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Depression in Mothers 1
Depression in Women who are Mothers: An Integrative Model of Risk for the Development of
Psychopathology in their Sons and Daughters
Sherryl H. Goodman and Erin Tully
Emory University
A chapter to appear in C.L.M. Keyes and S.H. Goodman, Editors, Women and Depression: A
Handbook for the Social, Behavioral, and Biomedical Sciences, Cambridge University Press
The writing of this chapter was supported by NIMH funding (1P50MH58922-01A1) for the
Silvio O. Conte Center for the Neuroscience of Mental Disorders (C.B. Nemeroff, P.I.), Project
8: Maternal Depression: An adverse Event for Infants (S.H. Goodman, P.I.).
Depression in Mothers 2
Driven both by knowledge of higher rates of depression in women than men and
assumptions about incompatibilities between depression and good quality parenting, research on
children with depressed mothers has soared over the last few decades. In an attempt to account
for the many factors involved in the transmission of risk for psychopathology from depressed
mothers to their offspring, Goodman and Gotlib (1999) developed an integrative and
developmentally sensitive model for understanding mechanisms whereby children of depressed
parents might be at risk for the development of psychopathology. The model is consistent with
the premise for this book in that it takes a bio-psycho-social perspective on mechanisms and,
therefore, we use it as the framework for this chapter. We move beyond previous reviews by
examining the current empirical status of each of the proposed mechanisms within this
framework. Further, given this book’s focus on women and depression, we explore the extent to
which daughters may be more affected by their mothers’ depression than sons, i.e. gender
specificity in the intergenerational transmission of depression. Finally, we draw implications
from the current status of the model overall and of gender specificity, in particular, for further
research as well as potential steps for prevention, treatment, and social policy.
This chapter begins by briefly describing the reasons for concern about children with
depressed mothers, including the nature and extent of associations between depression in
mothers and adverse outcomes in children, across the full age range from infancy to adolescence.
Then, we examine evidence for each of the individual mechanisms proposed in the Goodman
and Gotlib model to explain adverse outcomes in the children. Next, we examine evidence for
gender specificity in the transmission of risk for the development of psychopathology in children
with depressed mothers. Finally, we elaborate on implications for prevention, treatment, and
policy from the conclusions we draw.
Depression in Mothers 3
Nature and Extent of Risks:
Adverse Outcomes in Children Associated with Maternal Depression
Why be concerned about children with depressed mothers?
Depression is common. Although estimates vary, probably between a quarter and a third
of women experience a clinically significant major depressive episode at some point during their
lives (Kendler & Prescott, 1999). Rates are about twice as high in women as in men (Kessler,
2000), with the rates for women increasing during adolescence, when hormonal changes and
other major psychosocial changes likely interact with underlying predispositions to precipitate
the depression (Angold, Costello, & Erkanli, 1999; Frank & Young, 2000). Depression is also
highly likely to recur, with one’s risk for a second episode being about 50% and for a third
episode as high as 80% (Angst, 1988; Piccinelli & Wilkinson, 1994). Over 50% relapse within
two years of recovery and later episodes require lower levels of precipitants compared to initial
levels (Keller, Shapiro, Lavori, & Wolfe, 1982; Kendler, Thornton, & Gardner, 2000). Given the
increase in rates of depression among girls during adolescence and the high likelihood of
recurrence, it should not be a surprise that depression rates are especially high among women of
child-bearing ages (Blazer, Kessler, McGonagle, & Swartz, 1994). Of particular concern,
depression occurs in about 10-15% of women during pregnancy and the post-partum (O'Hara,
Zekoski, Philipps, & Wright, 1990) and the highest rates of depression are in child-bearing age
women (Kessler, McGonagle, Swartz, Blazer, & Nelson, 1993). Thus, children are very likely to
be exposed to depression in their mothers very early in life and, moreover, to experience
repeated exposures throughout their infancy, childhood and adolescence.
