1 s2.0 S0272735809000221 Main PDF

Clinical Psychology Review 29 (2009) 294316
Contents lists available at ScienceDirect
Clinical Psychology Review
Family processes in the development of youth depression:

Translating the evidence to treatment
Kathleen Restifo a,, Susan Bgels b
a
b
Maastricht University, Department of Clinical Psychological Science, Postbox 616, 6200 MD, Maastricht, The Netherlands
University of Amsterdam, Department of Education, PO Box 94208, 1090GE Amsterdam, The Netherlands
a r t i c l e
i n f o
Article history:
Received 30 May 2008
Received in revised form 16 January 2009
Accepted 13 February 2009
Keywords:
Depression
Youth
Family processes
Family systems
Treatment
a b s t r a c t
There is strong evidence that family factors play a role in the development, maintenance and course of youth
depression. However, to date few clinical trials of psychotherapy for youth depression employ family therapy
interventions or target the known family risk factors. This is surprising given recent meta-analytic ndings
showing only modest effect sizes for psychotherapy for youth depression, and that cognitive therapies do not
outperform non-cognitive therapies. The aim of this review is to 1) use a developmental systems approach to
review empirical evidence on family risk factors for youth depression to identify potential targets for
treatment, 2) examine the extent to which these family risk factors have been targeted in clinical trials for
youth depression, and 3) provide a road map for the development of empirically validated family-based
interventions for youth depression.
Strong evidence was found supporting a relationship between family factors at multiple system levels and
depressive symptoms or disorders. Support for several different hypothesized causal mechanisms as well as
bidirectional effects was found. A comparison of the identied risk factors and psychotherapy trials for youth
depression indicated that few RCT's target family factors; among those that do, only a few of the family risk
factors are targeted. Recommendations for translation of empirical knowledge of family risk factors and
mechanisms to develop empirically valid family-based interventions to enhance existing treatments for
youth depression are provided.
2009 Elsevier Ltd. All rights reserved.
Contents
1.
2.
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.1.
A systems approach to the evidence . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2.
Why use a systemic model for youth depression? . . . . . . . . . . . . . . . . . . .
Part I. Risk factors and mechanisms in the development of youth depression . . . . . . . . . .
2.1.
Methodological note: Levels of evidence required for causal models . . . . . . . . . . .
2.1.1.
Cross-sectional vs. longitudinal design . . . . . . . . . . . . . . . . . . . . .
2.1.2.
Self-report vs. observational assessment. . . . . . . . . . . . . . . . . . . .
2.2.
Level 1: Individual factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2.1.
Child factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2.2.
Parent factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2.3.
Hypothesized risk mechanisms. . . . . . . . . . . . . . . . . . . . . . . .
2.3.
Level 2: Parentchild subsystem . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.3.1.
Attachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.3.2.
Level 2: Parental rearing, conict and support, autonomy and relatedness . . .
2.3.3.
Parental care and control in children and adolescents: Non-observational studies
2.4.
Level 3: Marital relationship . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.5.
Level 4: Whole family system . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.5.1.
Global family environment . . . . . . . . . . . . . . . . . . . . . . . . . .
2.5.2.
Relationships between multiple family subsystems . . . . . . . . . . . . . .
Corresponding author. Tel.: +31 43 388 1593; fax: +31 43 388 4155.
E-mail addresses: k.restifo@dmkep.unimaas.nl (K. Restifo), s.m.bogels@uva.nl (S. Bgels).
0272-7358/$ see front matter 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cpr.2009.02.005
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K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316
2.5.3.
Interaction patterns in families with a depressed member . . . . . . . . . . . . . . . . .
2.5.4.
Summary of whole family level . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.
Level 5: Extra-familial context: stress . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.7.
Summary of empirically supported family risk factors for youth depression . . . . . . . . . . . . .
3.
Part II. Targeting family risk factors in psychotherapy of youth depression: Evidence from clinical trials . . .
3.1.
Who is the target of treatment? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.
Which risk factors are targeted in psychotherapy for youth depression? . . . . . . . . . . . . . .
3.3.
Which family risk factors are targeted? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4.
What kinds of treatments have been tested in RCT's for youth depression? . . . . . . . . . . . . .
3.5.
Efcacy of interventions targeting family factors . . . . . . . . . . . . . . . . . . . . . . . . .
3.6.
Summary of family risk factors targeted in youth depression treatment . . . . . . . . . . . . . . .
4.
Part III. Road map for the development of empirically supported family treatments for depression . . . . .
4.1.
Which family factors should be targeted? . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.
Steps in the development and validation of family-based interventions for youth depression. . . . .
4.2.1.
Developing a model . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.2.
Developing a manual . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.3.
Evidence for validation of family-based interventions for youth depression . . . . . . . . .
4.2.4.
Further research directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.
Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.1.
Why have the ndings from family process research gone largely unheeded in clinical trials for youth
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Introduction
An extensive body of evidence supports the role of family
processes in the development, course and maintenance of depression
in children and adolescents (Sander & McCarty, 2005). Family
environment, marital and family relationships (Cummings, Keller, &
Davies, 2005), parenting behavior (Alloy, Abramson, Smith, Gibb, &
Neeren, 2006) and attachment (Sexson, Glanville, & Kaslow, 2001)
have been related to the development and maintenance of childhood
and adolescent depressive symptoms and disorders, as well as
treatment response and relapse among depressed adolescents
(Birmaher et al., 2000). This evidence comes from diverse research
traditions and populations, employing diverse methodologies, and
examining varying aspects of family relationships (Goodman & Gotlib,
1999; Sander & McCarty, 2005; Sheeber, Hops, & Davis, 2001).
Surprisingly, the direct translation of these research ndings into
specic techniques for treatment of depressive disorders has been
limited (Davies & Cummings, 2006). Few treatment studies of youth
depression include family-based interventions; those that do target
only a few of the specic family risk factors identied in the research
literature (Sander & McCarty, 2005; Weisz, McCarty, & Valeri, 2006).
Furthermore, the evidence for efcacy of current treatments for
youth depression may not be as strong as it once appeared (Weersing &
Brent, 2006). In a recent meta-analysis of treatments for youth
depression, Weisz et al. (2006) reported a modest overall effect size for
current treatments for youth depression, which was considerably
lower than effect sizes found for treatments of other child and
adolescent disorders. Cognitively based treatments, which make up
the majority of empirically tested treatments, were not signicantly
better than non-cognitively based treatments. Taken together, these
ndings suggest not only that there is considerable room for
improvement in the treatment of youth depression, but also the
possibility that treatment effects could be increased by also targeting
non-cognitive risk factors. Family factors would seem to be an obvious
candidate, given the strong evidence for family factors in depression.
Despite this, few treatment studies of youth depression have included
family interventions which target the wide variety of family risk factors
for youth depression (Sander & McCarty, 2005; Weisz et al., 2006). This
is in contrast to clinical trials research on externalizing disorders,
substance abuse and eating disorders, in which efcacy of family
interventions has been demonstrated (Diamond & Josephson, 2005).
The aim of this review is to address the gap in the translation of
research ndings on family processes in depression and treatment of
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youth depression. The rst goal is to examine the empirical evidence

on family risk factors and mechanisms in the development of youth
depression, in order to identify potential targets for treatment. The
second goal is to examine the extent to which these family risk factors
have been targeted in randomized controlled psychotherapy trials for
youth depression. The third goal is to provide a road map for the
development of family-based treatments for youth depression to
target the broad array of family risk factors identied in the empirical
literature.
Several considerations guide our approach. First, there is a need to
move beyond identifying separate risk factors, to developing models
of causal risk mechanisms (Garber, 2006). Research on family and
parental factors related to depression have tended to view parental
psychopathology, rearing styles, marital functioning and family
structure as separate domains, and often research is conducted on
only one of these variables at a time. Researchers are increasingly
using developmental and family systems theory to integrate diverse
ndings into models, which can describe the complex interrelationships between risk factors and specify possible causal pathways from
risk to outcome (Cowan & Cowan, 2002; Davies & Cummings, 2006;
Goodman & Gotlib, 1999; Sheeber et al., 2001). While developmental
and interpersonal models have been available for decades in the
developmental literature (Cicchetti & Toth, 1998), the adult literature
on depression (Gotlib, 1990), and within family therapy research
(Steinglass, 1987) these models have less frequently been applied to
the treatment of child and adolescent depression, where cognitive
models have been predominant.
1.1. A systems approach to the evidence
While the terms family systems or systemic have been used in
various ways in the literature, in this review, systemic refers to an
approach which views the individual in the context of his environment. Individual characteristics such as genes, temperament and
personality are assumed to unfold within, and in interaction with, a
particular environment. Environmental inuences can be conceived as
operating at varying degrees of proximity to the child, from the
immediate family (parents and siblings), to extended family, to the
broader social context outside the family (e.g., school, work, sociocultural factors) (Bronfenbrenner, 1986). It is important to note that
this approach makes no further assumptions about etiology or treatment of depression. Rather, the only assumption is that examining
multiple factors at various systemic levels will give a more complete
296
picture of the mechanisms involved in the development of youth

depression. Within this approach, the term subsystem refers to any
part of a larger system: for example, the individual child subsystem
refers to the child, the marital subsystem refers to the spousal
relationship, the whole family subsystem refers to the mother, father
and child(ren) unit.
1.2. Why use a systemic model for youth depression?
Systemic models allow for the integration of multiple types of data
and theories by viewing each as occurring at different levels of
analysis: individual, family, community and culture (Bronfenbrenner,
1986). The literature on family factors in depression has drawn from
several populations (depressed parents, depressed youth, and community samples), and includes diverse factors such as parental rearing
style, family environment, marital conict, attachment, support and
conict. Rather than viewing these as separate factors, organizing
these factors according to the different system levels facilitates model
building and clinical application. Moreover, this approach lends itself
to developing hypotheses about how individual risk factors interact to
produce risk mechanisms, and is consistent with current multivariate
approaches to studying risk processes in youth. Furthermore, placing
risk factor evidence at each level of the system generates hypotheses
about potential targets for treatment, including the level at which
targets should be addressed, which can be tested in clinical trials.
Fig. 1 illustrates a systemic model of risk for the development of

youth depression. In contrast to models which describe hypothesized
causal pathways from family factors to youth depression (Cummings
& Davies, 1994; Downey & Coyne, 1990; Goodman & Gotlib, 1999), the
purpose of this model is to describe the multiple factors which can
inuence or maintain the development of depression, the level at
which each factor operates, and the ways in which each factor may
interact with other factors at the same or different level of the system.
The model does not specify the direction of causality, but allows for
the possibility that relationships may be reciprocal and transactional
rather than unidirectional. The purpose of this model is twofold: to
integrate family risk factor evidence into hypothesized mechanisms of
transmission which can be tested in subsequent research, and to
promote the translation of this evidence into clinical interventions
targeting the hypothesized mechanisms at the appropriate system
level.
While several reviews of family factors in youth depression have
appeared recently, this is the rst to use a systemic framework to
integrate the empirical ndings in order to facilitate clinical application. Furthermore, we include a broader range of studies, including
some studies of normal populations which have bearing on theoretical
models but which have largely been ignored in the youth depression
treatment literature. We also address the question of specicity of
these family factors to depression, by including studies which examine
other psychopathological outcomes in addition to depression.
Fig. 1. Systemic model of youth depression.
297
2. Part I. Risk factors and mechanisms in the development of

youth depression
produce evidence of varying strength for causal hypotheses linking

specic family factors to youth depression.
In Table 1, family risk factors for depression are organized according to

system levels, from the individual level to the broader social level. Level 1,
the individual subsystem, focuses on risk factors related to characteristics
of each individual family member (mother, father, or child). This includes
genetic, temperamental, and cognitive or personality factors of parents or
child. Level 2, the parentchild subsystem, includes aspects of the
parentchild relationship such as attachment, rearing style, support and
conict. Level 3, the marital subsystem, includes aspects of the spousal
relationship such as marital conict. Level 4, the whole family system,
includes triadic relationships (i.e. mother, father and children in interaction together), as well as subsystems interacting with each other and
global family environment. Finally, Level 5, the extra-familial level,
includes factors beyond the family which impact on the family and its
members, such as socialeconomic factors and stress.
While it is beyond the scope of this review to cover all family risk
factors, we have selected the risk factors at each level which have
received the most attention in youth depression research. Therefore, at
Level 1, we briey review child factors such as genes, temperament, and
cognitive style of the child; and the parent factor of depression; at Level 2,
the parentchild relationship including attachment, rearing, support and
conict, autonomy and relatedness; at Level 3, the marital relationship;
at Level 4, global family environment, triadic relations and relationship
between subsystems within the family; and at Level 5, stress.
2.1.1. Cross-sectional vs. longitudinal design

Most studies of family factors and depression use cross-sectional
designs, which makes it impossible to prove etiological hypotheses,
since child factors (e.g. depression, negative affect, helplessness) may
inuence parenting, or a third factor such as marital quality or shared
genes could explain both. Prospective longitudinal designs provide
stronger evidence for causal hypotheses; however, longitudinal
designs cannot completely eliminate the possibility of a third variable
causing the association, or of subtle child factors inuencing parent
behaviors (Cowan & Cowan, 2002). Experimental and intervention
studies provide additional support for causal hypotheses, but
processes involved in etiology and treatment may be different, so it
cannot be assumed that mechanisms of change due to an intervention
are the same as those which led to the symptom in the rst place.
2.1. Methodological note: Levels of evidence required for causal models

In this review, we highlight the differences between crosssectional vs. prospective longitudinal designs, and between selfreport vs. observational assessment methods, because these designs
Table 1
Risk factors for youth depression at ve system levels.
Level of system
Risk factor
1. Individual (child or parent)
Parental factors
Depression or depressive symptoms/

other psychopathology
Personality/temperament
Cognitive style
Genetic factors
Attachment history
Child factors
Depression or depressive symptoms/
other psychopathology
Personality/temperament
Cognitive style
Genetic factors
2. Parentchild subsystem
Attachment
Rearing behaviour and style
Conict and support
Autonomy and relatedness
Expressed emotion
3. Marital subsystem
Marital discord
Marital conict
Marital satisfaction
Partner support
4. Whole family subsystem
Mother, father, child tryadic triadic system

