Chronic stress and stressful life events in the offspring of parents with bipolar disorder
The stress generation theory suggests that depressed individuals and children of depressed mothers are prone to create stressors that are interpersonal and dependent on their own behaviour. Exposure to "self-generated" stress is believed to increase the risk for onset and recurrence of depression. Much less is known about stress in the offspring of parents with bipolar disorder (OBD).
As part of a longitudinal study, 37 OBD and 33 offspring of parents with no affective disorder (13 to 26 years old) were interviewed using the UCLA Life Stress Interview, assessing their current life circumstances (chronic stress) and recent negative life events (episodic stress).
The OBD reported more difficulties in interpersonal and non-interpersonal domains of chronic stress than controls. The group differences remained significant after controlling for the presence of affective disorders, indicating that the effect of risk status on chronic stress is independent of the problems associated with having a disorder. With respect to episodic stress, the OBD were 3.9 times more likely to have experienced a moderate to severe interpersonal stressor compared to the control group. There was no group difference for dependent events, but the OBD experienced more severe independent events than controls.
Methodological limitations include a small sample size, large age range, and the absence of parent-reported stress and symptomatology.
Although the findings do not support the stress generation theory, they suggest that elevated levels of episodic and chronic stress may be important markers of risk for affective disorders in high-risk participants.
Chronic stress and stressful life events in the offspring of parents
with bipolar disorder
Caroline S. Ostiguya, Mark A. Ellenbogena,⁎, Anne-Marie Linnena, Elaine F. Walkerb,
Constance Hammenc, Sheilagh Hodginsd
aCentre for Research in Human Development, Concordia University, Montreal, Qc, Canada
bDepartment of Psychology, Emory University, Atlanta, GA, United States
cDepartment of Psychology, University of California at Los Angeles, Los Angeles, CA, United States
dDepartment of Forensic Mental Health, Institute of Psychiatry, King's College, London, UK
Received 27 February 2008; received in revised form 4 August 2008; accepted 7 August 2008
Available online 24 September 2008
Background: The stress generation theory suggests that depressed individuals and children of depressed mothers are prone to create
stressors that are interpersonal and dependent on their own behaviour. Exposure to “self-generated” stress is believed to increase the
risk for onset and recurrence of depression. Much less is known about stress in the offspring of parents with bipolar disorder
Methods: As part of a longitudinal study, 37 OBD and 33 offspring of parents with no affective disorder (13 to 26 years old) were
interviewed using the UCLA Life Stress Interview, assessing their current life circumstances (chronic stress) and recent negative
life events (episodic stress).
Results: The OBD reported more difficulties in interpersonal and non-interpersonal domains of chronic stress than controls. The
group differences remained significant after controlling for the presence of affective disorders, indicating that the effect of risk
status on chronic stress is independent of the problems associated with having a disorder. With respect to episodic stress, the OBD
were 3.9 times more likely to have experienced a moderate to severe interpersonal stressor compared to the control group. There
was no group difference for dependent events, but the OBD experienced more severe independent events than controls.
Limitations: Methodological limitations include a small sample size, large age range, and the absence of parent-reported stress and
Conclusions: Although the findings do not support the stress generation theory, they suggest that elevated levels of episodic and
chronic stress may be important markers of risk for affective disorders in high-risk participants.
© 2008 Elsevier B.V. All rights reserved.
Keywords: Bipolar disorder; Risk factors; Stressful life events; Chronic stress; Stress generation theory
The offspring of parents with bipolar disorder (OBD)
are at high risk for developing a range of mental
Journal of Affective Disorders 114 (2009) 74–84
⁎Corresponding author. Concordia University, Department of
Psychology, 7141 Sherbrooke W., Montreal, QC, Canada H4B 1R6.
Tel.: +1 514 848 2424x7543; fax: +1 514 848 2815.
E-mail address: email@example.com
0165-0327/$ - see front matter © 2008 Elsevier B.V. All rights reserved.
Journal of Affective Disorders, 2009, 114, 74-84; doi: 10.1016/j.jad.2008.08.006
The final version can be accessed at: www.elsevier.com/locate/jad
Corresponding author: M.A. Ellenbogen. Concordia University, Department of
Psychology, 7141 Sherbrooke W., Montreal, QC, Canada H4B 1R6.
Tel.: +1 514 848 2424x7543; fax: +1 514 848 2815.
E-mail address: firstname.lastname@example.org
disorders, as well as other problems such as deviant
school behaviours and suicidality (DelBello and Geller,
2001; Henin et al., 2005; Hillegers et al., 2005; Lapalme
et al., 1997; Reichart et al., 2004; Singh et al., 2007;
Waters et al., 1983; Zahn-Waxler et al., 1984). Although
hereditary influences are important in the etiology of
bipolar disorder (BD; McGuffin et al., 2003; Todd et al.,
1996), environmental factors also contribute to the
development of difficulties in these offspring, both
directly and by activating susceptibility genes during
development (DelBello and Geller, 2001; Walker et al.,
2004). Environmental stress such as marital discord,
poor quality of parenting, and psychopathology in the
non-BD parent have been associated with the develop-
ment of disorders in the OBD (DelBello and Geller,
2001). Overall, parents with BD tend to create a familial
environment that is unstable and lacking in structure
(Chang et al., 2001; Ellenbogen and Hodgins, 2004;
Ellenbogen et al., 2006; Hodgins et al., 2002; Romero
et al., 2005). These findings suggest that the OBD, in
addition to being at genetic risk for the development of
mental disorders, are exposed to a stressful familial
environment that increases the risk of psychopathology
Stress can be conceptualized as the result of a
perceived imbalance between the demands made on
the individuals and their ability to cope with them
(Lazarus and Folkman, 1984). Exposure to stress
includes the occurrence of severe negative stressful life
events (SLEs) and the cumulative load of minor, day-to-
day difficulties. An important theoretical model of the
relationship between stress and affective disorders is the
stress generation theory (Hammen, 1991b). Hammen
examined SLEs in women who had either major
depressive disorder (MDD), BD, a chronic physical
illness, or no disorder. Relative to control participants,
depressed individuals experienced stressors that were
partly dependent on their own behaviour and inter-
personal in nature, even in remission (Hammen, 1991b;
Hammen and Brennan, 2002). This theory suggests that
depressed women “generate” SLEs in their environment
because of certain maladaptive stable characteristics,
such as high neuroticism (Hammen and Brennan, 2002;
Kendler and Karkowski-Shuman, 1997). Support for the
stress generation theory has been found in studies of
depressed adolescents (Hammen and Brennan, 2001;
Petti et al., 2004; Rudolph et al., 2000) and unaffected
offspring of parents with MDD (Adrian and Hammen,
1993; Hammen, 1991a).