Defining depression. Researchers define clinically significant depression using two
primary approaches, categorical and dimensional, as is described in other chapters in this
Depression in Mothers 4
Handbook. The important point here is that women who are identified as depressed based on
having high scores on dimensional scales, such as the commonly used Beck Depression
Inventory, now in its second edition (BDI-II) (Beck, Steer, & Brown, 1997), and the Centers for
Epidemiological Studies-Depression Scale (CES-D) (Radloff, 1977), may differ in important
ways from those who are diagnosed with a depressive disorder. High scores on these scales may
reflect general distress rather than depression as a specific disorder and may reveal more
transient depression than would meet diagnostic criteria (Coyne, 1994). Only a small percentage
of individuals in general population samples who score high on depression rating scales meet
diagnostic criteria for depression (Gotlib, Lewinsohn, & Seeley, 1995). Nonetheless, individuals
who score high on such scales have been found to have diminished parenting abilities (Harnish,
Dodge, Valente, & Group, 1995) and, thus, they are still of concern.
Impairment associated with depression. Depression is known to be an impairing
condition. As defined by DSM-IV, a depressive episode must be accompanied by “clinically
significant distress or impairment in social, occupational, or other important areas of
functioning” (p. 356) (American Psychiatric Association, 1994). While other chapters in this
Handbook address impairment in terms of costs to the individual and society, broadly defined, of
particular concern for this chapter is how depression interferes with quality of parenting. Several
researchers have directly observed depressed mothers interacting with their children across ages
ranging from infancy through adolescence and found impairments in functioning that raise
serious concerns. As has been reviewed recently (Gotlib & Goodman, 1999; Lovejoy, Graczyk,
O'Hare, & Neuman, 2000), compared to both nondepressed psychiatric and nonpsychiatric
controls, depressed mothers display less positive affect and more sad and irritable affect, engage
in more negative, intrusive, and hostile behaviors, and in discipline episodes tend to alternate
Depression in Mothers 5
between harsh, punitive discipline and lax and permissive parenting. Thus, there are ample
reasons to be concerned about children with depressed mothers. Next, we turn to the literature
on the nature and extent of associations between depression in mothers and adverse outcomes in
children, across the full age range from infancy to adolescence.
Adverse child outcomes associated with maternal depression: Potential precursors as well as
signs of psychopathology
A large body of research has accumulated showing that maternal depression is associated
with adverse outcomes for children. These outcomes include not only evidence of
psychopathology in the children, but also difficulties with or deficits in aspects of social,
cognitive, or behavioral functioning, which might indicate vulnerabilities for the development of
psychopathology or actual early signs of depression (Goodman & Gotlib, 1999). Because these
wide-ranging outcomes vary widely with the age of the children under study, the findings will be
reviewed separately for children in different developmental stages. Since some researchers have
investigated effects of depression during pregnancy on fetal development, we will begin there.
Fetal functioning. Researchers are beginning to recognize the need to be concerned
about depression during pregnancy. Depressed mood has been found to be at least as high
during pregnancy as during the postpartum (Evans et al., 2001; Green & Murray, 1994) and is of
particular concern given the potential effects on fetal development. Knowledge of biobehavioral
processes in fetal development, especially the role of corticotrophin releasing factor (CRF) in
both fetal development and in models of depression in adults, underscores the importance of
studying infants born to mothers who are depressed during pregnancy. In particular,
hypersecretion of CRF during pregnancy raises concern for potential dysfunctions in the
newborn’s neuroregulatory systems, i.e. frontal brain activity and HPA activity, in children who
Depression in Mothers 6
were exposed prenatally to their mothers’ depression (Wadhwa et al., 2002). Because of the
relative neglect of prenatal depression in the literature, few studies of infants with depressed
mothers began during pregnancy and, thus, we know little about the consequences to infants of
fetal exposure to maternal depression.
Of the few studies of maternal depression that began in pregnancy, one found that
mothers’ prenatal cortisol predicted newborns’ cortisol levels (Lundy et al., 1999). Elevated
cortisol in newborns is a concern because it reflects increased sensitivity to stress, which is
implicated in most leading etiological models of depression (Sanchez, Ladd, & Plotsky, 2001).
