Running Head STRESS GENERATION IN DEPRESSIVE.docx

Running
Head:
STRESS
GENERATION
IN
DEPRESSIVE
AND
ANXIETY
DISORDERS

1
Stress Generation in Depressive and Anxiety Disorders: Outline

One of the major aspects that has brought a tremendous
revolution in the field of abnormal
psychology is stress generation and how it leads to depressive
and anxiety disorders. Stress
STRESS
GENERATION
IN
DEPRESSIVE
AND
ANXIETY
DISORDERS

2
generation can be explained with both the stress causation
theory and stress continuation theory.
Moreover, episodic life stress is caused by depression that an
individual experiences over a short
period of time (Eberhart & Hammen, 2009). This paper presents

a comprehensive essay outline
on stress generation in depressive and anxiety disorders based
on a research case study that was
conducted to determine how depressive and anxiety disorders
affect stress generation.
The article journal first examines the two theories that explains
stress generation that are
fundamental in abnormal psychology using interviewed based
measures of episodic life stress as
well as interpersonal and non-interpersonal chronic life stress.
The two theories include:
a) Stress causation theory
According to this theory, various symptoms of depression
causes stress overtime. An individual
can exhibit episodic life stress. For example, the presence of
anxiety, fear and loneliness. These
episodic life stress results from depression and therefore cause
stress to the individual. Moreover,
chronic life stress can also occur if the depression causes stress
after a long period of time. Stress
causation theory gives an explanation of the existence of stress
from the occurrence of symptoms
of depression. According to the stress causation theory,
individuals can develop chronic life

stress due to the presence of different symptoms of depression
such as mood changes, aggressive
behavior and solitary life (Flynn, 2010).
b) Stress continuation theory
The stress continuation theory argues that the relationship
between depression and stress takes
place due to the continuity of stress over time. When the
symptoms of depression such as
aggression and anxiety persist over a long period of time, an
individual is likely to experience
stress. The occurrence of depression in relation to the stress
therefore results in the presence of
STRESS
GENERATION
IN
DEPRESSIVE
AND
ANXIETY
DISORDERS

3
traumatic conditions and longtime stress. Therefore there is this
theory posits that depression
does not results in long term life stress.
Other major aspects in stress and anxiety disorder that has been
examined include:

a) Neuroticism
Neuroticism is a personality based condition that is
characterized by the presence of
aggressiveness, anxiety and fear. An individual with
neuroticism often experiences episodic and
chronic life stress and is likely to experience trauma due to the
traits that are exhibited by the
condition. Neuroticism is a major risk factor in both stress and
anxiety disorders. According to
Uliaszek (2011), the personality trait has a great impact on
episodic life stress and chronic life
stress. Hence an individual who experiences the excessive
anxiety or fear in different situations
is likely to develop depression. The depression will thus lead to
a stress and anxiety disorder
after a long period of time. There is an interrelationship
between life stress, neuroticism and
disorder. This is because, the symptoms of neuroticism such as
excessive anxiety and fear results
into a depression that subsequently lead to life stress and finally
a disorder among individuals.
b) Extraversion
Extraversion is a personality trait that dictates the socialization

level of a person. The personality
trait is exhibited through the desire to interact and socialize
with other people. An extravert is
therefore an individual who likes socializing with others.
Extraversion also has a great impact on
depression.
People who are experiencing high levels of depression are
likely to record lower levels of
extraversion. This is because depressive symptoms such as
trauma, fear and loneliness will
trigger change the personality of the person. Such symptoms
will affect the emotion of the victim
STRESS
GENERATION
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and hence he or she will not develop a social trait. Such
individuals are likely to spend time in
lonely places as they also develops trauma. Extraversion
therefore is a major factor in stress and
disorder generation and continuity. Individuals experiencing a
reduced extraversion will tend to

withdraw from social life such as friends and family. Low levels
of extraversion is also likely to
develop into social phobias that contributes to depressive and
anxiety disorders.
Anxiety disorders
The article also described anxiety disorders and their role in
stress generation. Anxiety disorder
refers to a condition that is characterized by feelings of fear and
anxiety due to the occurrence of
daily life. Depression and neuroticism has a major impact in the
generation of anxiety disorders.
This is because the symptoms that are exhibited in neuroticism
such as loneliness and trauma
usually trigger depression in the victim. The presence of
depressive conditions will further lead
to stress disorders.
Different anxiety disorders such as social phobia occur due to
chronic life stress in which an
individual experiences extreme stress almost daily in his or her
life. Using the research from the
Youth Emotion Project, the article gives a comprehensive
analysis of the relationship between
anxiety disorders and depression and stress generation. The

study examined different forms of
stress generation and how they relate to various symptoms of
depression. Depression was found
to have a major impact on the occurrence of anxiety disorders.
Moreover, individuals who have
experienced anxiety disorder based symptoms such as social
phobia are likely to develop a
chronic life stress.
Findings and counterarguments
STRESS
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The study was conducted to demonstrate how stress is generated
in both depressive and anxiety
disorders using interviews and DSM-IV diagnosis. The results
found out that the generation of
stress is not specific to depressive disorder but it can also take
place in neuroticism and anxiety
disorders. This research has shown a relationship between stress
generation and anxiety

disorders. Through the stress continuation and stress causation
theories that explain stress
generation, it becomes clear that stress generation is dependent
in other variables such as the
occurrence of depression and anxiety disorders (Smith, 2016).
There are different symptoms that are exhibited by depressed
individuals that can be used to
explain the relationship between depression and major life
stress. For example, people who are
depressed usually develops fear of different situations,
loneliness and aggressive behavior among
others. These symptoms acts as the foundation for the
development of either episodic or chronic
life stress. Such victims are likely to develop episodic life
stress.
Moreover, such people are also likely to experience chronic life
stress, a condition that occurs for
a very long time almost daily in the life of an individual.
Neuroticism and extraversion also plays
a critical role in stress generation. Neuroticism leads to the
development of various symptoms
such as anxiety and fear. These personality characteristics can
immediately or gradually results
in depression and subsequent life stress.

In summary, the journal article has effectively examined the
various factors that contributes to
stress generation. Through comprehensive analysis of stress
continuation and stress causation
theories, the paper has presented the relationship between stress
generation and anxiety
disorders.
References
STRESS
GENERATION
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Eberhart, N. K., & Hammen, C. L. (2009). Interpersonal
predictors of
Stress generation. New York: McGraw Hill Press Flynn, M.,
Kecmanovic, J., & Alloy, L. B.
(2010). An examination of Integrated cognitive-interpersonal
vulnerability to depression: The
role Of rumination, perceived social support, and interpersonal
stress generation.
Cognitive Therapy and Research, 34, 456–466 Smith.