Exposure to chronic stress is also an important factor
in the development of affective disorders. Chronic stress
refers to long term disturbances and ongoing conditions
that do not have clear time boundaries; it is often used as
an index of a person's functioning. For example,
McGonagle and Kessler (1990) have found chronic
stress to be a better predictor of depressive symptoms
than episodic stress. Chronic stress was also found to be
predictive of school and social functioning, above and
beyond maternal diagnosis of MDD (Hammen et al.,
1987). Moreover, the presence of both chronic and
episodic stress in young women was associated with
elevated cortisol levels and worse immune function, but
the presence of episodic stress in the absence of chronic
stress had few negative biological effects (Marin et al.,
2007). In light of these findings, a comprehensive
investigation of stress should include a simultaneous
examination of both SLEs and chronic stress.
The association between MDD and stress has been
studied extensively (for review, see Hammen, 2005), but
much less is known about stress and BD. Adrian and
Hammen (1993) found that the OBD reported a similar
number of dependent stressors as the offspring of
depressed mothers. Petti et al. (2004) found that the
OBD who developed an affective disorder reported
more dependent SLEs before the onset of the disorder
than the OBD who did not develop a disorder. Similarly,
the OBD who were diagnosed with a disorder reported
more negative events within a 12-month period than
both the unaffected OBD and control offspring; the two
unaffected groups did not differ from each other (Duffy
et al., 2006). In terms of chronic stress, some studies
have found no impairment in functioning among the
OBD (Anderson and Hammen, 1993; Reichart et al.,
2007), while others have found evidence of maladjust-
ment (Henin et al., 2005; Hodgins et al., 2002). In a
recent study of 140 OBD using the youth and young
adult versions of the Child Behavior Checklist, social
functioning was impaired, relative to a large community
sample of youth, among those who were 18 years or
older and who were diagnosed with a mood disorder.
However, social functioning in younger or non-affected
OBD did not differ from control youth. Thus,
maladjustment in chronic functioning among the OBD
may be dependent on the presence of psychopathology.
The goal of the present study was to assess different
domains of chronic stress and the occurrence of SLEs in
the OBD and the offspring of parents with no affective
disorder (NAD). In contrast to studies using checklists
or questionnaires (e.g., Ellenbogen et al., 2006; Petti
et al., 2004), the present study uses the UCLA Life
Stress Interview, a well validated structured interview
(Adrian and Hammen, 1993; Hammen, 1991b). Struc-
tured interviews have been shown to be more effective
than checklists in stress research because they account
75 C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
for the influence of context and minimize mood-related
biases (Adrian and Hammen, 1993; Dohrenwend, 2006;
McQuaid et al., 2000). The UCLA Life Stress Interview
has been used in a number of studies to predict the
relationship between different types of stress and
negative outcomes (e.g., Espejo et al., 2006; Marin
et al., 2007).
Two hypotheses were put forth. First, it was predicted
that chronic stress would be higher in the OBD than in
the offspring of parents with NAD. Second, it was
hypothesized that the OBD, compared to control
participants, would experience a greater number of,
and more severe, episodic stressors that are interperso-
nal in nature and dependent on their behaviour.
The study sample was selected from a larger sample
of offspring who are participating in an ongoing
prospective study of families with a parent diagnosed
with BD or parents with NAD. Parents with a diagnosis
of BD, their spouses, and children were recruited from
psychiatric departments of general hospitals and from
consumer groups. Families in which parents had NAD
were also randomly recruited in the same geographic
sectors as the bipolar families. Control parents had no
current or lifetime axis I disorder except for one parent
diagnosed with a past episode of substance abuse and
one with a past anxiety disorder. At the time of family
recruitment, any parent suspected of having a “second-
ary” depression was excluded as a control (for more
information regarding the original sample, see Ellenbo-
gen and Hodgins, 2004).
The present study included 42 male and 28 female
participants, between 13 and 26 years (M=19.09;
SD=2.86), from 52 families. The groups did not differ
in age or gender composition. Thirty-three offspring
were diagnosed with one or more current or past
diagnoses (see Table 1). Overall, the OBD were more
likely to be diagnosed with any mental disorders or any
non-affective disorders compared to the controls
(χ2=8.57, p b 0.01 and χ2=7.68, p b 0.01, respec-
tively). However, the group difference in the number of
affective disorders was only a trend (χ2=3.21,
The study sample consisted of participants from two
different data collections.1Seventeen participants took
part in an event-contingent recording study of social
interactions conducted in 2005 (Linnen et al., 2008).
Fifty-three offspring participated in a data collection
between May 2006 and February 2007, as part of a
follow-up assessment of an ongoing longitudinal study.
Offspring who participated in the current study were
collected at the initial assessment when offspring were
between 4 and 12 years of age. No group differences
emerged on parent and teacher ratings on the Child
Behavior Checklist (Achenbach, 1991), clinician-rated
symptoms in the offspring, and measures of parents'
functioning, education, personality (i.e., neuroticism),
and intelligence (data not shown).