In another study that included data from pregnancy, number of prenatal months of exposure to
maternal depression marginally predicted left frontal lobe activation from electroencephalogram
(EEG) (Ashman & Dawson, 2002; Dawson, Frey, Panagiotides, Osterling, & Hessl, 1997). This
pattern of EEG asymmetry is associated with the experience of “withdrawal” emotions in
children and characterized depressed adults and adolescents (Davidson, Ekman, Saron, Senulis,
& Friesen, 1990; Dawson et al., 1999b; Dawson, Grofer Klinger, Panagiotides, Hill, & Spieker,
1992b; Finman, Davidson, Colton, Straus, & Kagan, 1989). The research may have been limited
by the fact that depression during pregnancy was measured retrospectively when the mothers
were 13-15 months postpartum, and included women who were in partial remission or
subthreshold. If this finding is corroborated, it suggests the need to examine mechanisms such as
genetics and intrauterine factors for the association between maternal depression and frontal
brain activity in prenatally exposed infants. Finally, a study is underway in our lab to test
associations between various indices of fetal exposure to maternal depression (diagnostic
interviews, self-report questionnaires, and cortisol) and infants’ neuroregulatory systems. We
are studying women who meet diagnostic criteria for depression at least once in the past and
Depression in Mothers 7
obtain multiple measures prospectively, one each month beginning typically in the third month
of pregnancy. We expect to find that prenatal exposure to maternal depression and its correlates
of stress and, possibly, hypersecretion of cortisol, will predict infants’ neuroregulatory
dysfunctions. It is the latter that we expect would impose on these high-risk children a
vulnerability to the development of psychopathology.
Infants. Compared to prenatal depression, much more is known about effects of postnatal
depression on infants with respect to emotional, behavioral, and biological functioning. Given
stage-salient needs of infants, limits on depressed mothers’ abilities to provide the sensitive,
responsive care needed for the development of healthy attachment relationships (Egeland &
Farber, 1984) and emotional self-regulation have been of particular concern (Tronick & Gianino,
1986). As predicted, maternal depression is associated with infants’ showing more negative
affect, more self-directed regulatory behaviors, and less secure attachment relationships (Gotlib
& Goodman, 1999; Tronick & Gianino, 1986; van IJzendoorn, Goldberg, Kroonenberg, &
Frenkel, 1992). Infants of depressed mothers have also been shown to have higher cortisol
levels, especially following interaction with their depressed mothers (Field, 1992); the harsh
parenting that is sometimes associated with maternal depression has also been linked to higher
cortisol levels in the children (Hertsgaard, Gunnar, Erickson, & Nachmias, 1995). Both findings
suggest an association between children’s HPA axis functioning and the depressed mothers’
failure to provide sensitive, responsive care.
There is also documentation of frontal EEG asymmetries in infants of depressed mothers.
Field and her colleagues report greater relative right frontal EEG asymmetry relative to controls
in infants of depressed mother as early as one week old, as well as in one month old infants,
which is correlated with infants’ EEG at 3-months and 3-years (Jones, Field, Davalos, &
Depression in Mothers 8
Pickens, 1997), suggestive of continuity of this effect. Dawson and her colleagues show similar
patterns in 18 month olds (Dawson et al., 1997). Thus, infants exposed to their mothers’
postpartum depression are showing longer-term disturbances in aspects of functioning that are
known vulnerabilities to the development of depression.
Toddlers and preschool-aged children (early childhood). Unlike the prenatal and infant
research, most of the studies of older children with depressed mothers are cross-sectional.
Researchers typically sample children in a particular age range and test for associations with
concurrent maternal depression. Thus, the studies are limited because one cannot determine if
the prior exposures may better explain the children’s functioning than the mother’s concurrent
depression. For example, children who had been exposed to maternal depression during fetal
development are expected to show various manifestations of behavioral and neurobiological
sequelae of such exposure later in development. Studies of toddlers or older aged children
typically are unable to determine the role of prior exposures. In our lab, we are using a
longitudinal design to study the consequences of fetal exposure to maternal depression on later
development. If consistent with stress responses in animals exposed to early adverse experiences
(e.g. maternal separation) and with knowledge of early human neurodevelopment (Graham,
Heim, Goodman, Miller, & Nemeroff, 1999; Matthews, 2002), we expect that fetal exposure to
maternal depression will be associated in preschool-age children, for example, with increased
sensitivity to stress, a predilection to experience negative or “withdrawal” emotions, and with
early signs of vulnerability to the development of stress-related psychopathology. That is,
depression during pregnancy might set the biological and cognitive ‘stage’ for children’s later
development of depression. Thus, it is important to interpret these findings with the caveat in
mind that what is usually unknown or untested is the contribution of any earlier exposures to
Depression in Mothers 9
maternal depression, having had the initial exposure at an earlier stage, and the effects of
repeated or continuous exposure.