Co-parenting
Global family environment (incl. grandparents)
Relations between subsystems
5. Extra-familial subsystem
Stress
Poverty
Ses
Culture, ethnicity
Community
2.1.2. Self-report vs. observational assessment

The majority of studies of family processes in depression assess
family functioning via self-report questionnaires, which have several
limitations. Many studies rely on youth report of family factors and
depressive symptoms, which can lead to over ination of the
association due to shared-method variance (i.e. same informant for
both the predictor and the outcome variable) (Ge, Conger, Lorenz, &
Simons, 1994). Furthermore, adolescents and parents often perceive
their relationship quite differently (Sheeber et al., 2001) and this
difference is difcult to interpret. Depressed adolescents' negative
cognitive bias may inuence their views of themselves as well as their
parents as excessively negative, leading to a spurious correlation
between perceived parenting and depression (Alloy et al., 2006). On
the other hand, social desirability may lead to an ination of parents'
report of their own positive rearing behaviors. In addition, adolescents
and parents bring to bear different sets of data when reporting on
their relationship, both of which may be valuable even if discrepant, as
they reect the different perspectives, history of interactions and the
emotional meanings attached to them (Sheeber et al., 2001).
Observational studies help ll this gap by objectively measuring
parentchild interactions, and by allowing the sequential analysis of
behaviors within an interaction, to provide a closer, real-time view of
how adolescents and parents reciprocally affect each other. Data from
observational studies can help elucidate what actually occurs (i.e.
behaviorally), and to compare to parent and youth perceptions.
Furthermore, observational data lend themselves to the development
of intervention strategies, by suggesting specic points in the interaction sequence to target for change. In contrast, global perceptions of
relationships such as warmth and control may be more difcult to
target (Sheeber et al., 2001). While multi-method, multi-informant,
longitudinal designs are clearly the gold standard; in practice we seek
an accumulation of converging evidence from studies of varying
methodological design and quality.
2.2. Level 1: Individual factors
2.2.1. Child factors
Characteristics of the individual child such as genetic and
biological factors, temperament, cognitive vulnerability, self-image
and personality fall at level 1 and are clearly important in the
development of depression (Alloy et al., 2001). However, since the
focus of this review is family factors in youth depression, and since
several excellent reviews have examined individual child factors in
depth (Alloy et al., 2001; Garber & Robinson, 1997; Goodman & Gotlib,
1999) we will limit our discussion to studies which examine the
interaction between child and family factors in depression.
Depressive disorders in children and adolescents have been associated with the cognitive triad described by Beck (1967) of negative
298
self-image, negative view of the world, and negative expectations of

the future (Beck, 1967; Stark, Schmidt, & Joiner, 1996). Beck (1967)
hypothesized that early parentchild interactions play an etiological
role in the development of maladaptive cognitive processes. The
mechanisms underlying the link between parentchild relationship
and maladaptive cognitions are increasingly receiving attention (Blatt
& Homann, 1992). Dysfunctional cognitive styles in children have been
associated with negative parenting practices in both cross-sectional
and prospective designs, and there is evidence that dysfunctional
cognitions may mediate the relationship between negative parenting
and childhood depression (Alloy et al., 2006). In their review, Alloy et
al. (2006) concluded that one mechanism through which negative
parenting leads to depression is through the development of a negative
cognitive style which increases vulnerability for depression (the
cognitive vulnerability hypothesis). In contrast, there has been less
support for the hypothesis that children's negative cognitive style is
related to the parents' negative cognitive style via modeling (Stark et
al., 1996). Children with a negative cognitive style have been found to
interpret family interactions more negatively; this may in turn lead to
more (actual) negative family interactions, in a negative feedback loop
which maintains depressive symptoms (Sheeber et al., 2001).
There is increasing evidence that environments may affect children
in different ways, due to temperamental differences, differential
susceptibility for environmental inuences (Belsky, 2005) or through
geneenvironment interactions (Eley, Sugden, Corsico, Gregory, Sham,
& McGufn et al., 2004). Children with negative temperaments may be
more sensitive to the effects of parental criticism, parental depression,
and family conict, and may need more parental support than children
with an optimistic or positive temperament (Belsky, 2005). Youth with
difcult or negative temperaments were found to be more sensitive to
the effects of interparental discord on adolescent delinquency and
depressive symptoms (Davies & Windle, 2001). Child temperament
has also been found to interact with environmental and genetic factors
to create increased risk for depressive and other disorders (Mufson,
Nomura, & Warner, 2002). Furthermore, there is accumulating
evidence that genetic predisposition may interact with adverse environmental events to increase risk for the development of depression in
adults (Caspi, Sugden, Moftt, Taylor, Craig, & Harrington et al., 2003)
and children (Eley et al., 2004). Thus individual genetic vulnerability
appears to require some kind of environmental stress to be fully
potentiated into a depressive disorder.
Finally, individual and family factors may interact in different ways,
depending on the developmental phase of the child. For example,
Nolen-Hoeksema, Girgus and Seligman (1992) found that negative
family events were more predictive of depressive outcomes in early
childhood, whereas pessimistic cognitive style combined with
negative events to predict depressive symptoms in later childhood.
2.2.2. Parent factors
The individual characteristics of parents, such as psychopathology,
personality, and cognitive style, may inuence the development of
child depression (Beardslee, Versage, & Gladstone, 1998; Goodman &
Gotlib, 1999). In this section we will examine the impact of parental
depression on the development of youth depression, as that has
formed the basis of many of the explanatory models of family factors
in child depression.
Children of depressed parents are at increased risk for a variety of
poor behavioral and psychological outcomes relative to children of
non-psychiatrically impaired parents (Beardslee et al., 1998; Downey
& Coyne, 1990; Goodman & Gotlib, 1999; Weissman & Jensen, 2002).
This increased risk can be observed throughout the developmental
course, from infancy to toddlerhood, childhood, adolescence and
adulthood (Goodman & Gotlib, 1999). For example, based on data
from their 10 year longitudinal follow-up study of children of
depressed parents, Weissman, Warner, Wickramaratne, Moreau, and
Olfson (1997) concluded that children of depressed parents are at
increased risk for anxiety disorder and major depression in childhood,

major depression in adolescence, alcohol dependence in adolescence
and early adulthood, and social impairment. Risk for major depression
and phobia's was three times greater compared to children of
nondepressed parents, while risk for panic disorder and alcohol
dependence was ve times higher. Hammen, Burge, and Stansbury
(1990) likewise found increased rates of psychiatric disorder in
children of unipolar depressed mothers compared to children of
bipolar depressed, chronically medically ill or healthy mothers. Many
of these children had multiple diagnoses, more than half met criteria
for an affective disorder, and 45% met criteria for major depression,
compared to 11% of the children of healthy mothers (Hammen et al.,
1990). Effects of parental depression have even been documented
across three generations: children in families with two generations of
depression (parents and grandparents) were found to be at highest
risk for psychopathology compared to children of depressed parents
only. Subclinical impairment across the developmental spectrum has
also been observed in the children of depressed parents, including in
infancy increased fussiness, more difcult temperaments, less secure
attachments to mothers, and lower functioning on motor and mental
development tests; in toddlerhood, increased stress reactivity and
delayed self-regulation skills; and in childhood and adolescence, more
school problems, lower social competence, lower self-esteem and
more behavior problems (Goodman & Gotlib, 1999).
2.2.3. Hypothesized risk mechanisms
While genetic factors partly explain the transmission of depression
from parent to child, genetic factors do not account for all of the
variance (Rice, Harold, & Thapar, 2002), suggesting that environmental mechanisms also play a role (Goodman & Gotlib, 1999).
Adverse family environments may be necessary to potentiate a genetic
risk factor into the development of adolescent depression (Eley et al.,
2004), or adult depression (Caspi et al., 2003).
One hypothesized environmental mechanism is that the symptoms of depression directly interfere with the tasks of parenting, such
as responding appropriately to children's needs and maintaining
emotional involvement (Goodman & Gotlib, 1999). For example,
depressed mothers displayed more negative/hostile and disengaged
behavior, and less positive social behavior compared to nondepressed
mothers, in a meta-analysis of 46 observational studies examining
parenting behavior among depressed mothers (Lovejoy, Graczyk,
O'Hare, & Neuman, 2000). Effect sizes (averaged across studies) were
moderate for negative and disengaged behaviors, and small for
positive behaviors, suggesting that the presence of negative behaviors
rather than the absence of positive social interactions best differentiated depressed from nondepressed mothers.
Other investigators hypothesize that the impaired social and
interpersonal skills of depressed parents, rather than specic symptoms, may lead to difculties in parenting (Berg-Nielsen, Vikan, &
Dahl, 2002; Hammen, Shih, Altman, & Brennan, 2003). Additionally,
the depressed parent's negative cognitive style may explain the
transmission of depression from parent to child (Alloy et al., 2001).
Finally, other aspects of family environment such as marital difculties
(Cummings et al., 2005) and stress (Goodman & Gotlib, 1999) may
partly or fully account for the relationship between parental depression and child outcomes (Downey & Coyne, 1990; Emery, Weintraub,
& Neale, 1982; Rutter & Quinton, 1984).
2.3. Level 2: Parentchild subsystem
The parentchild subsystem level of the family has received the
most theoretical and empirical attention in relation to the development of child depression (Sander & McCarty, 2005). Attachment
theory (Bowlby, 1969, 1980), cognitive theory (Beck, 1967), and
psychodynamic theory (Blatt & Homann, 1992) all postulate disturbances in the early parentchild relationship as an underlying
cause of depression. While systemic theory also assumes that parent

child relationships impact on the development of depression, parent
child relationships are viewed as one of several subsystem within the
family, which may interacts with other subsystems.
In this section we consider several different constructs which have
been used to describe the parentchild relationship and which have
been linked to youth depression: attachment, parental warmth and
control, parental support and parent-adolescent conict, autonomy and
relatedness, and expressed emotion.
2.3.1. Attachment
Bowlby (1980) made the rst theoretical argument for the
relationship between attachment and depression. According to his
theory, the infant's repeated experience of the primary caretaker's
response to his needs leads to a mental representation of the self in
relation to others, the Internalized Working Model. The internalized
working model forms the basis for later expectations about relationships with others, and shapes the child's behavior toward signicant
others, and his capacity to regulate his emotional states. According to
this theory, securely attached children will develop a self-concept as
being worthy of being loved and cared for, of others as being reliable,
caring and available, and an expectation of their needs being met in
interpersonal relationships in the future. In contrast, insecurely
attached individuals will develop a self-concept characterized by
feeling unworthy of being loved, and of signicant others as being
unavailable to meet emotional needs in the future. Bowlby (1973)
conceptualized attachment processes as extending throughout development, and attachment can be assessed at various stages of
development, from early infancy (Ainsworth, Blehar, Waters, & Wall,
1978) to early and middle childhood, adolescence and adulthood
(Ungerer & McMahon, 2005).
Two types of designs have been used to test the relationship
between attachment and depression: prospective longitudinal studies
which examine the relationship between infant attachment and later
psychopathology, and studies assessing attachment in children and
adolescents with depression.
2.3.1.1. Infant attachment and later psychopathology: prospective longitudinal studies. Several prospective longitudinal studies have
examined the relationship between infant attachment classication
and subsequent internalizing and externalizing psychopathology.
While the focus of this review is on depression, prospective studies
often assess both internalizing and externalizing symptoms as
outcomes. Furthermore, these data can help determine the specicity
of the relationship between attachment and depression, compared to
other disorders. Using the Strange Situation paradigm (Ainsworth
et al., 1978) infant attachment can be classied as either secure,
avoidant, ambivalent/resistant, or disorganized (Sroufe, Carlson, Levy,
& Egeland, 1999). In general, stronger relationships between infant
attachment and later psychopathology have been found in high risk
compared to low risk samples. For example, in a high-risk sample of
teenage mothers and their infants, avoidant attachment was associated with aggression in middle childhood, and aggression and
antisocial behavior in adolescence, whereas ambivalent attachment
was related to anxiety and depressive disorders (Sroufe, Egeland,
Carlson, & Collins, 2005; Warren, Huston, Egeland, & Sroufe, 1997). In
contrast, studies using low risk samples have failed to demonstrate a
clear relationship between infant attachment status and later
psychopathology (for review, see Ungerer & McMahon, 2005).
Disorganized attachment has been found to predict later internalizing
as well as externalizing behavior problems (Lyons-Ruth & Jacobvitz,
1999). Thus the evidence does not support a specic, one to one
relationship between attachment and depression. Rather, attachment
relationships appear to confer risk or protective effects in a
cumulative, incremental fashion, in combination with individual risk
factors and other environmental factors. These data also suggest the
299
hypothesis that the negative impact of insecure attachment is more

