Child-, adolescent- and young adult-onsetdepressions differ.docx

Child-, adolescent- and young adult-onset
depressions: differential risk factors in development?
L. Shanahan1*, W. E. Copeland2, E. J. Costello2 and A.
Angold2
1 Department of Psychology, University of North Carolina at
Greensboro, NC, USA
2 Developmental Epidemiology Program, Duke University
Medical Center, Durham, NC, USA
Background. Previous research reported that childhood
adversity predicts juvenile- onset but not adult-onset
depression, but studies confounded potentially genuine
differences in adversity with differences in the recency with
which adversity was experienced. The current study paper took
into account the recency of risk when testing for
differences among child-, adolescent- and young adult-onset
depressions.
Method. Up to nine waves of data were used per subject from
two cohorts of the Great Smoky Mountains Study
(GSMS; n=1004), covering children in the community aged 9–
16, 19 and 21 years. Youth and one of their parents
were interviewed using the Child and Adolescent Psychiatric
Assessment (CAPA) between ages 9 and 16 ; these same
youth were interviewed using the Young Adult Psychiatric

Assessment (YAPA) at ages 19 and 21. The most common
psychosocial risk factors for depression were assessed : poverty,
life events, parental psychopathology, maltreatment,
and family dysfunction.
Results. Consistent with previous research, most childhood
psychosocial risk factors were more strongly associated
with child-onset than with adolescent-/adult-onset depression.
When potentially genuine risk differences among the
depression-onset groups were disentangled from differences due
to the recency of risk, child- and young adult-onset
depression were no longer different from one another.
Adolescent-onset depression was associated with few
psychosocial risk factors.
Conclusions. There were no differences in putative risk factors
between child- and young adult-onset depression
when the recency of risk was taken into account. Adolescent-
onset depression was associated with few psychosocial
risk factors. It is possible that some adolescent-onset depression
cases differ in terms of risk from child- and young
adult-onset depression.
Received 23 September 2010 ; Revised 4 April 2011 ; Accepted
9 April 2011 ; First published online 6 May 2011
Key words : Depression, development, epidemiology, onset,

psychosocial risk factors.
Introduction
Do child-, adolescent- and adult-onset depression
have the same risk correlates and precursors
(Kaufman et al. 2001)? The answer to this question is
unclear. Neurobiological and treatment research has
found that usually two, but not all three, of these
depression-onset groups share common correlates
(Kaufman et al. 2001), suggesting a complex picture of
both shared and non-shared pathways to the onset
of depression at different points in development.
If developmental subtypes of depression differed in
terms of risk, examining them separately for purposes
of biosocial research, prevention and intervention
would be important, as has been shown by research on
developmental subtypes of antisocial behaviors (for a
review, see Moffitt, 2006).
Psychosocial risk for child-, adolescent- and young

adult-onset depression
Juvenile-onset depression is associated with a range of
early psychosocial risk factors, including childhood
poverty (Gilman et al. 2003), life events (Jaffee et al.
2002), parental psychopathology (Jaffee et al. 2002),
maltreatment (Jaffee et al. 2002 ; Hill et al. 2004) and
family dysfunction (Hill et al. 2004). Indeed, youth
with early-onset depression seem to be characterized
by pervasive dysfunction throughout life (Jaffee et al.
2002 ; Hill et al. 2004 ; see also Kovacs et al. 1984 ;
Christie et al. 1988 ; Giaconia et al. 1994 ; Rao et al. 1995 ;
Kasch & Klein, 1996; Weissman et al. 1999). By con-
trast, the childhood psychosocial risk factor profile for
adult-onset depression has been found to be ‘similar
to that of the never-depressed’ (Jaffee et al. 2002,
* Address for correspondence : L. Shanahan, Ph.D., University
of
North Carolina at Greensboro, Department of Psychology, PO
Box

26170, Greensboro, NC 27402, USA.
(Email : [email protected])
Psychological Medicine (2011), 41, 2265–2274. f Cambridge
University Press 2011
doi:10.1017/S0033291711000675
ORIGINAL ARTICLE
p. 215; Hill et al. 2004). These findings have been in-
terpreted as indicating that child- and adult-onset de-
pressions are likely to be etiologically distinct.
However, such a conclusion is premature because
such apparent differences in risk might merely reflect
differences in how recently risk factors were experi-
enced. Risk factors in the key studies were typically
assessed in childhood, but the depressogenic effects of
adversities are strongest during the period immedi-
ately following their occurrence (e.g. Brown & Harris,
1978 ; Kessler et al. 1997), so perhaps we should
not be surprised that childhood risk factors exerted

most of their effects in childhood. Fig. 1a illustrates
that potentially genuine differences in risk were con-
founded with differences in the recency of risk occur-
rence because the time elapsed between childhood
risk and juvenile-onset depression (path ‘a’) was
much less than the time elapsed between childhood
risk and adult-onset depression (path ‘b’).
We propose to test a ‘recency hypothesis ’, which
posits that the lack of strong associations between
childhood adversity and adult-onset depression oc-
curs not because child- and adult-onset depressions
genuinely differ in terms of risk, but because at every
age the depressogenic effects of adversities are mostly
time limited. For example, family dysfunction might
have depressogenic effects for a number of months or
years, but not longer. Thus, if measured in childhood,
it would be linked with child-onset depression, and
perhaps with adolescent-onset depression (Hill et al.

2004), but not with young adult-onset depression.
If measured in adolescence or young adulthood,
family dysfunction would, however, be linked with
adolescent- and perhaps with young adult-onset
depression.
Studies have used cut-offs ranging from 14 to
20 years of age to distinguish between juvenile- and
adult-onset depression (e.g. Jaffee et al. 2002 ; Gilman
et al. 2003 ; Hill et al. 2004). However, the major
increase in the prevalence of depression in females
occurs around age 13 in Western populations (e.g.
Angold et al. 2002), and research increasingly suggests
that adolescent-onset depressions may constitute their
own category (e.g. Kaufman et al. 2001 ; Copeland et al.
2009). Thus, placing adolescent-onset depressions
with either the child- or the adult-onset depressions
could mask adversity-onset links.
The present study attempts to eliminate the con-

found between the recency and risk differences
hypotheses by measuring the same psychosocial risk
factors occurring concurrently with and antecedently
to child-, adolescent- and young adult-onset de-
pressions (see Fig. 1b). According to the recency
hypothesis, the odds ratios (ORs) for paths ‘c ’ should
be similar in size to one another, as should the
ORs for paths ‘d’. According to the risk differences
(a)
(b)
Childhood Adolescence Adulthood
Childhood Adolescence
Adolescent risk
Adolescent-onset
Adult risk
Young adulthood
Childhood risk
Childhood risk

Childhood-onset
a b
Juvenile-onset Adult-onset
Adult-onset
Age
Age
c
d
c c
d
Fig. 1. Timing of risk in relation to depression onset. (a) The
design of previous studies, with childhood risk predicting
juvenile- and adult-onset depression. (b) The design of the
present study, with concurrent and antecedent risk predicting
child-, adolescent- and young adult-onset depression.
2266 L. Shanahan et al.
hypothesis, ORs for paths ‘c ’ should differ in size from
one another, as should the ORs for paths ‘d’.
Method

Sample and procedures
The Great Smoky Mountains Study (GSMS) is a
longitudinal study of the development of psychiatric
disorders in youth (Costello et al. 1996, 2003). The ac-
celerated cohort (Schaie, 1965), two-phase sampling
design and measures are described in detail elsewhere
(Costello et al. 1996). In brief, a representative sample
of 9-, 11- and 13-year-olds in western North Carolina
was selected using a household equal probability
design. In the screening phase the primary caregiver
completed a questionnaire containing items regarding
behavioral disorders from the Child Behavior Check-
list (Achenbach & Edelbrock, 1983). The interview
phase included all children scoring above a predefined
cut-off on this screen (designed to identify the most
pathological 25% of the population), along with a
10% random sample of the remainder. All age-eligible
American Indian children from the area were also

recruited. Data were collected on one cohort at ages
9 and 10, two cohorts at ages 11, 12 and 13, and all three
cohorts at ages 14, 15, 16, 19 and 21 years. Of the 1777
children recruited, 1420 agreed to participate (80%).
Across waves, an average of 82% of possible inter-
views were completed (75–94%). The present study
focuses on the two youngest GSMS cohorts (first as-
sessed at ages 9 and 11 respectively ; n=1004) because
childhood assessments were available for these two
cohorts. Each subject was interviewed up to nine times.
Before each interview began, parent and child signed
informed consent/assent forms approved by the
Institutional Review Boards of Duke University
Medical Center and the Eastern Band of Cherokee
Indians.
Measures
Psychiatric disorders were assessed using (1) the
Child and Adolescent Psychiatric Assessment (CAPA;
Angold & Costello, 1995, 2000) up to age 16, and (2)

the upward extension of the CAPA, the Young Adult
Psychiatric Assessment (YAPA), at ages 19 and 21
(Angold et al. 1999). To minimize recall bias, the time
frame for determining the presence of most psychi-
atric symptoms is the 3 months immediately preced-
ing the interview. Scoring programs for the CAPA and
YAPA, written in SAS (SAS Institute, 2004), combined
information about the date of onset, duration and in-
tensity of each symptom to create diagnoses according
to DSM-IV. A symptom was counted as present if
reported by either parent or child up to age 16 or
by the young adult at ages o19 years. The 2-week
test–retest reliability of CAPA diagnoses for 10- to
18-year-olds is comparable to that of other structured
diagnostic interviews (K values for individual dis-
orders range from 0.56 to 1.0 ; Angold & Costello,
1995). Consistent with previous relevant research, we
used age to distinguish among the depression-onset

groups (Jaffee et al. 2002; Hill et al. 2004). Using pub-
ertal status to define these groups resulted in only
minor changes. Child-onset depression was defined
as first reported diagnosis between ages 9 to <13,
adolescent-onset as first reported diagnosis between
the ages of 13 to 16, and young adult-onset as first
reported diagnosis at ages 19 or 21. We included major
depression, dysthymia and depression not otherwise
specified (NOS) in our depression category. Table 1
describes the depression-onset groups in terms of sex
Table 1. Characteristics of the depression-onset groups. The
percentages for male and female refer to weighted percentages
within the
respective depression (or never-depressed) groups
Child-onset
First diagnosed at
age 9 to <13
Adolescent-onset
First diagnosed
at age 13–16

