx.doi.org/10.1097/00005053-198508000-00003
Coryell, W., Winokur, G., Shea, T., Maser, J. D., Endicott, J., Hagpop, S., & Akiskal, H. S.
(1994). The long-term stability of depressive subtypes. American Journal of Psychiatry,
151, 199-204. doi: http://dx.doi.org/10.1176/ajp.151.2.199
Couyoumdjian, A., Ottaviani, C., Trincas, R., Spitoni, G., Tenore, K., & Mancini, F. (2012). The
role of personal goals in depressive reaction to adverse life events. Scientific World
Journal, 2012, 1-8. doi: http://dx.doi.org/10.1100/2012/810341
Cronbach, L. J., (1951). Coefficient alpha and the internal structure of tests. Psychometrika,
16(3), 297-334. doi: http://dx.doi.org/10.1007/BF02310555
Derogatis, L. R. (1983). SCL-90-R: Administration, Scoring, and Procedures Manual, II.
Towson, Maryland: Clinical Psychometric Research.
Dohrenwend, B. S., Krasnoff, L., Askenasy, A. R., & Dohrenwend, B. P. (1978).
Exemplification of a method for scaling life events: The PERI life events scale. Journal
of Health and Social Behavior, 19, 205-229. doi: http://dx.doi.org/10.2307/2136536
Dolan, R. J., Calloway, S. P., Fonag, P., deSouza, F. V. A., & Wakeling, A. (1985). Life events,
depression, and hypothalamic-pituitary-adrenal axis function. British Journal of
Psychiatry, 147, 429-433. doi: http://dx.doi.org/10.1192/bjp.147.4.429
Eaton, W. W., Smith, C., Ybarra, M., Muntaner, C., Tien, A. (2004). Center for Epidemiologic
Studies Depression Scale: review and revision (CESD and CESD-R). In M. E. Maruish
(Ed.), The use of psychological testing for treatment planning and outcomes assessment
(3rd Ed.), (pp. 363-377). Mahwah, NJ: Lawrence Erlbaum.

Fava, G. A. (1983). Assessing depressive symptoms across cultures: Italian validation of the
CES-D self-rating scale. Journal of Clinical Psychology, 39(2), 249-251. doi:
http://dx.doi.org/10.1002/1097-4679(198303)39:2<249::AID-
JCLP2270390218>3.0.CO;2-Y
Fennig, S., Naisberg-Fennig, S., Craig, T. J., Tanenberg-Karant, M., & Bromet, E. J. (1996).
Comparison of clinical and research diagnoses of substance use disorders in first-
admission psychotic sample. American Journal on Addictions, 5(1), 40-48. doi:
http://dx.doi.org/10.1111/j.1521-0391.1996.tb00282.x
Finlay-Jones, R., & Brown, G. W. (1981). Types of stressful life events and the onset of anxiety
and depressive disorders. Psychological Medicine, 11, 803-815. doi:
http://dx.doi.org/10.1017/S0033291700041301
First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B. W. (2002). Structured Clinical
Interview for DSM-IV-TR Axis I Disorders-Patient Edition (SCID-I/P, 11/2002 revision).
New York: New York State Psychiatric Unit, Biometrics Research Department.
Fisher, R. A. (1921). On the “probable error” of a coefficient of correlation deduced from a small
sample. Metron, 1, 205-235.
Fountoulakis, K. N., Iacovides, A., Kaprinis, S., & Kaprinis, G. (2006). Life events and clinical
subtypes of major depression: A cross-sectional study. Psychiatry Research, 143, 235-
244. doi: http://dx.doi.org/10.1016/j.psychres.2005.09.018
Frank, E., Anderson, B., Reynolds, C. F., Ritenour, A., & Kupfer, D. J. (1994). Life events and
the Research Diagnostic Criteria endogenous subtype. Archives of General Psychiatry,
51, 519-524. doi: http://dx.doi.org/10.1001/archpsyc.1994.03950070011005

Fredrickson, B. L. (2001). The role of positive emotions in positive psychology: The broaden-
and-build theory of positive emotions. American Psychologist, 57, 218-226. doi:
http://dx.doi.org/10.1037/0003-066X.56.3.218
Frijda, N. H. (1986). The emotions. New York: Cambridge University Press.
Gilbert, P. (1992). Depression: The evolution of powerlessness. New York: Guilford.
Gilbert, P. (2013). Depression: The challenges of an integrative biopsychosocial evolutionary
approach. In M. Power (Ed.), The Wiley-Blackwell handbook of mood disorders (pp. 229-
288). West Sussex, UK: John Wiley & Sons. doi:
http://dx.doi.org/10.1002/9781118316153.ch10
Giosan, C., Muresan, V., & Moldovan, R. (2014). Cognitive evolutionary therapy for depression:
A case study. Clinical Case Reports, 2(5), 228-236. doi:
http://dx.doi.org/10.1002/ccr3.131
Giosan, C., Cobeanu, O., Mogoase, C., Muresan, V., Malta, L. S., Wyka, K., Szentagotai, A.
(2014). Evolutionary cognitive therapy versus standard cognitive therapy for depression:
A protocol for a blinded, randomized, superiority clinical trial. Trials, 15(83), 1-12. doi:
http://dx.doi.org/10.1186/1745-6215-15-83
Goodman, S. H., & Brand, S. H. (2009). Depression and early adverse experiences. In I. H.
Gotlib & C. L. Hammen, (Eds.) Handbook of Depression (2nd ed.), pp. 249-274. New
York, NY: The Guilford Press.
Gotlib, I. H., & Hammen, C. L. (2009). Handbook of Depression (2nd ed.). New York, NY: The
Guilford Press.
Grant, I., Gerst, M., & Yager, J. (1976). Scaling of life events by psychiatric patients and
normals. Journal of Psychosomatic Research, 20, 141-149. doi:
http://dx.doi.org/10.1016/0022-3999(76)90041-6
Hagen, E. H. (1999). The functions of postpartum depression. Evolution and Human Behavior,
20, 325-359. doi: http://dx.doi.org/10.1016/S1090-5138(99)00016-1
Hamilton, M. (1960). A rating scale for depression. Journal of Neurology, Neurosurgery, and
Psychiatry, 23, 56-62. doi: http://dx.doi.org/10.1136/jnnp.23.1.56
Hammen, C. (2005). Stress and depression. Annual Review of Clinical Psychology, 1, 293-319.
doi: http://dx.doi.org/10.1146/annurev.clinpsy.1.102803.143938
Hammen, C. L. (2009). Children of depressed parents. In I. H. Gotlib & C. L. Hammen, (Eds.)
Handbook of Depression (2nd ed.), pp. 275-297. New York, NY: The Guilford Press.
Hathaway, S. R., & McKinley, J. C. (1942). A multiphasic personality schedule (Minnesota): III,
The measurement of symptomatic depression. Journal of Psychology, 14, 73-84. doi:
http://dx.doi.org/10.1080/00223980.1942.9917111
Hayes, A. F., Cai, L. (2007). Using heteroscedasticity-consistent standard error estimators in
OLS regression: an introduction and software implementation. Behavior Research
Methods, 4, 709-722. doi: http://dx.doi.org/10.3758/BF03192961
Helgeson, V. S., Fritz, H. L. (1999). Unmitigated agency and unmitigated communion:
Distinctions from agency and communion. Journal of Research in Personality, 33, 131-
158. doi: http://dx.doi.org/10.1006/jrpe.1999.2241
Henry, B., Moffitt, T. E., Caspi, A., Langley, J., & Silva, P. A. (1994). On the "remembrance of
things past": A longitudinal evaluation of the retrospective method. Psychological
Assessment, 6, 92-101. doi: http://dx.doi.org/10.1037/1040-3590.6.2.92
Hill, D. (1968). Depression: Disease, reaction, or posture. American Journal of Psychiatry, 125,
445-456. doi: http://dx.doi.org/10.1176/ajp.125.4.445