2.2.1. UCLA Life Stress Interview: chronic stress
The chronic stress interview (Adrian and Hammen,
1993; Hammen, 1991b) assesses nine domains of
functioning over the last 6 months (see Table 2). Each
domain is coded on a five-point scale by the interviewer,
Demographic information for the OBD and offspring of parents with
OBDOffspring of parents
Mean age (years) ± SD
Major depressive disorder
Bipolar disorder I
Bipolar disorder II
Adjustment disorder with
Substance use disorders
Oppositional defiant disorder 0
19.46 ± 2.63 18.67 ± 3.09
OBD = Offspring of a parent with bipolar disorder; SD = standard
deviation; NAD = no affective disorder.
1The two samples differed significantly on some study variables.
The offspring from the social interaction study (nine OBD and eight
controls) reported more dependent SLEs, more interpersonal SLEs,
and more severe interpersonal SLEs than the offspring in the second
study (28 OBD and 25 controls). We thus included a “study”
dichotomous variable in all our analyses to control for these
76C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
using behaviour-specific anchor points. Higher scores
reflect worse circumstances and impairment. Inter-
viewers were trained by Dr. Hammen or by a senior
graduate student trained by Dr. Hammen. Interrater
reliability was evaluated using the intraclass correlation
coefficient for consistency. Using independent inter-
viewers' ratings of 20 participants, intraclass correlation
coefficients revealed high reliability for all domains,
with a mean of 0.85, which is similar to what has been
obtained in other studies using the same instrument
(Eberhart and Hammen, 2006; Hammen and Brennan,
2002; Shih et al., 2006).
2.2.2. UCLA Life Stress Interview: episodic stress
This part of the interview assesses episodic life events
(having a clear beginning and end) that have occurred
within the last 12 months. Circumstances surrounding
each event were documented (e.g., duration, conse-
quences, functional impairment, etc.), but information
regarding the subjective emotional response to the event
was excluded. Events recorded by interviewers were then
coded by a team of raters who were blind to the group or
clinical status of the participant. Events were coded on
two dimensions (severity and independence) using a 5-
point scale. Independence refers to the degree to which
someone has contributed to an event. For analysis of
categorical data, ratings of 3 or above are considered as
dependent SLEs (Daley et al., 1997; Rudolph and
Hammen, 1999). Each event was also categorized as
interpersonal or non-interpersonal. Final ratings for each
event were determined by group consensus. Separate
indexes were computed for independent, dependent,
interpersonal, and non-interpersonal events by summing
the objective severity ratings across the relevant events.
Interrater reliability was not calculated for the SLEs'
ratings in this study because only one team of raters was
used. However, the interview has excellent reliability and
has been extensively used in different adult and
adolescent populations (Adrian and Hammen, 1993;
Hammen, 1991a; Hammen and Brennan, 2001; Kim
et al., 2007).
First et al., 2001)
The SCID-I is a semi-structured interview designed
assess clinical diagnoses according to the Diagnostic
and Statistical Manual of Mental Disorders (DSM
4th ed.; APA, 1994). The SCID-I was used in the
present sample with offspring aged 19 or above (n=40).
One limitation of this interview is that it is not well-
designed for capturing cyclothymia or BD NOS, two
particularly impairing disorders that are relevant for the
sample at hand (e.g., Birmaher et al., 2006).
2.2.4. Kiddie-Schedule for Affective Disorders and
Schizophrenia — Present and Lifetime version
(K-SADS-PL; Kaufman et al., 1997)
The K-SADS-PL is a semi-structured interview
designed to assess clinical diagnoses in children aged
7 to 18 years old (n=30). It has been shown to generate
Mean (standard deviation) for chronic stress domains on the UCLA Life Stress Interview
Chronic stress domainsOBDOffspring of parents with NADFa
Health of the Self
Health of the family
Total chronic stress20.79 (3.40)18.42 (2.16)17.39 (2.09)16.43 (1.70)15.10***0.20
Higher scores represent worse functioning. OBD = Offspring of a parent with BD; NAD = no affective disorder. ηp
** p b 0.01; *** p b 0.001.
aMain effect of group (difference between the OBD and control offspring).
bGender × Group Interaction, p b 0.05.
2= Partial eta squared.
77C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
reliable diagnoses, particularly with respect to the
affective disorders (Kaufman et al., 2004).
In the current study, both the SCID-I and K-SADS-
PL were administered by experienced clinicians or
clinical graduate students with extensive training and
experience in the administration of the interviews.
Reliability was assessed in 15 participants who are
part of the ongoing longitudinal study. Kappa was 0.82
for assigning affective disorder diagnoses, 0.71 for
anxiety disorders, and 1.0 for substance use disorders.
As described previously, participants' data for the
current study were obtained from two different projects.
For both projects, offspring were contacted by telephone
and those interested in participating in the study were
scheduled for a laboratory visit. For the social interac-
tion study, participants underwent a structured diagnos-
tic interview and filled out questionnaires. At a later
date, they were contacted and underwent the UCLA Life
Stress Interview. For the second study, both the
diagnostic interview and the UCLA Life Stress Inter-
view were conducted during the same visit. All
participants gave written consent, and parental consent
was obtained for participants 17 years of age or younger.
Depending on the study, participants received an
honorarium of $100 or $150 (CAN). All procedures
were approved by the Human Research Ethics Commit-
tee of Concordia University.
2.4. Data analyses
Data were screened for the presence of outliers,
defined as scores at least three standard deviations from
the mean, and violations of normality. One participant's
total severity of SLEs met this criterion. Analyses were
performed with and without this participant, and the
results did not differ. Therefore, the participant was
included in the analyses. Scores for the nine domains of
the chronic stress interview, as well as the three
aggregated scores, were positively skewed and therefore
were log-transformed. To facilitate the interpretation of
results, data in Table 2 are not transformed.
