Running Head: PARENT AND CHILD DEPRESSION
Relation between parent and child depression:
Sex, age, pubertal status, and parent-child conflict as moderators
Claire E. Borgschulte
Vanderbilt University
Research Advisors: Sarah A. Frankel, M.S., and Judy Garber, Ph.D.
Abstract
Children of depressed parents are at increased risk for developing depression themselves.
Children’s sex, age, pubertal development, and parent-child conflict all have been shown to be
related to depressive symptoms in children. The current study examined the relation between
parental depression and children’s depressive symptoms, and explored possible moderators
including children’s sex, age, pubertal development, and parent-child conflict. Participants were
227 parent-child dyads; of these, 129 parents were in treatment for depression (high risk); the
remaining 98 parents were lifetime free of depression (low risk). Linear regression analyses
revealed that high-risk children reported significantly higher levels of depressive symptoms than
low-risk children. Sex significantly moderated the relation between risk and children’s
depressive symptoms, such that high-risk girls reported higher levels of depressive symptoms
than low-risk girls. Pubertal development also was a significant moderator, whereas age was not.
More advanced pubertal development was associated with higher depressive symptoms in the
high-risk group, but not in the low risk group. Finally, the relation between risk and children’s
depressive symptoms also was moderated by parent-child conflict; the relation between parent
and child depression was stronger in high as compared to low conflict dyads. Thus, children of
depressed parents who were female, more advanced pubertally, or had greater parent-child
conflict may be at increased risk for depression and therefore should be targeted for intervention.
Offspring of depressed parents are at increased risk for emotional and behavioral
problems, especially depression, compared to children of non-depressed parents (Beardslee,
Versage, & Gladstone, 1998; Hammen & Brennan, 2003; Lieb, Isensee, Hofler, Pfister, &
Wittchen 2002). Children of depressed mothers are twice as likely to be diagnosed with
depression as are children of non-depressed mothers (Hammen & Brennan, 2003); 40% of
children of affectively ill parents experience a major depressive episode by age twenty
(Beardslee et al., 1998). The purpose of the current study was to examine possible moderators of
the link between current major depressive disorder (MDD) in parents and children’s depressive
symptoms. Several factors have been associated with depression in children and adolescents,
including children’s sex, age, pubertal development, and conflict with the depressed parent. The
extent to which these risk factors moderate the relation between parental depression and child
depressive symptoms is less clear, however.
Sex
Depression is more prevalent among females than males (Bouma, Ormel, Verhulst, &
Oldehinkel, 2007; Hankin & Abramson, 1999). After age fifteen, females are twice as likely as
males to experience a major depressive episode (Cyranowski, Frank, Young, & Shear, 2000).
One possible explanation for this sex difference is that females may be more sensitive to
interpersonal stressors than males (Leadbeater, Sidney, & Quinlan, 1995). Indeed, Gore, Asletine
and Colton (1993) found that high levels of interpersonal caring and involvement in the problems
of others accounted for 25% of this sex difference in depression. Females also may exhibit a
more negative cognitive style, which would make them more vulnerable to depression. For
example, Hankin and Abramson (2002) showed that girls’ higher levels of negative cognitions
including negative attributional style and self-perceptions (especially about appearance),
accounted for elevated levels of depressive symptoms.
The findings on sex differences in depression among offspring of depressed parents,
however, have been mixed. Some studies have found that female offspring of depressed parents
are more likely to develop depression than males (Cortes, Fleming, Catalano, & Brown, 2006;
Fergusson, Horwood, & Lynskey, 1995). Daughters of depressed mothers may be more likely
than sons to model their mothers’ depressive cognitions and behavior, and increasingly identify
with their depressed mother over time (Hops et al., 1996). Moreover, girls may be socialized to
develop characteristics typical of depression, such as helplessness, submissiveness, and emotionfocused coping (Hops et al., 1996). In contrast, other studies have not found sex differences in
the relation between parents’ and children’s depression (e.g., Brennan, LeBrocque, & Hammen,
2003). Thus, being female is associated with increased risk for depression, but whether the
relation between parent and child depression varies by sex remains to be explored.