Hoffman, L., & Rovine, M. J. (2007). Multilevel models for the experimental psychologist:
Foundations and illustrative examples. Behavior Research Methods, 39(1), 101-117. doi:
http://dx.doi.org/10.3758/BF03192848
Huber, P. J. (1967). The behavior of maximum likelihood estimates under non-standard
conditions. In Proceedings of the Fifth Berkeley Symposium on Mathematical Statistics
and Probability (pp. 221-233). Berkeley, CA: University of California Press.
Ingram, R. E., & Siegle, G. J. (2009). Methodological issues in the study of depression. In I. H.
Gotlib & C. L. Hammen, (Eds.) Handbook of Depression (2nd ed.), pp. 69-92. New York,
NY: The Guilford Press.
Izard, C. E. (1977). Human emotions. New York: Plenum. doi: http://dx.doi.org/10.1007/978-1-
4899-2209-0
Joiner, T. E., & Timmons, K. A. (2009). Depression in its interpersonal context. In I. H. Gotlib &
C. L. Hammen, (Eds.), Handbook of Depression (2nd ed.), pp. 322-339. New York, NY:
The Guilford Press.
Joorman, J. (2009). Cognitive aspects of depression. In I. H. Gotlib & C. L. Hammen, (Eds.)
Handbook of Depression (2nd ed.), pp. 298-321. New York, NY: The Guilford Press.
Judd, L., Akiskal, H. S., & Paulus, M. (1997). The role and clinical significance of subsyndromal
depressive symptoms (SDS) in unipolar major depressive disorder. Journal of Affective
Disorders, 45, 5-18.
Judd, L. L., Schettler, P. J., & Akiskal, H. S. (2002). The prevalence, clinical relevance, and
public health significance of subthreshold depressions. Psychiatric Clinics of North
America, 25(4), 685-698.
Katschnig, H., Pakesch, G., & Egger-Zeidner, E. (1986). Life stress and depressive subtypes: A
review of present diagnostic criteria and recent research results. In H. Katschnig (Ed.)
Life events and psychiatric disorders—Controversial issues (pp. 201-245). Cambridge,
UK: Cambridge University Press.
Keller, M. C., & Nesse, R. M. (2005). Is low mood an adaptation? Evidence for subtypes with
symptoms that match precipitants. Journal of Affective Disorders, 86, 27-35. doi:
http://dx.doi.org/10.1016/j.jad.2004.12.005
Keller, M. C. (2005). Event Coding Book. Retrieved January 2, 2009, from
http://matthewckeller.com/EventCodingBook.xls
Keller, M. C., & Nesse, R. M. (2006). The evolutionary significance of depressive symptoms:
different adverse situations lead to different depressive symptom patterns. Journal of
Personality and Social Psychology, 91(2), 316-330. doi: http://dx.doi.org/10.1037/0022-
3514.91.2.316
Keller, M. C., Neale, M. C., & Kendler, K. S. (2007). Association of different ALEs with distinct
patterns of depressive symptoms. American Journal of Psychiatry, 164(10), 1521-1529.
doi: http://dx.doi.org/10.1176/appi.ajp.2007.06091564
Kendler, K. S., Gardner, C. O., & Prescott, C. A. (2002). Toward a comprehensive
developmental model for major depression. American Journal of Psychiatry, 159, 1133-
1145. doi: http://dx.doi.org/10.1176/appi.ajp.159.7.1133
Kendler, K. S., Karkowski, L. M., Prescott, C. A. (1999). Causal relationship between stressful
life events and the onset of major depression. American Journal of Psychiatry, 156, 837-
841. doi: http://dx.doi.org/10.1176/ajp.156.6.837
Kendler, K. S., & Prescott, C. A. (2006). Genes, environment, and psychopathology:
understanding the causes of psychiatric and substance use disorders. New York:
Guilford.
Kennair, L. E. O. (2003). Evolutionary psychology and psychopathology. Current Opinion in
Psychology, 16, 691-699. doi: http://dx.doi.org/10.1097/00001504-200311000-00015
Klinger, E. (1975). Consequences of commitment to and disengagement from incentives.
Psychological Review, 82(1), 1-25. doi: http://dx.doi.org/10.1037/h0076171
Kranzler, H. R., Kadden, R. M., Burleson, J. A., Babor, T. F., Apter, A., & Rounsaville, B. J.
(1995). Validity of psychiatric diagnoses in patients with substance use disorders: Is the
disorder more important than the interviewer? Comprehensive Psychiatry, 36(4), 278-
288. doi: http://dx.doi.org/10.1016/S0010-440X(95)90073-X
Kranzler, H. R., Kadden, R. M., Babor, T. F., Tennen, H., & Rounsaville, B. J. (1996). Validity
of the SCID in substance abuse patients. Addiction, 91(6), 859-868. doi:
http://dx.doi.org/10.1046/j.1360-0443.1996.91685911.x
Labbot, S. M., Martin, R. B., Eason, P. S., & Berkey, E. Y. (1991). Social reactions to the
expression of emotion. Cognition and Emotion, 5, 397-417. doi:
http://dx.doi.org/10.1080/02699939108411050
Landis, J. R., & Koch, G. G. (1977). The measurement of observer agreement for categorical
data. Biometrics, 33, 159-174. doi: http://dx.doi.org/10.2307/2529310
Lazarus, R. S., Konner, A. D., & Folkman, S. (1980). Emotions: A cognitive-phenoneurological
analysis. In R. Plutchik & H. Kellerman (Eds.), Theories of emotion. Emotion: Theory,
research, and experience (pp. 189-215). New York: Academic Press. doi:
http://dx.doi.org/10.1016/B978-0-12-558701-3.50014-4
Levinson, D. F. (2005). The genetics of depression: A review. Biological Psychiatry, (50)2, 84-
92.
Lewis, A. J. (1934). Melancholia: A clinical survey of depressive states. Journal of Mental
Science, 80, 277-378. doi: http://dx.doi.org/10.1192/bjp.80.329.277

Little, R. J. A., & Rubin, D. B. (1987). Statistical analysis with missing data. New York, NY:
John Wiley and Sons.
Lloyd, C. (1980). Life events and depressive disorder reviewed: II. Events as precipitating
factors. Archives of General Psychiatry, 37, 541-548. doi:
Lobbestael, J., Leurgans, M., & Arntz, A. (2011). Inter-rater reliability of the Structured Clinical
Interview for DSM-IV Axis I Disorders (SCID I) and Axis II Disorders (SCID II)
Clinical Psychology and Psychotherapy, 18, 75-79. doi:
http://dx.doi.org/10.1002/cpp.693
Maas, C. J. M., & Hox, J. J., (2004). The influence of violations of assumptions on multilevel
parameter estimates and their standard errors. Computational Statistics and Data
Analysis, 46, 427-440. doi: http://dx.doi.org/10.1016/j.csda.2003.08.006
Matussek, P., & Neuner, R. (1981). Loss events preceding endogenous and neurotic depressions.
Acta Psychiatrica Scandinavica, 64, 340-350. doi: http://dx.doi.org/10.1111/j.1600-
0447.1981.tb00791.x
Mazure, C. M. (1998). Life stressors as risk factors in depression. Clinical Psychology: Science
and Practice, 5(3), 291-313. doi: http://dx.doi.org/10.1111/j.1468-2850.1998.tb00151.x
Mitchell, P. B., Parker, G. B., Gladstone, G. L., Wihelm, K., & Austin, M. P. (2003). Severity of
stressful life events in first and subsequent episodes of depression: The relevance of
depressive subtype. Journal of Affective Disorders, 73(3), 245-252. doi:
http://dx.doi.org/10.1016/S0165-0327(01)00479-7
Monroe, S. M. (1990). Psychosocial factors in anxiety and depression. In J. D. Maser & C. R.
Cloninger (Eds.), Comorbidity in anxiety and mood disorders (pp. 463-497). Washington,
DC: American Psychiatric Press.