Within these constraints, we find accumulating evidence that maternal depression is
associated with toddlers’ and preschoolers’ greater resistance to mothers’ control efforts, more
comforting behavior when the mother is distressed, and more of early signs of depression and
anxiety (Gotlib & Goodman, 1999). For example, toddlers of depressed mothers show more
dysregulated aggression and heightened emotionality and have more externalizing problems at
age five (Zahn-Waxler, Cummings, Iannotti, & Radke-Yarrow, 1984; Zahn-Waxler, Iannotti,
Cummings, & Denham, 1990). Maternal depression was associated with higher rates of
internalizing problems (e.g. depression or anxiety) in four-year-old boys and girls, but with
externalizing problems (e.g. conduct disorder or attention deficit disorder) only in girls
(Marchand & Hock, 1998). Mothers who reported high levels of depression symptoms reported
higher levels of behavior problems in their five-year-old children, with even stronger
associations when whose symptoms were severe, chronic and recent (Brennan, 2000). In
addition to these outcomes, there is evidence for the continuing association between maternal
depression and abnormal EEG patterns, as was noted in infants with depressed mothers. Dawson
and colleagues recently showed abnormal, albeit a more generalized abnormal brain electrical
activity pattern, at age 3 and ½ in the form of reduced activation from both right and left frontal
and parietal regions (Dawson et al., 2003). Overall, these findings are of particular concern
because emotional and behavioral problems identified during early childhood are predictive of
ongoing problems in later years (Campbell, 1995)
School-aged children. Beginning when children enter school, it is possible to reliably
measure psychopathology using diagnostic interviews and other instruments with the children,
Depression in Mothers 10
their parents and teachers. From several studies, we know that rates of depression are higher in
children with depressed mothers relative to a variety of controls (Beardslee, 1988; Billings &
Moos, 1985; Goodman, Adamson, Riniti, & Cole, 1994; Lee & Gotlib, 1989; Malcarne,
Hamilton, Ingram, & Taylor, 2000; Orvaschel, Walsh-Allis, & Ye, 1988; Weissman, 1984;
Welner, Welner, McCrary, & Leonard, 1977). Rates of depression in the school-aged children of
depressed mothers vary from 20 to 41%, depending on the severity or impairment of the parent’s
depression, whether both parents are depressed, and a number of other sociodemographic
variables (Gotlib & Goodman, 1999). Psychopathology in children with depressed mothers is
not limited to depression. Researchers have also found higher rates of social phobia, separation
anxiety and other anxiety disorders, attention deficit disorders, disruptive behavior disorders,
overall levels of behavior problems, and poorer social functioning relative to controls
(Biederman, 2001; Luoma et al., 2001; Weissman, 1984). In addition, children with depressed
mothers, in comparison to children whose mothers are medically ill or have other psychiatric
disorders, also have poorer academic performance and other behavioral problems in school
(Anderson & Hammen, 1993).