Adult-onset
First diagnosed at
age 19 or 21
Never-
depressed
Total, n (%) 46 (2.5) 55 (5.6) 44 (3.6) 860 (88.3)
M, n (%) 27 (58.8) 24 (35.1) 20 (40.6) 497 (52.8)
F, n (%) 19 (41.2) 31 (64.9) 24 (59.4) 363 (47.2)
OR (95% CI) M/F 1.35 (0.53–3.47) 0.49 (0.19–1.24) 0.63
(0.22–1.80) 1.55 (0.85–2.85)
Depressive disorders, n (%)
Minor depression 42 (2.3) 50 (5.5) 34 (2.5)
Dysthymia 4 (0.2) 15 (1.6) 17 (1.7)
Major depression 9 (0.4) 18 (2.0) 16 (1.3)
M, Male ; F, female ; OR, odds ratio ; CI, confidence interval.
Values given as unweighted n and weighted prevalence (%).
Risk for depression onset 2267

and specific depression diagnoses. Several subjects
had multiple diagnoses of depression within one
developmental period (e.g. depression NOS in one
childhood year, and major depression in another
childhood year).
Other disorders were also assessed in the CAPA/
YAPA. The unweighted n values and weighted
prevalence were 204 (11.6%) for childhood behavioral
disorders, 99 (6.4%) for childhood anxiety disorders,
203 (18.8%) for adolescent behavioral disorders
(including substance disorders), 48 (4.3%) for ado-
lescent anxiety disorders, and 211 (27.7%) for young
adult antisocial personality disorder and substance
use disorders, and 65 (9.3%) for young adult anxiety
disorders.
Psychosocial risk factors were also collected in the
CAPA and YAPA unless otherwise specified. Here,
we included putative psychosocial risk domains that

have been commonly identified for depression across
development : poverty, stressful life events, parental
psychopathology, maltreatment, and family dysfunc-
tion (Birmaher et al. 1996 ; Cicchetti & Toth, 1998 ;
Goodyer, 2001; Harrington, 2006 ; Zalsman et al.
2006). Individual risk factors (e.g. low income, ma-
terial hardship, and low education in the domain
of poverty) were coded as 1 (present) if reported by
either parent or child (CAPA), and as 0 when not
present. During the adult assessments with the YAPA,
the subject was the sole reporter of all risk factors.
With the exception of lifetime parental psychopath-
ology, all risk factors were assessed at the time of
the interview (e.g. poverty) or over the preceding 3
months (e.g. life events), and were aggregated across
childhood (i.e. any observation from ages 9 to <13),
adolescence (i.e. any observation from ages 13 to 16),
and young adulthood (e.g. any observation at ages 19
and 21). For example, if the subject had experienced

material hardship at any assessment between the ages
of 9 to<13, they received a 1 on the childhood version
of material hardship. Because the time frame for as-
sessing depression was also the 3 months immediately
preceding the interview, temporal overlap between
childhood putative risk factors and depression onset
in the same developmental period was possible (e.g.
childhood risk and child-onset depression). Indeed,
associations between risks and depression onset
within the same developmental period can only es-
tablish putative risk factor status (Kraemer et al. 2001).
To increase the parsimony of our analyses and our
power to detect differences between the depression-
onset groups, we created a sum score for each risk
domain.
The poverty scale ranged from 0 to 3, summing low
income, material hardship, and low education. Low
income was coded when the household income was

below the federal poverty level. Material hardship was
coded when the family (CAPA) or the subject (YAPA)
were unable to meet basic needs, having no health
insurance, financial problems, residential instability,
or no insurance for mental health or substance abuse
care. Low education was coded when the subject’s
parents (CAPA) or the subject (YAPA) did not
graduate from high school.
The loss and violence events scale ranged from
0 to 2, summing the occurrence of loss and violence
events. Loss events included parental divorce/
separation; death of a loved one, sibling, or peer ;
romantic breakup; breakup with or loss of best friend;
pregnancy loss ; and job loss (YAPA only). Violence
events included death of a loved one by violence, war,
terrorism, witness to a violent life event, and cause of
death or severe harm. Details of the construction and
psychometric testing of the Life Events section of the

CAPA are contained elsewhere (Costello et al. 1998).
Lifetime parental psychopathology ranged from
0 to 3 and summed whether biological parents had
ever sought or received treatment for mental health or
drug problems, and whether the parent had been
arrested and/or prosecuted for a crime since parent’s
age 18. [Arrests for driving under the influence (DUI)
and/or drug related charges were not coded here.]
This risk factor was only assessed using a lifetime time
frame.
Maltreatment ranged from 0 to 2 and summed
sexual abuse/violence (including rape) and physical
abuse/captivity. In the YAPA, spousal abuse was in-
cluded in the physical abuse variable. Finally, family
dysfunction ranged from 0 to 3, and included parent–
child conflict, interparental conflict, scapegoating
(CAPA only), and subject’s marital conflict (YAPA
only). Parent–child conflict was coded when children

scored in the top 25% of parent–child conflict within a
given wave. Interparental conflict was coded when the
relationship between parents was characterized by
high conflict, poor communication and/or violence.
Scapegoating (parental differential treatment) was
coded when children were regarded/treated more
negatively by a parent compared to other children in
the family. Subject’s marital conflict was coded when
subjects reported having conflict with a spouse.
Some individual risk factors were assessed in the
CAPA, but not in the YAPA, because they were no
longer relevant in young adulthood. For example,
scapegoating (i.e. parental differential treatment of
children in the home) was no longer coded in the
young adult assessments because many subjects no
longer resided with parents and siblings. Other risk
factors were only age appropriate for young adults,
including subject’s job loss, and marital violence and

conflict. Table 2 describes the depression-onset groups
in terms of (putative) risk factors. When identical risk
domain scores across developmental periods were
created or risk domain scores were standardized
within developmental period, our overall findings did
not change systematically.
Statistical analyses
Weighted logistic regression models were estimated
using generalized estimating equations (GEEs) imple-
mented by SAS PROC GENMOD. Robust (sandwich-type)
variance estimates adjusted the standard errors of the
parameter estimates for the design effects. All analyses
included sampling weights that were inversely pro-
portional to selection probability ; therefore, the results
are representative of the population from which the
sample was drawn. First, each depression-onset group

was examined separately, with child-onset versus never-
depressed, adolescent-onset versus never-depressed,
and young adult-onset versus never-depressed vari-
ables serving as outcome variables. Each (putative)
risk factor sum score was examined individually for
each depression-onset group in univariate regression
models. [The results for individual risk factors (as op-
posed to the sum scores) are available from the first
author upon request.] Next, we also directly tested
differences in the effect sizes of psychosocial risk
factors among the depression-onset groups. For ex-
ample, we tested whether recent risk factors were
more strongly associated with child- than with
adolescent-onset depression. To test for these differ-
ences, we stacked childhood, adolescence and young
adulthood data, and tested interaction terms between
risk factor sum scores and dummy variables indicat-
ing the timing of onset in the prediction of depression.

Because we conducted a large number of statistical
tests, we focus on patterns of results rather than on
single significant coefficients. We emphasize coeff-
icients that are significant using two-tailed significance
testing (i.e. at p<0.05). However, considering that the
hypotheses are directional in nature (i.e. higher levels
of risk are associated with depression), coefficients
significant at p<0.10 are discussed when they are
consistent with a larger pattern of significant results.
Results
Replicating previous findings for adult-onset
depression
To replicate previous findings regarding adult-onset
depression, we combined the adolescent- and young
adult-onset groups into one group, a strategy used
in previous research (see Fig. 1a). Compared to the
never-depressed, childhood poverty was the only
childhood risk domain predicting adolescent-/adult-
onset depression at p<0.05 [OR 1.65, 95% confidence
interval (CI) 1.17–2.30, p<0.01 ; see path ‘b’ in Fig. 1a].

Table 2. Weighted means (standard deviations) of child,
adolescent and young adult risk factors by depression-onset
group
Psychosocial risk factors
Possible
range
Overall
mean
(n=1004)
Child-
onset
(n=46)
Adolescent-
onset
(n=55)
Adult-
onset
(n=44)
Never-

depressed
(n=859)
Childhood risk
Poverty 0–3 1.00 (1.00) 1.72 (0.63) 1.43 (1.10) 1.51 (1.00) 0.93
(0.98)
Loss and violence events 0–2 0.32 (0.53) 0.81 (0.61) 0.40 (0.55)
0.53 (0.50) 0.29 (0.52)
Lifetime parental psychopathology 0–3 0.99 (0.90) 1.73 (0.73)
1.19 (0.99) 1.00 (0.49) 0.95 (0.91)
Maltreatment 0–2 0.10 (0.30) 0.44 (0.37) 0.11 (0.33) 0.13 (0.31)
0.09 (0.29)
Family dysfunction 0–3 0.87 (0.83) 1.48 (0.66) 0.80 (0.73) 1.01
(0.73) 0.85 (0.84)
Adolescent risk
Poverty 0–3 0.82 (0.89) 0.89 (1.04) 0.97 (0.73) 0.79 (0.90)
0.43 (0.61)
1.18 (0.51) 1.05 (0.85)
Maltreatment 0–2 0.19 (0.39) 0.51 (0.51) 0.20 (0.37) 0.15 (0.36)
Family dysfunction 0–3 0.80 (0.80) 1.28 (0.85) 1.44 (0.96) 0.72
(0.75)