Monroe, S. M., & Depue, R. A. (1991). Life stress and depression. In J. Becker & A. Kleinman
(Eds.), Psychosocial aspects of depression (pp. 101-130). Hillsdale, NJ: Erlbaum.
Monroe, S. M., Harkness, K., Simons, A. D., Thase, M. E. (2001). Life stress and the symptoms
of major depression. Journal of Nervous and Mental Disease, 189(3), 168-175. doi:
http://dx.doi.org/10.1097/00005053-200103000-00005
Monroe, S. M., Slavich, G. M, Georgiades, K. (2009). The social environment and life stress in
depression. In I. H. Gotlib & C. L. Hammen, (Eds.) Handbook of Depression (2nd ed.),
pp. 340-360. New York, NY: The Guilford Press.
Monroe, S. M., Thase, M. E., Hersen, M., Himmelhoch, J. M., & Bellack, A. S. (1985). Life
events and the endogenous-nonendogenous distinction in the treatment and posttreatment
course of depression. Comprehensive Psychiatry, 26, 175-184. doi:
http://dx.doi.org/10.1016/0010-440X(85)90038-0
Monroe, S. M., & Simons, A. D. (1991). Diathesis-stress theories in the context of life stress
research: Implications for depressive disorders. Psychological Bulletin, 110(3), 406-425.
doi: http://dx.doi.org/10.1037/0033-2909.110.3.406
Moscicki, E. K. (2001). Epidemiology of completed and attempted suicide: toward a new
framework for prevention. Clinical Neuroscience Research, 1, 310-323. doi:
http://dx.doi.org/10.1016/S1566-2772(01)00032-9
Muscatell, K. A., Slavich, G. M., Monroe, S. M., & Gotlib, I. H. (2009). Stressful life events,
chronic difficulties, and the symptoms of clinical depression. Journal of Nervous and
Mental Disease, 197(3), 154-160. doi:
http://dx.doi.org/10.1097/NMD.0b013e318199f77b
Muthén, L. K., & Muthén, B. O. (1998-2002). Mplus User’s Guide (7th ed.) Los Angeles, CA:
Muthén & Muthén.

Nesse, R. M. (1990). Evolutionary explanations of emotions. Human Nature, 1(3), 261-289. doi:
http://dx.doi.org/10.1007/BF02733986
Nesse, R. M. (2000). Is depression an adaptation? Archives of General Psychiatry, 57, 14-20.
doi: http://dx.doi.org/10.1001/archpsyc.57.1.14
Nesse, R. M. (2005). Natural selection and the regulation of defenses: A signal detection analysis
of the smoke detector principle. Evolution and Human Behavior, 26, 88-105. doi:
http://dx.doi.org/10.1016/j.evolhumbehav.2004.08.002
Nesse, R. M. (2009). Explaining depression: Neuroscience is not enough, evolution is essential.
In C. M. Pariente, R. M. Nesse, D. Nutt, & L. Wolpert (Eds.), Understanding depression:
A translational approach (pp. 17-35). New York, NY: Oxford University Press. doi:
http://dx.doi.org/10.1093/med/9780199533077.003.0003
Nesse, R. M. (2009). Why does depression exist at all? Practical implications of an evolutionary
explanation for mood. Grand Rounds. Archives of the Department of Psychiatry,
University of Michigan, Ann Arbor, MI. Retrieved from
http://www.randolphnesse.com/videos
Nesse, R. M., & Williams, G. C. (1994). Why we get sick: The new science of Darwinian
medicine. New York, NY: Times Books.
Oquendo, M. A., Barrera, A., Ellis, S. P., Li, S., Burke, A. K., Grunebaum, M., . . . Mann, J. J.
(2004). Instability of symptoms in recurrent major depression: A prospective study.
American Journal of Psychiatry, 161, 255-261. doi:
http://dx.doi.org/10.1176/appi.ajp.161.2.255
Paykel, E. S. (1982). Life events and early environment. In E. S. Paykel (Ed.), Handbook of
affective disorders. New York: Guilford Press.

Paykel, E. S. (1983). Methodological aspects of life events research. Journal of Psychosomatic
Research, 27, 341-352. doi: http://dx.doi.org/10.1016/0022-3999(83)90065-X
Paykel, E. S. (1997). The Interview for Recent Life Events. Psychological Medicine, 27(2), 301-
310. doi: http://dx.doi.org/10.1017/S0033291796004424
Paykel, E. S. (2003). Life events and affective disorders. Acta Psychiatrica Scandinavica, 108,
61-66. doi: http://dx.doi.org/10.1034/j.1600-0447.108.s418.13.x
Paykel, E. S., Myers, J. K., Dienelt, M. N., Klerman, G. L., Lindenthal, J. J., & Pepper, M. P.
(1969). Life events and depression: A controlled study. Archives of General Psychiatry,
21, 753-760. doi: http://dx.doi.org/10.1001/archpsyc.1969.01740240113014
Paykel, E. S., Rao, B. M., & Taylor, C. N. (1984). Life stress and symptom patterns in out-
patient depression. Psychological Medicine, 14, 559-568. doi:
http://dx.doi.org/10.1017/S0033291700015166
Plutchik, R. (1980). Emotion: A psychoevolutionary synthesis. New York: Harper and Row.
Powles, W. E. (1992). Human development and homeostasis: The science of psychiatry. Madison
CT: International Universities Press.
Price, J., Sloman, L., Gardner, R., Gilbert, P., & Rohde, P. (1994). The social competition
hypothesis of depression. British Journal of Psychiatry, 164, 309-315. doi:
http://dx.doi.org/10.1192/bjp.164.3.309
Qualtrics Labs, Inc. (2012). Qualtrics Survey Software (Version 52716). Available from
Qualtrics website: http://www.qualtrics.com/academic-solutions/usc-rossier-school-of-
education.
Radloff, L. S. (1977). The CES-D scale: a self-report depression scale for research in the general
population. Applied Psychological Measurement, 1, 385-401. doi:
http://dx.doi.org/10.1177/014662167700100306
Raftery, A. L. (1995). Bayesian model selection in social research. Sociological Methodology,
25, 111-163. doi: http://dx.doi.org/10.2307/271063
Raine, A., & Benishay, D. (1995). The SPQ-B: A brief screening instrument for schizotypal
personality disorder. Journal of Personality Disorders, 9, 346-355. doi:
http://dx.doi.org/10.1521/pedi.1995.9.4.346
Ree, M. J., Macleod, C., French, D., & Locke, V. (2000, November). The State-Trait Inventory
for Cognitive and Somatic Anxiety: Development and validation. Poster session presented
at the annual meeting of the Association for the Advancement of Behavior Therapy, New
Orleans, LA
Ross, M., & Fletcher, G. J. O. (1985). Attribution and social perception. In G. Lindzey & E.
Aronson (Eds.), The handbook of social psychology (3rd ed.) (pp. 73-122). Reading, MA:
Addison-Wessley.
Roy, A., Breier, A., Doran, A. R., & Pickar, D. (1985). Life events in depression: Relationships
to subtypes. Journal of Affective Disorders, 9, 143-148. doi:
http://dx.doi.org/10.1016/0165-0327(85)90093-X
Sadek, N, & Bona, J. (2000). Subsyndromal symptomatic depression: A new concept.
Depression and Anxiety, 12(1), 30-39. doi: http://dx.doi.org/10.1002/1520-
6394(2000)12:1<30::AID-DA4>3.0.CO;2-P
Savalei, V. (2014). Understanding robust corrections in structural equation modeling. Structural
Equation Modeling: A Multidisciplinary Journal, 21, 149-160. doi:
http://dx.doi.org/10.1080/10705511.2013.824793
Schwarz, G. (1978). Estimating the dimension of a model. The Annals of Statistics, 6(2), 461-
464. doi: http://dx.doi.org/10.1214/aos/1176344136