Hierarchical multiple regressions were performed on
total, interpersonal, and non-interpersonal chronic
stress. Gender × Group analyses of covariance (ANCO-
VAs) were performed on the total severity and total
number of SLEs. Gender × Group multivariate analyses
of covariance (MANCOVAs) were used to analyze
individual chronic stress domains and the severity and
frequency of different types of SLEs. Wilks' criterion
was used to evaluate the significance of the multivariate
effects. When main effects of group or gender were
significant, analyses of variance (ANOVAs) were
conducted on each of the dependent variables. Age,
the study from which the data were taken, and
offspring's affective disorder were included as covari-
ates for all ANCOVAs and MANCOVAs. For the
analyses involving categorical outcome variables,
logistic regressions were used.
The use of siblings in the data analyses poses
statistical problems because of the possibility of a
violation of the independence assumption among the
offspring data. Analyses were conducted with and
without siblings (using random deletion) to determine
if the inclusion of siblings may have biased the results.
Both analyses yielded similar findings; we therefore
included all participants in the analyses.
3.1. Chronic stress: interpersonal and non-interpersonal
Hierarchical multiple regressions were conducted to
parcel out the variance associated with having a parent
with BD from that of having an affective disorder on
measures of total, interpersonal, and non-interpersonal
chronic stress. We controlled for affective disorders
because they are associated with higher levels of chronic
stress (e.g., Hammen and Brennan, 2001; Rudolph et al.,
2000). Independent variables were entered in the
following steps: (1) study from which the data were
taken, (2) age, gender, and offspring affective disorder,
(3) group, (4) group by gender interaction. The
regression equation predicting total chronic stress was
significant [R=0.67, F(6, 63)=8.51, p b 0.001],
accounting for 40% (adjusted R2) of the variance.
Group (β=−0.42; t=−4.34, p b 0.001) was predictive
of 16.6% of the variance in chronic stress, even after
offspring, gender, and age. Gender (β=−0.29; t=−3.05,
p b 0.01) was also a significant predictor; male
participants had higher levels of chronic stress than
The results of the regressions for chronic interperso-
nal and non-interpersonal stress were similar to that
described for total stress. The regressions on inter-
personal [R=0.56, F(6, 63)=4.84, p b 0.001] and non-
interpersonal [R=0.61, F(6, 63)=6.36, p b 0.001] stress
were both significant. Group status was a significant
predictor, accounting for 9.4% and 14.6% of the
variance for interpersonal and non-interpersonal chronic
78C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
stress respectively, even after controlling for affective
disorders in the offspring. The gender by group
interaction was a significant predictor of interpersonal
chronic stress (β=0.20; t=2.28, p b 0.05), accounting
for 5.6% of the variance. Post-hoc comparisons revealed
that male OBD reported more interpersonal stress than
male control [t(40)=3.61, p b 0.001] and female OBD
participants [t(35)=1.97, p=0.057], although the latter
difference fell short of conventional statistical signifi-
cance. No differences in interpersonal stress were
observed between male and female control participants
or between female OBD and female control participants.
To determine if this interaction was due to the presence
of three male participants diagnosed with BD, the
regression analysis on interpersonal chronic stress was
repeated excluding these subjects. The gender by group
interaction fell short of conventional levels of signifi-
cance (β=0.15; t=1.85, p=0.069), but still accounted
for 4.4% of the variance.
3.2. Chronic stress: individual domains of functioning
MANCOVAs were conducted to examine the
individual domains of chronic stress (see Table 2). A
significant main effect of group was found, but there
were no significant gender or group by gender effects.
Among interpersonal domains, the OBD experienced
significantly greater stress than controls in the area of
family relationships [F(1, 59)=12.85, p b 0.001].
Among the non-interpersonal domains, the OBD
reported more difficulties in the spheres of finances
[F(1, 59)=21.63, p b 0.001]. There was also a trend for
the OBD to report more stress in the domain of personal
health [F(1, 59)=3.31, p=0.074].
3.3. Stressful life events
Analyses yielded no main effects or interaction in the
frequency of independent, dependent, interpersonal, and
non-interpersonal SLEs (see Table 3). Therefore, the
hypothesis that the OBD would experience more
interpersonal and dependent SLEs was not supported.
Analyses revealed no group or gender differences on
mean ratings of severity for dependent, interpersonal,
and non-interpersonal SLEs (see Table 3). However, the
OBD were found to experience independent SLEs that
were on average more severe than the control offspring
[F(1, 61)=6.82, p b 0.05].
Based on the previous finding, we examined whether
the OBD had experienced more SLEs of moderate to
of parents with NAD. In the logistic regression,
independent variables were entered as follows:
and 3) group. The results indicated that only group status
(Wald=4.71; 1 df; p b 0.05) significantly predicted the
last 12 months. The odds ratio indicated that the OBD
were 3.1 times more likely to experience a moderate to
Means and standard deviations for frequency and severity of stressful
life events (SLEs)
Stress variablesOBD Offspring of
Episodic stress — frequency
Episodic stress — mean severity
OBD = Offspring of a parent with BD; NAD = no affective disorder.
aGroup significantly different at pb0.05.
2= Partial eta squared.
Fig. 1. Percentage of OBD and offspring of parents with no affective
disorder (NAD) who experienced at least one event of moderate to
severe impact in the last 12 months, subdivided in independent,
dependent, interpersonal, and non-interpersonal stressful life events
(SLEs). Logistic regressions showed that the OBD are more likely to
experience interpersonal events of moderate to severe impact than
control offspring. ⁎pb0.05.
79C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
severe life event in the last 12 months than the control
We repeated the logistic regression described above
to predict the presence of the different types of SLEs
(see Fig. 1). There were no significant predictors of
independent, dependent, and non-interpersonal events.
However, group (Wald=4.62; 1 df; p b 0.05) signifi-
cantly predicted the presence of interpersonal events: the
OBD were 3.9 times more likely to experience a
moderate to severe interpersonal SLE in the last 12
months than offspring of parents with NAD.