M.,(2016). Anxiety Disorders and Anxiety
Attacks. Retrieved
from:http://www.helpguide.org/articles/anxiety/anxiety-attacks-
and-anxiety-
disorders.htm
Uliaszek, A. A., Zinbarg, R. E., Mineka, S., Craske, M. G.,
Griffith, J. W., Sutton, J. M.,
Epstein,A., & Hammen, C. (2011). A Longitudinal Examination
of Stress Generation in
Depressive and Anxiety Disorders. Journal of Abnormal
Psychology. Advance online
Publication. doi: 10.1037/a0025835
Journal of Abnormal Psychology
A Longitudinal Examination of Stress Generation in
Depressive and Anxiety Disorders
Amanda A. Uliaszek, Richard E. Zinbarg, Susan Mineka,
Michelle G. Craske, James W.
Griffith, Jonathan M. Sutton, Alyssa Epstein, and Constance

Hammen
Online First Publication, October 17, 2011. doi:
10.1037/a0025835
CITATION
Uliaszek, A. A., Zinbarg, R. E., Mineka, S., Craske, M. G.,
Griffith, J. W., Sutton, J. M., Epstein,
A., & Hammen, C. (2011, October 17). A Longitudinal
Examination of Stress Generation in
Depressive and Anxiety Disorders. Journal of Abnormal
Psychology. Advance online
publication. doi: 10.1037/a0025835
A Longitudinal Examination of Stress Generation in Depressive
and
Anxiety Disorders
Amanda A. Uliaszek
Northwestern University
Richard E. Zinbarg
Northwestern University and the Family Institute at
Susan Mineka
Michelle G. Craske
University of California, Los Angeles
James W. Griffith and Jonathan M. Sutton

Alyssa Epstein and Constance Hammen
University of California, Los Angeles
The current study compared two competing theories of the
stress generation model of depression (stress
causation vs. stress continuation) using interview-based
measures of episodic life stress, as well as
interpersonal and noninterpersonal chronic life stress. We also
expanded on past research by examining
anxiety disorders as well as depressive disorders. In addition,
we examined the role of neuroticism and
extraversion in these relationships. Participants were 627
adolescents enrolled in a two-site, longitudinal
study of risk factors for depressive and anxiety disorders.
Baseline and follow-up assessments were
approximately one year apart. Results supported the stress
causation theory for episodic stress generation
for anxiety disorders, with neuroticism partially accounting for
this relationship. The stress causation
theory was also supported for depression, but only for more
moderate to severe stressors; neuroticism
partially accounted for this relationship as well. Finally, we
found evidence for interpersonal and
noninterpersonal chronic life stress continuation in both
depressive and anxiety disorders. The present
findings have implications regarding the specificity of the stress
generation model to depressive
disorders, as well as variables involved in the stress generation
process.
Keywords: stress generation, depression, anxiety, personality
Research has consistently shown that major stressful life events
often precede the onset of an initial depressive episode (e.g.,
Hammen, 2005; Monroe, Slavich, & Georgiades, 2009). The
stress

generation model of depression (Hammen, 1991), which states
that
depression also predicts future stress, has less often been the
focus
of study. The body of research on stress generation has grown
in
recent years, with results suggesting that depressed individuals
tend to generate primarily dependent interpersonal stress (for a
recent review, see Liu & Alloy, 2010). Hypothesized
mechanisms
of stress generation also have been examined, with a focus on
specific cognitive and interpersonal styles, as well as family
vari-
ables (e.g., Liu & Alloy, 2010). However, there are still many
unanswered questions concerning these relationships. For exam-
ple, recent reviews suggest a closer examination of chronic life
stress because most research has focused solely on episodic life
stress (e.g., Liu & Alloy, 2010). In addition, little is known
about
whether stress generation is found in other closely related
condi-
tions (such as anxiety disorders) or whether stress generation is
specific to depressive disorders. Moreover, we present two
theo-
retically distinct interpretations of the stress generation model:
the
stress continuation theory versus the stress causation theory.
This
is the first study to explicitly articulate and compare two
interpre-
tations of stress generation. Finally, additional third variables in
the stress generation relationships, such as personality traits,
may
help inform our understanding of stress generation. The present

Amanda A. Uliaszek, Susan Mineka, James W. Griffith, and
Jonathan
M. Sutton, Department of Psychology, Northwestern University;
Richard
E. Zinbarg, Department of Psychology, Northwestern
University, Patricia
M. Nielson Research chair and Director of Anxiety and Panic
Treatment
Program, The Family Institute at Northwestern University;
Michelle G.
Craske, Alyssa Epstein, and Constance Hammen, Department of
Psychol-
ogy, University of California, Los Angeles.
James W. Griffith is now at the Department of Medical Social
Sciences,
Northwestern University; Jonathan M. Sutton is now at Edward
Hines, Jr. VA
Hospital, Hines, IL; and Amanda A. Uliaszek is now at the
University of
Toronto, Scarborough.
This research was supported by National Institute of Mental
Health Grants
R01 MH65651 to Richard Zinbarg and Susan Mineka
(Northwestern Univer-
sity) and R01 MH65652 to Michelle Craske (University of
California, Los
Angeles). Richard Zinbarg was also supported by the Patricia M
Nielsen
Research Chair of the Family Institute at Northwestern
University.
Correspondence concerning this article should be addressed to
Amanda A.

Uliaszek, Department of Psychology, University of Toronto,
Scarborough, 1265
Military Trail, Toronto, Ontario, M1C 1A4. E-mail:
[email protected]
Journal of Abnormal Psychology © 2011 American
Psychological Association
2011, Vol. ●●, No. ●, 000 – 000 0021-843X/11/$12.00 DOI:
10.1037/a0025835
1
study addresses each of these issues in a large sample of adoles-
cents.
Dimensions of Life Stress
The majority of stress research has focused on episodic life
stress, which refers to events that take place within discrete,
limited time periods. In contrast, chronic life stress is defined
as
ongoing life difficulties (e.g., Wheaton, 1994). Chronic life
stress
has been shown to be cross-sectionally related to depressive
symp-
toms in adults (e.g., McGonagle & Kessler, 1990), depressive
disorders in children and adolescents (e.g., Rudolph et al.,
2000;
Uliaszek et al., 2010), and anxiety disorders in adolescents
(e.g.,
Uliaszek et al., 2010). A few prospective studies have also
found
that chronic life stress predicted the severity of depression and
the
first onset of depression (e.g., Daley, Hammen, & Rao, 2000;

Hammen, Davila, Brown, Ellicott, & Gitlin, 1992).
Life stress can be characterized by two additional dimensions:
independent/dependent and interpersonal/noninterpersonal.
Inde-
pendent stress refers to events that are beyond one’s control;
examples include natural disasters, being in a plane crash, or
the
death of a loved one. Dependent stress occurs, at least in part,
as
a result of the individual’s own actions (Daley et al., 1997).
Examples include financial, marital, or academic difficulties
(al-
though these examples could be independent stressors under
cer-
tain circumstances). Interpersonal stress is defined as
difficulties
with family, peers, or significant others, whereas
noninterpersonal
stress refers to occupational, educational, and health problems
(Hammen, 1991).
Stress Generation
Research has shown that those with a history of depression tend
to experience higher levels of interpersonal life stress, even
when
euthymic, than do those without a history of depression (e.g.,
Chun, Cronkite, & Moos, 2004; Harkness & Stewart, 2009; Ru-
dolph, 2008; Rudolph, Flynn, Abaied, Groot, & Thompson,
2009).
Such effects of baseline depression on later stress have been
found
in clinical, collegiate, and community samples (Chun et al.,
2004;
Daley et al., 1997; Hammen, 1991; Shih, 2006), child and