Schwarz, N., & Sudman, S. (1994). Autobiographical memory and the validity of retrospective
reports. New York, NY: Spring-Verlag. doi: http://dx.doi.org/10.1007/978-1-4612-2624-
Shear, M. K., Greeno, C., Kang, J., Ludewig, D., Frank, E., Swartz, H. A., & Hanekamp, M.
(2000). Diagnosis of nonpsychotic patients in community clinics. American Journal of
Psychiatry, 157, 581-587. Psychiatry, 157, 581-587.
doi: http://dx.doi.org/10.1176/appi.ajp.157.4.581
Siegert, R. (2003). Clinical Psychology and Evolutionary Psychology: Strange Bedfellows?. In
K. Sterelny, & J. Fitness (Eds.), From Mating to Mentality: Evaluating Evolutionary
Psychology (pp. 227-246). New York, NY: Psychology Press.
Singer, J. D., & Willett, J. B., (2003). Applied longitudinal data analysis: Modeling change and
event occurrence. New York, NY: Oxford University Press. doi:
http://dx.doi.org/10.1093/acprof:oso/9780195152968.001.0001
Smith, R. E., Leffingwell, T. R., & Ptacek, J. T. (1999). Can people remember how they coped?
Factors associated with discordance between same-day and retrospective reports. Journal
of Personality and Social Psychology, 76, 1050-1061. doi:
http://dx.doi.org/10.1037/0022-3514.76.6.1050
Soszynski, D. (2003). The pathogenesis and the adaptive value of fever. Postepy Higieny I
Medycyny Doswiadczalnej, 57, 531-554.
Spitzer, R. L. (1983). Psychiatric Diagnosis: Are clinicans still necessary? Comprehensive
Psychiatry, 24(5), 399-411. doi: http://dx.doi.org/10.1016/0010-440X(83)90032-9
Spitzer, R. L., & Williams, J. B. W. (1985). Structured Clinical Interview for DSM-III-R (SCID).
New York: New York State Psychiatric Institute, Biometrics Research.

Steiger, J. H. (1980). Tests for comparing elements of a correlation matrix. Psychological
Bulletin, 87(2), 245-251. doi: http://dx.doi.org/10.1037/0033-2909.87.2.245
Steiner, J. L., Tebes, J. K., Sledge, W. H., & Walker, M. L. (1995). A comparison of the
structured clinical interview for DSM-III-R and clinical diagnoses. Journal of Nervous
and Mental Disorder, 183(6), 365-369. doi: http://dx.doi.org/10.1097/00005053-
199506000-00003
Strongman, K. T. (1987). The psychology of emotion. New York: Wiley Press.
Tanouye, E. (2001, June 13). Depression takes annual toll of $70 billion on employers. The Wall
Street Journal. Retrieved from http://www.wsj.com/articles/SB992387505347125993
Tennant, C. (2002). Life events, stress, and depression: A review of recent findings. The
Australian and New Zealand Journal of Psychiatry, 36(2), 173-182. doi:
http://dx.doi.org/10.1046/j.1440-1614.2002.01007.x
Tomkins, S. S. (1980). Affect as amplification: Some modifications in theory. In R. Plutchik &
H. Kellerman (Eds.), Theories of emotion. Emotion: Theory, research, and experience
(Vol. 1, pp. 141-164). New York: Academic Press. doi: http://dx.doi.org/10.1016/B978-
0-12-558701-3.50012-0
Thase, M. E. (2009). Neurobiological aspects of depression. In I. H. Gotlib & C. L. Hammen,
(Eds.) Handbook of Depression (2nd ed.), pp. 187-217. New York, NY: The Guilford
Press.
Thomson, K. C., & Hendrie, H. C. (1972). Environmental stress in primary depressive illness.
Archives of General Psychiatry, 26, 130-132. doi:
Van Dam, N. T., & Earleywine, M. (2011). Validation of the Center for Epidemiologic Studies
Depression Scale—Revised (CESD-R): Pragmatic depression assessment in the general

population. Psychiatry Research, 186(1), 128-132. doi:
http://dx.doi.org/10.1016/j.psychres.2010.08.018
VandenBos, G. R. (Ed.). (2007). APA dictionary of psychology (1st ed.). Washington, DC:
American Psychological Association.
Watson, D., Clark, L. A., & Tellegen, A. (1988). Development and validation of brief measures
of positive and negative affect: The PANAS scales. Journal of Personality and Social
Psychology, 54(6), 1063-1070. doi: http://dx.doi.org/10.1037/0022-3514.54.6.1063
Watson, P. J., & Andrews, P. W. (2002). Toward a revised evolutionary adaptationist analysis of
depression: The social navigation hypothesis. Journal of Affective Disorders, 72, 1-14.
doi: http://dx.doi.org/10.1016/S0165-0327(01)00459-1
White, H. (1980). A heteroscedasticity–consistent covariance matrix estimator and a direct test
for heteroscedasticity. Econometrica, 48, 817-838. doi:
http://dx.doi.org/10.2307/1912934
White, H. (1982). Maximum likelihood estimation of misspecified models. Econometrica, 50, 1-
25. doi: http://dx.doi.org/10.2307/1912526
World Health Organization (2004). The World Health Report 2004: Changing History, Annex
Table 3: Burden of disease in DALYs by cause, sex, and mortality stratum in WHO
regions, estimates for 2002. Geneva: WHO.
Young, J. Z. (1979). Programs of the brain. Oxford: Oxford University Press.
Zanarini, M. C., Skodol, A. E., Bender, D., Dolan, R., Sanislow, C., Schaefer, E., et al. (2000).
The Collaborative Longitudinal Personality Disorders Study: reliability of axis I and II
disorders. Journal of Personality Disorders, 14(4), 291-299. doi:
http://dx.doi.org/10.1521/pedi.2000.14.4.291
Zimmerman, M., Coryell, W., & Pfohl, B. (1986). Validity of familial subtypes of primary
unipolar depression: Clinical, demographic, familial, and psychosocial correlates.
Archives of General Psychiatry, 43, 1090-1096. doi:
Zorn, C. (2006). Comparing GEE and robust standard errors for conditionally dependent data.
Political Research Quarterly, 59(3), 329-341. doi:
http://dx.doi.org/10.1177/106591290605900301
Zung, W. W. K. (1965). A self-rating depression scale. Archives of General Psychiatry, 12(1),
63-70. doi: http://dx.doi.org/10.1001/archpsyc.1965.01720310065008

APPENDIX A
Informed Consent Agreement

California School of Professional Psychology,

Alliant International University, San Diego
10455 Pomerado Road
San Diego, CA 92131
INFORMED CONSENT AGREEMENT
Daily Events and Mood
You are being asked to participate in a research study. Before giving your consent to participate
in this study, you must read this form and ask as many questions as is necessary for you to
understand what your participation will involve.
INVESTIGATORS
The principal investigator of this research study is Alissa Maitino, M.A. Miss Maitino is a
doctoral student in the Clinical Psychology Ph.D. Program at Alliant International University in
San Diego, California. Miss Maitino is conducting this study as part of her dissertation project.
Irwin Rosenfarb, Ph.D., is Miss Maitino’s dissertation supervisor. Dr. Rosenfarb is a licensed
psychologist (PSY 15174) and professor of psychology at Alliant International University in San
Diego, California.
Alissa Maitino, M.A. / (949) 235-6063 / alissamaitino@gmail.com