The results of this study partially supported our
hypotheses regarding SLEs and chronic stress in the
OBD. First, we hypothesized that the OBD would
experience deficits in multiple domains of functioning.
To our knowledge, no previous study has examined
chronic stress, as assessed with a clinician-administered
interview, in the OBD. Consistent with our prediction, the
OBD reported more interpersonal and non-interpersonal
difficulties than the offspring of parents with NAD, even
the offspring. With respect to the individual domains, the
OBD reported more chronic stress in the areas of family
relationships, finances, personal health, and health of
family members than control offspring. The presence of
chronic stress in family relationships is consistent with the
literature suggesting that parents with BD create an
unstable familial environment (Chang et al., 2001;
Ellenbogen and Hodgins, 2004; Hodgins et al., 2002;
Inoff-Germain et al., 1992; Meyer et al., 2006; Romero
et al., 2005). Since we do not have data on the parents'
stress in this wave of data collection, it is not known what
due directly to the parents' behaviours. Nonetheless, the
the association between parent–child dysfunctional rela-
tionships and vulnerability for depression (for review, see
Burbach and Borduin, 1986; Holmes and Robins, 1987).
However, it is important to note that the OBD,
despite having overall deficits in interpersonal function-
ing, did not differ from the control offspring in the areas
of social life, close friendships, and romantic relation-
ships. The absence of deficits in those areas of
interpersonal functioning is notable given the well-
documented problems in the offspring of parents with
MDD. The latter tend to have more childhood social-
emotional maladjustment (Murray et al., 1999) followed
by global interpersonal impairments during adolescence
(Rudolph et al., 2000). The difference between the OBD
and the offspring of parents with MDD is not easily
explicable. However, other studies have reported similar
results (Kutcher et al., 1998; Petti et al., 2004). Reichart
et al. (2007) found that the OBD's social functioning
was impaired only in those who were aged 18 or over
and were diagnosed with a mood disorder. Similarly,
Anderson and Hammen (1993) found that social
competence was lower for the offspring of parents
with MDD compared to the OBD and control offspring.
Because the present study did not include a sub-sample
of offspring of parents with MDD, we make these
comparisons with due caution.
A significant group by gender interaction indicated
that men in the high-risk group experienced more
chronic interpersonal stress than men in the control
due to the presence of three men with BD in the OBD
group, the interaction was still present, albeit as a trend,
when the analyses were conducted excluding these
participants. Most past research in this area has focused
on the children of parents with MDD. In these studies,
high-risk girls experience more interpersonal stress
than high-risk boys (Hammen, 2003), a finding often
explained by the importance that girls give to
interpersonal relationships, support, and intimacy
(Cyranowski et al.,2000; Nolen-HoeksemaandGirgus,
1994; Rudolph and Hammen, 1999). Unfortunately,
few studies have examined chronic stress in the OBD
and, among these, none have reported significant
gender differences among high-risk youth (Reichart
et al., 2007; Wals et al., 2005). However, a recent study
of social interactions in the natural environment, assessed
over two weeks, revealed that male OBD were more
quarrelsome and less agreeable than female OBD, while
parents with NAD (Linnen et al., 2008). Although the
direction of the gender difference reported in this study
and the present one are inconsistent with the literature on
the children of depressed parents, studies examining the
in women than men (e.g., Reichart et al., 2007),
suggesting that the OBD might differ in meaningful
ways from the children of depressed parents.
In the chronic non-interpersonal stress domains,
more physical health and financial problems were
reported by the OBD than control participants. Since
the area of physical health excludes questions on mental
health, the higher incidence of mental disorders in the
OBD does not account for the finding. Rather, this
domain examines eating habits, illicit drug, cigarette,
and alcohol use, physical exercise, acute illnesses, and
chronic physical conditions. Unfortunately, it is not
80C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
possible to determine exactly which of these areas is
different between the groups. Previously, we found
increased cannabis use, but not tobacco or other drugs,
in the OBD relative to controls (Taylor et al., 2008).
Given that psychopathology is often associated with
poor health habits (Kilbourne et al., 2007), the present
finding may indicate an early or premorbid role of health
risk factors in the development of psychopathology (De
Genna et al., 2006). With respect to financial problems,
we have previously found that that the parents with BD
were characterized by lower income and lower levels
of educational attainment than the control parents
(Ellenbogen and Hodgins, 2004). Therefore, the finan-
cial situation of the BD families could account in partfor
the monetary difficulties reported by the OBD, but more
research is needed to examine spending habits, risky
behaviours, and education attainment in the offspring.
Our second hypothesis was that the OBD would
experience a greater number of, and more severe,
interpersonal and dependent episodic stressors than the
offspring of parents with NAD. The prediction was
partially supported. Although the mean number and
severity of interpersonal and dependent events did not
differ by group, the OBD were more likely to report
interpersonal SLEs of moderate to severe negative
impact. However, since we did not find any differences
in the frequency of dependent interpersonal SLEs, the
present results do not support Hammen's (1991b)
stress generation theory. Hammen's seminal study on
stress generation provided support for the theory in
depressed women, but not in women with BD (Ham-
men, 1991b). A study of young adults with bipolar
spectrum disorder found minimal support of the stress
generation theory using a retrospective self-report
measure of SLEs in childhood (Grandin et al., 2007).