Young adult risk
Poverty 0–3 1.25 (0.90) 1.55 (0.63) 1.18 (0.91)
1.05 (0.81)
Maltreatment 0–2 0.01 (0.11) 0.03 (0.15) 0.01 (0.09)
Family dysfunction 0–3 0.24 (0.46) 0.63 (0.60) 0.20 (0.45)
A total of 1004 subjects had data on childhood (putative) risk
factors ; 877 subjects had data on adolescent (putative) risk
factors ; 837 had data on young adult putative risk factors.
Thus, overall similarities in childhood psychosocial
risk between the adult-onset depressed and the never-
depressed were confirmed. To examine differences
in childhood psychosocial risk between child- and
adolescent-/adult-onset depression, we also tested
interactions between risk factors and the timing of
onset in the prediction of depression. Several factors

were more predictive of child- than of adolescent-/
adult-onset depression, including parental psycho-
pathology (OR 1.94, 95% CI 1.09–3.46, p<0.01 for
the interaction term), maltreatment (OR 8.55, 95% CI
1.51–48.48, p<0.05), and family dysfunction (OR 2.36,
95% CI 1.40–4.00, p<0.05), but not childhood poverty
and loss and violence events (OR 1.21, 95% CI
0.79–1.86, p>0.10, and OR 2.22, 95% CI 0.77–6.37,
p>0.10, respectively). As in previous research, child-
onset depression and adolescent-/adult-onset de-
pression were mostly different in terms of childhood
psychosocial risk, a finding previously interpreted as
consistent with the risk differences hypothesis.
Recency versus potentially genuine risk differences
To disentangle differences in predictors among the
depression-onset groups caused by recency from
potentially genuine risk differences, we first examined
links between concurrent putative risk factors and
the respective depression onsets (paths ‘c ’ in Fig. 1b).
Next we examined links between antecedent risk

factors and depression onsets (i.e. childhood risk for
adolescent-onset and adolescent risk for young adult-
onset depression ; paths ‘d’ in Fig. 1b). The results are
shown in Table 3.
Concurrent putative risk factors
According to the recency hypothesis, concurrently
assessed risk factors (paths ‘c ’ in Fig. 1b, shown in the
shaded cells of Table 3) should be similar in size for
the three depression-onset groups, and should have
the strongest and most consistent links with de-
pression onset. That is, childhood risk factors should
Table 3. Psychosocial risk factors predicting depression onset
(compared to the never-depressed)
Risk factor
Child-onset Adolescent-onset Young adult-onset
OR (95% CI) p OR (95% CI) p OR (95% CI) p
Poverty
Childhood 2.08 (1.62–2.69) <0.001 1.61 (1.04–2.49) 0.03a 1.71
(1.06–2.76) 0.03
Adolescence 1.12 (0.68–1.88) 0.64 1.23 (0.84–1.81) 0.28

Young adulthood 1.58 (1.10–2.28) 0.01a
Loss and violence events
Childhood 3.53 (1.49–8.35) 0.004 1.43 (0.72–2.83) 0.31 2.03
(1.03–4.03) 0.04
Adolescence 1.35 (0.67–2.71) 0.40 2.16 (1.02–4.58) 0.04
Lifetime parental psychopathology
Childhood 2.31 (1.43–3.73) 0.001 1.32 (0.84–2.06) 0.23 1.06
(0.88–1.27) 0.56
Adolescence 1.55 (0.86–2.78) 0.15 1.20 (0.86–1.68) 0.29
Young adulthood 1.96 (1.07–3.62) 0.03
Maltreatment
Childhood 9.28 (2.63–32.78) 0.001 0.25 (0.03–2.14) 0.20 2.95
(0.64–13.65) 0.17
Adolescence 7.24 (1.71–30.62) 0.007 1.65 (0.39–6.94) 0.50
Family dysfunction
Childhood 2.34 (1.54–3.54) <0.001 0.88 (0.58–1.35) 0.55 1.25
(0.75–2.08) 0.39
Adolescence 2.42 (1.39–4.20) 0.002 3.02 (1.35–6.75) 0.007

Young adulthood 3.85 (1.66–8.94) 0.002
OR, Odds ratio (unadjusted) ; CI, confidence interval.
A total of 1004 subjects had data on childhood (putative) risk
factors ; 877 subjects had data on adolescent (putative) risk
factors ; 837 had data on young adult putative risk factors.
Values in bold were significant at p<0.05. Values in bold and
italics were significant at p<0.10. Shaded values represent
associations between concurrent risk factors and depression
onset.
a No longer significant at p<0.10 or less when co-morbidity (i.e.
concurrent anxiety and behavioral disorders) was taken into
account.
have the strongest links with child-onset depression,
adolescent risk factors should have the strongest links
with adolescent-onset depression, and young adult
risk factors should have the strongest links with young
adult-onset depression.
The pattern of results suggest that, consistent with
the recency hypothesis, all childhood putative risk

factors were associated with child-onset depression,
and young adult risk factors were associated
with young adult-onset depression. Only adolescent
maltreatment and family dysfunction (but not
adolescent poverty, loss and violence events, and life-
time parental psychopathology) were associated with
adolescent-onset depression.
Because several concurrent putative risk factors
were linked with child- and young adult-onset de-
pression, but not with adolescent-onset depression,
we tested for putative risk differences between
adolescent-onset depression and the other two
depression-onset groups. For example, to examine
whether concurrent poverty was indeedmore strongly
associated with child- than with adolescent-onset
depression, we examined the interaction between
poverty and timing of depression onset in the predic-
tion of depression, essentially testing whether the ORs

for concurrent risk factors reported in Table 3 differed
between child- and adolescent-onset depression.
Concurrent poverty was more strongly linked with
child- than with adolescent-onset depression (OR 1.82,
95% CI 1.02–3.46, p<0.01 for the interaction term).
Similarly, concurrent loss and violence events were
more strongly linked with child- than with adolescent-
onset depression at the statistical trend level (OR 2.75,
95% CI 0.88–8.58, p<0.10 for the interaction term).
No other differences in concurrent risk between child-
and adolescent-onset and adolescent- and young
adult-onset depression were significant. Summarizing
results regarding concurrent putative risk factors
(paths ‘c ’ in Fig. 1b), the child- and young-adult onset
depression groups were similar in terms of concurrent
psychosocial risk. Indeed, follow-up analyses did not
identify significant differences in concurrent risk for
child- versus adult-onset depression. Adolescent-onset
depression, however, seemed to have some differences

in risk from these groups.
Antecedent risk factors
According to the recency hypothesis, some modest
associations would be expected between risk factors
from a previous developmental period and depression
onset. That is, some childhood risk factors may mod-
estly predict adolescent-onset depression, and some
adolescent risk factors may modestly predict young
adult-onset depression (paths ‘d’ in Fig. 1b). The
results showed that childhood poverty predicted
adolescent-onset depression, and that adolescent loss
and violence events and family dysfunction predicted
young adult-onset depression (see Table 3). Analyses
examining potential differences in risk (i.e. differences
in ORs) in antecedent risk factors between adolescent-
and young adult-onset depression showed that
antecedent family dysfunction was more predictive of
young adult-onset than of adolescent-onset depression

(OR 3.12, 95% CI 1.42–7.29, p<0.05). Summarizing the
results regarding antecedent risk factors, adolescent-
onset depression and young adult-onset depression
were mostly similar in terms of antecedent psycho-
social risk.
Childhood risk factors and young adult-onset depression
Finally, the recency hypothesis would predict weak
links between childhood risk factors and young adult-
onset depression. In fact, most childhood risk factors
did not predict young adult-onset depression, with the
exceptions of childhood poverty and childhood loss
and violence events (see Table 3).
Follow-up analyses
In multivariate models we included corresponding
risk factors from childhood and adolescence to
predict adolescent-onset depression, and from child-
hood, adolescence and young adulthood to predict
young adult-onset depression. The results show that
when concurrent risk factors were included, the pre-

viously significant corresponding risk factors from
previous developmental periods continued to predict
adolescent- and young adult-onset depression with
similar effect sizes. Thus, the effects of earlier risk
factors were not mediated by identical later risk. In
another set of multivariate analyses we controlled for
concurrent co-morbidity. For example, for adolescent-
onset depression we controlled for adolescent anxiety
and behavioral disorders. Most associations remained
significant (see coefficients marked with superscript
‘a ’ in Table 3 for exceptions).
Discussion
This is the first epidemiological study to focus
specifically on associations of psychosocial adversity
with child-, adolescent- and young adult-onset de-
pression in order to disentangle differences due to
recency from potentially genuine risk differences.
We also used age-of-onset cut-offs for child- and

adolescent-onset depression that correspond with the
points at which changes in the prevalence of major
depression occur (e.g. Angold et al. 2002).
Consistent with previous research, most childhood
psychosocial risk factors were more predictive of
child-onset than of adolescent-/adult-onset depres-
sion. When we attempted to disentangle potentially
genuine differences in risk from differences due to the
recency with which risk factors had been experienced,
our pattern of results was mostly consistent with the
recency hypothesis, particularly for child- and young
adult-onset depression. All childhood putative risk
factors were associated with child-onset depression;
and corresponding young adult putative risk factors
were associated with young adult-onset depression.
Only two of five adolescent putative risk factors were

linked with adolescent-onset depression. Overall,
our findings show that differences in childhood risk
reported in previous studies mostly reflected differ-
ences in the recency with which the risk factors
had been experienced rather than genuine risk differ-
ences.
A few noteworthy inconsistencies with the recency
hypothesis emerged. First, childhood poverty had
long-lasting effects, and did not differentiate child-
from later-onset depression. This finding was not en-
tirely surprising. In the work of Jaffee et al. (2002),
childhood socio-economic status did not differentiate
between child- and adult-onset depression. Gilman
et al. (2003) also found that childhood low socio-
economic status did not differentiate among child-,
adolescent- and adult-onset depression. Our follow-
up analyses that controlled for later corresponding
risk factors showed that the pathway from childhood