Age
The relation between parent and child depression also may vary as a function of
children’s age. Older daughters of depressed mothers show more depressive symptoms than
both same-age peers of non-depressed mothers and younger daughters of depressed mothers
(Hops et al., 1990). In addition, onset of depression is earlier for children of depressed parents
(mean age 12-13) than for children of non-depressed parents (mean age 16-17; Weissman et al.,
1987). Thus, symptoms of depression may onset at an earlier age in offspring of depressed
parents, and continue to worsen over time, leading older children of depressed parents to
experience more severe depressive symptoms than their non-depressed counterparts.
Additionally, child sex and age may interact to predict children’s risk for depressive
symptoms. Sex differences in the rates of depression begin to emerge during early adolescence,
with at least twice as many adolescent girls as boys displaying depressive symptoms (Hankin et
al., 1998; Ge, Lorenz, Conger, Elder, & Simons, 1994). Hankin and colleagues found that the
rates of depression increased between the ages of 15 and 18 years (from 2.7% to 16.8%,
respectively), and this increase was greater for girls (from 4.4% to 23.2%) than for boys (from
1% to 10.7%).
Some studies have shown that preadolescent boys have higher rates of depression than
preadolescent girls (Rutter, 1986), whereas others have not observed this pattern (Kashani et al.,
1982). The extent to which sex and age independently and then together potentially moderate the
link between parent and child depression in children of depressed parents is not known. Maternal
depression may be more strongly associated with girls’ depressive symptoms than with boys’ as
children enter adolescence (Cortes et al., 2006), but this possibility needs to be addressed
empirically.
Pubertal Development
Pubertal development also has been linked with depression (Angold, Costello, &
Worthman, 1998). Although age and puberty are related, and both have been linked to increases
in depression in girls, their independent relation to depression in high risk youth is less clear. The
gender intensification hypothesis proposes that following puberty, the disparity between the
stereotype of the “perfect” female body and girls’ actual bodies increases, which may, in part,
explain the rise in depressive symptoms among adolescent girls (Hankin & Abramson, 1999).
That is, for girls as their bodies mature and conform less to the “ideal female physique” (e.g.
thin, small hips) puberty may become a stressor. In contrast, puberty in males typically results in
a smaller disparity between their bodies and the “ideal male” physique (e.g. muscular, tall). In
addition, females may be more sensitive or reactive to life stressors and transitions, so the
biological and psychosocial changes associated with early adolescence may trigger more distress
for females than for males (Ge, Conger, & Elder, 2001).
Timing of puberty, that is, the interaction between a child’s age and the onset of puberty,
has been linked with the onset of depressive symptoms. In a longitudinal study, Ge and
colleagues (2001) found that pubertal status in seventh grade predicted later depressive
symptoms, whereas pubertal status in eighth through tenth grade did not predict depressive
symptoms over time. Thus, early maturation when divergent from the norm may provoke social
ridicule or rejection, which, in turn, may increase the chances of depressive symptoms. Ge et al.
(2001) also showed that early maturing girls had higher levels of depressive symptoms than other
girls and boys their age, and suggested that early maturing girls with depression were at a greater
risk for recurrent episodes later in life. Thus, early maturation may be particularly associated
with depression in girls.
The relations among age, pubertal timing, and depressive symptoms also vary by sex.
For example, Angold and colleagues (1998) reported that reaching mid-puberty (i.e., girls have
begun menstruation, are growing rapidly, and show notable breast development) was the best
predictor of depression, regardless of how quickly or at what age girls reached this stage.
Moreover, depressive symptoms in boys began to decrease once they entered puberty, and there
was a sharp decrease in boys’ depressive symptoms shortly after they had reached mid-puberty
(Angold et al., 1998). Thus, the relations among sex, age, pubertal development and children’s
depressive symptoms are complex, and have not yet been studied in children of depressed
parents.
Family Conflict
Levels of conflict are higher in families with a depressed parent (Cummings & Davies,
1994; Garber, 2005), and family discord is associated with depressive symptoms in children
(Davies & Windle, 1997). Moreover, children of depressed parents also have been found to be
particularly sensitive to stress (Bouma, Ormal, Verhulst, & Oldehinkel, 2008). Davies and
Windle (1997) noted that high levels of conflict may mediate the relation between parent and
child depression (Davies & Windle, 1997). It also is possible that family conflict acts as a
moderator of this relation. That is, the relation between parent and child depression may be
stronger in families with a depressed parent where there is more as compared to less conflict.