adoles-
cent samples (Cole, Girgus, Paul, & Nolen-Hoeksema, 2004;
Ru-
dolph, 2008; Rudolph et al., 2000, 2009), and a late middle-
aged
sample (Holahan, Moos, Holahan, Brennan, & Schutte, 2005).
Rudolph and colleagues (2009) found that stress generated by
depression partially accounted for the continuity of depression
over time in female youth. These results are consistent with
stress
generation being a potential mechanism explaining the high rate
of
relapse in major depression (e.g., Daley et al., 1997). We
empha-
size that stress generation does not imply that the mean level of
stress continues to increase over time. Instead, stress generation
implies that a heightened level of stress continues to be
maintained
for a time period after a depressive episode relative to what
would
be expected with nondepressed individuals with high levels of
stress over the same time period.
Two Contrasting Interpretations of Stress Generation
There is an abundance of evidence supporting stress generation
in depression when this phenomenon is construed broadly. How-
ever, there are at least two plausible theoretical interpretations
of
stress generation that differ in terms of whether intraindividual
characteristics (e.g., depression or neuroticism) exert a causal
influence on subsequent life stress and there is a paucity of data
that would allow us to choose among the two interpretations.
The

first, which we refer to as the stress causation theory is similar
to
the way stress generation is typically described (e.g., Hammen,
1991). In stress causation, the characteristics of the depressed
person (symptoms of depression or other predictors of
depression)
are thought to play a causal role in generating stress over time.
In
contrast, the second interpretation, which is referred to as stress
continuation theory, posits that the prospective relationship be-
tween depression and stress is actually accounted for by the
continuity of stress over time. According to this view, there is
no
causal influence of depression on subsequent life stress.
Instead,
there is a cross-sectional relationship between depression and
life
stress at baseline (e.g., Rudolph et al., 2000; Uliaszek et al.,
2010)
and that stress demonstrates a large degree of temporal stability.
Thus, the partial correlation between depression and subsequent
life stress should not be significant when accounting for
baseline
stress.
A comparison of these two interpretations of stress generation is
important from both a theoretical and an applied standpoint. If
the
stress continuation theory is supported, then we might see
evidence
of stress continuation in other disorders associated with life
stress,
as well as in people without a diagnosed disorder who are expe-
riencing heightened life stress. However, if the stress causation
theory is supported, future studies should focus on depression-
specific characteristics as variables of interest in understanding

stress generation. These characteristics may be specific to the
symptoms of depression (e.g., anhedonia, irritable mood) or to
specific correlates of depression. However, it is important to
note
that if specific correlates of depression (e.g., social withdrawal,
high neuroticism) are salient third variables, then other
disorders
related to these correlates (e.g., anxiety disorders) may be
associ-
ated with stress causation as well. Regardless of which theory is
supported, the applied consequences are the same: those with a
history of depression are prone to later stress and this stress
might
well cause further depression (Rudolph et al., 2009).
Given that the distinction between the stress causation and
stress
continuation theories has not previously been articulated, it is
not
surprising that previous studies have adopted analytic strategies
that are insufficient for testing both interpretations. That is,
many
previous studies have only reported the direct relationship
between
depression and future stress without accounting for baseline
stress
(e.g., Daley et al., 1997; Hammen, 1991; Shih, 2006), while a
small number of studies have only reported results where
baseline
stress has been taken into account. Thus, the present study
reports
results relevant to both theories in a single sample.
Neuroticism and Extraversion
Researchers have noted that depressive symptoms alone do not

seem to explain the continued elevated stress following the
onset
of a depressive episode (Chun et al., 2004; Daley et al., 1997;
Hammen, 1991). For example, some past studies have found that
people who were depressed at a baseline assessment often
contin-
ued to have elevated levels of stress long after the depressive
episode ends (e.g., Chun et al., 2004). Evidence supports
negative
2 ULIASZEK ET AL.
cognitive styles, family factors, and interpersonal styles as
impor-
tant explanatory factors in stress generation (for a review, see
Lui
& Alloy, 2010). There is also some evidence pointing to
neuroti-
cism and extraversion as potential explanatory factors in stress
generation.
Neuroticism is conceptualized as a core general risk factor for
depression (e.g., Clark, Watson, & Mineka, 1994; Klein,
Durbin,
& Shankman, 2009), with neuroticism prospectively predicting
increased risk for depression (e.g., Kendler, Kuhn, & Prescott,
2004; Krueger, 1999). In cross-sectional analyses, neuroticism
is
associated with both episodic life stress (Kendler, Gardner, &
Prescott, 2003; Saudino, Pederson, Lichtenstein, McClearn, &
Plomin, 1997) and chronic life stress (Ormel, Oldehinkel, &
Bril-
man, 2001; Uliaszek et al., 2010). Moreover, one study found
that

neuroticism prospectively predicted dependent episodic life
stress
(Magnus, Diener, Fujita, & Pavot, 1993). Research has also ex-
amined the interrelationships among neuroticism, life stress,
and
depression, with cross-sectional findings demonstrating that
neu-
roticism partially accounts for the relationship between
interper-
sonal chronic life stress and depression (Uliaszek et al., 2010).
Concerning extraversion, some studies have shown that de-
pressed individuals report lower levels of extraversion than con-
trols (Reich, Noyes, Hirschfeld, Coryell, & O’Gorman, 1987;
Trull
& Sher, 1994) and that extraversion is inversely related to risk
for
a first onset of depression (e.g., Hirschfeld, Klerman, Lavori &
Keller, 1989), although the results are mixed (e.g., Kendler,
Neale,
Kessler, Heath, & Eaves, 1993). At least one study has demon-
strated low extraversion to be concurrently associated with
chronic
life stress in an adolescent sample (Uliaszek et al., 2010).
Based on the above literature, it is possible that these
personality
variables partially account for the relationship between stress
and
depression. Specifically, heightened neuroticism and/or low
extra-
version could be third variables in the relationship between ele-
vated stress and depression. Concerning neuroticism, this might
be
caused by an increase in emotion sensitivity and negative mood
states that make interpersonal interactions conflictual. In the

case
of low extraversion, this might result from withdrawal from
friends, family, or work life.
Anxiety Disorders
Depression is the disorder most frequently examined in stress
generation research (Hammen, 2005). However, because anxiety
disorders are conceptually and empirically related to
depression,
they are promising candidates for further exploration. First, de-
pressive and anxiety disorders are highly comorbid and have
many
overlapping features (e.g., Kessler, Chiu, Demler, & Walters,
2005; Mineka, Watson, & Clark, 1998). Thus, certain character-
istics of depression that have been shown to be important in
stress
generation may also be present in some anxiety disorders. For
example, negative interpersonal characteristics such as an
avoidant
coping style act as third variables in stress generation in
depression
(for review, see Liu & Alloy, 2010). There is also evidence that
similar negative interpersonal characteristics are present in
anxiety
disorders (e.g., Heering & Kring, 2007). Second, as with
depres-
sion, neuroticism is a risk factor for many anxiety disorders
(e.g.,
Clark et al., 1994; Hayward, Killen, Kraemer, & Taylor, 2000).
Some research also supports a relationship between low
extraver-
sion and several anxiety disorders (see Trull & Sher, 1994),
although other research points to a specific relationship between
extraversion and social phobia (Uliaszek et al., 2010; Watson et

al., 2005). Thus, if neuroticism and/or extraversion are
important
third variables in stress generation, then we might see stress
generation in anxiety disorders because of their relationship to
those personality variables. Third, if the temporal stability of
stress
is an important factor in stress generation, as posited by the
stress
continuation theory, and anxiety disorders have a cross-
sectional
relationship with stress, this would constitute a further reason
why
we would hypothesize stress continuation in anxiety disorders.
Some studies have indeed reported an association between anx-
iety and life stress. For example, social phobia was cross-
sectionally associated with interpersonal chronic life stress in
our
sample of adolescents (Uliaszek et al., 2010). This relationship
was
partially accounted for by neuroticism and extraversion. In a
series
of prospective studies examining college students, negative
events
were shown to be risk factors for anxiety symptoms (Hankin,
Abramson, Miller, & Haeffel, 2004). However, at least one
study
has examined stress generation in self-reported anxiety
symptoms
utilizing a checklist measure of life stress; this study failed to
find
evidence of stress generation (Joiner, Wingate, Gencoz &
Gencoz,
2005). Liu and Alloy (2010) concluded that more research is
needed to further explore these relationships.