Similarly, adolescent offspring of depressed parents have been found to have higher rates
of depression (Beardslee, 1988; Beardslee, Schultz, & Selman, 1987; Hammen et al., 1987;
Hirsch, Moos, & Reischl, 1985) as well as higher rates of other disorders (Orvaschel, 1988;
Weissman, 1984) relative to controls. Moreover, depression in offspring of depressed parents,
compared with same-age offspring of non-depressed parents, has an earlier age of onset, longer
duration, and is associated with greater functional impairment and higher likelihood of
recurrence (Hammen & Brennan, 2001; Hammen, 1990; Hammen, Shih, Altman, & Brennan,
2003; Keller et al., 1986; Lieb, Isensee, Hofler, Pfister, & Wittchen, 2002; Warner, Weissman,
Depression in Mothers 11
Fendrich, Wickramaratne, & Moreau, 1992). In addition, levels of internalizing and
externalizing behavior problems are higher in children with depressed mothers relative to
controls (Brennan, Hammen, Katz, & Le Brocque, 2002; Fergusson, Lynskey, & Horwood,
1993; Forehand, 1988). Thus, depression in offspring of depressed parents appears to be
pernicious.
Adolescence is a particularly important stage of development for studying the effects of
maternal depression, because rates of depression increase in girls and the gender gap between
girls and boys emerges during this period. Thus, it is intriguing that one study found an
association between maternal depression and rates of depressive symptoms during middle
childhood and adolescence for girls, but not boys (Fergusson, 1995), although others do not find
differences between sons and daughters in the association between maternal depression and
adolescent behavior problems (Fowler, 2002). Gender specific findings are discussed in a later
section of this chapter. In addition to studies of depression and other disorders in adolescent
offspring, researchers have also studied aspects of functioning that might reveal vulnerabilities to
the later development of depression. For example, adolescents with depressed mothers, and the
daughters in particular, display more dysphoric and less happy affect (Hops, Sherman, & Biglan,
1990), and show early signs of cognitive vulnerability to depression, such as being more likely
than other adolescents to blame themselves for negative outcomes and less likely to recall
positive self-descriptive adjectives (Hammen & Brennan, 2001; Jaenicke et al., 1987). Evidence
for interpersonal vulnerabilities comes from studies showing that adolescent offspring of
depressed mothers have poorer peer relationships and less adequate social skills than teens of
nondepressed control mothers (Beardslee et al., 1987; Billings & Moos, 1986; Forehand &
McCombs, 1988; Hammen & Brennan, 2003).
Depression in Mothers 12
In sum, there is strong evidence at all ages, even beginning prenatally, that offspring of
depressed mothers are at risk for the development of psychopathology as well as delays and
deficiencies in emotional, social, and cognitive development. Next, we examine evidence for
each of the individual mechanisms proposed in the Goodman and Gotlib model to explain
adverse outcomes in the children.
Etiological Mechanisms Linking Maternal Depression and Adverse Child Outcomes
The Goodman and Gotlib model
Goodman and Gotlib (1999) proposed an integrative, developmentally sensitive model
for understanding how maternal depression impairs child development. Consistent with the
premise of this book, the model is integrative in the sense that it cuts across lines that have
traditionally separated studies of genetic, neuroendocrine, and other biological factors from
research in cognitive or interpersonal factors in depression. The model also makes essential the
consideration of principles of developmental psychopathology, such as the normative tasks that
children are undertaking at each developmental stage, the parenting and other supports that are
needed to facilitate that development, and how those tasks and the necessary supports might be
negatively affected by different manifestations of maternal depression.
As shown in Figure 1, the model begins with the mother. The model progresses from the
depressed mother to a set of mediators and moderators of the association between maternal
depression and adverse child outcomes. A major motivation for proposing the model was to
guide the identification of those variables that might mediate and moderate the association
between maternal depression and the development of psychopathology in the children (Baron &
Kenny, 1986). Empirically established mediators would reveal the mechanisms through which
maternal depression comes to be associated with adverse child outcomes. Potential mediators
Depression in Mothers 13
include any of the ways in which children or families with a depressed mother differ from those
without a depressed mother.
The theory- and research-based mediators proposed in the model include: (a) heritability
of depression; (b) innate dysfunctional neuroregulatory mechanisms; (c) exposure to negative
maternal cognitions, behaviors, and affect; and (d) the stressful context of the children’s lives.
Research on mediators holds promise for revealing the pernicious processes for which targeted
interventions might be developed to prevent the development of psychopathology in the children.
Also important are potential moderators, defined as variables that affect the strength or
direction of the association between maternal depression and the development of child
psychopathology. Among the moderators proposed in the model are children’s age and gender.