In summary, sex, age, pubertal development, parental depression, and family conflict all
have been shown to be associated with depression in children. The purpose of the present study
was to examine the extent to which each of these variables further conditioned (i.e., moderated)
the link between parent and child depression in a sample of high and low-risk families. We
hypothesized that: (1) current depression (MDD) in parents would be related to children’s
depressive symptoms; (2) girls of depressed parents would be more likely to have depressive
symptoms than boys of depressed parents and than girls of non-depressed parents; (3) older
children of depressed parents would display more depressive symptoms than younger children of
depressed parents and older children of non-depressed parents; (4) more pubertally developed
children of depressed parents would show more depressive symptoms than less pubertally
developed children of depressed parents and more pubertally developed children of nondepressed parents; and (5) children in high-risk, high conflict families would show higher levels
of depressive symptoms than children in high-risk, low conflict families and children in low-risk,
high conflict families. Finally, we also explored the interactions among these variables. In
particular, we investigated whether (1) high-risk older daughters and (2) high-risk daughters who
were more pubertally developed, experience higher levels of depressive symptoms.
Method
Participants
Participants were 227 parent-child dyads (one parent and one child per family). The
“high-risk” group consisted of 129 families in which a parent (72.9% mothers) was receiving
treatment for a current Major Depressive Disorder (MDD) according to the Diagnostic and
Statistical Manual of Mental Disorders (4th edition; American Psychiatric Association, 1994),
and scored 14 or higher on the 17-item Hamilton Rating Scale for Depression (HRSD17;
Hamilton, 1967). Exclusion criteria included a lifetime diagnosis of any psychotic or paranoid
disorder, organic brain syndrome, intellectual disability, bipolar I or II, current or primary
diagnosis of substance abuse or dependence, obsessive-compulsive disorder, eating disorder,
certain personality disorders (antisocial, borderline, schizotypal).
The comparison “low-risk” group included 98 families with parents (79.4% mothers)
who were lifetime-free of mood disorders, psychotic disorder, organic brain syndromes, or
personality disorders, and during the child’s life were free of adjustment disorders, anxiety
disorders, substance abuse/dependence, psychotherapy longer than two months or eight sessions,
and psychotropic medication use.
Child participants were between 7 and 17 years old (Mean = 12.53, SD = 2.33).
Exclusion criteria included a developmental disability or significant chronic medical conditions.
Among the depressed parents, if more than one child was eligible, the child closest to age 12
years old was recruited. For the non-depressed families, the enrolled child was the one who was
most similar to an offspring of a depressed parent in terms of age, sex, and race. The overall
sample of child participants was 54.6% female; 69.6% Caucasian, 21.6% African-American, 1%
Asian, and 6.9% multi-racial. High- and low-risk children did not differ significantly in age, sex,
or race.
Procedure
Participants were obtained from three cities in the southeast, northeast, and northwest
United States. Depressed parents were recruited from clinics when they first presented for
treatment. Recruitment of comparison families involved advertisements and coordination with
local schools, health maintenance organizations, and community agencies. These parents were
initially screened over the phone, and if eligible, then were scheduled for an evaluation to further
assess eligibility criteria. High-risk children were assessed at the beginning of the parents’
treatment, by different evaluators than those assessing and treating the parent. Low-risk children
were assessed within two weeks after the parent was found to be eligible for the study.
Measures
Parent Psychopathology. The Structured Clinical Interview for DSM-IV Axis I Disorders
(SCID-I; First, Spitzer, Gibbon, & Williams, 1997) and Axis II Personality Disorders (SCID-II;
First, Spitzer, Gibbons, Williams, & Benjamin, 1996) was used to assess current and past
psychiatric disorders and personality disorders. Inter-rater reliability of the SCID has been found
to be good (e.g., Zanarini et al., 2000). For this study, a randomly selected subset of taped
interviews was used to assess inter-rater reliability yielding kappa coefficients >.80.
The Hamilton Rating Scale for Depression (HRSD; Hamilton, 1967) is an interviewbased measure of the severity of depression during the previous week. The 17-item version
yields scores ranging from 0 to 52; higher scores indicate greater severity. The HRSD has high
inter-rater reliability (i.e., > .84). Intra-class correlation in this study was .96.
Children’s Depressive Symptoms. The Children's Depression Inventory (CDI; Kovacs,
1992) was used to measure children’s self-reported symptoms of depression. Each of the 27
items lists three statements in order of symptom severity. Total scores can range from 0 to 54,
with higher scores indicating more depressive symptoms. Internal consistency, test-retest
reliability, and convergent validity have been well-documented for the CDI (Kovacs, 1992). In
this sample, internal consistency was high (α =.84).