poverty to later depression onset was not explained
by poverty in adolescence or in young adulthood.
Childhood may be a sensitive period during which the
experience of poverty creates lasting changes in the
organism’s stress response (Power et al. 1999 ; Danese
et al. 2009 ; Miller et al. 2009), and, thus, vulnerability
to depression. Second, childhood loss and violence
events predicted young adult-onset depression.
Although parental loss predicted juvenile- but not
adult-onset depression in a previous paper (Jaffee et al.
2002), others have described the long-lasting mental
health effects of childhood loss events (Brown &
Harris, 1978).
Third, all differences among the depression-onset
groups involved adolescent-onset depression, sug-
gesting that there could be some genuine differences
in risk between adolescent-onset depression and
the other onset groups. Alternative pathways to

adolescent-onset depression, particularly for females,
have been suggested, including low birthweight
(Costello et al. 2007), early pubertal timing (Copeland
et al. 2010), increases in pubertal hormones (Angold
et al. 2003), and biopsychosocial and cognitive inter-
actions (e.g. Susman, 1997 ; Ge et al. 2001).
Limitations and directions for future research
First, although the study’s focus was limited to
psychosocial risk factors, the findings have important
implications for gene–environment (GrE) interaction
research. For example, taking into account that devel-
opmental nuances of environmental risk such as
their timing in relation to depression onset may be
important for increasing rates of replications in GrE
research involving the serotonin-transporter-linked
polymorphic region 5-HTTLPR (Canli & Lesch, 2007).
Second, our assessments began at age 9, but we will
have missed cases with depression onset before age 9,
depression onset in the 9 months of the year that

the CAPA/YAPA interviews did not cover, and de-
pression onset during years when interviews were not
conducted. Third, the depression-onset groups were
relatively small, limiting our statistical power. We also
did not distinguish between juvenile-onset groups
with recurrence versus those without recurrence ;
however, previous work had found few early ad-
versity differences between such groups (Jaffee et al.
2002). Fourth, our last available age for this study was
21, so the findings may be specific to the narrow young
adult age range assessed here.
Fifth, several of our risk factors were assessed con-
currently with depression, and therefore could be
indicative only of ‘putative’ risk similarities and dif-
ferences among depression-onset groups. We also
did not assess risk factors antecedent to child-onset
depression. Sixth, our findings are not informative
with respect to causal chains leading to the onset of

depression. Risk factors can also be heterogeneous
in terms of their developmental history, and future
research should examine interactions between risk
factors at different developmental periods in the pre-
diction of depression onset. Finally, to capture each
risk domain in the most age-appropriate, devel-
opmentally valid way, some individual risk factors
included in each risk domain varied somewhat be-
tween childhood/adolescence and young adulthood.
These slight changes in the composition of risk do-
mains could allow for an alternative interpretation
of findings: that apparent similarities in associations
between child/adolescent and young adult risk
factors nevertheless disguise potential risk differences.
Additional analyses showed, however, that when risk
factors were forced to be identical across develop-
mental periods or when risk factors were standardized
within each developmental period, the overall find-

ings did not change.
These limitations were balanced by the prospective
longitudinal design of our study, and the reliability of
CAPA and YAPA symptom assessment. Furthermore,
they were not unique to our study. Indeed, the only
other prospective longitudinal study of depression-
onset groups assessed depression at only six waves
per subject, starting at age 10, and interviewed
participants every 2, 3 or 5 years, using 12-month time
frames for symptom assessments (Jaffee et al. 2002).
Future prospective longitudinal studies should aim
for continuous coverage of depression-onset data.
This would determine whether findings are specific to
depression onset at particular ages, and not just to any
diagnosis of depression at these ages.
Despite these limitations, our study shows that,

when potentially genuine risk differences were disen-
tangled from differences in the recency of risk, the
number of putative psychosocial risk differences
among developmentally defined depression-onset
groups is relatively small. Although distinguishing
among developmental subtypes has been useful for
other disorders (Moffitt et al. 2008), our findings sug-
gest that assuming distinctions between child- and
young adult-onset depression based on differences in
psychosocial risk factors is unwarranted. Differences
between adolescent-onset depression and the two
other depression-onset groups may be consistent with
studies showing that adolescent-onset depression is
predicted by biological factors.
Acknowledgments
The work presented here was supported by the
National Institute of Mental Health (MH63970,
MH63671, MH48085), the National Institute on Drug

Abuse (DA/MH11301), and the William T. Grant
Foundation. All authors had full access to all in this
study and Dr Shanahan takes responsibility for the
integrity of the data, and the accuracy of the data
analysis.
Declaration of Interest
None.
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Discussion Board Forum 1 Instructions
Upon completing Module/Week 1’s Reading & Study items, you
will be well-equipped to respond with a thread and at least 2
replies by objectively applying critical thinking strategies and
articulating the importance of knowing what you believe and
why you believe it. (Syllabus MLOs: A, C, D and Module/Week
1 LOs 1, 2).
Discussion Board Forum 1 will have 2 parts: a thread in
response to the instructor’s prompt and replies to at least 2
other classmates’ threads. Review the Discussion Board Forum
1 – Thread Grading Rubric and the Discussion Board Forum 1 –

Replies Grading Rubric for a list of criteria and the breakdown
of points for each part of these assignments. To complete
Discussion Board Forum 1, adhere to the following:
General Instructions:
1. Submit your discussion board thread directly into the forum.
Do not attach your submissions as documents.
2. First person (e.g., “I” or “we”) is allowed in all posts.
3. See the Student Expectations for guidelines on proper
netiquette.
4. All threads in response to the instructor’s prompt must be
100–200 words (50–100 words per question). This parameter
helps to promote writing that is thorough, yet concise enough to
permit other classmates to read all the submissions. (Note:
Submissions fewer than 75 words will receive no credit.)
5. All threads must be supported with Scripture, course content,
or research. Quotations or the use of ideas addressed in course
content or found in research must be properly cited using
current APA, MLA, or Turabian formatting (whichever
corresponds to your degree program). All content used in your
forum that is not considered “common knowledge: must be
cited. Do not plagiarize.
6. Your replies to at least 2 other classmates’ threads must be
50–100 words each. (Note: Submissions fewer than 25 words
will receive no credit.)
7. Title the subject line of the replies “Reply to John Smith,”
“Reply to Jane Doe,” etc. so that it will be clear to whom you
are responding.
8. Each reply must contain:
· At least 2 positive comments or observations about the post.
· At least 1 suggestion on how your classmate could have
improved his or her post or ask him or her a question to think
about which specifically relates to the thread prompt questions.
Note that “I like what you said,” “That’s a good comment,” and
“I disagree with your comment” in and of themselves do not
count as complete replies. Instead, state why you liked or
disliked the comment, add additional thoughts or ideas to the

original comment, or provide alternative thoughts or ideas when
you disagree.
Replies:
1. COLLAPSE
Top of Form
I think that it is important to know what you believe so you
can help teach others and explain to people the way you feel
about the religion. "How then will they call on him in whom
they have not believed? And how are they to believe in him of
whom they have never heard? And how are they to hear without
someone preaching?" (Romans 10:14). I chose this passage as a
reference because I believe that God wants us to spread His
story and to help spread Christianity. If no one knew what they
believed, how would they be able to have faith in God? It is just
as important to be able to explain to someone why you believe
the things you do. In order to help spread the word of God,
especially those who are unsure of any religion, you must
provide support for your beliefs so it helps others gain your
trust and can start to have faith in God. I think it is important to
stick with what I believe and spread my beliefs, even if they
differ from someone else.
I believe that God has created this world for us to live in.
He wants us to treat it with respect, as it is a gift and a blessing
to us. I believe He watches over all of us all the time and is
important to recognize Him through religious practices. I
believe that the Bible was created in order to tell the story of
God and His followers. It gives us insight into periods of time
where none of us were present. I think some people have a hard
time putting their faith in God because some things in the Bible
are confusing and sound crazy. I think it is important to have a
strong faith in order to understand the Bible and trust in His
story. I believe that Jesus Christ is an extension of God and that
God created his only son, himself as a human. Jesus Christ died

on the cross for our sins and I believe that we must appreciate
the world we live in. It is important to ask for forgiveness and
put your trust in Jesus Christ for allowing you to be forgiven.
The Holy Bible ESV: English Standard Version: Containing the
Old and New Testaments. (2007). Wheaton, IL: Crossway
Bibles.
Bottom of Form
2. 1. Why is it important to know what you believe and why you
believe it?
Knowing what you believe and understanding why is
necessary to fulfill our Christian duty of spreading the gospel.
When telling others about God, our text says, "They ought to be
totally convinced that you yourself totally believe in what you
are saying with all your heart!” (Weider & Gutierrez, 2013) You
cannot tell about God if you have doubts. The devil will find
cracks to slither through. “Let us hold fast the confession of our
hope without wavering, for he who promised is faithful.”
(Hebrews 10:23 King James Version) If you trust and believe in
God, He will not let you slip.
2. Identify what you believe about God, the Bible and Jesus
Christ. Why do you believe these things?
I believe there is one God who created everything. I
believe in the Trinity that is God the Father, God the Son and
God the Holy Spirit. I believe that the Bible is the only book
authored by God, for us. “It shapes our worldview because of its
absolute truth, which transcends any other “truth” we can
create.” (Hindson, Etzel & Gutierrez, 2016) The Word of God is
alive and only when I rely on God and His Word do I find
peace. It is because of His faithfulness that I believe.
References:
Weider, L., & Gutierrez, B. (2013). Finding Your Worldview:
Thinking Christianly About the World [Ebook] (1st ed., p. 9).