Research on moderators is important for its potential to clarify how it is that some children with
depressed mothers develop normally, whereas others do not. With knowledge of which children
are most at risk, predictive efficacy is improved, as is our understanding of the circumstances
under which maternal depression is more or less strongly associated with negative outcomes in
the children.
Also essential to a developmental psychopathology perspective is a consideration of the
developmental pathways to disorder. Depression and other disorders for which these children
are at risk are known to unfold over time (Cicchetti & Toth, 1998). Thus, we propose a set of
vulnerability factors, characteristics or tendencies of the children, including behavioral, affective,
and psychobiological functioning, which may be risk factors or early signs of a disorder that has
not yet emerged. Each of the four proposed mechanisms in the model might lead to one or more
of the vulnerabilities, including physiological (especially the hypothalamic-pituitary-
adrenocortical [HPA] axis), cognitive (e.g., dysfunctional cognitions, low self-esteem,
Depression in Mothers 14
helplessness or hopelessness, negatively biased attention or memory functions), and behavioral
or interpersonal (e.g., inadequate social and social-cognitive skills, over- or under-regulated
behavior, problems with concentration, low mastery motivation).
The strength of the model lies in its potential to guide research that will facilitate an
understanding of the complexities of the associations between mothers’ depression and
children’s outcomes. Although each aspect of the model is important, the proposed mechanisms
are the component that holds the most promise for furthering our understanding of the
development of psychopathology in children with depressed mothers, and they provide the
foundation for studying the other components of the model, such as how gender and age of the
child affect the associations. Thus, the mediators are an appropriate focus for this chapter,
especially given that this component has been the subject of much of the research in this area of
study that has been published since the model was proposed. In contrast to earlier research that
sought to determine the extent to which children of depressed mothers are at risk for the
development of psychopathology, much of the recent work has attempted to reveal what it is
about being the child of a depressed mother that places one at risk. Accordingly, in the next
section of this chapter, we examine empirical evidence for each of the four mechanisms
proposed to explain adverse outcomes in the children in the Goodman and Gotlib model.
We preface the review of the support for the mechanisms with a brief discussion of the
nature of evidence needed to demonstrate that a variable functions as a mediator. Figure 2 shows
a mediated effects model for maternal depression and child functioning. As clarified by
Holmbeck, a mediator “specifies how (or the mechanism by which) a given effect occurs” (p.
599) (Holmbeck, 1997). Inherent in that definition is the idea that tests of mediation are based
on the assumption that the independent or predictor variable (A), in our case depression in
Depression in Mothers 15
mothers, is significantly associated with the dependent variable (C), which in our case is any
aspect of child psychological functioning that is of concern. It is that now well-established
association for which we seek the mediator. Then, three further significant associations must be
found in order for mediation to be established (Baron & Kenny, 1986). First, maternal
depression must be significantly associated with the proposed mediator (B). Second, the
proposed mediator must be significantly associated with the child outcome measure. And third,
the association between the predictor (maternal depression) and the child outcome measure must
be significantly less after controlling for the mediator, which indicates that a significant
proportion of that association is accounted for by the proposed mediator.
Mechanism 1: Genetic Influences
The criteria for support of genetic mediation, then, are that (a) depression in child-bearing
aged women is highly heritable; (b) heritability is also associated with depression in children, as
well as with the other disorders and the vulnerabilities that have been associated with maternal
depression; and (c) controlling for heritability of depression, the association between maternal
depression and children’s depression and other outcomes decreases significantly.