Irwin Rosenfarb, Ph.D. / (858) 635-4782 / irosenfa@alliant.edu
PURPOSE OF THE RESEARCH

This study is looking at the relationship between daily events and mood in order to increase our
understanding of the relationship between daily events and mood.
PROCEDURES TO BE FOLLOWED DURING THE RESEARCH

This study will take place primarily on the internet at a location of your choice over a period of
10 days. This study will include approximately 70 participants.
On day 1, you will complete a survey that includes questions about your mood along with a
demographic questionnaire. The demographic questionnaire includes questions about your age,
ethnicity, education, employment, psychological history, and family members’ psychological
history. In addition, the investigator will call you to answer any questions you have about the
study, and may ask you some additional questions about your mood and thoughts. Day 1
participation will take approximately 25 minutes.
On days 2 – 10, you will receive a daily text message prompt at a random time. The daily text
message prompt will contain the following statement: “Complete & submit your daily survey as
soon as possible within 3 hours.” (Please see the section below titled “Costs” for additional
information about these text messages.) When you receive the daily text message prompt, you
will be required to log on to the study website as soon as possible within 3 hours to complete
your daily survey. The daily survey will include questions about your mood and daily events
that were stressful for you. Two hours after you receive the daily text message prompt, you will
receive a follow-up text message that contains the following statement: “If you have not
submitted your daily survey, please do so as soon as possible.” On days 2 – 10, you will spend
approximately 8 - 10 minutes per day completing surveys. On the 10th and final day, you will
spend an additional 5 minutes completing a final survey that includes questions about your
mood.
RISKS
There are some risks involved in participating in this study. In particular, answering questions
about your mood or stressful events you have experienced may cause you to experience some
emotional discomfort. If you experience emotional discomfort, or any other unusual or
unexpected side effects during your participation, you may refuse to answer any question or stop
participating at any time. In addition, you should call the investigator to discuss what you are
experiencing. If necessary, the investigator will refer you for psychological help to a mental
health professional who provides low, medium, or high cost services, depending on your
preference. Please note that you will be financially responsible for any costs incurred for any
psychological help you receive. Again, your participation in this study is voluntary. You are not
required to participate in this study.
COSTS
There are some costs involved in participating in this study. One cost is your time. Over the
course of 10 days, you will spend approximately 2 hours participating in this study. A second
cost involves receiving telephone calls from the investigator. You will most likely only receive
one telephone call that lasts approximately 10 minutes. You are responsible for paying any
charges you incur for any telephone calls you receive related to this study. If you are not willing
and able to receive telephone calls and pay any charges you incur, do not participate in this
study. A third cost involves receiving text messages. You will receive approximately 20 text
messages over a period of 10 days. As a result, you must have a cellular phone with text
message capability in order to participate in this study. You will be financially responsible for
any charges you incur for receiving these text messages. If you are not willing and able to
receive approximately 20 text messages, and pay any charges you incur for receiving these text
messages, do not participate in this study.
INCENTIVES
There are some incentives for participating in this study. One incentive is that you could
participate in a raffle in which you could earn up to four $100 Visa gift cards. More specifically,
if you complete days 1 - 6 of the study, you will receive two raffle tickets. If you complete days
7 – 8, you will receive a third raffle ticket. If you complete days 9 - 10, you will receive a fourth
raffle ticket. At the end of the study, there will be a drawing for four raffle tickets. Each chosen
raffle ticket will be worth one $100 Visa gift card. This means that if you complete all 10 days
of the study, you could win up to four $100 Visa gift cards.
Another incentive is that you may be eligible for course credit/extra credit if the investigator
recruited you during a college/graduate class and your professor agreed to offer such credit for
your participation. Please note that you will have to fulfill the predetermined requirements in
order to receive such course credit/extra credit.
BENEFITS OF THE RESEARCH

You may benefit from participating in this study by learning about how psychological research
studies are conducted, and discovering more about the relationship between daily events and
mood. Both you and society may benefit from this study through a better understanding of the
mood states a person experiences following different types of daily events.
ALTERNATIVES TO THIS RESEARCH

The alternative is not to participate in this study.
CONFIDENTIALITY
You have a right to privacy. All information identifying you will remain confidential (private)
unless otherwise required by law. For example, if at any point during this study you indicate that
you are a danger to yourself or others, the investigators may be required to report this to the
appropriate authorities in order to keep you or other people safe. Aside from these types of
circumstances, the only individuals who will have access to your identifying information are the
study investigators, a research assistant who is a fellow doctoral student in the clinical
psychology program at Alliant International University, and members of the Institutional Review
Board at Alliant International University. With the exception of the Informed Consent
Agreement and the contact information form, the documents and surveys you complete during
this study will not contain your name or other identifying information. Instead, you will be
assigned a unique identification (ID) that will be listed on all of your surveys and documents. In
addition, the documents and surveys you complete will be kept separately from your Informed
Consent Agreement and contact information form.
With the exception of one possible phone interview (discussed below), you will complete all
documents and surveys online on a secure internet server. In order to ensure that your responses
remain private, you should complete each set of daily surveys in one sitting, and log off
completely if you are using a public computer. One week after your participation ends, your data
will be removed from the secure internet server and downloaded into two separate password-
protected files on a password-protected computer. One password-protected file will contain your
Informed Consent Agreement and contact information form while the other password-
protected file will contain all remaining documents and surveys. After all data for the study has
been collected and analyzed, it will be removed from the password-protected computer and
downloaded onto two separate password-protected external storage devices. The external
storage devices will be kept in two separate locked file cabinets. Within five years of the date
you sign this Informed Consent Agreement, the external storage devices will be destroyed.
The data you provide will only be presented to others when combined with the responses of other
participants. The results of this study may be published in scientific journals or presented at
professional meetings so long as you are not identified and cannot be reasonably identified by
doing so. Although extremely unlikely, it is possible that data could be subpoenaed by court
order. However, the circumstances required for this to happen are very rare.
It is possible that you will called by the principal investigator for a brief interview in which you
will be asked questions about your mood and thoughts. If so, your interview will be recorded to
make sure that the principal investigator has an accurate understanding of your mood and
thoughts. This will be accomplished by having a qualified colleague listen to your interview to
determine if he or she has the same understanding of your responses. The colleague will be
either the other investigator in this study or a research assistant who is a fellow doctoral student
in the clinical psychology Ph.D. program at Alliant International University. If you are
interviewed, the recording of your interview will only be used in conjunction with this study in
the manner described above. The recording will not contain your name or any other information
that might identify you such as your age, ethnicity, or background. Instead, you will be assigned
a unique identification (ID) that will be included in the recording. In addition, the recording will
be kept separately from all other documents and surveys you complete during this study. The
responses you provide will not be presented to others, published in scientific journals, or
presented at professional meetings. If you are interviewed, your interview will be recorded using
a portable digital recorder. Immediately following the interview, the recording will be removed
from the portable digital recorder and downloaded into a password-protected file on a password-
protected external storage device. The external storage device will be kept in a locked file
cabinet. Within five years of the date you provide consent, the external storage device will be
destroyed. Please note that by providing your consent to participate in this study, you are also
providing your consent to be audiotaped for the purposes of this study. If you are not willing to
be audiotaped for such purposes, do not provide your consent to participate in this study.
You will receive approximately one phone call and 18 - 24 text messages from the investigator
during your participation. The investigator will call you through her cellular telephone service
provider, Sprint, on her personal cellular telephone. As a result, Sprint will have records of a
phone call from the principal investigator to you. The investigator will send you text messages
via the internet through a company called MessageMedia, Inc. MessageMedia, Inc., a corporate
gateway provider, is a company that provides software that allows a person or business to send
text messages from their computer to another person’s cellular telephone. As a result,
MessageMedia, Inc. will have records of your phone number and the text messages you receive
from the principal investigator. However, MessageMedia, Inc. treats such information as strictly
confidential. MessageMedia, Inc. has a range of corporate clients (including but not limited to
UCLA, Coca Cola, HP, DELL, REMAX, and financial institutions), and adheres to strict
security and privacy policies. To learn more about MessageMedia, Inc., please visit their wesite
at http://www.message-media.com. To learn more about MessageMedia, Inc.’s privacy and
security policies, click the following link (or copy and paste it into your web browswer): <
http://files.message-media.com/docs/privacypolicy.pdf >. Please note that your cellular
telephone service provider will also have records of the phone calls and text messages that you
receive from the principal investigator.
PSYCHOLOGICAL TREATMENT
If you need psychological treatment while participating in this study, you should contact the
principal investigator, Alissa Maitino, who will make an appropriate referral. Miss Maitino can
be reached at (949) 235-6063. Miss Maitino can refer you to a mental health professional who
provides low, medium, or high cost services, depending on your preference. Please note that you
will be financially responsible for any costs incurred for any psychological help you receive.
Again, your participation in this study is voluntary. You are not required to participate in this
study. You may also call Dr. Irwin Rosenfarb at (858) 635-4782 between 8:00 AM and 4:00
PM. Should you have any additional concerns, please call the Institutional Review Board at
Alliant International University at (858) 635-4448 between 8:00 AM and 4:00 PM.
While you are participating in this study, you must agree to follow the instructions of the
research and to call the investigator immediately if you begin to experience emotional distress or
any unusual or unexpected side effects.
While enrolled in this study, you must agree not to participate in any other research studies at the
same time. Are you currently involved in any other research projects?
____YES ____NO
Please list any research studies in which you have participated over the last three months:
______________________________________________________________________________
______________________________________________________________________________
QUESTIONS ABOUT THE RESEARCH