Present Study
The present study utilized data from the Youth Emotion Proj-
ect—a large multiyear, two-site prospective study examining
risk
factors for psychopathology in late adolescence (see Zinbarg et
al.,
2010, for more details). The present analyses used data from
two
time points, collected approximately one year apart. A goal of
this
study was to expand on previous stress generation research by
examining both interpersonal and noninterpersonal chronic life
stress, as well as dependent episodic life stress. Only dependent
events were examined because, based on the definition of
independent life stress, we believe that a person’s direct actions
cannot cause these events. These relationships were examined
for both depressive and anxiety disorders. This study also
examined the competing hypotheses of the stress continuation
and stress causation theories for both depression and anxiety
disorders. We also sought to test the role of personality traits in
stress generation. Given the abundance of research demonstrat-
ing the relationships among personality with depressive and
anxiety disorders and the relationships between personality and
life stress, we hypothesized that neuroticism and extraversion
would at least partially account for stress generation in depres-
sive and anxiety disorders.
Method
Participants
Participants were from the Youth Emotion Project, a multiyear,
two-site prospective study designed to identify risk factors for
emotional disorders in a large sample of late adolescents (see
Zinbarg et al., 2010 for more details). The present study

included
two assessment points, collected approximately 1 year apart. A
total of 627 participants were recruited for the Time 1
assessment
(T1). These participants, all in their junior year of high school,
3STRESS, PERSONALITY, EMOTIONAL DISORDERS
were recruited over three years based on scores from the neurot-
icism scale of the revised Eysenck Personality Questionnaire
(EPQ-R-N; Eysenck & Eysenck, 1975), which was administered
during mass screening sessions (see Zinbarg et al., 2010).
Because
neuroticism has been shown to be a risk factor for depressive
and
anxiety disorders (e.g., Clark et al., 1994; Klein et al., 2009),
participants scoring in the top third on the EPQ-R-N were over-
sampled. This behavioral high-risk design was intended to over-
come statistical problems associated with the low base rates of
particular disorders in community samples (Hauner, Revelle &
Zinbarg, 2011).1 Of the participants who were invited and who
participated in the T1 assessment (n � 627), 368 had high, 145
had
medium, and 114 had low scores on the EPQ-R-N (58.7, 23.1,
and
18.2%, respectively).
Participants were recruited from two large metropolitan areas
(suburban Chicago and suburban Los Angeles). There were 305
participants drawn from the Northwestern University site and
322
participants from the University of California, Los Angeles site.
The racial makeup of the total sample was as follows:
Caucasian,

n � 302 (48.2%); Hispanic/Latin American, n � 96 (15.3%);
African American, n � 82 (13.1%); more than one ethnicity, n
�
82 (13.1%); other, n � 34 (5.4%); Asian American, n � 27
(4.3%); Pacific Islander, n � 4 (0.6%).
At T1, the participants ranged in age from 15 to 18 years, with
a mean (M) age of 16.91 (standard deviation [SD] � .39). The
participants included 195 males (31.1%) and 432 females. This
gender difference in participation was unintentional and
occurred
for several reasons, such as females being more likely to agree
to
complete the screening questionnaire and to participate in the
study if invited. Because females tend to score higher on
neurot-
icism (see Costa et al., 2001) and due to our behavioral high
risk
design, more females were invited to participate.
Measures
Structured Clinical Interview for the Diagnostic and Statis-
tical Manual for Mental Disorders–IV (DSM)–IV. (SCID; First,
Spitzer, Gibbons, & Williams, 2002). Diagnoses of current
Axis I disorders were made using the SCID. SCID interviewers
were graduate students, postdoctoral fellows, and bachelor’s
level
research assistants. Training included approximately 60 hours
of
didactics, matching gold standard ratings, role-playing, and live
observations. Each diagnosis was presented at a supervision and
consensus meeting led by doctoral-level supervisors. To
maintain
consistency across sites, difficult cases were presented at
weekly

teleconferences that were periodically attended by supervisors
from the other site.
Interrater reliability for categorical DSM–IV (American Psychi-
atric Association, 2004) diagnoses was assessed by having
trained
interviewers observe live SCIDs on a subset of 69 cases.
Cohen’s
(1960) kappa was acceptable to good when aggregated across all
disorders (� � .82) and for the individual disorders, including
major depressive disorder (� � .83), social phobia (� � .65),
generalized anxiety disorder (� � .85), and obsessive–
compulsive
disorder (� � .85). Kappa estimates are only available for these
disorders because they were the only ones rated frequently
enough
(at least five cases) in this subset of cases.
The depressive and anxiety disorder variables included in the
present study required the participant to meet criteria for the
disorder and demonstrate clinically significant distress and/or
im-
pairment. Participants with a not-otherwise-specified depressive
or
anxiety diagnosis were labeled as not having the specific
disorder
(n � 44). Each diagnostic variable was labeled as present or
absent
for every participant. Participants with no present diagnoses
were
not excluded from analyses. The depressive disorders variable
in
the current study consisted of current cases of major depressive
disorder (n � 23) and dysthymia (n � 7). The anxiety disorders
variable consisted of current cases of the following disorders:

social phobia (n � 52); posttraumatic stress disorder (n � 4);
obsessive– compulsive disorder (n � 9); generalized anxiety
dis-
order (n � 17); specific phobia (n � 37); and panic disorder (n
�
3). Sixteen participants met criteria for both a current
depressive
and anxiety disorder.
Life Stress Interview (LSI; Hammen et al., 1987). Life
stress was evaluated using the LSI, a semistructured interview
that
assesses chronic life stress and episodic life stress. The chronic
life
stress portion assessed the level of ongoing objective stress
expe-
rienced by the participant in 10 domains over the past year. This
version of the LSI contains chronic life stress domains relevant
to
an adolescent population, including four interpersonal domains
(close friendship, social life, romantic relationships, and
family)
and six noninterpersonal domains (neighborhood, school, work,
finances, personal health, and health of close family members).
Unlike the episodic stressors, the chronic life stress domains
can-
not be separated by dependence. To determine chronic life
stress
scores, the interviewer used suggested general probes to elicit
relevant objective information. Subjective impressions offered
by
the participant were not probed for and were disregarded if
offered.
Ratings ranged in half-point intervals from 1 (ideal
circumstances)
to 5 (most stressful circumstances), with specific behavioral an-

chors for each point on the scale. Training of interviewers
involved
approximately 30 hours of didactics, matching gold standard
rat-
ings, role-plays, and live observations. T1 reliability was
assessed
by rating 76 intersite and intrasite audio recorded interviews.
Intraclass correlation coefficients (ICCs) ranged from .58 for
health-other to .92 for neighborhood. Averaged across all
domains,
the ICC was .70.
Episodic events were probed for within each chronic life stress
domain. Interviewers obtained details concerning the
description
and date of the event, the degree, duration, and impact of its
consequences, the participant’s prior experience with the event,
and availability of social support. This information was later
presented by the interviewer to an independent team of two
raters
who evaluated the event on its level of contextual threat. Any
subjective impressions the participants offered about the
stressful-
ness of an event, as well as any diagnostic information about
the
participant, were not presented to the raters. Contextual threat
was
assessed by objectively rating how much impact a particular
epi-
1 To ensure that our results were not biased due to the
behavioral
high-risk design, all analyses were also completed including
sampling
weights to adjust for the differing distributions of neuroticism,
sex, and