Both family studies and quantitative genetic studies (those using twin or adoption
designs) provide evidence for heritability of depression in adults (Kendler et al., 1995; Kendler,
Myers, & Prescott, 2000; Sullivan, Neale, & Kendler, 2000). Heritability of major depression
broadly defined (using DSM-III-R criteria, which did not require impairment) is significantly
greater in women than in men, but when impairment is required as a criterion, heritability
contributes to depression about equally in men as in women (Kendler, Gardner, Neale, &
Prescott, 2001; Kendler & Prescott, 1999). Also, postpartum depression itself has been found to
be heritable (O'Hara, 1986). Finally, recent molecular genetics studies also provide supporting
Depression in Mothers 16
evidence for heritability of depression. Recently published findings implicate a region of
chromosome 2 containing the CREB1gene as a susceptibility gene for unipolar depression in
women in particular (Levinson, in press; Zubenko, Hughs, Stiffler, Zubenko, & Kaplan, 2002;
Zubenko et al., 2003). Kendler and colleagues’ findings (Kendler et al., 2001; Kendler &
Prescott, 1999) are consistent with the possibility that at least some genes may be related to risk
for depression differently in men compared to women. Also promising is the serotonin
transporter (5-HTTLPR) gene, which is particularly interesting given the accumulating evidence
for the role of the serotonin system in major depression and in the effectiveness of serotonin
reuptake-inhibitor drugs in the treatment of depression (Ressler & Nemeroff, 2000). In a birth
cohort sample of young adults, a functional polymorphism of this gene moderated the
prospective association between stressful life events and depression (Caspi et al., 2003). Thus,
the first step to establish mediation is satisfied, given the strong support for heritability of
depression in adults.
The second step to establish heritability as a mediator is to show that heritability is also
associated with depression in children, as well as with the other disorders and the vulnerabilities
that have been associated with maternal depression. Due to the methodological complexities of
measuring depression in children, evidence for the strength of heritability of depression in
children is less clear than in adults (Happonen et al., 2002; Rice, Harold, & Thapar, 2002).
Harrington and colleagues reviewed the evidence from family studies and found that depression
in children, especially when strictly defined, is associated with increased rates of depression in
relatives (Harrington, 1996; Harrington et al., 1997). Twin studies find partial support for
heritability of depression in children, with heritability estimates higher for levels of symptoms
that were below clinical cut-offs (Rende, Plomin, Reiss, & Hetherington, 1993), for depression in
Depression in Mothers 17
adolescents rather than in children (Eley & Stevenson, 1999; Murray & Sines, 1996; Scourfield
et al., 2003; Silberg et al., 2001; Thapar & McGuffin, 1994), for parent-reported symptoms
relative to child-reported symptoms (Eaves et al., 1997), and for girls more than boys, especially
based on parent report (Murray & Sines, 1996; Scourfield et al., 2003). Thus, while there is no
single estimate of heritability of depression in children, heritability likely plays an important role
in at least a subset of children with depression. Moreover, since heritability of depression may
not be specific to depression, other disorders found in higher rates in children with depressed
mothers compared to controls may be explained by the mechanism of heritability (Moldin, 1999;
Tsuang & Faraone, 1990). Finally, behavior genetics studies have also found that heritability is
high for several of the proposed vulnerabilities in the Goodman and Gotlib model, lending
further support to the idea that children with depressed mothers inherit vulnerabilities to
depression, rather than inheriting depression as a disorder (Goodman & Gotlib, 1999). For
example, behavioral inhibition and shyness (Cherny, Fulker, Corley, Plomin, & DeFries, 1994),
low self-esteem (Loehlin & Nichols, 1976), neuroticism (Tellegen et al., 1988), sociability
(Plomin et al., 1993), subjective well-being (Lykken & Tellegen, 1996), and expression of
negative emotion (Plomin et al., 1993) are all highly heritable.
In sum, there is strong evidence for genetics as one mechanism to explain the association
between depression in mothers and at least the vulnerabilities that have been implicated in the
pathway to depression in children, and, with several qualifiers, to depression itself, the first and
second steps in establishing mediation. As for the third step, in order to determine if the
association between maternal depression and child outcome decreases after controlling for
heritability, genetic mechanisms for the transmission of depression that could serve as the
mediator need to be identified. As reviewed earlier in this section, the potential of soon being
Depression in Mothers 18
able to identify susceptibility genes for major depression would lead to studies of the biological
mechanisms regulated by these genes, revealing how it is that children who inherit these gene
variations are at greater risk for the development of depression relative to others.