Lew Weider and Ben Gutierrez. Database. Retrieved from
http://www.mywsb.com
Hindson, E., Etzel, G., & Gutierrez, B. (2016). Everyday:
Biblical Worldview [Ebook] (p. 10 of 1,224). Nashville,
Tennessee: LIfeway Church Resources, B&H Publishing Group.
Retrieved from https://www.mywsb.com/reader
The Relations among Maternal Depressive Disorder,
Maternal Expressed Emotion, and Toddler Behavior
Problems and Attachment
Julie A. Gravener & Fred A. Rogosch & Assaf Oshri &
Angela J. Narayan & Dante Cicchetti & Sheree L. Toth
Published online: 7 December 2011
# Springer Science+Business Media, LLC 2011
Abstract Direct and indirect relations among maternal
depression, maternal Expressed Emotion (EE: Self- and
Child-Criticism), child internalizing and externalizing symp-
toms, and child attachment were examined. Participants were
mothers with depression (n=130) and comparison mothers
(n=68) and their toddlers (M age=20 mo.; 53% male).
Assessments included the Diagnostic Interview Schedule
(maternal depression); the Five Minute Speech Sample (EE);
the Child Behavior Checklist (toddler behavior problems);
the Strange Situation (child attachment). Direct relations
were significant linking: 1) maternal depression with both
EE and child functioning; 2) Child-Criticism with child
internalizing and externalizing symptoms; 3) Self-Criticism
with child attachment. Significant indirect relations were
found linking maternal depression with: 1) child externaliz-

ing behaviors via Child-Criticism; 2) child internalizing
behaviors via Self- and Child-Criticism; and 3) child
attachment via Self-Criticism. Findings are consistent with
a conceptual model in which maternal EE mediates relations
between maternal depression and toddler socio-emotional
functioning.
Keywords Maternal depression . Expressed emotion .
Attachment . Internalizing behaviors . Externalizing
behaviors . Criticism
Maternal depression poses significant risks for the social and
emotional development of offspring (Goodman and Tully
2006; Lovejoy et al. 2000). Children of mothers with
depression are at increased risk for developing an insecure
attachment with caregivers (Coyl et al. 2002), increased
internalizing and externalizing symptoms during childhood
(Silk et al. 2006), and clinically significant psychopathology
during childhood and adolescence (Hammen and Brennan
2003). Although the adverse effects of maternal depression
are well documented, the underlying processes by which
maternal depression impacts child functioning have been less
clearly elucidated (Cicchetti and Toth 1998; Goodman and
Gotlib 1999). The purpose of this study is to examine the
direct relations between maternal depression, maternal
Expressed Emotion (EE), and toddler attachment security
and behavior problems, and to investigate the role of
maternal EE as a mediator of the relations between maternal
depression and toddler socio-emotional functioning.
Expressed Emotion
Depression is a debilitating mental disorder that is often
characterized by negative thoughts and emotions regarding

self and the world (Beck 1976; Beck 2002). In mothers
with depression, this tendency towards negativity may
J. A. Gravener : F. A. Rogosch :A. Oshri :D. Cicchetti :
S. L. Toth
Clinical and Social Sciences in Psychology,
University of Rochester, Mt. Hope Family Center,
Rochester, NY, USA
A. J. Narayan
Institute of Child Development, University of Minnesota,
Minneapolis, MN, USA
D. Cicchetti
Institute of Child Development and Department of Psychiatry,
University of Minnesota,
Minneapolis, MN, USA
J. A. Gravener (*)
Mt. Hope Family Center,
187 Edinburgh St.,
Rochester, NY 14608, USA
e-mail: [email protected]
J Abnorm Child Psychol (2012) 40:803–813
DOI 10.1007/s10802-011-9598-z
create a child-rearing environment characterized by criti-
cism. The Five Minute Speech Sample (FMSS; Magana et
al. 1986) provides one way to assess maternal representa-
tions of the child. In the FMSS, individuals are asked to
speak uninterrupted for 5 min on their thoughts and feelings
about a specified individual without knowledge of what
constructs will be coded from their speech. The content and
tone of the speech sample are assessed to rate EE, which

serves as an index of an individual’s affective expression.
An overall EE rating is made from the speech sample along
with sub-ratings of Criticism and Emotional Over-
Involvement. The EE construct was initially developed in
the context of predicting relapse after treatment in adults
with schizophrenia (Brown et al. 1972; Brown and Rutter
1966), and high EE measured in family members has been
found to predict relapse in adults with schizophrenia
(Moline et al. 1985; Yang et al. 2004) as well as other
mental illnesses (Hooley 2007; O’Farrell et al. 1998; Yan et
al. 2004).
More recently, research on EE has been extended to
assess the emotional climate of the relationship between
parents and young children. High EE-Criticism has been
found to be associated with maladaptive parental behaviors
such as antagonism, negativity, disgust, harshness and
decreased responsiveness in the context of the parent–child
relationship (McCarty et al. 2004). Previous research has
found that high EE-Criticism is associated with adverse
functioning in children and adolescents, including higher
levels of internalizing and externalizing symptoms (Frye
and Garber 2005), affective disorders (Schwartz et al. 1990;
Silk et al. 2009), substance abuse and conduct disorder
(Schwartz et al. 1990), antisocial behavior problems (Caspi
et al. 2004), and self injurious thoughts and behaviors
(Wedig and Nock 2007). With few exceptions (e.g.,
Hirshfeld et al. 1997; Raishevich et al. 2010), high EE-
Emotional Over-Involvement has been found to be less
predictive of child behavior problems (Baker et al. 2000;
Nelson et al. 2003), and may lack construct validity in the
context of the relationship between parents and young
offspring where it has been found to be unrelated to
observed behaviors during parent–child interactions
(McCarty et al. 2004).

Expressed Emotion and Parental Psychopathology
EE has traditionally been coded from parental speech
samples as a way to predict mental illness or relapse in
offspring; however EE is also a useful tool for understand-
ing mental representations of self and other in an individual
with psychopathology and the emotional climate experi-
enced by those around the individual. It is unique from
many other assessments of parenting in that it focuses on
how a parent thinks about their child rather than explicit
parental behavior. Higher EE-Criticism measured in regard
to offspring is significantly associated with maternal
depression diagnosis and symptoms (Bolton et al. 2003;
Frye and Garber 2005; Green et al. 2007; Nelson et al.
2003; Rogosch et al. 2004; Tompson et al. 2010). One
study found that mothers of toddlers with a history of
depression also express more EE-Criticism when speaking
about themselves and their spouses using the FMSS
(Rogosch et al. 2004). This finding suggests that represen-
tations of both other and self are likely to be characterized
by negativity in mothers diagnosed with depression, and
more research is necessary to understand how maternal
Self-Criticism and Child-Criticism are differentially associated
with child socio-emotional functioning.
The documented associations between EE-Criticism,
maternal depression, and child psychopathology and be-
havior problems suggest that maternal EE-Criticism may be
involved in the underlying process by which maternal
depression can negatively impact child socio-emotional
development. A handful of studies have examined this
hypothesis using child behavior problems as an assessment
of child adaptation. One study found that EE-Criticism
partially mediated the association between degree of
maternal depression and adolescent externalizing symptoms

but not internalizing symptoms in a study employing a
concurrent design; notably, there also continued to be a
direct effect for maternal depression on child externalizing
symptoms after controlling for EE-Criticism (Nelson et al.
2003). EE-Criticism was also found to significantly mediate
the association between maternal depressive symptoms and
child externalizing behaviors in a cross-sectional study of
children ages four to 11 (Bolton et al. 2003). In contrast, a
longitudinal study that focused on adolescent aged off-
spring found no support for EE-Criticism as a mediator of
the association between maternal depression and adolescent
internalizing and externalizing symptoms (Frye and Garber
2005). Rather, support was found for adolescent external-
izing behaviors as a mediator of the association between
maternal depression history and EE-Criticism (Frye and
Garber 2005). In a conceptually related area of research,
longitudinal associations have been demonstrated between
harsh and rejecting parenting during early childhood and
child behavior problems in subsequent years (Campbell et
al. 1996; Shaw et al. 2003; Shaw et al. 1998). Studies of
school age children have also found significant indirect
relations between maternal depression and child behavior
problems via harsh parenting (Chang et al. 2004; Harnish et
al. 1995). Collectively, these findings highlight the impor-
tance of examining both negative parental behaviors and
representations during early development. However, to
date, research on maternal critical representations of the
child as assessed by EE has focused exclusively on older
804 J Abnorm Child Psychol (2012) 40:803–813
children and adolescents, leaving unanswered questions
about the role of EE-Criticism in the association between
maternal depression and child behavior problems in very

young children. Studying these processes in younger
children may better elucidate the way in which the
associations between maternal depression, EE-Criticism,
and child behavior problems develop. Additionally, to our
knowledge, the role of maternal EE-Criticism towards self
in the association between maternal depression and child
behavior problems has yet to be investigated. Examining
each of these associations will allow us to evaluate whether
it is child criticism specifically that poses a risk factor for
child behavior problems or if children’s behaviors at this
young age are also related to maternal self-criticality.
An important task during the first 2 years of life involves
developing a secure attachment relationship with the parent.
Research has repeatedly shown that children of mothers with
depression or elevated depressive symptoms evidence higher
rates of insecure and disorganized attachment than do
children of non-depressed mothers (Carter et al. 2001;
Lyons-Ruth et al. 1990; Teti et al. 1995; Toth et al. 2009).
However, the process by which maternal depression
impacts child attachment is yet to be fully understood.
Little research has examined the association between
maternal EE and child attachment. Findings from two
studies suggest significant associations between disorga-
nized attachment and high maternal EE assessed in both a
clinically referred (Green et al. 2007) and normative sample
of children (Jacobsen et al. 2000). To our knowledge, no
study to date has examined maternal EE as a potential
mediator of the association between maternal depression
and child attachment. Through early interactions with his or
her primary caregiver, the child develops a sense of self and
other, influenced by the child’s perceptions of his or her
needs being met in the context of the caregiving relation-
ship (Bowlby 1969). Negative self-representations may
impact a mother’s perceptions of her ability to meet her
child’s needs. Additionally, mothers’ negative child repre-

sentations could impact maternal perceptions of child
soothability when the child is distressed. Thus, EE-
Criticism towards self and child may be associated with
maternal efforts towards or success at serving as a secure
base, and the role of EE has yet to be explored in the relation
between maternal depression and child attachment security.
Aims of the Current Study
Previous research on the current sample has demonstrated
that compared to nondepressed mothers, depressed mothers
have higher levels of EE. Additionally, children of
depressed mothers have higher levels of behavior problems
and attachment insecurity than children of nondepressed
mothers, and there is a significant relation between
maternal EE and child problem behaviors (Rogosch et al.
2004; Toth et al. 2006). The present study aims to elaborate
on previous research by using a path analytic technique to
test hypotheses regarding significant direct positive associ-
ations between maternal depression and (a) maternal EE
Self-Criticism, (b) maternal EE Child-Criticism, (c) child
internalizing and externalizing behaviors, (d) and attach-
ment insecurity. Additionally, we hypothesize that there
will be positive direct associations between EE Self- and
Child-Criticism and (a) child internalizing and externalizing
behaviors and (b) attachment insecurity. Subsequently, we
test a model in which maternal EE Self- and Child-
Criticism are each conceptualized as mediators of the
association between maternal depression and (a) child
internalizing and externalizing behaviors and (b) attachment
insecurity in toddler aged children. We hypothesize that
there will be significant indirect relationships between
maternal depression and child behavior problems and
attachment via maternal EE Self- and Child-Criticism.