likely to be potentiated in environments with high degree of adversity
or stress.
2.3.1.2. Attachment and depression in childhood and adolescence. The
majority of studies of attachment in childhood and adolescence assess
attachment as measured by the youth's report of attachment. Two
measures have been frequently used: the Inventory of Parent and Peer
Attachment (Armsden, McCauley, Greenberg, Burke, & Mitchell,
1990), a self-report measure which assesses affective and cognitive
dimensions of adolescents' relationships with parents and close
friends, particularly in terms of psychological security, and the Adult
Attachment Interview (AAI) (George, Kaplan, & Main, 1985), which
assesses the adolescent's memories of childhood experiences with
parents, and the impact of these experiences on current relationships.
Thus, the operationalization of attachment in youth is based on the
youth's self-reported affective and cognitive schemas about attachment, in contrast to the behavioral and interactive assessment used in
the Strange Situation paradigm for assessing infant attachment. While
this is consistent with Bowlby's theory that the actual attachment
relationship will be internalized as the internal working model, the
types of data yielded by these two designs are quite different.
Essau (2004) found that perceived attachment to parents but not
peers on the IPPA was signicantly worse in depressed adolescents
compared to adolescents with no psychiatric disorder in a community
sample. Armsden et al. (1990) compared self-reported attachment
security in early adolescents who were either currently depressed,
depressed remitted, nondepressed psychiatric controls or maternal
illness controls. Depressed adolescents reported less secure parent
attachment compared to nondepressed psychiatric controls, nonpsychiatric controls, and less secure peer attachment compared to
nonpsychiatric controls. However, the attachment security of the
adolescents with remitted depression was not signicantly different
from the nonpsychiatric control group. This nding suggests that the
negative bias during the depressive episode may account for the lower
self-reported attachment of the depressed children.
While the above studies suggest a relationship between selfreported youth attachment and depression, they do not address the
actual relationship between parent and child, making it impossible to
rule out negative attributional bias as the cause of the correlation. Selfreported measures of attachment strategies presumably reect the
accumulation over time of interactions with attachment gures as
perceived by the child, consolidated into a relatively stable, cognitive
affective perceptual schema which then shapes the interpretation of
new interactions with signicant others (Kobak, Sudler, & Gamble,
1991). However, the actual quality of the current relationship with the
parent may also affect the individual's experience, and may serve to
either conrm or disconrm the attachment schema. For example,
Sroufe et al. (1999) found that individuals whose attachment patterns
switched from insecure in infancy to secure in adolescence had a
better prognosis than those who were insecure at both time points, or
secure as infants but insecure as adolescents.
Studies which examine both perceived attachment strategy and
observational measures of parentchild interaction can help disentangle these issues, and elucidate possible mechanisms through
which attachment in childhood and adolescence is related to actual
interactions with parents and peers. For example, Kobak, Cole, FerenzGillies, Fleming, and Gamble (1993) tested the hypothesis that secure
adolescents would be better able to negotiate age-appropriate autonomy from parents, while maintaining a cooperative relationship with
parents. Consistent with their hypothesis, in a disagreement task with
parents, adolescents with secure attachment were able to assert their
own point of view while still listening to their mothers (balanced
assertiveness) and showed less avoidance and dysfunctional anger
than insecure adolescents (Kobak et al., 1993). In a related study, both
insecure and preoccupied attachment as measured by the Adult
300
Attachment Interview (AAI) were signicantly related to depressive

symptoms, and the interactions of depressed teens and their mothers
were characterized by maternal dominance and dysfunctional anger
(Kobak et al., 1991).
Abela, Hankin, Haigh, Adams, Vinokuroff, and Trayhern (2005)
hypothesized that excessive reassurance-seeking behavior may interact with insecure attachment, leading to child depression. That is,
insecurely attached children may be prone to ask for excessive
reassurance from their parents; parents in turn may feel irritated and
respond in a rejecting manner, thereby reinforcing the child's
insecurity and low self-esteem, and increasing depressive symptoms.
They examined children's self-reported attachment to parents,
reassurance-seeking behavior, and depression in 614 year old
children of depressed parents. Children who reported both insecure
attachment and high excessive reassurance seeking had higher levels
of current depressive symptoms, were more likely to have a past
history of depression, and had greater severity of depressive episodes,
compared to those that had just one (insecure attachment or excessive
reassurance seeking).
Similarly, Allen, Moore, Kuperminc, and Bell (1998) have hypothesized that insecurely attached adolescents will have more difculty
establishing autonomy from parents while maintaining a sense of
relatedness, and that difculty establishing autonomy will increase
risk for internalizing and externalizing symptoms. Consistent with the
rst part of their model, adolescents with secure attachment
strategies on the AAI had current adolescentmother relationships
characterized by autonomy and relatedness: they could disagree
amicably with their mothers, had a realistic rather than idealizing
view of their mothers, felt supported by their mothers, and had
mothers who were attuned to their self-perceptions (Allen et al.,
2003). A strength of this study was that the adolescentmother
relationship was assessed with a combination of observational,
adolescent-reported and mother-reported measures. In a related
study, securely attached adolescents reported higher competence
with peers, lower self-reported internalizing symptoms, and lower
peer- and mother-reported deviant behaviors, supporting the
hypothesized link between attachment security and adolescent
psychosocial functioning (Allen et al., 1998). Turning to the role of
the father in attachment and autonomy processes in adolescents,
Allen, Porter, McFarland, McElhaney, and Marsh (2007) found that
adolescents' relationships with their fathers and peers signicantly
contributed to attachment security, even after controlling for maternal
relationship factors. Furthermore, attachment insecurity was linked to
higher levels of depressive symptoms across adolescence, primarily in
females. In contrast, Pavlidis and McCauley (2001) found that while
depressed adolescents reported poor attachment to parents, observed
parentadolescent attachment quality was not found to be signicantly different from nonclinical adolescents.
Finally, attachment representations may be changeable, for example through new positive relationships in therapy (van Ijzendoorn,
1995), or through improvements in the attachment relationship with
parents.
2.3.1.3. Attachment and youth depression: Summary. In summary,
although a direct causal link between infant attachment and
depressive symptoms is not supported, the available evidence
suggests that early attachment may operate as a risk or protective
factor for the development of both internalizing disorders and
externalizing disorders, with the strongest relationships being found
in high-risk samples, and with infants with a disorganized attachment
pattern. It may be that severe disruptions of attachment, or
disruptions of attachment within the context of highly stressful,
chaotic or aversive environments, are necessary to potentiate the
development of disorder, although further evidence is required. In
adolescence, perceived insecure attachment to parents has been
related to cognitive processes such as maladaptive attributional style,
observed parentchild interactions such as excessive reassurance

seeking and autonomous behavior, and symptoms of psychopathology
such as depression, internalizing and externalizing symptoms. Two
models have been suggested in the literature: the mediation model, in
which parentchild relationship decits lead to insecure attachment
strategies which in turn leads to internalizing or externalizing
behavior, and the moderation model, in which adolescent attachment
style interacts with actual parentchild relationship to produce
depressive or other symptoms. While the data are not inconsistent
with either hypothesis, they do not denitively conrm one over the
other. What is clear, however, is that in adolescence, self-reported
attachment and observed parentchild relationships, while correlated, are constructs which can be separately measured, and should be
differentiated in studies examining adolescent attachment.
Finally, the available evidence cannot rule out the hypothesis that
the attributional bias of depressed adolescents accounts for the lower
self-reported attachment security. While these ndings are consistent
with Bowlby's original model linking decient early caretaking
with insecure attachment and a negative sense of self in relation to
others, further research is required to establish causal links between
attachment processes as they unfold over time, actual parentchild
relationships, cognitiveaffective schemas, and the development of
depressive symptoms.
2.3.2. Level 2: Parental rearing, conict and support, autonomy
and relatedness
Many different aspects of the parentchild relationship have been
examined in relation to youth depression, but most fall under one of
two broad dimensions: warmth/support and control/autonomy. A
third dimension, conict, has also been examined, most often in
relation to parental support, and usually in adolescent as opposed to
child samples. While overlapping, each of these terms has been
dened and operationalized in somewhat different ways, which will
briey be described before discussing specic ndings.
Warmth and control. Broadly dened, parental warmth or care
refers to acceptance and responsiveness, emotional closeness, and
availability on the positive end, and criticism, rejection, lack of
warmth or acceptance on the negative end (Gladstone & Parker,
2005). Two forms of parental control have been differentiated: psychological control, which refers to over protectiveness, guilt-induction,
shaming, threats of withdrawal of love, or intrusiveness, and behavioral control, which refers to consistency in limit-setting, supervision
and monitoring of children (Barber, Olsen, & Shagle, 1994).Whereas
studies of parenting in community samples have found associations
between behavioral control and positive outcomes, studies of
psychopathology have more often focused on the negative consequences of high psychological control combined with low warmth, or
the so-called affectionless control style (Rapee, 1997).
Support and conict. Parental support is a variable frequently
examined in studies of adolescents, usually in combination with conict. While similar to warmth, it is typically operationalized with
different measures. Several aspects of conict have been examined:
severity, tactics and resolution.
Autonomy and relatedness. While the construct of autonomy is
similar to the positive side of psychological control, and the concept of
relatedness to warmth and support, studies employing these variables
are grounded in developmental theory which views establishment of
autonomy as the central psychological task of adolescence (Allen,
Hauser, Bell, & O'Connor, 1994). Furthermore, autonomy and relatedness are often operationalized using observational measures of the
parentchild interaction.
Expressed emotion. Expressed emotion (EE) refers to the degree of
criticism and emotional involvement expressed in the verbal descriptions of patients with schizophrenia and depression by their family
members (Asarnow, Thompson, Hamilton, Goldstein, & Guthrie,
1994), and has been shown to correlate strongly with relapse. These
constructs are similar to the constructs of rejection (warmth) and

psychological control, but are assessed differently.
In the following section the empirical evidence on the association
between the parentchild relationship and youth depression will be
reviewed, beginning with non-observational (self-report) studies,
followed by observational studies.
2.3.3. Parental care and control in children and adolescents:
Non-observational studies
Cross-sectional studies. Depressed adults consistently have reported
greater perceived parental rejection and psychological control compared to nondepressed adults in retrospective studies of the parent
child relationship (Gladstone & Parker, 2005; Parker, 1983). However,
since retrospective designs cannot rule out the possibility that this is due
to the known negative cognitive and attentional bias of depressed
individuals, only studies of depressed youth will be included in this
section.
In one of the rst studies directly assessing current interpersonal
relationships of depressed children, Puig-Antich, Lukens, Davies,
Goetz, Brennan-Quattrock, and Todak (1985a) interviewed the
mothers of prepubertal depressed children. The psychosocial functioning of the depressed children was signicantly worse than both
psychiatric and normal control children (including poorer communication, less warmth and greater rejection in the motherchild
relationship). Fatherchild relationships were also signicantly
poorer in the depressed and psychiatric children compared to normal
controls. Even after the children had fully recovered, including normal
school functioning, the parentchild relationships, though improved,
did not reach the level of the control group, suggesting some enduring
family relationship difculties even after remission of symptoms
(Puig-Antich et al., 1985b).
Two comprehensive reviews of parental rearing and youth
depression have found consistent evidence for a relationship between
low care and high psychological control parenting style (affectionless
control) and depression; however, the evidence is stronger for care
than control (Alloy et al., 2006; Rapee, 1997). Reviewing crosssectional studies, Alloy, Abramson, Smith, Gibb, and Neeren (2006)
found consistent support for an association between low parental care
and depressive symptoms in children and adolescents, whereas
ndings for control/overprotection were mixed: two out of three
studies reported a signicant relationship between high control and
depressive symptoms (Garber, Robinson, & Valentiner, 1997) and one
failed to nd an association (Greaven, Santor, Thompson, & Zuroff,
2000). In studies examining rearing and depressive disorders, ve out
of six studies found a signicant association between affectionless
control parenting and youth diagnosis of depression, with one study
(Burbach, Kashani, & Rosenberg, 1989) nding that affectionless
control was not associated with depression, but rather with other
psychiatric disorders (Alloy et al., 2006). In a study examining
psychological as well as behavioral control, Barber et al. (1994)
found parental psychological control to be related to internalizing
symptoms, whereas low behavioral control was related to externalizing symptoms.
Prospective studies. Three longitudinal studies have examined
parental support and parentadolescent conict in relationship to
onset, course, and remission of depressive symptoms or disorder, in
order to test the causal hypothesis that increases in parentadolescent
disagreement are related to increases in depressive symptoms over
time. Rueter, Scaramella, Wallace, and Conger (1999) found that
increases in parent-reported parentadolescent disagreements from
age 12/13 to age 14/15, predicted increase in adolescent-reported
internalizing symptoms in the same time period, which in turn
predicted rst onset of diagnosis of depressive or anxiety disorder at
age 19. The authors statistically tested and rejected several alternative
hypotheses, including the bidirectional hypothesis that emotionally
distressed adolescents induce more conict in family members. In
301
addition, by using parent reports of parentadolescent conict to

predict youth reports of symptoms, they avoided shared-method
variance problems. Similarly, Stice, Ragan, and Randall (2004) found
that decits in perceived parental but not peer support in 1115 year
old girls were related to increases in depressive symptoms and rst
onset of major depression two years later. They also found that youth
depressive behavior led to decreases in perceived peer social support,
but not perceived parent social support, suggesting support erosion
due to depression occurs more in peer social relations than with
parents. Sandford et al. (1995) looked at factors which predicted
persistence of major depression one year later in a sample of clinically
depressed adolescents, and found that adolescents who continued to
be depressed were less involved with their fathers, and less responsive
to maternal discipline compared to remitters. In a related nding from
a treatment study, parentchild conict and low affective involvement
at baseline and follow-up predicted lack of recovery, chronicity and
recurrence of depression at two year follow-up in a randomized
controlled trial comparing cognitivebehavior therapy to family
therapy for depressed adolescents (Birmaher et al., 2000).
Several studies have examined prospective relationships between
parental care and control and child depression. In a ten year follow-up
study of offspring of depressed and nondepressed parents, Nomura,
Wickramaratne, Warner, Mufson, and Weissman (2002) found
affectionless control parenting to be associated with a six-fold
increased risk of major depressive disorder (MDD) and parentchild
discord with a four-fold increased risk of MDD, but only among
offspring of nondepressed parents. In contrast, among offspring of
depressed parents, parental affectionless control was not associated
with offspring diagnosis of MDD, anxiety or substance abuse.
Affectionless control also predicted a 12 fold risk of substance abuse
in children of nondepressed parents, suggesting a lack of specicity of
affectionless control for depression. Multivariate analyses indicated
that parental depression was more important than family discord for
predicting offspring MDD or anxiety disorders, whereas family discord
was more important for predicting substance abuse disorders.
Reporting on the same sample, Miller, Warner, Wickramaratne, and
Weissman (1999) found that maternal affectionless control was
associated with daughter low self-esteem, which in turn was related
to daughter depression at 10 year follow-up, but only among
daughters of depressed mothers.
Similarly, Liu (2003) found that perceived parental care and
indifference of 6th grade Taiwanese schoolchildren predicted depression scores one year later, with children's self-esteem fully mediating
the relationship between low care and depression and partially
mediating that between indifference and depression. Furthermore,
girls and boys may respond differentially to parenting from mothers
vs. fathers: In a prospective study of parental care and control,
mothers' reports of their own rejecting and controlling behavior
toward their 5 year old children predicted self-criticism in the
daughters at age 12, whereas mother-reported paternal control and
rejection predicted self-criticism in the sons at age 12 (Koestner,
Zuroff, & Powers, 1991).
Finally, Hale, van der Valk, Akse, and Meeus (2008) tested a
bidirectional model of perceived parental rejection and adolescent
depressive and aggressive symptoms over four yearly assessments in
young adolescents. In the rst two assessments, perceived parental
rejection predicted adolescents' depressive symptoms, and adolescent
depressive symptoms predicted perceived parental rejection, supporting bidirectional effects between parental rejection and adolescent depressive symptoms. However, in the last two assessments,
adolescent depression predicted parental rejection, but parental
rejection did not predict adolescent depression, suggesting that by
later adolescence, the depressive behavior of the adolescent was
inuencing the parental rejection, not vice-versa. Interestingly,
parental rejection predicted adolescent aggression at all four time
periods. The authors hypothesize that in early adolescence, parental
302
rejection and adolescent depression are reciprocally related, but by