Pubertal Development. The Pubertal Development Scale (PDS; Petersen, Crockett,
Richards, & Boxer, 1988) is a self-report measure of children’s pubertal development. It consists
of 5 items each coded on a four-point Likert scale, with higher scores indicating more advanced
development. The PDS contains gender-specific questions pertaining to signs of physical
development, such as growth in height, skin changes, and body hair. It has been shown to have a
high internal consistency (Petersen et al., 1988) and high criterion validity (Brooks-Gunn et al.,
1987). Internal consistency for this sample was .87.
Family Conflict. Children completed the Conflict Behavior Questionnaire (CBQ; Prinz,
Foster, Kent, & O’Leary). This 20-item, true-false measure of perceived parent-child conflict
includes items such as “The talks we have are frustrating,” and “We almost never seem to
agree.” The CBQ has been shown to have good reliability and validity (Robin & Foster, 1989).
In the current sample, internal consistency was high (α = .87).
Results
Correlations among Study Variables
Table 1 displays means and standard deviations for all study variables.
Correlations among study variables are presented in Table 2. Child age was significantly
associated with family conflict, indicating that levels of parent-child conflict were higher for
older child ages. Age also was significantly associated with pubertal development. Higher levels
of depressive symptoms were significantly associated with more advanced pubertal development
and greater family conflict.
Data Analysis
First, a linear regression analysis was conducted with risk as the independent variable and
children’s depressive symptoms (i.e., CDI) as the dependent variable. Next, separate regression
analyses were conducted for each potential moderator, with risk and the moderator (i.e., child
sex, age, pubertal development, and family conflict) as independent variables, and CDI score as
the dependent variable. All main effects and two-way interactions were tested. Next, two
multiple regression analyses were conducted to examine the three-way interactions of (a) risk,
sex, and age, and (b) risk, sex, and pubertal development, on CDI scores. Simple slope analyses
were conducted on all significant interactions (Aiken & West, 1991).
Relation of Risk to Children’s Depressive Symptoms
There was a significant main effect of risk on children’s depressive symptoms (β= 3.58;
pr=.30, p<.001), such that high-risk was associated with significantly higher levels of depressive
symptoms than low-risk.
Does Sex Moderate the Relation between Risk and Children’s Depressive Symptoms?
Regression analyses revealed a significant risk by sex interaction predicting depressive
symptoms (β = -3.05; pr = -.13; p = .05). Simple slope analyses revealed that for girls, risk
significantly predicted depressive symptoms (β = 4.99; pr = .30; p < .001), with high-risk girls
reporting significantly higher levels of depressive symptoms than low-risk girls (see Figure 1).
For boys, risk was not significantly associated with depressive symptoms (β=1.94; pr=.11;
p=.09). Within the high-risk group the difference between girls and boys showed a
nonsignificant trend (β=-1.87; pr=-.12; p =.07); within the low risk group sex was not
significantly related to depressive symptoms (β=1.19; pr=.07; p=.32).
Does Age Moderate the Relation between Risk and Children’s Depressive Symptoms?
The interaction of risk and age did not significantly predict children’s depressive
symptoms (β=.31; pr=.06; p=.36). The main effect of age on depressive symptoms showed a
nonsignificant trend (β=.30; pr=.12; p=.07) for older age to be associated with higher levels of
depressive symptoms.
Does Pubertal Development Moderate the Relation between Risk and Children’s Depressive
Symptoms?
The interaction of risk and pubertal status significantly predicted children’s depressive
symptoms (β= 2.16; pr=.17; p < .05). Simple slope analyses revealed that within the high-risk
offspring group, more advanced pubertal development was associated with higher levels of
depressive symptoms (β=1.86; pr=.23; p = .001). For low-risk children, extent of pubertal
development was not significantly related to level of depressive symptoms (β=-.30; pr=-.03;
p=.66). At both more advanced (β=.50; pr=.02; p=.75) and less advanced (β=-3.28; pr=-.08;
p=.28) pubertal development, the relation between risk and children’s depressive symptoms was
not significant (see Figure 2).
Does Conflict Moderate the Relation between Risk and Children’s Depressive Symptoms?