Methods
Participants
Mothers (n=198) ages 21 to 41 (M=31.68, SD=4.68) with
and without a history of major depressive disorder since the
birth of their child and their toddlers (53% male) were
recruited as part of a larger study of the effects of maternal
depression on child development. All study procedures
were approved by the University of Rochester human
subjects institutional review board, and mothers provided
informed consent and permission for their child’s partici-
pation in the project before study procedures were initiated.
Mothers who had experienced a major depressive episode
(n=130) since the birth of their child were recruited through
newspaper and community publication notices and flyers
placed in medical offices and on community bulletin
boards. A comparison group of mothers (n=68) without a
current or past history of any major mental disorders was
recruited by contacting families who lived in the same
neighborhoods as the mothers in the depressed group. Birth
records were utilized to identify families with toddler-age
children. Inclusion criteria for mothers in the depressed
group included meeting the Diagnostic and Statistical
Manual of Mental Disorders (3rd ed., rev.; DSM-III-R;
American Psychiatric Association 1987) criteria for major
depression since their child’s birth according to the
Diagnostic Interview Schedule (Robins et al. 1989) and
having a child approximately 20 months (M=20.32, SD=
2.50 months) of age at the time of recruitment. Mothers in
the depressed group were excluded if they met criteria for
J Abnorm Child Psychol (2012) 40:803–813 805

bipolar disorder. Mothers were included in the nonde-
pressed group if they had a toddler of approximately
20 months of age at the time of recruitment and did not
meet criteria for any current or past major psychiatric
disorder as determined by the DIS-III-R. To minimize co-
occurring risk factors, only families of middle or higher
socioeconomic status were included. Accordingly, mothers
in both groups were required to have a minimum of a high
school education and could not be receiving public
assistance at the time of recruitment.
Participants in the depressed and nondepressed
groups were comparable on a number of variables.
Family socioeconomic status did not differ between
groups, t(196)=1.19, p=0.24, nor did child gender, χ2(1,
N=198)=0.08, p=0.78. The majority (92.9%) of mothers
in the sample were Caucasian, and the percentage of mothers
of non European-American race/ethnicity did not differ
between groups, χ2(1, N=198)=1.11, p=0.29. Maternal age
differed significantly between the two groups, with mothers
in the nondepressed group being slightly older (M=32.8,
SD=4.0) than mothers in the depressed group (M=31.0,
SD=4.9), t(196)=2.58, p=0.01. The majority of mothers in
the sample were married (87.9%). However, mothers in the
depressed group were more likely to be currently unmarried
or separated than the nondepressed group mothers, χ2(1, N=
198)=11.03, p=0.001; this finding is consistent with reports
of marital difficulties associated with depression (Coyne and
Downey 1991).
Measures
Diagnostic Interview Schedule (DIS-III-R; Robins et al.
1989) The DIS-III-R is a structured interview designed to
assess diagnostic criteria for Axis I disorders according to
the DSM-III-R (American Psychiatric Association 1987)

and allows for the diagnosis of 48 DSM-III-R disorders.
The DIS-III-R version was chosen for use in this study as it
was the current diagnostic interview at the initiation of the
investigation. The interview consists of modules that
inquire on symptom history for different categories of
DSM-III-R Axis I disorders. Questions are answered in a
“yes” or “no” format, reducing the need for interviewer
interpretation. Given the highly structured format of the
DIS-III-R, sensitive clinical judgments are not necessary
and trained nonprofessional interviewers can conduct the
interview. Demographic information was also collected
during the administration of the DIS-III-R.
Beck Depression Inventory (BDI; Beck et al. 1961) The
BDI is a widely used self-report measure of current
depressive symptoms, including cognitive, affective, moti-
vational and physiological symptoms. It contains 21 items,
and each lists four self-evaluative statements that are scored
from 0 to 3, with higher scores indicating greater severity.
Cutoff scores have been established to indicate different
levels of depression (0–9: none or minimal; 10–18: mild to
moderate; 19–29: moderate to severe; 30–63: severe) (Beck
et al. 1988). The validity of the BDI has been supported by
previous research (Beck et al. 1988), and internal consis-
tency of the measure in this sample was 0.92.
Five Minute Speech Sample (FMSS; Magana et al. 1986)
The FMSS was conducted to assess EE in regard to self and
child. EE has traditionally been coded from the Camberwell
Family Interview, but the FMSS is a valid alternative
method that reduces the burden of assessment on the
research participant as well as the time necessary to code
EE (Magana et al. 1986).
Mothers were asked to speak for 5 min without

interruption on their thoughts and feelings about their child
using standard administration procedures. They were then
asked to speak for 5 min about themselves in a separate
speech sample. They were unaware of what constructs
would be coded from their speech. Based on audio
recordings of the speech samples, EE was coded based on
verbal content and tone using the Magana et al. (1986)
coding manual. A three-point scale was used to indicate
whether the mother’s level of EE-Criticism was low,
borderline, or high. A high EE-Criticism rating is made if
the mother starts the FMSS with a negative comment,
expresses one or more criticisms, or describes a negative
relationship (the latter used only for the speech sample
regarding the child). A borderline rating is made if the
mother expresses one or more dissatisfactions in the
absence of any of the following: critical comments, a
negative initial statement, and a negative description of the
relationship with the child. A low rating is made in the
absence of dissatisfaction, criticism, a negative initial
statement, and a negative relationship description. Indepen-
dent ratings were obtained for the mother speaking on her
child (Child-Criticism) and herself (Self-Criticism). The
primary coder for all samples met reliability according to
the standards established by the UCLA Family Project and
was unaware of group status of the mother and the
hypotheses of the study. A second trained coder indepen-
dently rated a random subsample of 20% of the self and
child speech samples to obtain inter-rater reliability.
Quadratic weighted kappas (Fleiss et al. 2003) were
calculated, obtaining 0.74 for Child-Criticism and 0.70 for
Self-Criticism, indicating good inter-rater agreement.
Strange Situation (Ainsworth et al. 1978) Attachment
security in toddlers was assessed using Ainsworth’s Strange
Situation, a standardized laboratory procedure designed to
activate the attachment relationship in a controlled setting.

Two trained raters coded the videotapes to determine
attachment classifications: insecure-avoidant (A), secure
(B), insecure-resistant (C), or disorganized (D). Given that
the children in this sample were on average 20 months of
age and the Strange Situation was originally developed for
infants of approximately 12 months of age, developmen-
tally informed modifications to the coding of toddler
attachment were made based on previously published
recommendations (Schneider-Rosen et al. 1985). Each rater
coded the videotaped Strange Situation for each toddler,
and agreement between raters was 90% (see Toth et al.
2006 for an elaboration). Due to small cell sizes for the A and
C classifications, insecure and disorganized categories were
combined for the current study and comparisons were made
betweens secure and insecure attachment classifications.
Child Behavior Checklist (CBCL; Achenbach 1992) The
CBCL was used to obtain maternal assessment of child
behavioral and emotional problems. It is a widely used and
psychometrically valid and reliable instrument. The version
designed to assess 2- and 3-year-old children was used for
this study. Parents rate their child’s current functioning as
well as that of the previous 2 months on 100 items which
are scored from 0 (not true of the child) to 2 (very true or
often true of the child). Standardized T-scores for internal-
izing and externalizing behavior problems were obtained
from these ratings.
Data Analysis Plan
Analyses were performed using Mplus Version 6.00