If you have questions about this research or your participation, you may call Alissa Maitino at
(949) 235-6063 between 9:00 AM and 5:00 PM or Professor Irwin Rosenfarb at (858) 635-4782
between 8:00 AM and 4:00 PM. Should you have any additional concerns, please call the
Institutional Review Board at Alliant International University at (858) 635-4448 between 8:00
AM and 4:00 PM.
MANDATORY REPORTING OF CHILD, DEPENDENT ADULT, AND ELDER ABUSE

California law mandates the filing and reporting of reasonable suspicions of child, dependent
adult, and elder abuse. Participation in this research could result in the investigator being
required to report child, dependent adult, or elder abuse.
PARTICIPANT RIGHTS AND RESEARCH WITHDRAWAL

Your participation in this study is voluntary. You may refuse to participate in this study. If you
choose not to participate, you will not be penalized or lose benefits to which you are otherwise
entitled. In addition, you can end your participation at any point during the study by contacting
the investigator. Refusing to participate or ending your participation will not affect your
relationship with Alliant International University or any participating institution, website,
organization, or other entity. You may also refuse to answer any questions you do not wish to
answer.
We have tried to explain all the important details about this study to you. If you have any
questions that have not been answered here, please call the investigator for more information
before giving your consent to participate in this study.
To print a copy of this Informed Consent Agreement for your own records, click [here].
ACKNOWLEDGEMENT AND CONSENT TO PARTICIPATE

By clicking the I CONSENT link below, I am acknowledging that
I am at least 18 years of age.

I am a citizen of the United States of America, and I speak English fluently.
I have had a chance to ask questions to help me understand what my participation will involve.
I have read and understand all of the information in this Informed Consent Agreement.
I printed a copy of this Informed Consent Agreement for my own records.
I have been told that I can end my participation at any point during this study.
I agree to be audiotaped for the purposes of this study.
I agree to participate in this study until I decide otherwise.
[I CONSENT]
----------------------------------------------
For Research Office Only: IRB# _______
This study is valid from: _______ until _______

APPENDIX B
Demographic Questionnaire
Demographic Questionnaire
1. What is your last name? ___________________
2. What is your first name? ___________________
3. Attention: In order to participate in this study, you must have a United States cell phone
number from an actual cell phone that you will have with you throughout your participation.
If it is anything other than an actual cell phone that you will have with your throughout your
participation, you will be disqualified from participating. You will also be disqualified if it is
not a United States cell phone number. The cell phone number you provide will be used to
send you daily text messages indicating that it is time to complete your daily surveys.
Please provide the US cell phone number we should use to text and potentially call you
during your participation. Enter your 3 digit area code and 7 digit cell phone number in the
following format: XXX-XXX-XXXX.
________ - ________ - ____________
4. Please enter your current home address. Include the street address (including unit number, if
applicable), city, state, zip code, and country. NOTE: You must currently live in the United
States to participate in this study.
Street Address _____________________________
Unit/Apt. #
(if applicable) _____________________________
City _____________________________
State _____________________________
Zip Code _____________________________
Country _____________________________
5. Please enter an email address we can use to contact you (if necessary) during your
participation, and about the raffle ticket results after your participation.
________________________________
6. What is your age? _________
7. What is your gender?
Male
Female
8. Which category best represents your ethnicity?
African American / Black
Latino / Hispanic American
Non-Hispanic White / Caucasian / European American
Middle Eastern / Arab / Arab American
Asian / Asian American
Native Hawaiian / other Pacific Islander
Native American / American Indian / Alaskan Native
Indian / Asian Indian / East Indian / Indian American
Other (please specify) ____________________
9. Which category best represents your racial heritage?
White / Caucasian
African American / Black
Asian
Native Hawaiian / other Pacific Islander
Native American / American Indian / Alaskan Native

10. What is your marital/relationship status?
Single
Married / Civil Union / Domestic partnership
Separated
Divorced
Widowed
11. What is the highest level of education you have completed?
Less than High School
Some High School
High School / GED
Some College
Vocational or Professional Certificate
Associate's Degree
Bachelor's Degree
Master's Degree
Doctoral Degree
Professional Degree (JD, MD, etc.)
12. Are you currently employed?
Yes
No
13. What is your occupation? ______________________________