The risk by conflict interaction was significant (β=.34; pr=.14; p < .05). Simple slope
analyses revealed that in families with high conflict, risk was significantly associated with higher
levels of depressive symptoms (β=3.07; pr=.30; p < .001), whereas for low conflict families, risk
was not significantly associated with children’s depressive symptoms (β = .32; pr = .02; p = .82)
(see Figure 3). For both high (β=.96; pr= .57; p <.001) and low (β = .63; pr = .30; p < .001) risk
children, conflict was significantly associated with depressive symptoms.
Do the interactions between sex and age or between sex and pubertal development moderate the
relation between risk and children’s depressive symptoms?
Regression analyses revealed that neither the risk by sex by age interaction (β=-1.09; pr=.11; p=.11), nor the risk by sex by pubertal development interaction (β=-1.98; pr=.-08 ; p=.30)
significantly predicted children’s depressive symptoms.
Discussion
The current study found several interesting relations among parental depression,
children’s depressive symptoms, and children’s sex, age, pubertal development, and parent-child
conflict. As expected, depressive disorder in parents was significantly associated with children’s
depressive symptoms. In addition, sex, pubertal status, and conflict significantly moderated the
relation between parental MDD and children’s depressive symptoms. Consistent with previous
research (Cortes, Fleming, Catalano, & Brown, 2006; Fergusson, Horwood, & Lynskey, 1995;
Weissman et al., 1987), daughters of depressed parents reported higher levels of depressive
symptoms than daughters of non-depressed parents. In contrast, no difference was found in
levels of depressive symptoms for sons of depressed versus nondepressed parents.
Interestingly, pubertal status significantly moderated the relation between risk and
depressive symptoms, whereas age did not. Among high-risk youth, more advanced pubertal
development was associated with higher levels of depressive symptoms. In contrast, for low-risk
children, puberty was not significantly related to depressive symptoms. Thus, the combination of
living with a depressed parent and experiencing the potential stressors associated with puberty
may be particularly difficult, leading to higher rates of depressive symptoms. It is possible that
the experience of pubertal development differs between high- and low-risk offspring. Depressed
parents may react more negatively to advancing pubertal development. Also, depressed parents
might be less available to support the teen during the normative challenges of puberty.
Consistent with previous findings, (Davies & Windle, 1997; Garber, 2005) family
conflict significantly moderated the relation between risk and depressive symptoms. Specifically,
high-risk children in high conflict homes reported more depressive symptoms than high-risk
children in low conflict homes or low-risk children in high conflict homes. Low-risk children in
high conflict homes also reported more depressive symptoms than low-risk children in lowconflict homes. Thus, high family conflict was an important risk factor for depressive symptoms,
regardless of parental depression; when combined with the risks associated with having a
depressed parent (e.g., genetic vulnerability, maternal criticism), high family conflict may make
high-risk children even more vulnerable to developing depression. The finding that high-risk
children with less parent-child conflict had lower levels of depressive symptoms than those in
high conflict homes, suggests that reducing conflict may be an important target for intervention.
The interactions of neither sex and age nor sex and pubertal development moderated the
relation between parent and child depressive symptoms. Several explanations for these findings
are possible. First, these variables may not interact to predict child depression in a high-risk
sample. For example, in children of depressed parents, the moderating effect of pubertal
development may be the same for girls and for boys. Second, our measure of pubertal
development may not have assessed aspects of pubertal development particularly relevant to risk
for depressive symptoms. Pubertal timing and/or course may be better predictors of depressive
symptoms than pubertal development alone (Ge, Conger, & Elder, 2001; Angold et al., 1998).
The measure of pubertal development used here was a continuous measure based on one time
point, and we were unable to assess timing of the onset of pubertal development. Finally, the
relation between parental depression and child depressive symptoms may vary as a function of
child sex, age, and pubertal development. It is possible that all four of these factors interact to
form the most complete predictor of depressive symptoms in children. Given the sample size in
the current study, however, we likely would not have had sufficient power to test this four way
interaction.
Limitations and Future Directions
Limitations of this study highlight important directions for future research. First, data
about children’s depressive symptoms, pubertal status, and parent-child conflict were based on
self-report questionnaires completed by the children. As a result, relations among these measures
could have been due, in part, to shared method variance. Given that the relations among these
variables differed as a function of which particular moderator was being analyzed, however, it is
not clear why “rater bias” would affect some of these relations more than others. Moreover, the
measures of the most important relation in this study – between parents’ MDD and children’s
depressive symptoms – were based on different informants (i.e., parents and children,
respectively). Nevertheless, whenever possible, multiple methods and measures (e.g., parent
report; behavioral observation) of the constructs being studied should be used.