According to the authors, the results were consistent
with a “harsh environment” or stress exposure hypoth-
esis, which states that people who develop BD are
exposed to more negative SLEs (e.g., maltreatment)
that contribute to the onset of their disorder. In contrast,
parents with BD from the present sample have
previously reported higher dependent, but not inde-
pendent, SLEs using a self-report life event checklist
(Ellenbogen et al., 2006), which is consistent with the
stress generation theory. It is important to note that the
stress generation patterns have been based mostly on
female populations (Hammen, 2003); the small sample
of female offspring in the present study might have
diminished our statistical ability to detect group
differences in dependent SLEs. Although the lack of
support of the stress generation hypothesis may be
surprising, it is consistent with the pattern of results
reported previously for chronic stress, which indicated
no impairment in important areas of interpersonal
functioning. Moreover, we have recently observed no
robust group differences between the OBD and the
offspring of parents with NAD on ratings of social
interactions in the natural environment (Linnen et al.,
2008). In contrast with the stress generation theory, the
OBD experienced independent SLEs that were on
average more severe than those reported by control
offspring. This finding suggests that the OBD do not
generate stress in their lives, but rather are exposed to
stress that may in part be due to the unstable
environment of living with an affected parent. Clearly,
there is a need for studies comparing groups of parents
with BD and parents with MDD to further understand
how differences in stress exposure and stress genera-
tion arise and how they affect vulnerability to
There were several limitations to this study. First, the
sample size (i.e., statistical power) may not have been
therefore negative findings should be interpreted with
caution. The group means for dependent SLEs, for
example, are in the expected direction: perhaps with a
group differences. In addition, this sample size did not
of high-risk populations. There may be substantial
differences in premorbid functioning between those
high-risk offspring who develop psychopathology and
those who remain unaffected (Ellenbogen et al., 1999).
Although we controlled for age, participants in early
adolescence are unlikely to experience the same types of
it is expected that some currently asymptomatic or
previously depressed OBD will be diagnosed with BD
2008; Hillegers et al., 2005). Thus, the large range in age
among study participants may have decreased our ability
to detect overall group differences in the number and
severity of SLEs. Third, the present study does not report
recent data on parents' chronic functioning or diagnostic
status. We found that the OBD experienced high levels of
chronic stress in the family relationships, but it is difficult
to determine whether this effect is due to offspring
behaviour or to parent functioning and/or the conse-
quences of affective episodes. Finally, it is possible that
cyclothymia orBDNOS inthe OBD werenot adequately
assessed in the present study. Perhaps undetected
symptoms have influenced measures of chronic inter-
personal stress and SLEs in high-risk offspring.
81C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
This study was the first to examine both chronic and
episodic stress in a sample of OBD, using a clinician-
administered interview. We found that the OBD
experienced more difficulties in interpersonal and non-
interpersonal domains of functioning compared to
offspring of parents with NAD, even after controlling
for the presence of affective disorders in the offspring.
The OBD were also more likely to experience
interpersonal SLEs of moderate to severe intensity.
Overall, the results of this study do not support the stress
generation theory as it applies to BD. However, our
sample size was modest and larger samples may be
needed to detect group differences that are small in
magnitude. Future work in this area should directly
compare the OBD with the offspring of parents with
MDD. Yet, the present findings underline the impor-
tance of examining indices of chronic stress and SLEs in
high-risk youth, as both may represent important risk
factors for the development of affective disorders.
Role of funding source
Funding for this study was provided by grants to Mark Ellenbogen
from the Canadian Institutes of Health Research and Fonds Québecois
de la Recherche sur la Société et la Culture. Caroline Ostiguy was
supported with a fellowship from the Social Sciences and Humanities
Research Council of Canada and Fonds Québecois de la Recherche
sur la Société et la Culture. The agencies had no further role in the
design of the study, collection, analysis, and interpretation of data,
writing of the report, and in the decision to submit the paper for
Conflict of interest
All authors declare that they do not have any conflicts of interest.
are grateful to the anonymous reviewers, who provided
the study. In addition, this project would not have been
possible without the gracious participation of families
involved in this longitudinal project, who have been
collaborating with us for over 10 years.
Achenbach, T.M., 1991.Manual for the ChildBehaviorChecklist/4-18
and 1991 Profile. University of Vermont, Department of
Psychiatry, Burlington, VT.
Adrian, C., Hammen, C., 1993. Stress exposure and stress generation
in children of depressed mothers. J. Consult. Clin. Psychol. 61,
American Psychiatric Association, 1994. Diagnostic and Statistical
Manual of Mental Disorders, 4th edition. American Psychiatric
Press, Washington, D.C.
Anderson, C.A., Hammen, C.L., 1993. Psychosocial outcomes of
children of unipolar depressed, bipolar, medically ill, and normal
women: a longitudinal study. J. Consult. Clin. Psychol. 61,
Benazzi, F., Akiskal, H.S., 2008. How best to identify a bipolar-related
subtype among major depressive patients without spontaneous
hypomania: superiority of age at onset criterion over recurrence
and polarity? J. Affect. Disord. 107, 77–88.
Birmaher, B., Axelson, D., Strober, M., Gill, M.K., Valeri, S.,
Chiappetta, L., Ryan, N., Leonard, H., Hunt, J., Iyengar, S., Keller,
M., 2006. Clinical course of children and adolescents with bipolar
spectrum disorders. Arch. Gen. Psychiatry 63, 175–183.
Burbach, D.J., Borduin, C.M., 1986. Parent–child relations and the
etiology of depression a review of methods and findings. Clin.
Psychol. Rev. 6, 133–153.
Chang, K.D., Blasey, C., Ketter, T.A., Steiner, H., 2001. Family
environment of children and adolescents with bipolar parents.
Bipolar Disord. 3, 73–78.
Cyranowski, J.M., Frank, E., Young, E., Shear, M.K., 2000.
Adolescent onset of the gender difference in lifetime rates of
major depression: a theoretical model. Arch. Gen. Psychiatry 57,
Herzberg, D.S., 1997. Predictors of the generation of episodic
stress: a longitudinal study of late adolescent women. J. Abnorm.
Psychology 106, 251–259.
De Genna, N.M., Stack, D.M., Serbin, L.A., Ledingham, J.E.,
Schwartzman, A.E., 2006. From risky behavior to health risk:
continuity across two generations. J. Dev. Behav. Pediatr. 27,
DelBello, M.P., Geller, B., 2001. Review of studies of child and
adolescent offspring of bipolar parents. Bipolar Disord. 3,
Dohrenwend, B.P., 2006. Inventorying stressful life events as risk
factors for psychopathology: toward resolution of the problem of
intracategory variability. Psychol. Bull. 132, 477–495.