14. Are you currently a student?
Yes
No
15. What level of education are you currently pursuing?
Less than High School
High School / GED
Some College
Vocational or Professional Certificate
Associate's Degree
Bachelor's Degree
Master's Degree
Doctoral Degree
Professional Degree (JD, MD, etc.)
16. Have you ever been diagnosed with Schizophrenia, Schizoaffective Disorder, or any type
of Psychotic Disorder?
Yes
No
17. Have you ever been diagnosed with any other psychological disorders or substance use
disorders? Some examples of psychological disorders and substance use disorders include
the following: Major Depressive Disorder (Depression), Bipolar Disorder (Manic-
Depression), Schizophrenia, Generalized Anxiety Disorder, Borderline Personality Disorder,
Panic Disorder, Alcohol Abuse or Dependence, Opioid Abuse or Dependence, Cocaine
Abuse or Dependence, and Post-Traumatic Stress Disorder (PTSD).
Yes
No
18. You indicated that you have been diagnosed with one or more psychological disorders or
substance use disorders. Please answer the following questions about each disorder.
What is the name of Are you currently If not, when was the
disorder? experiencing this last time? (Please
disorder? specify whether
your answer is in
weeks, months, or
years.)
Psychological
Disorder # 1
Psychological
Disorder # 2
Psychological
Disorder # 3
Psychological
Disorder # 4
Psychological
Disorder # 5
Psychological
Disorder # 6
Psychological
Disorder # 7
Psychological
Disorder # 8
Psychological
Disorder # 9
Psychological
Disorder # 10
19. Do you currently drink alcohol or take drugs (illegal or prescription)? Please DO NOT
include medications that you take as prescribed.
Yes
No
20. You indicated that you currently drink alcohol or take drugs. Please answer the following
questions about each substance you currently use. Begin with the substances you use the
most.
What is the Do you have or About how many On a typical day that
substance? think you may days per month you use this
have a problem do you use this substance, how much
with this substance? do you use (e.g., five
substance? beers, 2 grams
cocaine, etc.)?
Substance # 1
Substance # 2
Substance # 3
Substance # 4
Substance # 5
Substance # 6
Substance # 7
Substance # 8
Substance # 9
Substance # 10
21. Are you currently taking any prescribed medication(s)?
Yes
No
22. Please answer the following questions about the prescribed medication(s) you are currently
taking. Please be as specific and accurate as possible.
What is the name of What issue is the medication How often do you
the medication? supposed to be treating? take the medication?
Medication # 1
Medication # 2
Medication # 3
Medication # 4
Medication # 5
Medication # 6
Medication # 7
Medication # 8
Medication # 9
Medication # 10
23. Are you currently seeing a psychologist, psychiatrist, or any other type of mental health
professional?
* NOTE * Some examples of mental health professionals include the following:
psychiatrists, psychologists, psychoanalysts, marital and family therapist, nurse
psychotherapist, psychiatric/mental health nurse, clinical social worker, certified alcohol and
drug abuse counselor, pastoral counselor, licensed professional counselor, mental
health counselor, etc.
Yes
No
24. Please answer the questions below about the mental health professional(s) you are currently
seeing. Please be as specific and accurate as possible. Some examples of mental health
professionals include the following: psychiatrist, psychologist, psychoanalyst, marital and
family therapist, nurse psychotherapist, psychiatric/mental health nurse, clinical social
worker, certified alcohol and drug abuse counselor, pastoral counselor, licensed professional
counselor, and mental health counselor.
What type of mental health Are you seeing How often do you
professional are you seeing? this person for see this person?
depression?
Mental Health
Professional # 1
Mental Health
Professional # 2
Mental Health
Professional # 3
Mental Health
Professional # 4
Mental Health
Professional # 5
Mental Health
Professional # 6
Mental Health
Professional # 7
Mental Health
Professional # 8
Mental Health
Professional # 9
Mental Health
Professional # 10
APPENDIX C
Center for Epidemiologic Studies Depression Scale - Revised

Center for Epidemiologic Studies Depression Scale – Revised
Last Week
Not at Nearly
Below is a list of the ways you might have felt or
all or every
behaved. Please check the boxes to tell me how 1–2 3–4 5–7
Less day for
often you have felt this way in the past week or so. days days days
than 1 2 weeks
day
My appetite was poor. 0 1 2 3 4
I could not shake off the blues. 0 1 2 3 4
I had trouble keeping my mind on what I was doing. 0 1 2 3 4
I felt depressed. 0 1 2 3 4
My sleep was restless. 0 1 2 3 4
I felt sad. 0 1 2 3 4
I could not get going. 0 1 2 3 4
Nothing made me happy. 0 1 2 3 4
I felt like a bad person. 0 1 2 3 4
I lost interest in my usual activities. 0 1 2 3 4
I slept more than usual. 0 1 2 3 4
I felt like I was moving too slowly. 0 1 2 3 4
I felt fidgety. 0 1 2 3 4
I wished I were dead. 0 1 2 3 4
I wanted to hurt myself. 0 1 2 3 4
I was tired all the time. 0 1 2 3 4
I did not like myself. 0 1 2 3 4
I lost a lot of weight without trying to. 0 1 2 3 4
I had a lot of trouble getting to sleep. 0 1 2 3 4
I could not focus on the important things. 0 1 2 3 4
APPENDIX D
Depressive Symptoms Scale: Instructions, Scales, and Items

Depressive Symptoms Scale: Instructions, Scales, and Items
Instructions: Please think carefully about how you are feeling. After each statement, indicate
the extent to which you feel the way described. Remember: (a) all responses are completely
anonymous, so be as honest as possible; (b) answer each item separately from all others, even if
some questions seem redundant; (c) there are no right or wrong answers; try to indicate how you
actually feel rather than how you think you “should” feel.
1 = Not at all 2 = A little bit 3 = Moderately 4 = Quite a bit 5 = Extremely
Scales and Items
Emotional Pain
1. I feel really sad.
2. I “hurt” inside, even though the pain isn’t physical.
3. I feel fine emotionally.
4. I am in agony.
5. I am free from emotional pain.
Pessimism
6. Things seem hopeless.
7. I feel pessimistic about the future.
8. I feel like things are going to turn out really well.
9. I feel discouraged about things.
10. I feel hopeful for the future.
Fatigue
11. I feel as energetic as I normally do.
12. Everything seems like such an effort.
13. I feel active and full of “pep.”
14. I can’t “get going.”
15. It is easy to get a lot of things done.
Anhedonia
16. I am still able to feel happy.
17. I enjoy life.
18. Nothing can make me smile.
19. Things that normally give me joy continue to give me joy.
20. I am incapable of feeling anything pleasant.
Rumination
21. I can’t “let go” of certain thoughts.
22. I am able to clear problems from my mind.
23. I think about how I could have done things differently.
24. I catch myself thinking about the same issue.
Crying
25. I feel like crying.
26. I cry really hard.
27. I get teary-eyed.
28. I sob.
29. I take effort to fight off tears.
Guilt
30. I feel ashamed.
31. I feel guilt-free.
32. I am angry at myself.
33. Rational or not, I blame myself.
Low Appetite
34. The thought of food is not appealing.
35. I don’t have my normal appetite.
36. Food doesn’t taste as good as it usually does.
Anxiety
37. I am free from fear.
38. Things make me nervous.
39. I am free from worrying.
40. I am more afraid than usual.
41. I feel anxious.
Sleepiness
42. I want to sleep all day.
43. I sleep more than I normally do.
44. I feel sleepy even though I’ve had plenty of sleep.
Desire for Social Support
45. I feel like having a heart-to-heart with a close friend or relative.
46. I want to share how I feel with someone.
47. I want to be with close friends or family for support
APPENDIX E
Modified Version of the Depressive Symptoms Scale

Modified Version of the Depressive Symptoms Scale
Instructions: Please think carefully about how you have been feeling since the last time you
completed this questionnaire (yesterday). If you did not complete this questionnaire yesterday,
then please think about how you have been feeling over the past 24 hours. After each statement,
indicate the extent to which you have been feeling the way described by selecting 0 – 4 (0 = Not
at all, 1 = A little bit, 2 = Moderately, 3 = Quite a bit, 4 = Entirely).
Remember: (a) all responses are completely anonymous, so be as honest as possible; (b) answer
each item separately from all others, even if some questions seem redundant; (c) there are no
right or wrong answers; try to indicate how you actually feel rather than how you think you
should feel.
1. I have “hurt” inside, even though the pain isn’t physical.

0 ...... Not at all
1 ...... A little bit
2 ...... Moderately
3 ...... Quite a bit
4 ...... Entirely
2. I have felt anxious.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
3. I have felt as energetic as I normally do.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
4. I have wanted to sleep all day.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
5. I have been in agony.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
6. I have felt like having a heart-to-heart with a close friend or relative.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
7. I have been free from emotional pain.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
8. I haven’t been able to get going.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
9. I have felt like things are going to turn out really well.
0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
10. I have felt fine emotionally.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
11. I have felt discouraged about things.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
12. I have felt hopeful for the future.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
13. I have felt active and full of “pep.”