(Muthen and Muthen 1998–2010). To account for non-
normality, we used a maximum likelihood estimator with
robust standard errors (MLR) using a numerical integration
algorithm (Muthen and Muthen 1998–2010). Maximum
likelihood parameter estimates with standard errors and a
chi-square test statistic are robust to non-normality and non-
independence of observations. Traditional maximum likeli-
hood methods assume the distributions of the continuous
variables in the model are multivariate normal. The normal
distribution assumption is problematic in mediation models
as the product coefficients used to evaluate mediation rarely
meet this assumption (Preacher and Hayes 2008; Shrout
and Bolger 2002). Thus, in the current study, maternal Self-
Criticism and Child-Criticism were examined as mediators
of the association between maternal depression and child
behavior problems using 2,000 bootstrap replicates to
obtain bias-corrected bootstrap confidence intervals for the
product coefficients of the indirect effects (MacKinnon et
al. 2007). Maternal Child-Criticism and Self-Criticism were
examined as mediators of the association between maternal
depression and child attachment insecurity using the Joint
Significance Test (JST), given that attachment was a
dichotomous variable. Monte Carlo studies suggest that
the JST offers the best compromise between statistical
power and Type I error (MacKinnon et al. 2002). Missing
data varied by indicator, ranging from 0% to 3%, and was
determined to be missing at random using a full information
maximum likelihood approach (Little and Rubin 2002).
Results
Of the 130 mothers who met DSM criteria for MDD since
the birth of their child, 97 met criteria for MDD in the last
6 months and 51 met criteria in the month prior to
assessment. The mean BDI score of the depressed group

was in the mild depression range (M=16.1, SD=9.2).
Importantly, more than 70% of the depressed group reported
that they had experienced symptoms of MDD prior to the
birth of their child with a mean of 8.6 years since onset,
suggesting the chronic nature of depression in this group.
The depressed and nondepressed groups differed
significantly on main study variables, with depressed
mothers evidencing higher Child-Criticism and Self-
Criticism and having toddlers with higher levels of
internalizing symptoms, externalizing symptoms, and
attachment insecurity. Extensive group comparisons have
been reported elsewhere (Rogosch et al. 2004; Toth et al.
2006). Pearson bivariate correlations for all study variables
are presented in Table 1. Correlation analyses indicated that
both maternal Child-Criticism and Self-Criticism were
significantly positively associated with internalizing and
externalizing behaviors. Maternal Self-Criticism was sig-
nificantly positively associated with toddler attachment
insecurity; maternal Child-Criticism and attachment inse-
curity were not significantly related. (See Table 1).
Children of mothers in the depressed group evidenced
primarily an insecure or disorganized attachment, with
32.3% being categorized as A, 19.2% as B, 9.2% as C, and
39.2% as D. In comparison, the majority of toddlers of
nondepressed mothers were securely attached: 19.1% were
categorized as A, 55.9% as B, 5.9% as C, and 19.1% as D.
The A, C, and D groups were combined into an insecure
group. Chi-square analyses indicated that there was a higher
proportion of insecurely attached toddlers in the depressed
group (80.7%) compared to the nondepressed group
(44.1%), χ2(1, N=198)=27.65, p<0.001.
Group differences on CBCL internalizing and external-
izing T-scores were tested using one-way ANOVAs.

Internalizing symptoms were significantly higher in chil-
dren of mothers in the depressed group (M=50.55, SD=
8.37) compared to toddlers of mothers in the nondepressed
group (M=46.72, SD=7.55), F(1, 194)=9.96, p=0.002.
Children of mothers in the MDD group were also higher on
externalizing symptoms (M=53.30, SD=8.19) compared to
children of nondepressed mothers (M=50.60, SD=7.62),
F(1, 194)=5.04, p=0.026.
Path Analyses
Analyses confirmed significant direct paths linking mater-
nal depression status to child internalizing (β=0.188, p=
0.005) and externalizing (β=0.139, p=0.048) symptoms, as
well as attachment insecurity (B=+1.671, p<0.001, Odds
ratio=5.32).
Behavior Problems Controlling for maternal marital status
and age and child age, bootstrapped bias corrected CIs were
used to examine the indirect effect between maternal
depression and child internalizing and externalizing behav-
iors via maternal Self-Criticism and Child-Criticism. All
traditional indices of global fit suggested good fit between
the data and the model tested (χ2(1, N=198)=2.7, p=0.10;
Comparative Fit Index, CFI=0.99; Root Mean Square Error
of Approximation, RMSEA=0.093; standardized root mean
residuals, SRMR=0.018). (See Table 2).
Table 2 shows estimates for the direct and indirect
effects. Maternal depression status was significantly asso-

ciated with Self-Criticism and Child-Criticism. Child-
Criticism was significantly associated with both internaliz-
ing and externalizing behaviors. Additionally, the indirect
paths between maternal depression and child externalizing
behaviors and between maternal depression and child
Table 1 Bivariate correlations between study variables
1. Dep. 2. BDI 3. Child-Crit. 4. Self-Crit. 5. Intern. 6. Extern. 7.
Attach. 8. Toddler age 9. Mother age 10. Marital status
1. Dep. –
2. BDI 0.64** –
3. Child-Crit. 0.17* 0.19** –
4. Self-Crit. 0.28** 0.25** 0.17* –
5. Intern. 0.22** 0.19** 0.24** 0.23** –
6. Extern. 0.16* 0.12 0.34** 0.20* 0.74** –
7. Attach. 0.37** 0.28** 0.12 0.21** 0.23** 0.16* –
8. Toddler age −0.17* −0.10 −0.01 0.05 −0.05 −0.02 −0.23** –
9. Mother age −0.17* −0.06 −0.12 −0.15* −0.29** −0.24**
−0.07 0.07 –
10. Marital Stat. −0.24** −0.30** −0.11 −0.05 −0.18* −0.12
−0.09 0.07 0.23** –
Dep. = Depression group status; BDI = Beck Depression
Inventory; Child-Crit. = EE Child-Criticism; Self-Crit. = EE
Self-Criticism; Intern. =
CBCL internalizing behaviors; Extern. = CBCL externalizing
behaviors; Attach. = Attachment insecurity; Marital Stat. =

Maternal marital status.
* p<0.05, ** p<0.01
Table 2 Path analyses estimates of direct and indirect effects
Independent variables Mediator variables Dependent variables β
B SE of meana 95% CIa (lower, upper)
Dep. → Internalizing 0.096 1.671 1.227 [−0.678, 4.109]
Dep. → Externalizing 0.047 0.800 1.242 [−1.621, 3.268]
Dep. → Self-Crit. 0.282 0.390 0.095 [0.194, 0.571]*
Dep. → Child-Crit. 0.142 0.170 0.081 [0.009, 0.333]*
Self-Crit. → Internalizing 0.142 1.783 0.942 [−0.039, 3.678]
Self-Crit. → Externalizing 0.112 1.365 0.934 [−0.491, 3.164]
Child-Crit. → Internalizing 0.163 2.361 0.904 [0.385, 4.004]*
Child-Crit. → Externalizing 0.285 4.025 0.922 [2.217, 5.757]*
Dep. → Self-Crit. → Internalizing 0.040 0.696 0.696 [0.026,
1.778]*
Dep. → Self-Crit. → Externalizing 0.032 0.533 0.420 [−0.124,
1.500]
Dep. → Child-Crit. → Internalizing 0.023 0.402 0.264 [0.033,
1.124]*
Dep. → Child-Crit. → Externalizing 0.041 0.685 0.392 [0.071,
1.651]*
CI = Confidence Interval; Dep. = depressed/nondepressed group
status; Child-Crit. = EE Child-Criticism; Self-Crit. = EE Self-
Criticism;
Internalizing = CBCL internalizing behaviors; Externalizing =

CBCL externalizing behaviors.
a These values are based on unstandardized boostrapped path
estimates.
*p<0.05
internalizing symptoms via Child-Criticism were both
significant. Whereas the direct path between Self-
Criticism and child internalizing problems approached
significance (p=0.059), the indirect path from maternal
depression to internalizing behaviors through Self-Criticism
was significant. There was no direct association between
Self-Criticism and child externalizing behaviors, and the
indirect path between maternal depression and child
externalizing symptoms by way of Self-Criticism was not
significant.
The direct effect for maternal depression on internalizing
symptoms was no longer significant after including Child-
Criticism and Self-Criticism in the model, consistent with a
full mediation interpretation. Similarly, the direct effect for
maternal depression on child externalizing symptoms was
no longer significant after including Child-Criticism in the
model, also consistent with a full mediation conceptual
interpretation. (See Fig. 1.)
Attachment Insecurity Maternal Self-Criticism and Child-
Criticism were examined separately as mediators of the
association between maternal depression and child
attachment insecurity, controlling for maternal marital
status and age and child age. Using the JST, significant
mediation is determined when the path from the

predictor to the hypothesized mediator (path a) and the
path from the hypothesized mediator to the dependent
variable (path b) are statistically significant after the direct
path from the independent variable to the outcome
variable is held constant (Cohen and Cohen 1983;
Mallinckrodt et al. 2006). Self-Criticism was examined
first as a mediator. Path a was tested by regressing
maternal Self-Criticism onto maternal depression status
and was significant (β=0.283, p<0.001). A logistic
regression was used to test path b. Controlling for the
direct pathway between maternal depression status and
attachment, attachment classification was regressed onto
maternal Self-Criticism. Results revealed that children of
mothers with higher Self-Criticism had a significantly
higher probability of being classified as insecurely
attached (β=0.369, p=0.025; Odds ratio=1.74). The
direct effect from maternal depression status to attachment
insecurity remained significant while accounting for Self-
Criticism as a mediator (β=0.680, p<0.001), suggesting a
partial mediation interpretation.
Child-Criticism was next tested as a mediator. Path a was
tested by regressing maternal Child-Criticism onto maternal
depression status and was significant (β=0.145, p=0.03).
Path b was tested using logistic regression; Child-Criticism
was not a significant predictor of attachment security versus
insecurity (β=0.182, p>0.05) while controlling for the
direct pathway between maternal group status and attach-
ment (β=0.788, p<0.001). Results do not support Child-
Criticism as a significant mediator of the association between
maternal depression and child attachment insecurity. (See
Figs. 2 and 3.)
Discussion

This study revealed important findings regarding the
relations between maternal depression, negative maternal
representations of self and child, and behavior problems
and attachment in toddler aged offspring. Consistent with
study hypotheses, maternal depression was significantly
positively associated with EE Self- and Child-Criticism,
child internalizing and externalizing behaviors, and attach-
ment insecurity. There was a direct relation between
maternal Child-Criticism and child internalizing and exter-
nalizing behaviors, but not attachment, partially congruent
with study hypotheses. Maternal Self-Criticism was posi-
tively associated with attachment insecurity, consistent with
our predictions. However, contrary to study hypotheses,
maternal Self-Criticism was associated with internalizing
symptoms only at the trend level and was not directly
associated with child externalizing behaviors. Importantly,
results are consistent with a conceptual model in which
Non-Dep (0)
vs.
Dep (1)
Maternal
EE Self-Crit
.39
0(.2
82)
***
Child
internalizing
symptoms