Duffy, A., Alda, M., Trinneer, A., Demidenko, N., Grof, P., Goodyer,
I.M., 2006. Temperament, life events, and psychopathology
among the offspring of bipolar parents. Eur. Child Adolesc.
Psychiatry 16, 222–228.
Eberhart, N.K., Hammen, C.L., 2006. Interpersonal predictors of onset
of depression during the transition to adulthood. Pers. Relatsh. 13,
Ellenbogen, M.A., Hodgins, S., 2004. The impact of high neuroticism
in parents on children's psychosocialfunctioningin a population at
high risk for major affective disorder: a family–environmental
pathway of intergenerational risk. Dev. Psychopathol. 16,
Ellenbogen, M.A., Young, S.N., Dean, P., Palmour, R.M.,
Benkelfat, C., 1999. Acute tryptophan depletion in healthy
young women with a family history of major affective disorder.
Psychol. Med. 29, 35–46.
Ellenbogen, M.A., Hodgins, S., Walker, C.D., Couture, S., Adam, S.,
2006. Daytime cortisol and stress reactivity in the offspring of
parents with bipolar disorder. Psychoneuroendocrinology 31,
82 C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
Bor, W., 2006. Stress sensitization and adolescent depressive severity
as a function of childhood adversity: a link to anxiety disorders.
J. Abnorm. Child Psychol. 35, 287–299.
First, M.B., Gibbon, M., Spitzer, R.L., Williams, J.B.W., 2001.
Structured Clinical Interview for the DSM-VI-TR Axis I Disorders,
Research Version, Patient Editionwith PsychoticScreen. Biometrics
Research, New York State Psychiatric Institute, New York.
Grandin, L.B., Alloy, L.B., Abramson, L.Y., 2007. Childhood stressful
life events and bipolar spectrum disorders. J. Soc. Clin. Psychol.
Hammen, C., 1991a. Depression Runs in Families: The Social Context
of Risk and Resilience in Children of Depressed Mothers.
Springer-Verlag Publishing, New York, NY, US.
Hammen, C., 1991b. Generation of stress in the course of unipolar
depression. J. Abnorm. Psychology 100, 555–561.
Hammen, C., 2003. Social stress and women's risk for recurrent
depression. Arch. Womens Ment. Health 6, 9–13.
Hammen, C., 2005. Stress and depression. Annu. Rev. Clin. Psychol.
Hammen, C., Brennan, P.A., 2001. Depressed adolescents of
depressed and nondepressed mothers: tests of an interpersonal
impairment hypothesis. J. Consult. Clin. Psychol. 69, 284–294.
Hammen, C., Brennan, P.A., 2002. Interpersonal dysfunction in
depressed women: impairments independent of depressive symp-
toms. J. Affect. Disord. 72, 145–156.
Hammen, C., Adrian, C., Gordon, D., Burge, D., Jaenicke, C., Hiroto,
D., 1987. Children of depressed mothers: maternal strain and
symptom predictors of dysfunction. J. Abnorm. Psychology 96,
Henin, A., Biederman, J., Mick,E.,Sachs, G.S., Hirshfeld-Becker,D.R.,
Siegel, R.S., McMurrich, S., Grandin, L., Nierenberg, A.A., 2005.
Psychopathology in the offspring of parents with bipolar disorder: a
controlled study. Biol. Psychiatry 58, 554–561.
Hillegers, M.H., Reichart, C.G., Wals, M., Verhulst, F.C., Ormel, J.,
Nolen, W.A., 2005. Five-year prospective outcome of psycho-
pathology in the adolescent offspring of bipolar parents. Bipolar
Disord. 7, 344–350.
Hodgins, S., Faucher, B., Zarac, A., Ellenbogen, M., 2002. Children of
parents with bipolar disorder. A population at high risk for major
affective disorders. Child Adolesc. Psychiatr. Clin. N. Am. 11,
Holmes, S.J., Robins, L.N., 1987. The influence of childhood
disciplinary experience on the development of alcoholism and
depression. J. Child Psychol. Psychiatry 28, 399–415.
Inoff-Germain, G., Nottelmann, E.D., Radke-Yarrow, M., 1992.
Evaluative communications between affectively ill and well mothers
and their children. J. Abnorm. Child Psychol. 20, 189–212.
Kaufman, J., Birmaher, B., Brent, D., Rao, U., 1997. Schedule for
Affective Disorders and Schizophrenia for School-Age Children-
Present and Lifetime version (K-SADS-PL): initial reliability and
validity data. J. Am. Acad. Child Adolesc. Psych. 36, 980–988.
Kaufman, J., Schweder, A.E., Hilsenroth, M.J., Segal, D.L., 2004. The
Schedule for Affective Disorders and Schizophrenia for School-
Age Children: Present and Lifetime version (K-SADS-PL). John
Wiley & Sons Inc, Hoboken, NJ, US.
Kendler, K.S., Karkowski-Shuman, L., 1997. Stressful life events and
genetic liability to major depression: genetic control of exposure to
the environment? Psychol. Med. 27, 539–547.
Kilbourne, A.M., Rofey, D.L., McCarthy, J.F., Post, E.P., Welsh, D.,
Blow, F.C., 2007. Nutrition and exercise behavior among patients
with bipolar disorder. Bipolar Disord. 9, 443–452.
Kim, E.Y., Miklowitz, D.J., Biuckians, A., Mullen, K., 2007. Life
stress and the course of early-onset bipolar disorder. J. Affect.
Disord. 99, 37–44.
Kutcher, S., Robertson, H.A.,Bird, D., 1998.Premorbidfunctioningin
adolescent onset bipolar I disorder: a preliminary report from an
ongoing study. J. Affect. Disord. 51, 137–144.