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
14. I have caught myself thinking about the same issue.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
15. Things have seemed hopeless.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
16. I have felt pessimistic about the future.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
17. I have felt sleepy even though I’ve had plenty of sleep.
0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
18. I have felt really sad.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
19. I have enjoyed life.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
20. Things that normally give me joy have continued to give me joy.
0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
21. The thought of food has not been appealing.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
22. Things have made me nervous.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
23. I have not had my normal appetite.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
24. I have been incapable of feeling anything pleasant.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
25. I haven’t been able to let go of certain thoughts.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
26. I have been able to clear problems from my mind.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
27. I have thought about how I could have done things differently.
0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
28. I have felt like crying.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
29. I have wanted to be with close family or friends for support.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
30. I have gotten teary-eyed.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
31. Everything has seemed like such an effort.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
32. I have taken effort to fight off tears.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
33. It has been easy to get a lot of things done.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
34. I have felt ashamed.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
35. I have still been able to be happy.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
36. Rational or not, I have blamed myself.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
37. Food has not tasted as good as it usually does.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
38. I have cried really hard.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
39. I have been free from fear.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
40. I have sobbed.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
41. I have been free from worrying.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
42. Nothing has been able to make me smile.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
43. I have been more afraid than usual.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
44. I have slept more than I normally do.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
45. I have felt guilt-free.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
46. I have been angry at myself.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
47. I have wanted to share how I feel with someone.

0 ...... Not at all
2 ...... Moderately
4 ...... Entirely
APPENDIX F
Adverse Life Events Measure

Adverse Life Events Measure
Instructions: Please take a moment to think about the MOST STRESSFUL event you have
experienced OR issue you have focused on since the last time you completed this survey
(yesterday). If you did not complete this questionnaire yesterday, then think about the MOST
STRESSFUL event you have experienced or issue you have focused on in the past 24 hours
instead.
As you do so, keep in mind that that event or issue could be any one of the following: something
stressful that happened since yesterday, something stressful that happened in your past but that
you have been thinking about since yesterday, something ongoing that started in the past and is
still happening today, or something stressful that never happened but that you have been thinking
about since yesterday.
1. Identify and describe the event or issue you came up with in the space provided.
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
Please take a moment to think about the event/issue you identified and then respond to the
following questions on a 5-point scale (Not at all or not applicable = 0; A little bit = 1;
Moderately = 2; Quite a bit = 3; Entirely = 4). Please do not select more than one response
number. Instead, select the one that you believe most accurately reflects how you feel.
2. To what extent did this event/issue negatively affect you?

0 ...... Not at all or N/A
2 ...... Moderately
4 ...... Entirely
3. To what extent does this event/issue represent a failure or a disappointment that is final (not
ongoing)?
2 ...... Moderately
4 ...... Entirely
4. To what extent does this event/issue involve problems related to your health or physical
functioning?
2 ...... Moderately
4 ...... Entirely
5. To what extent does this event/issue involve tension or conflict between you and a friend or
loved one, OR being let down by a friend or loved one?
2 ...... Moderately
4 ...... Entirely
6. To what extent does this event/issue involve the death of a loved one?
2 ...... Moderately
4 ...... Entirely
7. To what extent does this event/issue involve a romantic loss for you?
2 ...... Moderately
4 ...... Entirely
8. To what extent does this event/issue involve some type of ongoing stress, many things going
wrong, or a loved one’s failure(s)?
2 ...... Moderately
4 ...... Entirely
9. To what extent is this event/issue related to your need for greater social support, or feeling
isolated from other people?
2 ...... Moderately
4 ...... Entirely
10. To what extent is this issue/event related to the winter season?

2 ...... Moderately
4 ...... Entirely
11. To what extent does this event/issue involve something other than what has been mentioned
above?
2 ...... Moderately
4 ...... Entirely
12. To what extent is there really no stressful event/issue that you have experienced or focused
on?
2 ...... Moderately
4 ...... Entirely

An Evolutionary Investigation

Uploaded by

Document Information

Original Title

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

An Evolutionary Investigation

Uploaded by

Copyright:

Available Formats

AN EVOLUTIONARY INVESTIGATION OF DEPRESSED MOOD:

THE RELATIONSHIP BETWEEN ADVERSE LIFE EVENTS

AND DEPRESSIVE SYMPTOM PATTERNS

Dissertation presented to the Faculty of the

California School of Professional Psychology

Alliant International University

In partial fulfillment of the requirements for the degree of

Alissa Ann Maitino, M.A.

Irwin Rosenfarb, Ph.D.

Jack Maser, Ph.D.

Matthew Keller, Ph.D.

All rights reserved

INFORMATION TO ALL USERS

constructive suggestions for refining my research methodology. Professor Matthew Keller

different patterns of depressive symptoms. The situation-symptom congruence hypothesis

Chapter I: Introduction ................................................................................................................ 1

The Present Study ...................................................................................................................5

Chapter II: Literature Review ...................................................................................................... 7

Chapter III: Method .................................................................................................................. 48

Chapter IV: Results ................................................................................................................... 69

Sample Characteristics .......................................................................................................... 69

Chapter V: Discussion............................................................................................................. 168

Summary of Findings .......................................................................................................... 170

Hypothesis 1: Findings, Explanations, and Implications ...................................................... 171

References .............................................................................................................................. 203

APPENDIX A Informed Consent Agreement ........................................................................ 222

APPENDIX B Demographic Questionnaire .......................................................................... 229

APPENDIX E Modified Version of the Depressive Symptoms Scale .................................... 245

APPENDIX F Adverse Life Events Measure......................................................................... 256

Table 1 Predictions of the Situation-Symptom Congruence Hypothesis .......................... 24

Table 3 Sociodemographic Characteristics of Sample: Frequencies and Percentages ...... 71

Table 4 Results of Attrition Analyses ............................................................................. 73

Table 5 Frequencies and Percentages of Days Completed ............................................... 74

Table 8 Frequencies and Percentages of Responses to Death of a Loved One, Total

Table 9 Descriptive Statistics of Responses to Death of a Loved One, Total and by

Table 10 Frequencies and Percentages of Responses to Romantic Loss, Total and by

Table 12 Frequencies and Percentages of Responses to Chronic Stress, Total and by

Table 14 Frequencies and Percentages of Responses to Social Isolation, Total and by

Table 19 Results of Analyses Comparing Participants With and Without Major

Table 20 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 21 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 22 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 23 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 24 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 25 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 26 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 27 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 28 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 29 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 30 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 31 Descriptive Statistics of the Adaptive and Nonadaptive Symptom Cluster

Table 45 Hypothesis 2a Multilevel Model Results for Failure ......................................... 135

Table 50 Hypothesis 2f Multilevel Model Results for Winter ......................................... 162

DSM-V; American Psychiatric Association, 2013), approximately 7% of the population will

business is estimated to be approximately “$70 billion in medical expenditures, lost productivity,

and other costs” (Tanouye, 2001, para. 1).

mood to an extreme feeling of sadness, pessimism, and despondency” (American Psychological

depression/depressive disorders will refer collectively to the depressive disorders recognized by

the DSM-IV-TR. Subthreshold depression/depressive disorders will refer to dysphoric episodes

disorders will refer collectively to both clinical and subthreshold depression/depressive

disorders, or to the general phenomenon of depression/depressive disorders. We relied on

or chronic stress (Kendler et al., 2002).

associated with certain subtypes of MDD (hereinafter referred to as the subtype-based