later adolescence, a transactional process has been established
whereby parents react negatively to their adolescents' depressive
behavior, and adolescents who feel rejected react with aggression.
In summary, the ndings from prospective longitudinal studies
show that key aspects of the parentchild relationship such as care,
control, support and conict predict increases in depressive symptoms, rst onset of depressive disorder, increased risk for major
depression, and persistence, lack of recovery, chronicity or relapse of
major depression. The prospective design provides stronger evidence
compared to cross-sectional studies for a causal relationship between
parentchild relationship factors and risk for depression. While some
evidence supports unidirectional parentchild effects, there is also
evidence for bidirectional effects of child depressive symptoms and
parenting. Finally, strong support is lacking for a specic relationship
between parentyouth variables and depression. Rather, these
parentyouth variables are also related to anxiety, substance use,
and externalizing symptoms and disorders.
2.3.3.1. Observational studies of parentchild relations. In this section
studies using observational methods are reviewed.
Cross-sectional studies: support and conict. Several studies have
combined observational and self-report assessments to investigate
the relationship between perceived and observed parentyouth
relationships. For example, Sheeber and Sorensen (1998) found that
depressed adolescents and their mothers both described their families
as being less supportive and more conictual than non-distressed
adolescents and their mothers. In observed problem-solving interactions, the same depressed adolescentmother pairs demonstrated less
facilitative and more depressive interactions. However, neither
adolescent nor mother exhibited higher rates of aggressive behavior.
In a second study combining both self-report and observational
measures, Sheeber, Davis, Leve, Hops, and Tildesley (2007) found that
both clinically and sub-clinically depressed adolescents had less
supportive and more conictual relationships with their mothers as
well as fathers compared to healthy adolescents. Furthermore, a
supportive relationship with either father or mother did not moderate
the relationship between conict and depression. Self-report and
observational data were combined to create factors of support and
conict; interestingly, observational data did not load as highly as selfreport data on the two constructs.
McCarty, Lau, Valeri, and Weisz (2004) examined whether the two
dimensions of expressed emotion (EE), criticism and emotional
involvement, were correlated with observed parentchild interactions. Parents rated high on the critical dimension of EE were observed
to be higher on antagonism, negativity, disgust, harshness and to be
less responsive in their interaction with their children compared to
low or borderline critical parents. In contrast, none of the observed
parentchild interaction variables corresponded to the parental
emotional over-involvement dimension of EE. Similarly, parents of
depressed children have been found to score higher on the criticism
dimension of EE compared to parents of nonclinical (Schwartz, Dorer,
Beardslee, Lavori, & Keller, 1990) or schizophrenia spectrum disordered children (Asarnow et al., 1994) whereas the over-involvement
dimension did not differentiate depressed from nonclinical children
(Asarnow et al., 1994).
Parental support and conict: Prospective observational studies.
Finally, several studies have combined observational assessment of
parentchild interactions with prospective longitudinal design, which
provides the strongest test for causal hypotheses. Burge and Hammen
(1991) found observed critical interaction quality and low task
involvement during a motherchild disagreement task to be associated with children's depressive symptoms and maladaptive school
performance six months later in children aged 8 to 16. Positive
motherchild interactions were associated with good school performance six months later.
Ge, Lorenz, and Conger (1994) examined whether maternal

warmth and support moderated the relationship between stress and
depressive symptoms in girls and boys, in a longitudinal study
employing home observations of youth aged 917. Observed maternal
warmth and support moderated the relationship between stressful
life events and depressive symptoms in girls, not boys. Furthermore,
they found differences in the trajectories of girls and boys' depressive
symptoms and stress: Girls' depressive symptoms increased after age
13, whereas boys' depressive symptoms remained relatively stable
after age 13. Boys reported more stressful life events than girls before
age 12, but after 13, the pattern reversed, with girls' reporting a
greater increase in stressful life events, particularly between 13 and
15. The authors conclude that girls not only experience more stressful
life events during adolescence, but are also more sensitive to the
effects of these stressful events than boys, for whom the increases in
negative events were not associated with increased depressive
symptoms. This gender difference in experienced stressful life events
and vulnerability to these events may explain why the moderating
effect of maternal support was found for girls but not boys.
Prospective studies employing multi-method, multi-informant
measurement illustrate how parents and children perceive the
parentchild relationship differently. For example, Sagrestano, Paikoff,
Holmbeck, and Fendrich (2003) found that child reports of increases
in parentchild conict and decreases in parental monitoring were
associated with increases in depressive symptoms in low income,
African American youth aged 915. On the other hand, parentreported increases in positive parenting were associated with
decreases in child depression two years later. Increases in observed
peer relationship between parent and child (that is, a relationship
characterized by the child acting like a parent, and the parent acting
like a child), were related to increases in depressive symptoms at
follow-up. However, 12 other dimensions of observed parenting or
family atmosphere were not associated with increases in depression
scores.
Prospective observational studies: Autonomy and relatedness. Several
developmental researchers have hypothesized that difculty in
negotiating the central adolescent task of establishing autonomy
from parents can increase vulnerability to depression and other
disorders (Allen et al., 1994; Powers & Welsh, 1999). According to
Powers and Welsh's model, the transition into adolescence leads to
increases in the child's expression of autonomy, which in turn leads to
increases in conict with parents and decreases in the adolescent's
submissive behavior. Families which cannot tolerate conict or in
which conict is extreme, may not provide the necessary support for
the adolescent's developmental need to negotiate conict and a more
autonomous relationship with the parents (Powers & Welsh, 1999).
Furthermore, adolescent girls and their mothers may have particularly
difcult time with this phase of development, given girls' socialization
to be more submissive and conict-avoidant, and mothers' potential
loss of power as adolescent autonomy increases (Powers & Welsh,
1999).
To test this model, Powers and Welsh (1999) examined longitudinally the relationship between motherdaughter interactions
reecting autonomy, and daughters' internalizing symptoms. They
tested two directional models: a causal model in which mother
daughter interpersonal behaviors predicted increases in daughter's
internalizing symptoms one year later, and a reactive model in which
daughters' internalizing behaviors predicted difculty negotiating
autonomy. To combine subjective perception with objective interaction, mothers and daughters rated their own videotaped interaction.
Daughters high in internalizing symptoms rated themselves as having
high levels of conict and submission with mothers, whereas their
mothers, rating the same interaction, viewed their daughters'
behaviors as humorous rather than reecting conict or submission.
The daughters' perceived submissive behavior to mother was
associated with increased risk of internalizing symptoms one year
later, supporting the causal/maintaining model. Furthermore, both

too high and too low levels of mother's conict, humor and sarcasm
were related to daughter's internalizing symptoms one year later,
supporting their hypothesis that a moderate degree of conict is
protective (Powers & Welsh, 1999).
Allen et al. (1994) have conducted a series of longitudinal studies
examining the relationship between adolescent autonomy development and internalizing and externalizing symptoms. Observed
difculty establishing autonomy and relatedness with parents at age
14 and 16 was linked to observed depressed affect and self-reported
externalizing behaviors at age 17. Difculties with autonomy were
more strongly linked to depressed affect, and difculties maintaining
relatedness more strongly linked to externalizing behaviors. Lack of
hostile, relatedness-inhibiting behaviors in the parentadolescent dyad
was associated with adolescent depressive affect, similar to Power
and Welsh's (1999) nding of submissiveness in internalizing girls.
In a related longitudinal study, autonomy and relatedness with
both mother and peers contributed to increases in depressive
symptoms in adolescents (Allen et al., 2006). Specically, adolescentmother interactions in which the adolescent undermined
autonomy and relatedness in a disagreement task, and adolescent
peer interactions in which the adolescent was withdrawn, angry or
dependent, each independently predicted increases in depressive
symptoms one year later (Allen et al., 2006). In contrast, Pavlidis and
McCauley (2001) found no differences in observed autonomy and
relatedness between clinically depressed adolescentmother dyads
compared to nonclinical pairs, but lower self-reported attachment to
parents among the depressed adolescents.
In summary, ndings from observational studies of parentyouth
interactions are generally consistent with ndings from self-report
studies on care, support, conict, expressed emotion and autonomy.
Specically, there is evidence for the critical dimension of EE
corresponding to observed antagonistic and harsh parenting, for
observed critical and uninvolved parenting to be prospectively related
to depressive symptoms, and for observed difculty with autonomy
and relatedness between adolescents and parents to be prospectively
related to observed depressed affect. However, some interesting
discrepancies between self-report and observational data were also
found. In Sheeber and Sorensen's (1998) study, depressed adolescents
and their mothers experienced themselves as being more conictual
and less supportive; however, their interactions were not characterized by higher aggressive behavior, but rather by lower facilitative
behavior, and higher depressive behavior. The impact of parental
support is also unclear. Sheeber et al. (2007) found no evidence in
their cross-sectional study that father or mother support moderated
the relationship between conict and depressive symptoms, and
Powers and Welsh (1999) found that maternal support was not
prospectively related to adolescent girls' internalizing symptoms. In
contrast, Ge et al. (1994) found that observed maternal support
moderated the relationship between stress and later depressive
symptoms in girls, but not boys. Finally, observational measures
were found to be less related to outcome variables than self-report
(Sagrestano et al., 2003) and loaded less strongly than self-report
measures on combined variables (Sheeber et al., 2007). Powers and
Welsh's study (1999) provides some hypotheses for these discrepancies. Mothers and daughters perceived the same interaction quite
differently: the high internalizing girls felt submissive and in conict;
their mothers found them humorous. Mothers may interpret
submissive behavior in a positive light, as cooperative, helpful, or
close. Such an interpretation may be appropriate for younger children,
but may be less appropriate for adolescents, who may desire more
autonomy but be afraid to express it directly, leading to feelings of
resentment. Similarly, an explanation for the conicting results with
regard to maternal support is that too much maternal support in
adolescence may be related to a lack of autonomy and avoidance of
healthy levels of conict in the motheradolescent relationship.
303
Finally, these studies illustrate how the framework of adolescent

autonomy development helps integrate the ndings reviewed above
on parental rearing, conict and support, and leads to testable
hypotheses about the relationship between these variables.
2.4. Level 3: Marital relationship
In this section, the impact of the marital relationship on child
functioning will be reviewed. The majority of this evidence comes
from prospective longitudinal studies of community samples which
examine a broad range of outcomes, from adjustment problems to
internalizing and externalizing symptoms. These studies provide the
strongest evidence for causal models linking marital relationship to
child outcomes and allow investigators to determine the specicity of
the relationship between marital factors and depression (compared to
other symptoms such as aggression). While these studies are broader
in scope than this review's specic focus on depression, they are
included in this section as they provide data to test the hypothesis that
marital relations impact on child psychopathology.
There is clear evidence that marital discord and divorce are associated with child adjustment problems and psychopathology (Cummings, 1994; Emery, 1982). Studies examining marital discord and
divorce show that much of the deleterious effect of divorce on child
functioning can be explained by the high degree of marital discord in
divorcing families rather than the fact of the divorce or separation per
se (Emery, 1982). Among intact couples, marital conict may have the
most negative impact on children (Cummings, 1994; Hudson, 2005).
In response to interparental conict, children show behavioral distress, report feeling anger, sadness, fear, guilt, shame or worry, and
show physiological reactions (Cummings & Wilson, 1999). Interparental conict has been associated particularly with aggression,
conduct problems and other externalizing disorders, but also with
internalizing problems, impaired social skills, and childparent and
peer relationships (Cummings, 1994; Hudson, 2005).
Marital conict appears to play a role in the transmission of
psychological problems from depressed parent to child (Downey &
Coyne, 1990). For example, Emery et al. (1982) found little association
between parental unipolar or bipolar depression and children's
disturbed school behavior, after controlling for the effect of marital
discord. In their study of the children of psychiatrically ill parents,
Rutter and Quinton (1984) concluded that the main risk in most cases
stemmed from the associated psychosocial dysfunction in these
families. Thus, marital conict may explain part of the increased risk
for problems among children of depressed parents. In contrast,
Nomura et al. (2002) found parental depression to be a stronger
predictor of offspring depression compared to marital discord and
other family environment risk factors, suggesting a direct effect of
parental depression on offspring depression.
While the negative effects of marital conict on children have been
well documented, some amount of conict may be inevitable in family
relationships, and conict may serve a number of useful functions
within a family, such as resolving disagreements, developing
problem-solving skills, and modeling effective interpersonal problem
solving (Cummings, 1994; Cummings & Wilson, 1999). Determining
constructive as opposed to destructive interparental conict tactics
becomes the important question (Cummings & Wilson, 1999). Indeed,
the type of conict tactics used by parents appears to have an effect on
children. In general, interparental hostility and withdrawal have been
more strongly related to externalizing than internalizing problems in
children (Katz & Woodin, 2002). For example, interparental verbal
and nonverbal hostility, threat of physical aggression, and withdrawal
increased the likelihood of children's aggressive responding, whereas
interparental calm discussion, humor, support, affection and problem
solving decreased likelihood of children's aggressive responding in
children aged 816 (Cummings, Goeke-Morey, & Papp, 2004).
However, interparental conict was found to predict internalizing
304
problems when the husband was angry and withdrawn (Katz &
Gottman, 1993). Avoidant conict tactics have been found to be
related to higher rates of internalizing, but not externalizing problems
in children (Marchand & Hock, 2003).
Finally, conict resolution has been shown to ameliorate children's
distress in the face of interparental conict in experimental analogue
studies, in which children are exposed to videotapes depicting
parents (i.e. actors) ghting, with varying degrees of conict resolution (Davies & Cummings, 1994). Complete resolution of conict has
been shown to bring children's distress levels back to baseline levels,
but even partial resolution of conict reduces children's distress
(Cummings, 1994). Children's distress is also reduced when parents
resolve their conict off screen, or when they tell children that the
conict has been resolved (Cummings, Simpson, & Wilson, 1993).
In summary, marital discord, particularly marital conict, has been
related to both internalizing and externalizing problems in children in
cross-sectional, longitudinal and experimental studies, has been
found to be elevated in families of depressed children and depressed
parents, and may partially account for the relationship between
parental depression and child psychopathology, including depression.
How parents ght seems to matter, with actual or threatened physical
aggression, anger combined with withdrawal, and avoidant tactics
having particularly deleterious effects on children, and calm discussion, humor and problem solving decreasing negative effects.
Resolution of the conict, whether directly observed or only explained
by parents, has been found to ameliorate the negative impact of
interparental conict in analogue experiments. The bulk of this
research has been conducted in nonclinical populations, and stronger
relationships have been found between interparental conict and
externalizing symptoms than internalizing symptoms.
2.5. Level 4: Whole family system
In this section, we turn to studies which have examined interconnections between the above subsystems within the context of the broader
family system. Thus we move from consideration of the individual, dyadic
relationships (spouse-spouse or parentchild) to triadic relationships, that
is mother, father and child(ren). The shift from dyadic to triadic
relationships allows interrelationships between various subsystems to
be examined, which may impact on dyadic and individual processes
(Bronfenbrenner, 1986; Minuchin, 1974). By examining a broader level of
the system, transactional processes may be revealed which might
otherwise go unnoticed. For example, if a depressed mother is observed
to be withdrawn from and critical of her children, a causal relationship
may be hypothesized:
Maternal depressionYCritical withdrawn parentingYChild depression:
However, if the scope is broadened to include the father, we may