Maternal
EE Child-Crit
Child
externalizing
symptoms
.170(.142)*
1.783(.112)
4.025(.285)***
2.3
61(
.16
3)*
*
Fig. 1 Parameter estimates for
mediational model testing
maternal EE Self-Crit and EE
Child-Crit as mediators of the
association between maternal
depression group and child
internalizing and externalizing
symptoms; estimates reported as
unstandardized (standardized).
Non-Dep = nondepressed group;
Dep = depressed group.
† p<0.06. * p<0.05. ** p<0.01.
*** p<0.001

Self-Criticism partially mediates the association between
maternal depression and child attachment; although a full
mediation model was predicted, this finding is largely
compatible with study hypotheses. Contrary to our pre-
dictions, Child-Criticism was not significant in the pathway
between maternal depression and child attachment insecu-
rity. Child-Criticism, but not Self-Criticism, mediated the
association between maternal depression and child external-
izing behaviors; both Self- and Child-Criticism were signif-
icant in the path between maternal depression and child
internalizing behaviors, largely in line with study hypotheses.
The finding that mothers’ expressed criticism towards
their toddlers significantly mediated the pathway between
maternal depressive status and child externalizing symp-
toms is consistent with some research on older children and
adolescents (Bolton et al. 2003; Nelson et al. 2003). Results
suggest that mothers with depression who are critical of
their toddlers have offspring who may be at heightened risk
for developing externalizing symptoms, which can be a
precursor to later psychopathology, including oppositional
behavior and conduct problems (Campbell et al. 2000).
Contrary to our predictions, maternal Self-Criticism did not
emerge as a significant mediator of the pathway between
maternal depression and child externalizing symptoms.
Thus, it is representations of the child among mothers with
depression that appear to be related to the extent to which
children exhibit under-controlled, impulsive behavior.
Child-Criticism also emerged as a significant mediator of
the association between maternal depression and child
internalizing symptoms. This finding is inconsistent with
previous research that has not established Child-Criticism

as a mediator of the relation between maternal depression
and child internalizing symptoms in older children and
adolescents (Bolton et al. 2003; Nelson et al. 2003). These
results suggest that different factors may be operating in the
association between maternal depression and child inter-
nalizing symptoms in toddler-aged children compared to
older children and highlight the importance of considering
developmental stage when investigating processes influ-
encing child internalizing symptoms in the context of
maternal depression. Results may also be attributable to
behavior problems being less differentiated during the
toddler period than during childhood and adolescence.
Results were also consistent with a conceptual model in
which maternal Self-Criticism mediated the association
between maternal depressive status and child internalizing
symptoms, an indirect path that has not been examined in
previous research. Toddlers’ emerging sense of self and
associated affect may be sensitive to a relational environ-
ment where mothers are critical of the child and themselves
(cf. Cicchetti et al. 1997). Thus, high levels of maternally
expressed criticism towards both self and child may be
assimilated by young toddlers and manifest through
internalizing behaviors.
Non-Dep (0)
vs.
Dep (1)
Maternal
EE Child-Crit
a
.173 (.145)*

Secure (0)
vs.
Insecure (1)
b
n.s.
c
+1.671***
Fig. 3 Parameter estimates for mediational model testing
maternal EE
Child-Criticism as a mediator of the association between
maternal
depression group and child attachment security vs. insecurity;
estimates reported as unstandardized (standardized). Path c
denotes
the direct path from depression status to attachment quality, not
controlling for EE Child-Criticism. * p<0.05. Non-Dep = nonde-
pressed group; Dep = depressed group; n.s. = non- significant
Non-Dep (0)
vs.
Dep (1)
Maternal
EE Self-Crit
a

.390(.283)***
Secure (0)
vs.
Insecure (1)
b
+ +.553( .369)*
c
1.671***+
Fig. 2 Parameter estimates for mediational model testing
maternal EE
Self-Criticism as a mediator of the association between
maternal
depression group and child attachment security vs. insecurity;
estimates reported as unstandardized (standardized). Path c
denotes
the direct path from depression status to attachment quality, not
controlling for EE Self-Criticism. Non-Dep = nondepressed
group;
Dep = depressed group. * p<0.05. *** p<0.001
The finding that Self-Criticism, but not Child-Criticism,
partially mediated the association betweenmaternal depression
and child attachment suggests that a mother’s self-
representations may be more strongly related to the attachment

relationship than her representations of her child. Whereas
extensive research has highlighted mother’s representations of
her own caregiver (see van IJzendoorn 1995 for a meta-
analysis) and maternal sensitivity (see De Wolff and van
IJzendoorn 1997 for a meta-analysis) to explain the develop-
ment of the attachment relationship, these findings suggest
that a mother’s representation of herself may be an important
factor in explaining the association between maternal
depression and child attachment insecurity.
A limitation of the current study is the concurrent as-
sessment of primary study variables. Although theoretically-
informed meditational models were hypothesized, we are
unable to determine whether maternal depression precipitates
EE-Criticism, which in turn leads to child behavior problems
and insecure attachment, or whether maternal depression
leads to child behavior problems and attachment insecurity,
which then results in mothers being critical of themselves
and their children. It is also possible that the effects are
transactional, as has been suggested previously in regards to
externalizing behaviors in adolescents (Nelson et al. 2003).
Despite this limitation, the current study has established an
association between maternal depression, EE-Criticism and
important assessments of child functioning in toddler-aged
children, an essential first step before examining the relations
among these variables longitudinally.
Another potential limitation of the current research
involves utilization of maternal report to assess child
internalizing and externalizing symptoms. Although prior
research has found that maternal depression is associated
with ratings on the CBCL as it was in this study, previous
research established that maternal ratings distinguish
between children with and without psychiatric problems
even after controlling for maternal depression (Friedlander
et al. 1986). Additionally, because mothers provided the

FMSS from which Child-Criticism and Self-Criticism were
rated, information on their depressive symptoms in order to
make diagnoses using the DIS, and reports on child
behavior problems, inflation of associations between these
constructs cannot be ruled out. In an attempt to mitigate this
concern, mothers were not aware that coders would be
assessing levels of criticism from their speech, and coders
adhered to specific guidelines and rules for these ratings.
Further, a structured diagnostic interview was used in
addition to a self-report instrument to assess maternal
depression. Because Child-Criticism and Self-Criticism were
coded by the same rater, concerns about the independence of
these variables could be raised; to minimize these concerns,
speech samples were de-identified before rating occurred,
and ratings of all child speech samples were completed
before ratings of self speech samples were initiated. It should
also be noted that although toddlers of the depressed mothers
in this study had significantly higher internalizing and
externalizing symptoms than the children of the non-
depressed mothers, their mean symptom levels were still in
the normative range. Accordingly, interventions for behavior
problems were not yet indicated for the toddlers in this
sample. However, understanding processes associated with
the initial development of psychopathology, underscored by
the high rate of insecure and disorganized attachment found
among these toddlers, provides insight into the negative
developmental cascade that can eventuate from risk factors
such as maternal depression (Masten and Cicchetti 2010).
Despite these limitations, the current study represents a
significant contribution to the literature. This was the first
study to investigate the relations among maternal depression,
maternal Child-Criticism and internalizing and externalizing
symptoms in toddler-aged children and among maternal
depression, maternal Self-Criticism, and child problem

behaviors in children of any age. Importantly, it is also the
first study in children of any age to examine a conceptual
model in which EE-Criticism mediates the relation between
maternal depression and child attachment security. Additional
strengths include the large sample size, the clinical diagnosis
of MDD using a structured diagnostic interview, and the
inclusion of a non-psychiatric comparison group. Different
coders were utilized to assess attachment and EE, thereby
eliminating concerns regarding non-independence of coding
between the two paradigms.
Maternal depression is widely recognized as a risk factor
for the development of child behavior problems and
insecure attachment. Findings from this study contribute
to the understanding of processes that may be more
proximal to behavior problems and attachment insecurity
in children of mothers with depression, knowledge that can
inform interventions aimed at this population. The results
suggest that a focus on altering negative maternal repre-
sentations of self and child could deter the emergence of
child behavior problems. Reducing maternal Self-Criticism
may be especially relevant for interventions aimed at
strengthening the attachment relationship such as Child–
Parent Psychotherapy (Toth et al. 2006).
Future research should implement a longitudinal design
to test the mediational models reported in this study in
order to confirm the direction of hypothesized pathways.
The current work also highlights maternal self-representations
as an important area for future investigations of the develop-
ment of the attachment relationship between mother and
young offspring. Future studies should seek to more fully
understand the link between maternal Self-Criticism and child
attachment through examining maternal self-efficacy, self-
esteem, and other self-system processes likely also involved
in this association.

In conclusion, the current study extends previous research
linking maternal depression and maternal EE-Criticism to
internalizing and externalizing problems in toddler-aged
children and to the attachment relationship. Much research
suggests that supportive and responsive parenting is vital for
promoting resilient adaptation in children (Masten 2001).
Thus, research directed toward understanding ways that
maternal representations of their children and themselves
may be affected by depression and how these representations
are related to child socio-emotional functioning is of the
utmost importance for advancing our understanding of
processes leading to child risk for psychopathology and for
preventing these processes from unfolding.
References
Achenbach, T. M. (1992). Manual for the child behavior
checklist 2–3
and 1992 profile. Unpublished manuscript.
Ainsworth, M. D. S., Blehar, M. C., Waters, E., & Wall, S.
(1978).
Patterns of attachment; A psychological study of the strange
situation. Hillsdale: Erlbaum.
American Psychiatric Association. (1987). Diagnostic and
statistical
manual of mental disorders (3rd ed., rev. ed.). Washington:
American Psychiatric Press.
Baker, B. L., Heller, T. L., & Henker, B. (2000). Expressed

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