Second, the current study was cross-sectional, and therefore the direction of the relations
among the variables cannot be determined from these data. Parent and child depression can
reciprocally influence each other (Ge et al., 1995; Kouros & Garber, 2010). For example, the
relation between conflict and depressive symptoms in high-risk youth could have been due as
much to the child’s depression leading to the parent-child conflict as to the reverse (i.e., conflict
leading to depression in the youth). Moreover, the relation between parents’ and children’s
depression also could have been due to some third variable (e.g., genes, common stressors) not
assessed here. Prospective studies are needed to better understand the temporal relation between
risk and children’s depressive symptoms and the contribution of these moderators to this relation
across time.
Third, the relations among parent depression, child depression, and child sex may differ
as a function of parents’ sex (Hops, 1992; Luthar, Cushing, & McMahon, 1997). For example,
children of depressed mothers have been found to have higher levels of internalizing problems
than children of depressed fathers (Connell & Goodman, 2002). Given the small number of
depressed and nondepressed fathers in the current study, we likely would not have had sufficient
power to adequately test parent sex as another possible moderator.
Finally, the current study explored a variety of potential moderators separately. However,
these variables do not operate in isolation. Future research should examine how they are related
to each other, as well as which ones best explain the intergenerational transmission of depression
from parents to their children.
Overall, the present study identified several moderators of the relation between parental
MDD and children’s depressive symptoms. Some of these moderators may be appropriate targets
for prevention. As has been reported in community samples (e.g., Hankin et al., 1998), girls in
high-risk families may be particularly at risk for developing depressive symptoms. As such,
daughters of depressed parents may be especially important targets of intervention. More
advanced pubertal development also was significantly related to higher levels of depressive
symptoms for high-risk youth. Targeting youth based on extent of pubertal development rather
than age, per se, might be a better strategy for identifying those at greatest risk. Interventions
aimed at addressing the specific challenges that accompany puberty (e.g. managing hormonal
changes, understanding body development) could be particularly beneficial. Finally,
interventions focused on reducing the level of parent-child conflict in high-risk families may
prevent children from developing depressive symptoms or may lessen current symptoms. Future
research should examine the effectiveness of targeting these different variables for preventing
depression in high risk youth in particular.
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Table 1. Means and standard deviations for the study variables
Total
Low
Risk
Mean
(SD)
12.72
(2.22)
Girls
Boys
Mean
(SD)
12.53
(2.33)
High
Risk
Mean
(SD)
12.38
(2.40)
Mean
(SD)
12.64
(2.42)
Mean
(SD)
12.44
(2.24)
Pubertal Development
2.41
(0.87)
2.35
(.89)
2.48
(.85)
2.16
(.76)
2.62
(.91)
Conflict
3.45
(4.08)
3.90
(4.39)
2.86
(3.56)
3.00
(3.60)
3.83
(4.41)
Depressive Symptoms
6.56
(6.03)
8.10
(6.66)
4.52
(4.32)
6.30
(4.9)
6.79
(6.86)
Variable
Age
Table 2. Correlations among study variables
Risk
Sex
Age
Pubertal
Development
Conflict
Risk
--
Sex
.014
--
Age
-.073
.043
--
Pubertal
Development
Conflict
-.071
-.264***
.728***
--
.126~
-.102
.174**
.216*
--
CDI
.295***
-.040
.036
.129~
.600***
~p < .10; *p < .05; **p < .01, *** p < .001
CDI = Children’s Depression Inventory
CDI
--
Figure 1. Risk by Sex interaction predicting depressive symptoms (CDI Scores)
16
14
Boys
Girls
CDI Score
12
***
10
8
6
4
2
0
High Risk
***p < .001
Low Risk
Figure 2. Risk by pubertal development interaction predicting depressive symptoms (CDI
Scores)
16
14
More Pubertally Developed
CDI Score
12
Less Pubertally Developed
***
10
8
6
4
2
0
High Risk
***p < .001
Low Risk
Figure 3. Risk by Conflict interaction predicting depressive symptoms (CDI Scores)
16
High Conflict
14
CDI Score
12
Low Conflict
***
***
10
8
6
***
4
2
0
High Risk
***p < .001
Low Risk