notice a high degree of marital conict, with father alternating
between hostile and withdrawn behavior, and mother exhibiting
hostile, dependent, and withdrawn behavior. With this additional
data, several different levels of the system can be modeled: individual
(mother, father and child), marital relationship separate from child,
and marital relationship including child. The causal relationship
between these factors is not immediately evident, and can be modeled
in a series of competing hypotheses, or modeled as transactional,
circular causal models.
The shift from dyadic to triadic family processes also has important
implications for research design. In the above example, marital
conict can be included in a statistical model, as a third variable
which accounts for the relationship between maternal depression and
child depression, or as a moderator or mediator variable. For example,
marital conict may moderate the relationship between maternal
depression and child depression, such that the interaction between
maternal depression and marital conict leads to child depression.
Alternately, marital conict may mediate the relationship between

maternal depression and child depression, such that maternal
depression leads to increased marital conict, which leads to child
depression. Conversely, maternal depression may mediate the
relationship between marital conict and child depression, such that
marital conict leads to maternal depression, which leads to child
depression. Furthermore, reciprocal causal pathways can be tested.
Thus including more levels of the family system can lead to research
designs in which competing hypotheses are tested against each other.
Finally, there is greater ecological validity in studying triadic systems:
most families, even divorced or single-parent families, include some
variation of father, mother and children and how these parents
interact clearly affects child functioning (Emery, 1982).
2.5.1. Global family environment
Several studies have examined the perceived family environment
of depressed youth. Stark, Humphrey, Crook, and Lewis (1990)
compared the perceived family environment of depressed only,
anxious only, comorbid depressed/anxious, or normal 4th to 7th
grade children and found that all disordered children perceived their
families as less supportive, more conictual, less involved with
outside recreational activities, more enmeshed, and less involved in
decision making processes, compared to the normal controls. Children
with comorbid anxiety/depression and their mothers reported the
greatest degree of family disturbance compared to anxious only and
control children. Moreover, in a study of adolescent school refusers
comorbid for anxiety and depression, adolescents and their families
described their family environment as low in cohesion (disengaged)
and in adaptability (rigid) (Bernstein, Warren, Massie, & Thuras,
1999). Adolescents in extremely disengaged families were signicantly more depressed than adolescents in connected families, and
adolescents in extremely rigid families had higher somatic complaints. Finally, Kashani, Suarez, Jones, and Reid (1999) compared
perceived family environment of clinically depressed or anxious
youth, and found that depressed youth reported less pride in their
families; less trust, respect and loyalty between family members;
viewed their families as less adaptable when under stress; and felt less
supported by family members.
Studies of perceived family environment are limited by the
potential bias on the part of child or parent; however, observational
studies can address this limitation. In an observational longitudinal
study, Jacobvitz, Hazen, Curran and Hitchens (2004) examined
whether boundary disturbances in the family interactions of
24 month old children predicted depressive, anxiety and ADHD
symptoms at age 7. Both disengaged family patterns (low warmth,
affection, eye contact or emotional responsiveness between family
members), as well as by enmeshed family patterns, (one parent turns
to a child for inappropriate intimacy or guidance, or undermines the
authority of the spouse) predicted depressive symptoms at age 7, even
after controlling for maternal depression. In contrast, controlling
interactions predicted anxious symptoms, and hostility predicted
ADHD symptoms. Girls and boys showed different reactions to family
patterns: girls who experienced the enmeshed pattern were more
vulnerable to developing depressive symptoms, whereas boys were
more vulnerable to developing ADHD symptoms. The fact that
observed disengagement or enmeshment at age 2 predicts depressive
symptomatology at age 7 provides stronger evidence for a causal role
of actual, not only perceived, family processes in the development of
depressive symptoms. (However, the possibility of a third variable
such as genetic factors explaining both cannot be ruled out.)
Furthermore, it broadens the issue of warmth and control to the
larger family context; what has sometimes been treated as a measure
of parentchild relationship may in fact reect a broader family style,
which in turn may impact on parentchild relationships.
Similarly, Rueter and Conger (1995) hypothesized that an overall
family climate characterized by warmth and supportiveness in early
adolescence would buffer against the increased parentchild conict

in middle adolescence, by supporting conict resolution, and keeping
conict at low to moderate levels. Conversely, a hostile or coercive
environment would make it more difcult to resolve conicts, leading
to escalation of conict. Using prospective longitudinal data of
adolescents from age 12/13 to 15/16, they found that families which
displayed critical, coercive, and angry behavior towards each other
became more hostile one year later, which in turn predicted more
defensive and disruptive behavior during problem-solving tasks, and
which further predicted exacerbated parentchild disagreements. In
contrast, families strong in communication, attentive listening, and
warmth remained warm one year later, and these emotionally
supportive families' problem-solving abilities improved. Furthermore,
warmth and supportiveness directly and more strongly related to
reduction in parentadolescent conict from early to middle adolescence, than did parents' exibility in handling conict. While this
study was conducted in a community sample, and therefore does not
address the link between these family variables and youth depression,
it provides evidence of a relationship between family environment
and parentyouth conict, a known correlate of youth depression.
2.5.2. Relationships between multiple family subsystems
Families with depressed individuals often have multiple risk
factors for depression, occurring at different levels of the family
system (individual, marital dyad, parentchild dyad, entire family),
making it difcult to interpret ndings from bivariate analyses, or
determine causal mechanisms. Multivariate designs address these
limitations by simultaneously measuring several risk factors at
different levels, and testing competing causal models. For example,
Cummings et al. (2005) examined interrelationships between
maternal and paternal depressive symptoms, family functioning, and
child adjustment in a community sample of families with kindergarten children. Increased parental depressive symptoms were associated
with greater marital conict, insecure marital attachment, less
parental warmth, more psychological control in parenting, and with
children's internalizing and externalizing problems, peer exclusion,
and lower prosocial behavior. Marital conict mediated the relationship between maternal depressive symptoms and children's internalizing and externalizing problems and peer exclusion, whereas
marital attachment mediated between maternal depressive symptoms and peer exclusion. In fathers, marital conict and marital
attachment mediated the relationship between paternal depressive
symptoms and children's internalizing problems. While parental
depressive symptoms were related to less effective parenting,
parenting did not mediate the relationship between parental depression and child outcomes. Once again, girls and boys responded
differentially to mothers and fathers: mother's depressive symptoms
were more strongly associated with girls' peer exclusion than boys,
and father's depressive symptoms were more strongly and negatively
associated to boys' prosocial behavior than girls.
Similarly, Cox, Paley, Payne, and Burchinal (1999) examined the
effects of the marital relationship on parenting by measuring marital
interactions in couples expecting their rst baby. Marital withdrawal
rather than conict (assessed prior to the infant's birth) predicted less
sensitive parenting for both husbands and wives when their infants
were 3 and 12 months. For fathers, the interaction of marital conict
and withdrawal predicted less sensitive parenting at 12 months.
Interestingly, relationships between parental depressive symptoms
and parenting were relatively weaker.
Finally, Low and Stocker (2005) found that mother's and father's
marital hostility was linked to parentchild hostility, which was
linked to children's internalizing problems. There were different
patterns found for mothers and fathers: Mothers' marital hostility was
directly associated with child externalizing problems, whereas
fathers' marital hostility was indirectly associated with externalizing
problems via fatherchild hostility, and father's depressed mood was
305
related to child internalizing problems indirectly via fatherchild

hostility. Similarly, Hops, Biglan, Sherman, Arthur, Friedman, and
Osteen (1987) compared the children of depressed mothers with
marital distress to children of depressed mothers without marital
distress, and found that children of depressed mothers with marital
distress displayed signicantly higher irritable affect than children of
normal mothers, whereas children of depressed mothers without
marital distress did not. Taken together, these ndings suggest that
marital distress may be an important factor in the relationship
between maternal depression and youth depression, with interparental hostility directed at the child being one hypothesized mechanism of transmission.
In contrast, Nomura et al. (2002) examined the impact of several
measures of family discord (poor marital adjustment, parentchild
discord, low family cohesion, affectionless control, divorce) on risk for
psychiatric disorders among offspring of depressed and nondepressed
parents, in a prospective longitudinal study. While all family discord
measures were associated with a diagnosis of either major depression,
anxiety disorder or substance abuse among the offspring of
nondepressed parents, among the offspring of depressed parents,
family discord was not related to child diagnosis (with the exception
of low family cohesion increasing the risk of substance abuse).
Parental depression was more important than family discord for the
development of offspring major depression, whereas family discord
was more important than parental depression for the development of
substance use disorder in offspring.
2.5.3. Interaction patterns in families with a depressed member
Micro-analytic studies of interaction patterns in families with a
depressed member allow for the observation of reciprocal processes as
they unfold between several subsystems of the family, and shed light
on hypothesized interactional mechanisms which may promote or
maintain the development of depressive behavior. Two different
models have been hypothesized: 1) Reinforcement of depressive
behavior in the family, and 2) Effect of child's response to interparental
conict on the development of depressive symptoms.
2.5.3.1. Reinforcement models of depressive behavior. Social learning
theory models of depression hypothesize that depressive behavior
may be reinforced within the family (Davis, Sheeber, & Hops, 2000).
For example, mothers of depressed adolescents have been found to
increase facilitative behavior in response to the adolescent's depressive behaviors during a problem-solving task, compared to mothers of
nondepressed adolescents (Sheeber, Hops, Andrews, Alpert, & Davis,
1998). Further evidence comes from studies showing that depressed
affect in one family member can reduce or suppress subsequent
expression of aggression in other family members. For example, high
levels of depression in children have been found to be associated with
subsequent low levels of conict and aggression in family members of
both depressed and comorbid depressed/conduct disordered children
(Dadds, Sanders, Morrison, & Rebgetz, 1992). Dysphoric affect in
mothers has been found to suppress the expression of aggressive
affect from children or husbands, while aggressive affect from children
and fathers suppressed mother's dysphoric affect (Hops et al., 1987).
Thus, aversive behavior (both depressive and aggressive) may be
functional in that it decreases the aversive behavior of other family
members, and therefore may be reinforced within the family (Biglan,
Rothlind, Hops, & Sherman, 1989; Hops et al., 1987). In addition,
depressed children may receive less reinforcement for positive, nondepressive behavior. For example, mothers of depressed clinic children
rewarded their children at much lower rates than mothers of
nondepressed clinic children or nonclinical children during a challenging task (Cole & Rehm, 1986). Thus, not only do depressive disorders
appear to be reinforced in the family via positive and negative
reinforcement processes, depressed children appear to receive lower
levels of reinforcement for positive, problem-solving behaviors.
306
In contrast, some evidence suggests that depressed youth may

receive less attention due to their aversive behavior theorists, consistent with Coyne's (1976) interactional theory of depression, which
states that depressive behavior is aversive to others and elicits
negative interpersonal reactions. For example, Pineda, Cole, and Bruce
(2007) found that parents of depressed adolescents were less
attentive and reacted more negatively to their adolescents compared
to parents of nondepressed adolescents, consistent with Coyne's
interactional model rather than the social learning model of depression. However, these two theories are not necessarily incompatible.
For example, Biglan et al. (1989) found that while distressed behavior
in couples induced negative feelings in the long-term, in the short run,
it deterred hostile reactions. In their model, a husband who initially
suppresses his aggression towards his depressed wife becomes
resentful over time; however, the reinforcing effect of his suppressed
anger has already occurred. Furthermore, it may be precisely because
depressive behaviors are so aversive that they are so (negatively)
reinforcing. If family members reduce their aggressive behavior in
reaction to depressive behaviors as a way to escape from them or
reduce them in the short run, they may in the long run reinforce them.
2.5.3.2. Response to interparental ghting and aggression and development of depression. The way a child responds to interparental conict
and distress may mediate the relationship between marital conict
and the child's depressive symptoms (Davis, Hops, Alpert, & Sheeber,
1998). Children are more likely to intervene in interparental conict in
families with high levels of marital conict, and this has detrimental
effects (Cummings, 1994). For example, Davis et al. (1998) found that
adolescents became aggressive after involvement in interparental
conict, with differential patterns emerging for boys vs. girls. Boys
who responded to their mother's attack on the father by becoming
aggressive to the mother (defense of or alliance with father) were
more likely to show increased aggressive behavior one year later
(Davis et al., 1998). On the other hand, girls who responded to their
father's initiating conict with their mother by becoming aggressive
to their mother (attack of mother; alliance with father) were more
likely to display higher levels of aggressive functioning one year later.
The relation between response to interparental conict and later depressive symptoms was weaker than for aggressive symptoms. However,
suppression of sadness toward the mother when mother initiated
conict with father was related to an increase in depressive symptoms in
a subset of girls. Intervening in reaction to interparental depressive
behavior has been found to predict depressive symptoms in adolescents:
females who responded to interparental depressive behavior with either
facilitative or depressive behavior, or with the suppression of aggression
showed increases in depressive symptomatology one year later, whereas
for males, both depressive and aggressive responses to interparental
depressive behaviors related to increases in depressive symptoms
(Davis, Sheeber, Hops, & Tildesley, 2000).
2.5.4. Summary of whole family level
Family-level processes such as cohesion, enmeshment and warmth
have been associated with depressive symptoms in both self-report as
well as observational studies. Prospectively assessed family environment of very young children has been found to predict internalizing
and externalizing symptoms in middle childhood, and supportive
family environment in early adolescence predicted lower parentchild
conict during middle adolescence. Several studies have implicated
marital conict as one potential mechanism in the transmission of
depression from parent to child; however, one well-designed longitudinal study found stronger evidence for a direct effect of parental
depression on child depression. Micro-analytic studies suggest that
reinforcement processes may help maintain depressive behavior in
children and adolescents. Finally, intervening in interparental aggressive or depressive behavior appears to have negative consequences for
adolescents, with intervention in interparental conict associated
with later aggressive behavior, and intervention in interparental