ethnicity in our sample compared to the population. There were
no differ-
ences in statistical significance between results with or without
the inclu-
sion of sampling weights. Thus, we followed the
recommendation of
Winship and Radbill (1994) and presented the unweighted
results.
4 ULIASZEK ET AL.
sodic event would have for the average person in those exact
circumstances.
Ratings for episodic events were made on a 1–5 scale: 1 (min-
imal or no threat), 2 (mild threat), 3 (moderate threat), 4
(marked
impact with many consequences), and 5 (severe and catastrophic
negative impact). T1 reliability was assessed by rating 208
audio
recordings of life events across sites. The ICC was .82. In
addition
to a contextual threat rating for episodic events, raters assessed
the
dependence of the event, with 1 denoting complete
independence
and 5 signifying that the event was completely caused by
the respondent. Most interpersonal events were given a rating of
three with the assumption that the event was at least in part the
result of both parties. If raters could not reach consensus, the
episode was then presented to a third rater who helped the raters
reach consensus. The ICC was .90 for the dependence ratings
for
the same 208 events used to assess the reliability of the

contextual
threat ratings. The episodic life stress variable in the present
study
consisted of the average contextual threat ratings for all
dependent
events. Dependence ratings greater than 2 were included in the
present analyses based on the assumption that independent epi-
sodic life stress as defined here could not logically be
“generated”
by any type of individual difference variable. However, we do
acknowledge that there may be some examples where a person
might select themselves into an environment where independent
events are more likely to happen (i.e., not planning a proper
route,
ending up in a high crime neighborhood, and getting robbed) or
where a stable negative environment might contribute to both a
person’s mood state and the likelihood of independent events
(Harkness & Stewart, 2009).
Eysenck Personality Questionnaire—Revised, Neuroticism
Scale (EPQ-R; Eysenck & Eysenck, 1975). The neuroticism
scale of the EPQ-R was the initial screening questionnaire for
the
present study. It consists of 222 items in a yes–no format, with
higher scores indicative of higher levels of neuroticism. Coeffi-
cient alpha was .79 and coefficient omegahierarchical (�h;
Zinbarg,
Revelle, Yovel, & Li, 2005) was .66 (Mor et al., 2006). The
extensive construct validity for this instrument is reported in
the
EPQ-R manual (Eysenck & Eysenck, 1975).
International Personality Item Pool-NEO-PI-R (IPIP-N,
2000). The neuroticism scale from the IPIP-N consists of 60
items rated on a 1–5 Likert Scale. This scale was developed to
closely correspond with the neuroticism scale from the NEO-PI-

R
(Costa & McCrae, 1985). Goldberg (1999) reported that the
total
scores for the two scales correlate .93. A confirmatory factor
analysis completed on one half of the T1 data confirmed six
facets and one general factor underlying the IPIP-N (Uliaszek et
al., 2009). Because of fit indices below conventional levels of
acceptable fit, the model was modified. First, the sample was
randomly split and modifications were tested in the second
subsample suggesting correlated residuals. This resulted in 21
items being cut from the original measure. This altered model
was confirmed in the second half of the data, revealing a
satisfactory fit for this revised version and an �h estimate of
.86
on the full sample (for details, see Uliaszek et al., 2009).
Therefore, the 39 item IPIP-N measure was used in the current
analyses.
The Behavioral Inhibition Scale (BIS; Carver & White,
1994). The BIS, which measures concern over and sensitivity to
negative outcomes, consists of seven items rated on a 4-point
Likert scale. Carver and White (1994) have demonstrated the
convergent and divergent validity of the BIS. The coefficient
alpha
at T1 in this study was .75.
Big Five Mini-Markers Scale (Saucier, 1994). This 40-item
measure consists of eight items assessing each of the Big 5
personality traits: neuroticism, extraversion, agreeableness,
con-
scientiousness, and openness/intellect. The extraversion and
neu-
roticism scales were used in the present analyses. Each item is
rated on a 9-point Likert scale ranging from extremely
inaccurate

to extremely accurate. Saucier (1994) reported a coefficient
alpha
of .76 for the neuroticism scale and .85 for the extraversion
scale.
In this study, the coefficient alphas at T1 were .80 for both
neuroticism and extraversion.
Procedures
A mass screening of potential participants was completed during
school hours. For both T1 and Time 2 (T2) assessments, SCID
and
LSI interviews occurred after regular school hours throughout
the
entirety of the school year. Participants were interviewed in
person
for approximately 1.5 to 3 hr at each time point. Questionnaire
measures were completed either immediately after the
interviews
or arrangements were made for the participant to return to com-
plete the questionnaires, usually within the next week. All ques-
tionnaires were completed at both T1 and T2 except for the
EPQ-R-N, which was used only as the screening questionnaire
at
the beginning of T1.
A total of 497 participants from T1 also participated at T2.
Similar to the full T1 sample, T2 included 30.6% males (n �
152)
and 69.4% females (n � 345). T1 noninterpersonal chronic life
stress was the only variable in the present study to predict
attrition
at T2 (B � .54, standard error [SE] B � .25, Wald �2 � 4.42, p
�
.05, odds ratio � 1.71). When each noninterpersonal chronic
life

stress domain was looked at individually, the only domain to
predict attrition was the school domain (B � .38, SE B � .13,
Wald �2 � 8.43, p � .01, odds ratio � 1.46). Thus, participants
who experienced more school-related stress at T1 were less
likely
to complete the assessment at T2.
Data Analysis
The present analyses were completed using Mplus structural
equation modeling software (Muthén & Muthén, 2007) with full
information maximum likelihood estimation. The use of this
method allowed us to include all 627 participants in analyses
and
potentially corrected at least some of the biases that would
ensue
from including only participants with complete data (see
McArdle,
1994). Only neuroticism was modeled as a latent variable
because
it was the only variable to have multiple indicators. Thus, struc-
tural equation modeling was used for all analyses including neu-
roticism. All other analyses were conventional regressions con-
ducted using Mplus in order to handle missing data using full
information maximum likelihood. A description of the models is
2 The original EPQ Neuroticism Scale consists of 24 items. The
item
referring to suicidality was omitted based on recommendations
from the
Institutional Review Board. The item, “Do you worry about
your health”
was also omitted from scoring because it failed to load on any
factor in
preliminary analyses (Mor et al., 2008).

shown in Figure 1. First, we examined the zero-order path from
T1
disorder (depressive disorders or anxiety disorders) predicting
T2
stress (interpersonal chronic life stress, noninterpersonal
chronic
life stress, or episodic stress; Figure 1, Panel a). Second, we
examined the path from T1 disorder predicting T2 stress with
T1
stress as a covariate (Figure 2, Panel b, path a). The covariate
was
the same type of stress as the dependent variable. A significant
zero-order association of T1 disorder with T2 stress with a non-
significant path a provided support for stress continuation,
while a
significant path a provided support for stress causation. If we
found evidence for stress generation, we then completed an
addi-
tional analysis with neuroticism and/or extraversion included in
the model to test whether these two personality traits at least
partially accounted for the effect of T1 disorder on T2 stress
above
and beyond T1 stress (Panel c). We also examined the unique
relationships of these two T1 personality variables predicting
T2
life stress, accounting for T1 life stress, as a means of assessing
a
stress causation theory for these two personality variables, as
well
as these two personality traits as third variables partially
explain-
ing stress continuation (see Figure 2).