Lapalme, M., Hodgins, S., LaRoche, C., 1997. Children of parents
with bipolar disorder: a metaanalysis of risk for mental disorders.
Can. J. Psychiatry 42, 623–631.
Lazarus, R.S., Folkman, S., 1984. Stress, Appraisal and Coping.
Springer, New York.
Linnen, A., aan het Rot, M., Ellenbogen, M., Young, S., 2008.
Interpersonal functioning in the adolescent offspring of parents
with bipolar disorder. J. Affect. Disord. 114, 122–130.
Marin, T.J., Martin, T.M., Blackwell, E., Stetler, C., Miller, G.E., 2007.
Differentiating the impact of episodic and chronic stressors on
hypothalamic–pituitary–adrenocortical axis regulation in young
women. Health Psychol. 26, 447–455.
McGonagle, K.A., Kessler, R.C., 1990. Chronic stress, acute stress,
and depressive symptoms. Am. J. Community Psychol. 18,
McGuffin, P., Rijsdijk, F., Andrew, M., Sham, P., Katz, R., Cardno, A.,
2003. The heritability of bipolar affective disorder and the genetic
relationship to unipolar depression. Arch. Gen. Psychiatry 60,
McQuaid, J.R., Monroe, S.M., Roberts, J.E., Kupfer, D.J., Frank, E.,
2000. A comparison of two life stress assessment approaches:
prospective prediction of treatment outcome in recurrent depres-
sion. J. Abnorm. Psychology 109, 787–791.
Meyer, S.E., Carlson, G.A., Wiggs, E.A., Ronsaville, D.S., Martinez,
P.E., Klimes-Dougan, B., Gold, P.W., Radke-Yarrow, M., 2006. A
prospective high-risk study of the association among maternal
negativity, apparent frontal lobe dysfunction, and the development
of bipolar disorder. Dev. Psychopathol. 18, 573–589.
Murray, L., Sinclair, D., Cooper, P.,Ducournau, P., Turner, P., 1999.The
socioemotional development of 5-year-old children of postnatally
depressed mothers. J. Child Psychol. Psychiatry 40, 1259–1271.
Nolen-Hoeksema, S., Girgus, J.S., 1994. The emergence of gender
differences in depression during adolescence. Psychol. Bull. 115,
Petti, T., Reich, W., Todd, R.D., Joshi, P., Galvin, M., Reich, T.,
Raymond DePaulo, J., Nurnberger, J., 2004. Psychosocial
variables in children and teens of extended families identified
through bipolar affective disorder probands. Bipolar Disord. 6,
Reichart, C.G., Wals, M., Hillegers, M.H., Ormel, J., Nolen, W.A.,
Verhulst, F.C., 2004. Psychopathology in the adolescent offspring
of bipolar parents. J. Affect. Disord. 78, 67–71.
Reichart, C.G., van der Ende, J., Wals, M., Hillegers, M.H., Nolen, W.
A., Ormel, J., Verhulst, F.C., 2007. Social functioning of bipolar
offspring. J. Affect. Disord. 98, 207–213.
Romero, S., Delbello, M.P., Soutullo, C.A., Stanford, K., Strakowski,
S.M., 2005. Family environment in families with versus families
without parental bipolar disorder: a preliminary comparison study.
Bipolar Disord. 7, 617–622.
Rudolph,K.D., Hammen, C., 1999. Age and gender as determinants of
stress exposure, generation, and reactions in youngsters: a
transactional perspective. Child Dev. 70, 660–677.
Rudolph, K.D., Hammen, C., Burge, D., Lindberg, N., Herzberg, D.,
Daley, S.E., 2000. Toward an interpersonal life-stress model of
depression: the developmental context of stress generation. Dev.
Psychopathol. 12, 215–234.
83C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84
Shih, J.H., Eberhart, N.K., Hammen, C.L., Brennan, P.A., 2006.
Differential exposure and reactivity to interpersonal stress predict
sex differences in adolescent depression. J. Clin. Child Adolesc.
Psychol. 35, 103–115.
Singh, M.K., Delbello, M.P., Stanford, K.E., Soutullo, C.,
McDonough-Ryan, P., McElroy, S.L., Strakowski, S.M., 2007.
Psychopathology in children of bipolar parents. J. Affect.
Disord. 102, 131–136.
Taylor, V., Ostiguy, C., Linnen, A., Kadulina, Y., Ellenbogen, M.,
2008, August. Cannabis use, stress, and offspring of parents with
bipolar disorder. Poster presented at the meeting of the American
Psychological Association, Boston.
Todd, R.D., Reich, W., Petti, T.A., Joshi, P., DePaulo Jr., J.R.,
Nurnberger Jr., J., Reich, T., 1996. Psychiatric diagnoses in the
child and adolescent members of extended families identified
through adult bipolar affective disorder probands. J. Am. Acad.
Child Adolesc. Psych. 35, 664–671.
Walker, E.F., Sabuwalla, Z., Huot, R., 2004. Pubertal neuromaturation,
stress sensitivity, and psychopathology. Dev. Psychopathol. 16,
Wals, M., Hillegers,M.H., Reichart,C.G.,Verhulst,F.C.,Nolen,W.A.,
Ormel, J., 2005. Stressful life events and onset of mood disorders
inchildrenof bipolarparents during14-monthfollow-up. J. Affect.
Disord. 87, 253–263.
Waters, B., Marchenko, I., Smiley, D., 1983. Affective disorder,
paranatal and educational factors in the offspring of bipolar manic-
depressives. Can. J. Psychiatry 28, 527–531.
Zahn-Waxler, C., Cummings, E.M., McKnew, D.H., Radke-Yarrow,
M., 1984. Altruism, aggression, and social interactions in young
children with a manic-depressive parent. Child Dev. 55, 112–122.
84C.S. Ostiguy et al. / Journal of Affective Disorders 114 (2009) 74–84