depressive behavior associated with later depressive behavior.
2.6. Level 5: Extra-familial context: stress
Bronfenbrenner (1986) argued that developmental research
should examine how extra-familial factors may have direct or indirect
inuences on child and family functioning. Goodman and Gotlib
(1999) in their inuential review of the effect of maternal depression
on child functioning, highlight the overall stressful context of
depressed women's lives as an important level to investigate to
elucidate the underlying mechanism through which maternal depression leads to child psychopathology. We therefore briey discuss this
level, as it has implications for research as well as treatment.
Stress has broadly been dened as environmental events or
chronic conditions that objectively threaten the physical and/or
psychological health or well-being of individuals of a particular age in
a particular society (Grant et al., 2003). While stress can theoretically
occur at any level of a system, it is particularly useful to consider
stressful environmental events which impinge upon family functioning. In a comprehensive review of prospective studies, stressful events
were found to predict increases in both internalizing and externalizing
symptoms in youth in 53 out of 60 studies, with stronger associations
found with internalizing symptoms (Grant, Compas, Thurm, McMahon, & Gipson, 2004). Effect sizes ranged from 1% to 21%, with an
average of 4% for studies testing unique variance accounted for (Grant
et al., 2004). Families with depressed mothers are more likely to face
stresses such as poverty, single parenthood, or job or nancial
difculties (Goodman & Gotlib, 1999). Furthermore, families with a
depressed parent tend to be more isolated and less likely to encourage
their children to participate in social groups and activities outside the
immediate family, which may limit children's ability to develop social
relationships or receive extra-familial support, and which may
negatively impact on the separation-individuation process (Cummings & Davies, 1994).
While it is beyond the scope of this article to extensively review the
vast literature linking stress to youth depression, a study by Ge et al.
(1994) illustrates how stress can impact on family functioning and
youth depression, and how models linking stress to particular family
subsystem functioning and youth depression can be developed and
tested. In cross-sectional data from a community sample of 7th grade
students, stressful life events experienced by parents were related to
parents' depressed mood which then was found to disrupt parenting
practices (via harsh or inconsistent parenting), which in turn placed
adolescents at increased risk for developing depressive symptoms.
These results were found with all parentchild combinations: fathers
and sons, fathers and daughters, mothers and sons, and mothers and
daughters. The relevant point for researchers interested in the
development of youth depression is that the larger social context
may interact with aspects of the family environment to lead to
increased or decreased risk for depression. There are also policy
implications of such research: if extra-familial factors such as poverty,
social or ethnic identity, language, socio-economic status, school or
neighborhood have an impact on child depression, then interventions
at this level may be important for preventing or treating depression.
Psychologists tend to focus on the individual or family level of
intervention, but in some cases, interventions at a broader level may
prove to be more effective, and intervention trials should include tests
at this level as well.
2.7. Summary of empirically supported family risk factors for
youth depression
Family risk factors for youth depression were reviewed at ve
system levels. At Level 1 (individual parent), parental depression has
been associated with increased risk of psychiatric disorders among
Table 2
Family risk factors targeted and effect sizes in randomized controlled trials for youth depression1,2.
Level of family
system
Family risk factor

targeted
Authors
1 Individual
parent
Maternal depression3
Sample
Study design
Results (child outcomes)
Billings and Moos (1986); 249 b18 year old children of depressed
Timko et al. (2002)
parents already receiving treatment
and children of nondepressed parents
Depressed parents
Not randomized; compared

children of fully remitted,
partially remitted, or no
improvement, and children
of never depressed parents
At 1 year follow-up, children of remitted

depressed parents whose depression remitted
functioning better than children of parents
who remained depressed but worse than
children of never depressed; at 4-year followup, children of stably remitted comparable to
children of never depressed; children of nonremitters functioning most poorly; at 10 year
follow-up, offspring of remitted depressed
parents comparable to offspring of
nonremitted depressed parents, and sig. worse
than offspring of never depressed parents
Byrne et al. (2006)
260 416 year old children of

dysthymic mothers
Dysthymic mothers
Medication vs. IPT vs.

medication + IPT
Children of mothers with 40% reduction in

dysthymic symptoms had fewer internalizing
symptoms compared to children of mothers
with b 40% symptom reduction 2 years post
maternal treatment
Clark et al. (2003)
19 124 mo old infants of

depressed mothers
Depressed mothers
IPT vs. M-ITG vs. waitlist
Greater child adaptability in the two active

conditions compared to waitlist; no treatment
effects for children's cognitive and motor
development
Forman et al. (2007)
176 6 mo infants of postpartum

depressed mothers
Depressed mothers
IPT vs. waitlist
No association between reductions in maternal

postpartum depression and child behavior
problems, attachment, emotionality,
temperament
Lee and Gotlib

(1989, 1991)
75 713 year old children

of depressed, psychiatric or
medical patients (mothers)
Depressed, psychiatric or
medically ill mothers
No randomization; child
outcomes examined after
mothers began treatment
No differences in child internalizing or

externalizing symptoms between treatment
groups
Murray et al. (2003)
193 newborns of mothers with

postpartum depression
Depressed mothers
Nondirective counseling vs. CBT

vs. psychodynamic therapy
vs. routine primary care
Some short-term (4.5 and 18 mo) benet to

motherchild relationship and infant behavior
problems. No group differences for attachment,
or for cognitive or emotional development at
5 years.
Modell et al. (2001)

depressed mothers
Depressed mothers
Open trial medication
Reduction in maternal depression

associated with fewer child internalizing,
externalizing and learning problems
Verdeli et al. (2004)
9 618 year old depressed children

referred for outpatient treatment with
depressed mothers
Depressed mothers
Open trial IPT
Reduction in maternal depression associated

with improved child global functioning but not
child depressive symptoms
Verduyn et al. (2003)
119 24 year old children of depressed

mothers from the community
Depressed mothers
Parent CBT + parenting skills vs.

support group vs.
no intervention
No group differences on child behavior or

maternal depression; children of mothers in
CBT group showed prepost improvement
Weissman et al. (2006)

depressed mothers
Depressed mothers
Medication treatments
Maternal response to trt correlated with

reduction in child symptoms and diagnosis
307
(continued on next page)
Target of treatment
308
Table 2 (continued)
Family risk factor
targeted
Authors
Sample
Target of treatment
Study design
Support
Conict
Autonomy
Communication
Mufson et al. (1999)
33 1218 year old clinic-referred

depressed adolescents
Youth
IPT vs. clinical monitoring;

12 weekly sessions
Youth
Overall ES 4
.61 IPT
Depression ES
.54 IPT
IPTA vs. TAU (16 sessions)
.45 IPT
.44 IPT
Youth
IPT vs. CBT vs. WL
.11 CBT
.47 IPT
.37 CBT
.72 IPT
Parents + youth
ABFT (12 weeks) vs. WL (6 weeks)
.68 ABFT
.72 ABFT
CBT vs. SBFT vs. NST (12 weeks)
.32 CBT
.15 SBFT
.36 CBT
.18 SBFT
2 Parentyouth
63 1218 year old high school

students with depression, dysthymia,
depression NOS, adjustment disorder
w/depressed mood
Rosello and Bernal (1999) 71 1318 year old clinic clinic-referred
Results (child outcomes)
Attachment
Diamond et al. (2002)
Parental warmth/control
Support
Conict
Autonomy
Communication
32 1217 year old clinic clinic-referred

Parenting style
Conict
Communication
Problem solving
Communication
Problem solving
High expectations
Pos. reinforcement
Attachment
Brent et al. (1997)
107 1318 year old depressed adolescents Family (SBFT) youth (CBT)
(clinic referred and via advertisement)
Treatment of Adolescent
Depression Study
(TADS; March et al., 2004)
439 1217 year old depressed

adolescents (outpatients)
CBT vs. medication vs. CBT + Med

Youth (CBT, med) parent
(psychoed) youth + parent vs. placebo (psychoed and
(optional conjoint sessions) parentyouth sessions not
separately tested)
.09 CBT
.07 CBT
Conict
Communication
Problem solving
Clarke et al. (1999)
123 1418 year old depressed or

dysthymic adolescents
Youth (CWD-A) parent

(parent group)
CWD-A (16 sessions) vs. CWD-A

(16 sessions) + parent group
(8 group sessions) vs. WL
.32 CWD-A
.15 CWD-A + parent
group
.18 CBT
.14 CWD-A + parent
group
Conict
Communication
Problem solving
Support
Lewinsohn et al. (1990)

(major or minor) adolescents
Youth (CWD-A) parent

(parent group)
Asarnow et al. (2002)
23 4th6th graders with

depressive symptoms
Youth (CBT) youth +

parents (MFT)
CWD-A (14 sessions) vs. CWD-A

(14 sessions) + parent group
(7 group sessions) vs. WL
CBT + MFT vs. WL
.53 CWD-A
.73 CWD-A + parent
group
.41 CBT + MFT
.68 CWD-A
1.31 CWD-A + parent
Group
.25 CBT + MFT
Level of family
system
Parental warmth/control Sanford et al. (2006)

Communication
Support
41 1318 year old depressed adolescents
Family
TAU vs. TAU + family psychoeducation N .50 5 (TAU + FP)

(12 in-home sessions)
.64 (TAU + FP)
Marital conict
4 Entire family
system
Dysfunc. interactions
Brent et al. (1997)
107 1318 year old depressed adolescents Family (SBFT) youth (CBT)
(clinic referred and via advertisement)
CBT vs. SBFT vs. NST (12 weeks)
.32 CBT
.15 SBFT
.36 CBT
.18 SBFT
Expressed emotion
Cohesion/
disengagement

Parents + youth
.68 ABFT
.72 ABFT
Treatment of Adolescent
Depression Study
(TADS; March et al., 2004)

adolescents (outpatients)
CBT vs. medication vs. CBT + Med

Youth (CBT, med) parent
(psychoed) youth + parent vs. placebo (psychoed and parent
(optional conjoint sessions) youth sessions not separately tested)
.09 CBT
.07 CBT
Sanford et al. (2006)
41 1318 year old depressed adolescents
Family
TAU vs. TAU + family psychoeducation N .50 5 (TAU + FP)

(12 in-home sessions)
.64 (TAU + FP)

Youth
IPT vs. clinical monitoring;

12 weekly sessions
.61 IPT
.54 IPT
63 1218 year old high school

students with depression, dysthymia,
depression NOS, adjustment
disorder w/depressed mood
Youth
IPTA vs. TAU (16 sessions)
.45 IPT
.44 IPT
Rosselo & Bernal (1999)

Youth
IPT vs. CBT vs. WL
.11 CBT
.47 IPT
.37 CBT
.72 IPT

Parents + youth
.68 ABFT
.72 ABFT
5 Extra-familial
Communication
Expressed emotion
Problem solving
Stressful life events
IPT = Interpersonal Therapy; IPTA = Interpersonal Therapy Adolescent; M-ITG = MotherInfant Therapy Group; CBT = CognitiveBehavioral Therapy; TAU = Treatment As Usual; SBFT = Systematic Behavior Family Therapy; CWD-A =
Coping With Depression Adolescent; MFT = Multiple Family Therapy.
1
Studies can be listed more than once if family factors at multiple system levels are targeted.
2
Unless noted, all studies are RCT's.
3
Reported in Gunlicks & Weissman, 2008.
4
All effect sizes (ES) for overall outcomes and for depression outcomes from Weisz et al. (2006) unless otherwise noted.
5
Effect sizes for overall and depression outcomes from Sanford et al. (2006), not Weisz et al.
3 Marital
subsystem
309
310
offspring, including depression, anxiety, substance abuse, as well as