Results
Means and standard deviations are displayed in Table 1. Cor-
relations among T1 interpersonal chronic life stress,
noninterper-
sonal chronic life stress, the average contextual threat rating for
dependent episodic life stress, neuroticism, and extraversion are
displayed in Table 2. All correlations were significant with the
exception of the correlation between T1 extraversion and T1
episodic life stress. The T2 correlations among interpersonal
chronic life stress, noninterpersonal chronic life stress, and epi-
Figure 1. Panel a. Time 1 (T1) disorder predicting Time 2 (T2)
life stress.
Panel b. T1 disorder predicting T2 life stress. T1 life stress, the
same type
of stress as the dependent variable, is entered as a covariate.
Panel c. T1
disorder and T1 personality predicting T2 life stress with T1
life stress
entered as a covariate. Disorder and stress variables are in
square boxes
because they indicate observed variables. Personality is
represented by a
circle because, in the case of neuroticism, it is a latent variable
with
multiple indicators.
Figure 2. Time 1 (T1) personality predicting Time 2 (T2) life
stress. T1
life stress, the same type of stress as the dependent variable, is
entered as
a covariate. Stress variables are in square boxes because they
indicate
observed variables. Personality is represented by a circle

because, in the
case of neuroticism, it is a latent variable with multiple
indicators.
Table 1
Means and Standard Deviations for All Interpersonal Chronic
Life Stress Domains, Noninterpersonal Chronic Life Stress
Domains, the Average Contextual Threat Rating of Dependent
Episodic Life Stress, Neuroticism Measures, and Extraversion at
Time 1(T1) and Time 2 (T2)
T1 Mean (SD),
n � 697
T2 Mean (SD),
n � 497
Interpersonal chronic life stress 2.39 (.47) 2.31 (.44)
Noninterpersonal chronic life stress 2.20 (.38) 2.14 (.34)
Episodic life stress 1.30 (.80) 1.27 (.86)
Moderate episodic life stress .90 (1.30) .44 (1.02)
Neuroticism
EPQ-R-N 11.89 (4.52)
IPIP-N 2.65 (.65)
BIS 2.90 (.58)
Big Five Mini-Markers Scale-N 4.77 (1.42)
Extraversion 5.70 (1.34)
Note. EPQ-R-N � neuroticism scale of the revised Eysenck
Personality
Questionnaire; IPIP-N � neuroticism scale of the International
Personality
Item Pool; BIS � the Behavioral Inhibition Scale; SD �
standard devia-
tion. The range of scores is as follows: interpersonal chronic

life stress
(1–5), noninterpersonal chronic life stress (1–5), episodic life
stress (0 –5),
moderate episodic life stress (0 –5), EPQ-R-N (0 –22), IPIP-N
(0 –5), BIS
(0 – 4), Big Five Mini-Markers Scale-N (0 –9), extraversion (0
–9).
6 ULIASZEK ET AL.
sodic life stress also are shown in Table 2, above the diagonal.
All
T2 correlations were significant.
Neuroticism Measurement Model
A measurement model was estimated using full information
maximum likelihood to evaluate a unidimensional model of the
latent structure of T1 neuroticism as measured by the EPQ-R-N,
IPIP-N, BIS, and Big Five Mini-Markers N Scale. Standardized
factor loadings for each of these measures are as follows: EPQ-
R-N � .68, IPIP-N � .90, BIS � .65, and Mini-Markers � .77.
This model had excellent fit indices of �2(2) � 1.34,
nonsignifi-
cant, comparative fit index � 1.00, root mean square error of
approximation � .00 (90% confidence interval [CI]: .00 –.07),
and
standardized root mean square residual � .01.
Depression and Anxiety Predicting
Episodic Life Stress
First, we determined that there was a significant direct path
between T1 and T2 episodic life stress (standardized regression

weight � .18, SE � .04, p � .001). Next, we examined the
zero-order path between T1 depressive and anxiety disorders
pre-
dicting T2 episodic life stress (see Table 3). Both relationships
were significant. We then examined T1 depressive and anxiety
disorders predicting T2 episodic life stress with T1 episodic life
stress as a covariate (see Table 4). Only the relationship
between
T1 anxiety disorders and T2 episodic life stress remained
signifi-
cant after accounting for T1 episodic life stress. Together these
results supported the stress causation theory for anxiety
disorders
and the stress continuation theory for depressive disorders.
However, the above analyses included a high frequency of mild
stressors. Because research has often supported a specific role
of
only moderate to severe stress (and not mild stress) in the
predic-
tion of major depression (see Hammen, 2005; Monroe & Reid,
2009), we thought it was important to also examine the relation-
ship between depression and moderate to severe levels of stress.
This is because such results would provide stronger evidence
that
stress generation might play in the role of maintenance and/or
recurrence of depression. Thus we completed additional
analyses
with the focus on the generation of more moderate to severe
events
(average episodic life stress rating of 2.5 or higher on a 5-point
scale). We then repeated the above analyses including only
these
stressors. There was a significant direct path between T1 and T2
moderate episodic life stress (standardized regression weight �

.16, SE � .04, p � .001). Depressive disorders predicted
moderate
episodic life stress after accounting for baseline moderate
episodic
life stress, supporting the stress causation theory (see Table 3).
These analyses were repeated for the anxiety disorders, as well
as
the personality trait analyses (see below). In these cases, there
were no differences in results between the full range of episodic
stressors and only the moderate episodic stressors. Thus, they
are
not discussed further and follow-up analyses focus only on the
full
range of episodic stressors for these variables.
Depression and Anxiety Predicting Chronic Life Stress
For chronic life stress, we first determined that there was a
significant zero-order association between T1 and T2
interpersonal
Table 2
Correlations Among Time 1 Interpersonal Chronic Life Stress,
Noninterpersonal Chronic Life Stress, the Average Contextual
Threat
Rating of Dependent Episodic Life Stress, Neuroticism, and
Extraversion
Interpersonal chronic
life stress
Noninterpersonal chronic
life stress
Episodic life
stress Neuroticism

Interpersonal chronic life stress — .45�� .15�� —
Noninterpersonal chronic life stress .47�� — .17�� —
Episodic life stress .17�� .16�� — —
Neuroticism .38�� .05�� .14�� —
Extraversion �.22�� .13�� .08 �.47��
Note. The correlations above the diagonal represent the
correlations at Time 2, N � 627. Neuroticism is a latent
variable measured by the neuroticism
scale of the revised Eysenck Personality Questionnaire,
neuroticism scale of the International Personality Item Pool, Big
Five Minimarkers Scale-N, and
the Behavioral Inhibition Scale.
� p � .05. �� p � .01. �� p � .001.
Table 3
Results Examining the Longitudinal Relationships Between
Time 1 Disorders and Personality Predicting Time 2 Life Stress,
N � 627
Standardized regression
weight (SE)
Depressive disorders
Episodic life stress (all levels) .10 (.04)�
Moderate episodic life stress .12 (.04)��
Interpersonal chronic life stress .21 (.04)��
Noninterpersonal chronic life stress .20 (.04)��
Anxiety disorders
Episodic life stress .16 (.04)��

Moderate episodic life stress 16 (.04)��
Interpersonal chronic life stress .16 (.04)��
Noninterpersonal chronic life stress .16 (.04)��
Neuroticism
Episodic life stress .13 (.04)��
Moderate episodic life stress .14 (.05)��
Interpersonal life stress .35 (.04)��
Noninterpersonal life stress .09 (.05)
Extraversion
Episodic life stress �.04 (.03)
Moderate episodic life stress �.03 (.05)
Interpersonal life stress �.20 (.04)��
Noninterpersonal life stress �.14 (.05)��
Note. SE � standard error.
� p � .05. �� p � .01. �� p � .001.
chronic life stress (standardized regression weight � .55, SE �
.03, p � .001) and noninterpersonal chronic life stress
(standard-
ized regression weight � .68, SE � .02, p � .001). Next, we
examined the zero-order association between depressive and
anx-
iety disorders and T2 chronic life stress (see Table 3). We found

that T1 depressive disorders predicted both interpersonal and
non-
interpersonal chronic life stress at T2, but these relationships
did
not remain significant after accounting for T1 chronic life stress
(see Table 4). Concerning anxiety disorders, we also found evi-
dence for the stress continuation theory but not the stress
causation
theory in chronic life stress. Specifically, T1 anxiety disorders
significantly predicted both interpersonal and noninterpersonal
chronic life stress at T2 (see Table 3), but these relationships
did
not remain significant after accounting for T1 stress (see Table
4).
Effects of Personality Variables
We first examined the zero-order association of T1 personality
with T2 life stress. These results are displayed in Table 3. T1
neuroticism significantly predicted both T2 episodic life stress
and
T2 interpersonal chronic life stress. T1 extraversion also
signifi-
cantly predicted T2 interpersonal and noninterpersonal chronic
life
stress. We then examined these relationships while accounting
for
T1 life stress. The relationships between T1 neuroticism and T2
episodic life stress, and T2 interpersonal chronic life stress, re-
mained significant after accounting for T1 life stress (see Table
5),
supporting the stress causation theory. T1 extraversion was not
a
significant predictor of T2 stress after accounting for T1 stress,
supporting the stress continuation theory.

Our final set of analyses examined whether neuroticism at least
partially accounted for stress causation in the relationships be-
tween T1 depressive disorders and T2 moderate episodic life
stress
(accounting for T1 moderate episodic life stress) and T1 anxiety
disorders and T2 episodic life stress (accounting for T1 episodic
life stress). Only neuroticism was examined because we did not
find evidence that extraversion was associated with T1 or T2
episodic life stress. We completed the product of coefficients
test
using the program PRODCLIN (distribution of the PRODuct
Con-
fidence Limits for Indirect effects; MacKinnon, Fritz, Williams,
&
Lockwood, 2007). This program converts the regression weights
and standard errors from the analyses into z scores and finds
critical values based on the product of two random variables.
The
result is a nonsymmetrical confidence interval around the
product
of coefficients. If it includes zero, the effect is not significant
(MacKinnon, Lockwood, Hoffman, West, & Sheets, 2002;
MacK-
innon, Lockwood, & Williams, 2004). Although this test is
often
used in meditational analyses, it is also appropriate for tests of
confounding or third variables (MacKinnon, Krull, &
Lockwood,
2000). In these analyses, the � coefficient is the direct
relationship
between the disorder of interest (depression or anxiety) and
neu-
roticism. The � coefficient is the relationship between
neuroticism
and T2 life stress after accounting for the disorder of interest

and
T1 life stress. Thus, results (for the product of ��) indicate the
role
of neuroticism in the relationship between disorder and T2 life
stress, after accounting for T1 life stress.
The first analysis examined T1 depressive disorders (standard-
ized regression weight � .08, SE � .05, ns), moderate episodic
life
stress (standardized regression weight � .13, SE � .05, p �
.01),
and neuroticism (standardized regression weight � .11, SE �
.05,
p � .05) as predictors of T2 moderate episodic life stress. In
this
analysis, T1 neuroticism was significantly correlated with T1
depression (r � .18, SE � .04). The product of coefficients test
revealed that neuroticism partially accounted for the stress
causa-
tion effect in depression (�� .02, confidence interval �
.002–
.04). Next, we examined T1 anxiety disorders (standardized re-
gression weight � .11, SE � .05, p � .05), episodic life stress
(standardized regression weight � .15, SE � .04, p � .05), and
neuroticism (standardized regression weight � .08, SE � .05,
ns.)
as predictors of T2 episodic life stress. In this analysis, T1 neu-
roticism was significantly correlated with T1 anxiety disorders
(r � .37, SE � .04). The product of coefficients test revealed
that
Table 5
Time
1 Personality Variable and Time 2 Life Stress, Accounting for
T1 Life Stress, N � 627

a b
Standardized
regression
weight (SE)
Standardized
regression
weight (SE)
Neuroticism
Episodic life stress .13 (.05)� .16 (.04)��
Moderate episodic life stress .12 (.05)� .14 (.05)��
Interpersonal chronic life stress .15 (.04)�� .49 (.04)��
Extraversion
Interpersonal chronic life stress �.06 (.04) .54 (.03)��
Noninterpersonal chronic life stress �.01 (.03) .69 (.02)��
Note. In the column to the left, a
represents the relationship between T1
personality and T2 life stress, while accounting for T1 life
stress (see
Figure 2, Path a
). b
represents the relationship between T1 life stress and
T2 life stress within the specified relationship.
� p � .05. �� p � .01. �� p � .001.
Table 4

Time
1 Disorder and Time 2 Life Stress, Accounting for T1 Life
Stress, N � 627
a b
Standardized
regression
weight (SE)
Standardized
regression
weight (SE)
Depressive disorders
Episodic life stress .08 (.04) .16 (.04)��
Moderate episodic life stress .10 (.04)� .15 (.04)��
Interpersonal chronic life stress .05 (.04) .54 (.03)��
Noninterpersonal chronic life stress .05 (.03) .68 (.03)��
Anxiety disorders
Episodic life stress .14 (.04)�� .16 (.04)��
Moderate episodic life stress .15 (.04)�� .15 (.04)��
Interpersonal chronic life stress �.02 (.04) .54 (.03)��
Noninterpersonal chronic life stress �.004 (.03) .69 (.02)��
Note. In the column to the left, a represents the relationship

between T1
disorder and T2 life stress, while accounting for T1 life stress
(see Figure 1
Panel b, Path a). b represents the relationship between T1 life
stress and T2
life stress within the specified relationship.
� p � .05. �� p � .01. �� p � .001.
8 ULIASZEK ET AL.
neuroticism partially accounted for stress causation in anxiety
disorders (�� .04, confidence interval � .004 –.08).
Discussion
This is the first prospective study to demonstrate stress gener-
ation in both depressive and anxiety disorders using DSM–IV
diagnoses and an interview-based assessment of stress. In
addition,
we believe this is the first study to directly examine both the
stress
continuation and stress causation theories of stress generation in
the same study. These results also examined the role of neuroti-
cism and extraversion in stress generation, with neuroticism
par-
tially accounting for episodic stress generation in both
depressive
and anxiety disorders.
Our analyses supported the stress causation theory when exam-
ining stress generation in depressive disorders with moderate to
severe episodic life events. Thus, something specific to
depression
at baseline, apart from elevated concurrent stress, has a