social, emotional and behavioral problems. Several mechanisms have
been proposed to explain this increased risk, including impaired parenting skills, poor social skills, cognitive style of the parent, stressful
family environment, and genetic transmission. While support for a
causal relationship is strengthened by evidence from several prospective studies, the evidence does not denitively support one causal
mechanism over another, and the consensus is that several mechanisms of transmission are likely. The impact of parental depression is
not specic for child depression: while it increases risk for offspring
depression, it is also linked to other forms of psychopathology, such as
anxiety and substance use disorders. Individual characteristics of the
child, such as cognitive style, temperament and genetic vulnerability,
can increase risk for depression, either as a direct effect or in
interaction with adverse environmental factors.
The parentchild subsystem, level 2, has been most investigated in
the context of child depression. Evidence from cross-sectional and
prospective studies using self-report and observational methods has
supported an association between increased risk of depressive
symptoms and disorders in youth, and parental rearing style, low
parental support, attachment difculties, difculty establishing
autonomy and parentyouth conict. Evidence for the role of
psychological control and maternal support in predicting depressive
symptoms is mixed. Evidence for both unidirectional and bidirectional
effects has been found. While some parentchild relationship factors
have been specically linked to depressive or internalizing disorders,
studies which examine a wider range of outcomes do not tend to
support a specic relationship between these factors and depression.
At Level 3, the marital relationship, cross-sectional, prospective
longitudinal and experimental studies have supported a relationship
between marital conict and immediate distress in children and
adolescents, as well as later development of internalizing and
externalizing disorders. The type of conict strategy used by couples
appears to be important, with hostility and withdrawal associated
with more negative child outcomes including internalizing symptoms,
and calm discussion, humor, and physical contact associated with
more positive outcomes. Experimental evidence suggests that resolution of parental conict can help ameliorate the harmful effects on
children. While marital conict has been associated with both
internalizing and externalizing symptoms, stronger associations
have been found with externalizing symptoms.
At Level 4, the whole family system, disengaged as well as
enmeshed family patterns have been linked prospectively with
increased risk for symptoms of depression, anxiety and ADHD, with
disengaged patterns more strongly associated with internalizing
symptoms, and enmeshed patterns with ADHD symptoms. Supportive
family environment has been prospectively associated with lower
parentadolescent conict. Several multivariate studies found that
when adverse family environment is controlled for, the association
between parental depression and youth depression is reduced or
eliminated, suggesting that these other family factors may account for
the association. Similarly, marital conict has been found to be more
predictive of negative child outcomes than parental depression.
However, one longitudinal study found parental depression to be
more important in predicting youth depression than family discord. A
longitudinal observational study demonstrated negative consequences for adolescents who are involved in interparental conictual
or depressive behaviors, with involvement in interparental conict
more strongly linked to later adolescent aggressive behavior, and
involvement in interparental depressive behavior more strongly
linked to later depressive behavior.
Finally, at Level 5, the extra-family subsystem, there is evidence
from prospective longitudinal studies that stressful events increase
risk for youth internalizing or externalizing symptoms, either through
main effects or in interaction with other levels of the family system,
with stronger effects for internalizing symptoms.
3. Part II. Targeting family risk factors in psychotherapy of youth

depression: Evidence from clinical trials
In this section, we turn to the clinical trials research on psychotherapy for youth depression to examine which of the identied
family risk factors and mechanisms have been targeted in youth
depression trials. We rst examine who is the target of treatment (i.e.
youth, parent or family), and which risk factors at which system level
are targeted. We then briey describe the main types of psychotherapies tested for youth depression. Finally, we examine the evidence for
efcacy of youth treatments for depression at the ve system levels.
3.1. Who is the target of treatment?
The majority of treatments for youth depression target the
depressed child or adolescent. In a recent meta-analysis of the effects
of psychotherapy for youth depression (Weisz et al., 2006), the youth
alone was the focus of treatment in 30 out of 35 studies. Among the ve
studies which treated family members, two studies treated the youth
and parents, one study treated the youth primarily but also included
one family education group session, and two studies treated the entire
family (i.e. youth and family together). An additional study not
included in this meta-analysis targeted the entire family (Sanford et al.,
2006). Finally, 10 studies targeted depressed parents in order to reduce
symptoms of child depression or other psychopathology (Gunlicks &
Weissman, 2008).
3.2. Which risk factors are targeted in psychotherapy for
youth depression?
The majority of RCT's for psychotherapy for youth depression target
cognitive factors. 31 out of 35 studies in Weisz et al.'s (2006) metaanalysis involved a cognitive change element compared to 12 noncognitively based treatments. Only 8 out of 35 studies targeted family
processes. Of those eight, only ve interventions made family or interpersonal relationships the central focus, while three tested CBT interventions plus additional parent or family sessions. Of the ve emphasizing
relationships, only two actually treated the entire family (Brent et al.,
1997; Diamond, Reis, Diamond, Siqueland, & Isaacs, 2002), while the
remaining three treated the youth but made interpersonal issues central
(Mufson et al., 2004; Mufson, Weissman, Moreau, & Garnkel, 1999;
Rossello & Bernal, 1999). One major CBT trial included an optional family
component that was not separately tested (March et al., 2004).
3.3. Which family risk factors are targeted?
Among the few studies which address family risk factors, which of
the empirically supported risk factors have been targeted? Table 2
compares risk factors identied in Part I with the risk factors targeted
among the few psychotherapy trials which have addressed family
factors. The majority of studies have targeted risk factors of the individual parent (Level 1), or of the parentchild relationship (Level 2).
At Level 1, ten studies tested the effect of treating maternal depression
on child depression and psychopathology (Gunlicks & Weissman,
2008). Ten RCT's of psychotherapy for youth depression targeted
parentchild relationship factors (Level 2), such as conict resolution,
improving communication, and parental support. No studies targeted
marital conict (Level 3) to reduce youth depression. Three studies
targeted the entire family (Level 4). Finally, four studies targeted
stressful life events (Level 5).
3.4. What kinds of treatments have been tested in RCT's for
youth depression?
CBT. By far the most commonly used psychotherapy for youth
depression is cognitivebehavioral therapy (CBT). A recent meta-
analysis of psychotherapy trials for youth depression classied 31 out

of 35 studies as involving a cognitive change emphasis (Weisz et al.,
2006). Although many different variations of CBT for youth depression
have been developed, most include two main components: cognitive
restructuring and behavioral activation. Two studies also evaluated
the benet of adding a parent group to the youth CBT (Coping with
Depression) compared to youth CBT alone (Clarke, Rohde, Lewinsohn,
Hops, & Seeley, 1999; Lewinsohn, Clarke, Hops, & Andrews, 1990). The
parent group targets the interpersonal factors related to depression,
by increasing parental support of youth, and reducing negative
interactions and conict between parent and teens. Parents are taught
communication and conict resolution skills which they role play
with each other; in the last two sessions, they are joined with their
adolescents to practice these skills together. A CBT treatment for
prepubertal children, Stress Busters (Asarnow, Scott, & Mintz, 2002)
included one multiple family group session at the end of treatment
which focused on increasing parental support for child competency;
however, this was not separately tested.
Interpersonal Psychotherapy (IPTA). Three studies tested Interpersonal Therapy for Depression, adolescent version (Mufson et al., 2004;
Mufson et al., 1999; Rossello & Bernal, 1999), an individually-based
psychotherapy which targets the interpersonal difculties of adolescents identied in epidemiological and clinical research. Depressive
symptoms are assumed to be related to interpersonal conicts; thus
resolution of interpersonal conict and development of positive
interpersonal relationships is the presumed mechanism of recovery.
The treatment focuses on developmental issues common to adolescents with depression, such as separation and authority issues with
parents, interpersonal disputes, role transitions, loss, peer pressure,
single-parent families, and stressful life events.
Family therapy for depression. Three RCT's tested some form of
family therapy, and one included an optional family therapy
component which was not separately tested for efcacy.
Systemic Behavior Family Therapy. Systemic Behavior Family
Therapy (SBFT) was tested against CBT and Supportive Psychotherapy
in one study (Brent et al., 1997). SBFT combines techniques from
functional family therapy (Alexander & Parsons, 1982) and from
problem-solving therapy (Robin & Foster, 1989), and includes techniques such as reframing problematic behaviors, changing dysfunctional family interactional patterns, improving communication and
problem-solving skills, improving parenting skills and sensitivity to
developmental issues.
Attachment Based Family Therapy (ABFT). Attachment Based Family
Therapy (Diamond et al., 2002) stresses the role of attachment
problems in the development of adolescent depression, and addresses
several family risk factors which have been empirically linked to youth
depression: parental criticism, hostility and disengagement, parental
stress, ineffective parenting, parentadolescent conict and support,
and autonomy development. The goal of ABFT is to strengthen the
attachment relationship between parent and adolescent, by helping
the adolescent openly address longstanding conicts with parents
which have strained the attachment relationship, and by developing
appropriate autonomy from parents.
Family psychoeducation. One study compared family psychoeducation plus treatment as usual to treatment as usual for adolescent
depression (Sanford et al., 2006). Twelve 90 minute sessions were
conducted with all family members in the home, with one booster
session at 3 month follow-up. The goals of the sessions were to
increase knowledge about depression and its effect on the family,
strengthen family communication and reduce expressed emotion, and
to enhance coping, problem solving and crisis-management.
Treatment of Adolescent Depression Study (TADS) parent component.
The Treatment of Adolescent Depression Study (TADS) (March et al.,
2004) which compared the efcacy of medication to CBT alone and
CBT combined with medication, included a parent component which
was not separately tested but was considered essential to treatment
311
retention (Wells & Albano, 2005). The parent component included two
mandatory sessions of parent psychoeducation, as well as optional
parentyouth sessions which could be drawn from ve family therapy
modules which addressed 1) family problem-solving skills; warmth
and hostility 2) family communication skills, 3) behavioral contingency schedules 4) positive reinforcement, and 5) parentadolescent
attachment.
3.5. Efcacy of interventions targeting family factors
How effective are interventions that primarily target family and
interpersonal relationships? Table 2 displays results from treatment
studies targeting family factors in order to improve youth depression,
including ten studies which treated maternal depression to reduce
child psychopathology. Effect sizes from Weisz et al.'s (2006) metaanalysis are included. Unfortunately, the small number of studies
makes it difcult to draw rm conclusions. Weisz et al.'s (2006) metaanalysis of psychotherapy of youth depression found an average
effect size of .34 for all treatments, and cognitively based interventions
fared no better than non-cognitive interventions. Effect sizes for
family or parent-based treatments of youth depression varied widely,
from .14 to 1.31 for child CBT + parent group, from .18 to .72 for family
therapy, and from .44 to .72 for Interpersonal Therapy (IPT). Since
many factors independent of type of treatment can inuence effect
size, it is difcult to directly compare effect sizes. When family or
parenting interventions have been compared to individual, cognitively
based interventions, the ndings have been mixed. In the only
randomized controlled trial which directly compared CBT to family
therapy, Brent's group found cognitivebehavioral therapy (CBT) to be
more effective in the short term than systematic behavioral family
therapy (SBFT), however, at two year follow-up the treatment effects
were the same. Furthermore, SBFT was found to reduce parentchild
conict, which was a predictor of relapse. Rossello and Bernal (1999)
found larger effect sizes for IPT compared to CBT; however these
differences were not signicant. Among the cognitivebehavioral
trials, Lewinsohn's group found evidence for a marginally signicant
increase in effect by adding a parent group to a youth CBT group
(Lewinsohn et al., 1990); however a later study failed to replicate this
nding (Clarke et al., 1999).
How effective are treatments that target a depressed parent (Level 1)
at reducing symptoms of child depression or other psychopathology?
In their review, Gunlicks and Weissman (2008) found evidence that
reduction or remission of parental depressive symptoms was associated
with reduction in child symptoms. Specically, ve out of nine studies
found that treatment of parental depression was associated with
improvements in child psychopathology, and ve out of the six studies
examining psychosocial outcomes reported that mothers' treatment
was associated with child improvement, including better academic
functioning, better global functioning, better motherchild relationship.
In contrast, they found little evidence that treating postpartum depression has signicant positive effects on infant attachment, temperament,
and cognitive development.
3.6. Summary of family risk factors targeted in youth
depression treatment
In summary, the majority of tested treatments for youth depression do not target family factors or involve family members in the
treatment. Among those that do, the parentchild relationship (Level
2), is the main focus, particularly conict resolution, problem-solving
skills, communication and support, attachment, increasing warmth
and decreasing hostility, and increasing positive reinforcement of the
adolescent. Marital conict (Level 3) has not been targeted in RCT's for
youth depression, and whole family relations (Level 4) and stressful
life events (Level 5) are targeted in only a few studies. In a promising
trend, investigators have begun to target parental depression (Level 1)
312
as a means to reduce or limit child psychopathology, with positive

results. Family-based treatments as well as individual treatments
targeting family issues show clear promise in terms of efcacy
compared to waitlist, with effect sizes ranging from small to large.
However, the data are inconclusive with regard to relative efcacy of
targeting family factors vs. cognitive or behavioral factors, or the
relative efcacy of targeting the individual adolescent vs. including
other family members. Comparing the existing treatments which
target family factors, IPTA targets a broad range of family factors, but
involves only the youth, which may limit efcacy. ABFT demonstrates a strong effect size and targets the largest number of family
factors, but its primary focus on parentyouth attachment may not be
appropriate for all families. Lewinsohn and Clarke's Coping With
Depression group targets parentyouth conict, but provides minimal
direct practice between parent and teen, which may limit efcacy.
Finally, the TADS study demonstrates the feasibility of targeting
multiple family risk factors using exible modules, integrated with
standard individual CBT; however, the lack of efcacy data is a
limitation.
4. Part III. Road map for the development of empirically supported
family treatments for depression
In this section, we discuss recommendations for applying the
empirical ndings on family factors in depression to family treatment
for depression. We will address two questions: 1) Which family risk
factors should be targeted? 2) What are the steps needed to
empirically validate family-based treatments?
4.1. Which family factors should be targeted?
The evidence reviewed demonstrates that family factors at all
levels of the family system play a role in youth depression. These
family risk factors are highly intercorrelated, and although several
different models have been tested to identify causal risk processes,
there is insufcient evidence to support one model over another, or to
determine where in the process from family risk to disorder to
intervene. Furthermore, different family factors may be differentially
related to depressive symptoms. A meta-analysis examining which of
these factors has the strongest relationship to depressive symptoms
and changes in depressive symptoms would help identify potential
targets. There is also evidence for bidirectional pathways between risk
factors at the different system level (e.g. between parent factors and
child factors), making it difcult to determine causal priority, or where
to intervene. RCT's can help identify potential targets of treatment by
systematically varying the target (e.g. parent, child family) as well as
by testing hypothesized mechanisms related to outcome. For example,
since ABFT is presumed to operate by improving parentyouth
attachment, demonstrating that changes in attachment mediate
treatment outcome would provide empirical evidence for targeting
the parentyouth relationship.
Component prole analysis, an approach used to identify specic
techniques employed in effective treatments, can also be used to
identify potential targets for treatment (McCarty & Weisz, 2007).
Applying this method to youth depression treatments which target
family factors, four studies demonstrated the effect size criteria of.5 or
greater: ABFT (ES = .72; Diamond et al., 2002), IPTA (ES = .54; Mufson
et al), CBT plus parenting training (ES = 1.31; Lewinsohn et al., 1990);
and psychoeducation plus treatment as usual (ES = .64; Sanford et al.,
2006). Communication and problem solving were targeted in all four
studies; parentyouth conict and parental support in three out of
four studies, parental warmth and control, autonomy and expressed
emotion in two out of four studies, and attachment and cohesion/
disengagement in one out of four studies. Thus communication,
problem solving, parentyouth conict and parental support may be
key elements to target in family-based treatments.
4.2. Steps in the development and validation of family-based