predictive
relationship to later moderate to severe episodic stressors. One
such variable that we found to be important in this relationship
is
elevated neuroticism. Neuroticism partially accounted for the
stress
generation relationship between depression and moderate
episodic
stressors, even after accounting for baseline stress. These
results have
both theoretical and clinical implications. First, these results
show
that, relative to the nondepressed, people with depression are at
an
elevated risk for future dependent episodic stress of moderate to
severe intensity. These types of stressful life events may well
lead to
continued depressive symptoms and future recurrence of
depressive
episodes (e.g., Rudolph et al., 2009). This provides one possible
explanation for the high recurrence rate of depression (e.g.,
Boland
& Keller, 2009) and for subclinical depressive symptoms
between
episodes of depression (Judd et al., 1998). Second, these
findings
suggest that clinical interventions should target stress reduction
as
a means of preventing future depressive episodes.
It is important to note that a few other studies have found a
predictive relationship between depression and episodic stress,
even after accounting for baseline stress (e.g., Harkness &
Stewart,
2009; Holahan et al., 2005; Rudolph et al., 2009), that is,
support-

ing the stress causation theory. In our sample, this was only
replicated with moderate to severe episodic life stress. There
are
several possible explanations for why we did not replicate these
findings for analyses including all levels of episodic life stress.
First, our analyses did not separate interpersonal from noninter-
personal episodic life stress (although we did for chronic life
stress). Several studies have found stress generation for
depression
to be stronger for interpersonal episodic life stress (e.g.,
Rudolph
et al., 2000; Shih, 2006). Second, we used more rigorous
method-
ology than many other studies, including clinically significant
diagnoses for our disorder variables and an interview-based
mea-
sure of life stress. It is possible that more studies would have
failed
to support stress generation in depression if using such stringent
criteria.
The findings on episodic stress generation in anxiety disorders
are an exciting addition to the stress generation literature, with
this
evidence demonstrating that the phenomenon is not specific to
depression. Because we found evidence of stress generation in
anxiety disorders, we are led to believe that there is something
about the characteristics of anxiety disorders that lead to
elevated
levels of episodic stress. We found that high neuroticism is one
such characteristic, partially accounting for the relationship be-
tween T1 anxiety disorders and T2 episodic life stress, after
accounting for T1 episodic life stress. However, neuroticism did
not completely explain stress generation in anxiety. Another im-
portant characteristic to examine might be the interpersonal pro-

cesses similar to what is seen in depression. Much research
points
to an interpersonal theory of stress generation in depression,
with
a focus on interpersonal style and interpersonal stressors (e.g.,
Eberhart & Hammen, 2009; Flynn, Kecmanovic, & Alloy,
2010),
and how this process may lead to future depressive episodes
(Rudolph et al., 2009). Future studies examining stress
generation
in anxiety disorders might examine negative interpersonal
charac-
teristics as variables that might, at least in part, account for this
relationship.
A recent review article has noted the importance of examining
chronic life stress in stress generation research (Liu & Alloy,
2010). We found evidence for stress continuation theory, but
not
for stress causation, for both interpersonal and noninterpersonal
chronic life stress in both depressive and anxiety disorders.
These
results demonstrate that, although characteristics of depressive
and
anxiety disorders do not appear to be causal agents in the gener-
ation of chronic life stress, those with these disorders are prone
to
future elevated levels of chronic life stress nonetheless. This is
clinically and theoretically important when thinking about the
developmental course and prognosis of those with depressive
and
anxiety disorders. Similar to a scar effect, we expect those with
a
history of a depressive or anxiety disorder would continue to
experience elevated levels of chronic life stress relative to those
without such a history. It is possible that we did not find

support
for the stress causation theory with chronic life stress because it
is
by its nature enduring and so it may be more difficult to detect
changes. In fact, results supported the high stability of both
inter-
personal and noninterpersonal chronic life stress.
As mentioned above, neuroticism was a significant third vari-
able in stress generation for depressive and anxiety disorders.
Results looking solely at neuroticism also supported the stress
causation theory for both episodic life stress and interpersonal
chronic life stress. In other words, T1 neuroticism predicted
both
types of stress at T2, even after accounting for baseline stress.
Taken together, these findings demonstrate that being high in
neuroticism, at least in late adolescence, is a risk factor for later
chronic and episodic stress. We can at least partially attribute
this
continued elevation in stress to specific characteristics or corre-
lated behaviors of a person high in neuroticism. For example,
increased emotional sensitivity may lead a person to actions that
interfere with social and romantic relationships or school and
work
performance.
Extraversion was not associated with a significant stress causa-
tion effect for any type of stress. However, T1 extraversion did
predict both T2 interpersonal and noninterpersonal chronic life
stress, supporting the stress continuation theory. Support of this
theory does provide evidence that those displaying the
withdrawn,
nonassertive behavior characteristic of introversion are likely to
have continued elevated chronic life stress in the future, if only
due
to the cross-sectional relationship between chronic life stress

and
introversion and the temporal stability of chronic life stress.
There are several limitations of the current study. First, because
our sample consisted entirely of late adolescents and because
we
present several new findings, our results need to be replicated in
additional samples before firm conclusions can be drawn. This
is
also pertinent to the results concerning stress generation in
anxiety
disorders because this area of study is quite new. Second, there
was a large difference in the number of participants meeting
criteria for a depressive disorder (n � 28) versus an anxiety
disorder (n � 92). The resulting difference in power was
another
possible reason why the stress causation theory was supported
for
the full range of episodic stressors in anxiety disorders, but not
in
depressive disorders. In this regard, however, we also note that
the
effect size estimates for depressive disorders were consistently
smaller than those for the anxiety disorders suggesting that
power
alone cannot entirely explain the differences in results between
depressive disorders and anxiety disorders. Third, participants
reported an average of two dependent episodic life events in T1
(M � 1.90, SD � 1.63) and 1.5 in T2 (M � 1.54, SD � 1.48).
One
possible reason for the decrease is the socialization of the

partic-
ipants to the LSI; they may have learned that reporting fewer
episodic events results in a shorter interview. In addition,
attrition
was predicted by chronic life stress in the school domain
suggest-
ing that those having higher school stress were also likely to
drop
out of the study. A fourth limitation is that we only tested a
small
set of possible third variables. It is possible that there are other
third variables with some of them having even larger effects
than
the ones we examined. A final limitation is related to the
approx-
imate one-year time lag between assessments. This time lag was
a
matter of convenience; any shorter period of time would unduly
tax the participants, whereas a longer lag would make it too
difficult to recall the stress since the previous interview. Thus,
it is
possible that the results would be different if there were more or
less time between assessments.
In conclusion, we believe that this study provides some of the
most comprehensive evidence to date on stress generation. We
examined the effects of both depression and anxiety disorders
on
both chronic and episodic life stress. To our knowledge, ours is
the
first study to distinguish between and test both the stress
contin-
uation and stress causation theories of stress generation.
Moreover,
we examined the role of normal personality traits in stress
gener-

ation, with results showing that neuroticism partially accounted
for
the predictive relationship between depressive disorders and
mod-
erate episodic life stress, as well as the relationship between
anxiety disorders and episodic life stress. Finally, this study
pro-
vides new evidence demonstrating that stress generation is not
specific to depressive disorders, but also occurs in those with
anxiety disorders and elevated neuroticism.
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Received March 30, 2010
Revision received August 10, 2011
Accepted August 11, 2011 �
12 ULIASZEK ET AL.

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