interventions for youth depression
Validation of new psychotherapeutic treatments proceeds in a
series of standard phases including 1) model development, 2) manual
development, 3) efcacy testing, 4) effectiveness and implementation, and 5) testing moderation and mediation hypotheses. We rst
summarize recommendations based on this review for model and
manual development. We then examine to what extent family-based
interventions have been validated at each of these phases.
4.2.1. Developing a model
We have argued that a systemic framework can help facilitate the
translation of empirically supported family risk factors to interventions for youth depression, by integrating risk factor evidence at
multiple system levels into hypothesized risk mechanisms which can
be tested in intervention research. We propose an integrative rather
than competitive model: each of the competing theories of
depression can be seen as operating at different levels of analysis.
Determining the most effective level for intervention becomes an
empirical rather than theoretical question. Furthermore, a systemic
approach allows for the assessment of multiple risk factors at multiple
levels, from the individual, to the parentyouth dyad, to the family, to
the broader school and social environment. Not every family with a
depressed youth will present with the same constellation of risk
factors, and a systemic approach allows for exibility in tailoring
interventions to the needs of specic families.
Several excellent models of development of depression in the
family context have already been proposed by developmental and
family researchers (Cummings et al., 2005; Davis et al., 2000;
Sheeber et al., 2001) and by adult depression researchers (Gotlib,
1990). These models, while differing in specics, each propose that
depressive behavior develops in the context of family, interpersonal,
and social contingencies in interaction with genetic and cognitive
propensities of the child. While we do not dispute the importance of
individual processes in the development of depression, we focus on
family-level processes for several reasons. First, since both genetic
and environmental vulnerability may be required for the development of depression (Eley et al., 2004), addressing adverse environmental factors may be one way to prevent the development of
depression. Second, cognitive and interpersonal theories of depression place strong emphasis on the early parentchild relationship
in the development of vulnerability to depression (Beck, 1967).
Intervening directly in this interpersonal process could potentially
prevent the development of this vulnerability, or could help change
maladaptive relationship patterns which maintain depressive symptoms. Finally, we emphasize family-level interventions because the
application of the empirical evidence on family risk factors for
depression has lagged far behind application of individual cognitive
and interpersonal models of depression (Sander & McCarty, 2005). It
should be noted however that individual, cognitive or interpersonal
approaches can be integrated in this model at the individual level of
analysis.
From a clinical perspective, the family level may be the most
efcient point of entry into the family system as well. Depressed
adolescents are living within a family context, and the evidence
strongly supports the likelihood of problematic family relationships.
Depressed adolescents are usually referred to professionals by parents
who want to help, but may not know how. Beginning treatment with
the entire family may improve retention rates, by providing parents
with much needed support (e.g. Wells & Albano, 2005). Furthermore,
by beginning at the level of the whole family, the clinician can assess
the adolescent's individual vulnerability in the specic context of his
or her family, which may help identify features of his or her
environment that help maintain the depression. With this broader
view of the adolescent in his family context, the therapist can easily
move down to the level of individual cognitive vulnerability (e.g. by

recommending CBT), or up to the level of school environment
(by intervening with school staff) to address problems occurring at
multiple levels.
4.2.2. Developing a manual
Several manualized family therapy protocols are available for
youth depression: Diamond's Attachment Based Family Therapy
(Diamond et al., 2002), the TADS family modules (Wells & Albano,
2005), and Brent and colleagues' Systemic Behavioral Family Therapy
(Brent et al., 1997). Lewinsohn and Clarke's parenting intervention,
while targeting the parental subsystem rather than the entire family,
provides a good example of a highly structured and detailed program
targeting depressed youth and their parents.
4.2.3. Evidence for validation of family-based interventions for youth
depression
Table 3 shows studies which have been conducted to validate
family therapy for depression at each phase. With the exception of
Phase I, treatment development, there has been little empirical
research at the other phases. At Phase II, randomized controlled trials,
there have been only two trials: one trial comparing ABFT to waitlist
control (Diamond et al., 2002), and one randomized controlled clinical
trial against a known effective treatment, CBT (Brent et al., 1997).
There have been no studies comparing family therapy to treatment as
usual, or to medication. In Phase III, assessing the additive benet of
family therapy, three RCT's have been conducted (Lewinsohn et al.,
1990; Clarke et al., 1999; Sanford et al., 2006). Further questions such
as whether family therapy can improve efcacy in combination with
IPT or with medication have not been conducted. Only one study has
examined moderation effects (Phase IV) that is, whether there are
differential treatment effects for specic subpopulations (e.g. youth
Table 3
Phases in the validation of family-based interventions for youth depression.
Phase
I. Treatment development phase
Targeting of family risk factors, model
development, manual development, pilot
studies (e.g. open trials)
II. Randomized controlled trials (RCT's)

1. Family therapy vs. waitlist control
2. Family therapy vs. treatment as usual
3. Family therapy vs. effective
psychosocial treatments (e.g. CBT)
4. Family therapy vs. effective
psychopharmacological treatment
III. RCT to assess the additive benet of FT
5. CBT alone vs. CBT + FT
Studies
Brent group
(Brent et al., 1997)
TADS Group
Wells & Albano (2005)
Brent group

Clarke et al. (1999)
6. Treatment as usual vs. TAU + FT

7. IPT alone vs. IPT + FT
8. Medication alone vs. Med + FT
IV. RCT to assess specialized populations
(moderation variables)
9. Non-responders to CBT, IPT, med
10. Comorbid conditions (e.g. comorbid anxiety disorders) Brent group
11. Specic high-risk populations (abuse/neglect, poverty, Brent group
single-parent families, offspring of depressed parents,
clinic-referred patients, cognitive distortions)
V. Testing hypothesized mechanisms of change
(meditation models)
12. Cognitive and family mechanisms
Brent group
(Kolko et al., 2000)
VI. RCT to test relative efcacy of specic components
of family therapy treatments (dismantling studies)
313
with comorbid conditions, treatment-resistant depression, or adverse

family environments). Brent's group examined relative efcacy for
adolescents with comorbid anxiety compared to those with depression only, and for clinic referred compared to non-clinic referred
(Brent et al., 1998). Finally, only one study (Kolko, Brent, Baugher,
Bridge, & Birmaher, 2000) examined mediation effects (Phase V); that
is, whether the hypothesized therapy mechanisms mediate change
after psychotherapy. Finally, dismantling studies (Phase VI), or studies
which test the relative efcacy of specic components of family
treatments, have not yet been conducted.
4.2.4. Further research directions
Further evidence is needed to build an empirical basis for
determining which family risk factors or processes to target in
treatment of youth depression. One relatively simple approach
would be to conduct a meta-analysis to determine the relative
strength of the relationship between various family factors and
depressive symptoms and disorders. Since this may vary with the
age and gender of the child, moderation effects need to be included.
Component proling analysis is also recommended to identify the
components of effective family treatments; however, we rst need to
have a larger evidence base of family treatment studies (McCarty &
Weisz, 2007). Most importantly, we need more family intervention
studies for youth depression to test efcacy of family therapy, and to
begin to ll in the blank spaces in Table 3 to go beyond the basic
question of whether family therapy works, to examine the relative
efcacy of family treatments compared to other bona de treatments, to examine what combination of treatments is most effective
for which subgroups of patients, to evaluate whether the hypothesized mechanisms of change actually mediate therapeutic change,
and to identify the essential components of treatment. These studies
also have the potential to answer questions about the mechanisms of
change after psychotherapy, and to provide evidence for causal risk
models for the development of depression (Cowan & Cowan, 2002).
For example, the hypothesis that family therapy decreases youth
depression by reducing dysfunctional parentadolescent conict can
be tested in an RCT by examining whether parentadolescent
conict mediates improvement in depressive symptoms. If conrmed, this nding would lend support to the hypothesis that
parentadolescent conict leads to or maintains depression, which
in turn can be tested in basic developmental research into depression. Thus, family therapy intervention research has the potential to
improve evidence-based treatment of youth depression, and to
further our basic knowledge of the development of depression
within the family.
5. Discussion
The results of this review comparing family risk factors for youth
depression to current empirically evaluated treatments for youth
depression suggest indeed that there is a signicant gap in the
translation of basic research ndings to treatment studies. Put simply,
we know more than enough about family risk factors and possible
underlying mechanisms to begin to apply this information to treatment. Review after review article has documented this evidence, and
has recommended the application of these ndings to treatment. To
date, this has occurred to only a limited degree. This is all the more
striking given the lack of evidence that CBT is more effective than
other forms of treatment for youth depression, and lack of evidence
that cognitive processes mediate changes over the course of
psychotherapy for youth depression (Kolko et al., 2000; Spielmans,
Pasek, & McFall, 2007; Weersing & Weisz, 2002). Furthermore, the
relatively modest effect size for cognitive-based therapies for youth
depression compared to treatment of other youth disorders suggests
the need to enhance existing treatments by targeting other risk
factors.
314
5.1. Why have the ndings from family process research gone largely
unheeded in clinical trials for youth depression?
If the preference for individual, cognitive-based approaches is not
supported by the empirical evidence, on the one hand, and if there is
strong evidence that targeting family factors could improve treatment
of youth depression on the other, why has this been largely neglected
in the treatment literature? One explanation is that clinical applications always lag behind basic research ndings. Intervention
researchers may be less aware of the evidence from developmental
and family process research. Furthermore, whereas cognitive therapy
researchers have highlighted the importance of empirical validation,
family therapy proponents have been less concerned with empirically
demonstrating treatment efcacy or conrming hypothesized models.
However, the very success of the cognitive paradigm may also be a
factor. Scientic paradigms serve to dene the concepts and data for
inclusion in a particular eld, as well as dening what lies outside the
eld (Kuhn, 1962). The cognitive model has been tremendously inuential in the last forty years in organizing the selection and interpretation
of data about depression. During roughly the same time period, evidence
supporting family factors in depression has been accumulating. However, this evidence has not been as systematically applied to treatment of
youth depression. More than a dozen recent reviews of family factors in
depression have called for the application of these ndings to treatment
of youth depression (e.g., Alloy et al., 2006; Goodman & Gotlib, 1999;
Sander & McCarty, 2005; Sheeber et al., 2001). At the same time, recent
articles from experts within the eld of youth depression have questioned the evidence for the superiority of cognitive therapy for youth
depression compared to other therapies (Weersing & Brent, 2006;
Weersing, Iyengar, Kolko, Birmaher, & Brent, 2006; Weisz et al., 2006).
Thus the eld appears to be poised to integrate and apply these ndings
which have been available for several decades. There are promising signs
that this integration is beginning. There are manualized treatments
available to address the interpersonal and family relationships associated
with youth depression; however they need to be integrated into a developmental and family framework, and they need to be tested systematically. The fact that TADS included a comprehensive family component
as part of the rst study comparing CBT to medication indicates the
degree to which CBT researchers have incorporated concerns about
family processes into their study designs. Interventions targeting
parental depression as a means of reducing child psychopathology
represent another promising research trend. And nally, the fact that
leading CBT researchers are taking a critical look at the accumulated data
on CBT for youth depression is a welcome sign, which will improve
cognitivebehavioral treatments as well as open the eld to other
treatments for youth depression. We hope that this review, by organizing
the family evidence within a systemic framework, will contribute to the
further application of this evidence to treatment of youth depression.
The future of psychotherapy research may lie in integrative rather
than competitive models. Fortunately, there is enough to go around
for everyone interested in youth depression: from individual genetic
and cognitive factors, to the wide variety of family factors reviewed
here. Future research on psychotherapy of adolescent depression
should focus on which combination of interventions is most helpful
for which individuals and their families.
Acknowledgements
We are grateful to Marcus Huibers and David Bernstein for their
comments on earlier drafts of this article.
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Clinical Psychology Review 29 (2009) 294316

Contents lists available at ScienceDirect

Clinical Psychology Review

Family processes in the development of youth depression:

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

youth depression. The rst goal is to examine the empirical evidence

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

picture of the mechanisms involved in the development of youth

Fig. 1 illustrates a systemic model of risk for the development of

Fig. 1. Systemic model of youth depression.

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

2. Part I. Risk factors and mechanisms in the development of

produce evidence of varying strength for causal hypotheses linking

In Table 1, family risk factors for depression are organized according to

2.1.1. Cross-sectional vs. longitudinal design

2.1. Methodological note: Levels of evidence required for causal models

1. Individual (child or parent)

Depression or depressive symptoms/

4. Whole family subsystem

Mother, father, child tryadic triadic system

2.1.2. Self-report vs. observational assessment

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

self-image, negative view of the world, and negative expectations of

increased risk for anxiety disorder and major depression in childhood,

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

cause of depression. While systemic theory also assumes that parent

hypothesis that the negative impact of insecure attachment is more

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

Attachment Interview (AAI) were signicantly related to depressive

observed parentchild interactions such as excessive reassurance

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

constructs are similar to the constructs of rejection (warmth) and

addition, by using parent reports of parentadolescent conict to

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

rejection and adolescent depression are reciprocally related, but by

Ge, Lorenz, and Conger (1994) examined whether maternal

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

later, supporting the causal/maintaining model. Furthermore, both

Finally, these studies illustrate how the framework of adolescent

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

However, if the scope is broadened to include the father, we may

Alternately, marital conict may mediate the relationship between

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

adolescence would buffer against the increased parentchild conict

related to child internalizing problems indirectly via fatherchild

K. Restifo, S. Bgels / Clinical Psychology Review 29 (2009) 294316

In contrast, some evidence suggests that depressed youth may

with later aggressive behavior, and intervention in interparental

Family risk factor

Results (child outcomes)

Not randomized; compared

At 1 year follow-up, children of remitted

Byrne et al. (2006)

260 416 year old children of

Medication vs. IPT vs.

Children of mothers with 40% reduction in

Clark et al. (2003)

19 124 mo old infants of

IPT vs. M-ITG vs. waitlist

Greater child adaptability in the two active

Forman et al. (2007)

176 6 mo infants of postpartum

IPT vs. waitlist