Mechanism 2: Innate Dysfunctional Neuroregulatory Mechanisms
The second mechanism refers to neurobiological processes that are specific to infants
born to women depressed during pregnancy. The criteria to establish support for mediation
through innate dysfunctional neuroregulatory mechanisms are that (a) depression in child-
bearing aged women is associated with adverse influences on fetal development, with
implications for the offspring’s neuroregulatory processes; (b) neuroregulatory processes are
associated with depression in children, as well as with the other disorders and the vulnerabilities
that have been associated with maternal depression; and (c) controlling for measures of
neuroregulation, the association between maternal depression and children’s depression and
other outcomes decreases significantly.
The first criterion has been supported by a few studies in which aspects of the fetal
environment have been associated with depression in pregnant women. Levels of plasma and
urinary cortisol, norepinephrine, beta-endorphin, and corticotrophin releasing hormone (CRH)
are positively associated with depressed mood during pregnancy (Field, 2002; Handley, Dunn,
Waldron, & Baker, 1980; Smith et al., 1990). Of those, none is known to be associated with fetal
levels other than cortisol; maternal levels of cortisol account for 50% of the variance in the fetus’
levels of cortisol (Glover, Teixeira, Gitau, & Risk, 1998, April). Further, mothers’ prenatal
levels of cortisol predict newborns’ cortisol levels (Lundy et al., 1999) and number of months
depressed during pregnancy predict preschool-aged children’s baseline cortisol levels (Dawson,
1999, August) as cited in (Ashman & Dawson, 2002). These associations between mothers’ and
Depression in Mothers 19
children’s cortisol levels, and indices of hypothalamic-pituitary-adrenal (HPA) axis functioning,
may explain the role of early stress in the development of depression (Graham et al., 1999).
Ongoing research in our lab may reveal the extent to which, among women with histories of
major depressive episodes, cortisol levels during pregnancy are associated with infants’
dysregulated emotions.
Depression during pregnancy may also be related to adverse income outcomes due to
depressed women being less likely than other women to obtain adequate prenatal care, to report
healthy eating and sleeping patterns, and to avoid smoking (Milberger, Biederman, Faraone,
Chen, & Jones, 1996). Although an association between the use of antidepressants by depressed
women and abnormal fetal development has been suggested, the concern is probably unfounded.
Recent evidence suggests that women’s use of antidepressants during pregnancy does not
influence the offspring’s neuroregulatory abilities (Nulman et al., 1997). In sum, a few studies
show that maternal depression during pregnancy increases the level of fetal exposure to cortisol
and is associated with other likely risks to fetal development, each of which is likely to
compromise the offspring’s neuroregulatory processes. Replications of these findings are
needed. Also needed are findings from studies such as our current one which will examine the
associations between fetal exposure to cortisol, as well as inadequate prenatal care, and infants’
own neuroregulatory response to stress.1
1 Mechanism 2 specifies that dysfunctional neuroregulatory abilities are innate, i.e. present at birth, whether
inherited or acquired during fetal development. Evidence is also accumulating that postnatal exposure to maternal
depression is associated with children’s cortisol levels and abnormal EEG patterns, which could also be mechanisms
through which maternal depression is associated with children’s adverse outcomes (Ashman & Dawson, 2002).
Although important, these later acquired dysfunctions are not the focus of the dysfunctional neuroregulatory abilities
proposed as a mechanism in the Goodman and Gotlib (1999) model. They are discussed later in that there is
evidence that depressed mothers’ insensitive or unresponsive behavior (Mechanism 3) mediates the relation between
maternal depression and children’s emotion regulation abilities, increasing children’s vulnerability factor for the
later development of depression.
Depression in Mothers 20
Are neuroregulatory processes associated with depression in children, as well as with the
other disorders and the vulnerabilities in children that have been associated with maternal
depression? Neuroregulatory systems, including both frontal brain activity (abnormal EEG
patterns) and HPA functioning (abnormal cortisol responses to stress) have both been associated
with depression in adults (Davidson et al., 1990; Ressler & Nemeroff, 2000). In children,
supportive evidence is accumulating. Elevated CRH levels in pregnant women has been
associated with impaired neurodevelopment in the fetus (Wadhwa et al., 2002), which may be
the first indication of stress-related physiological dysregulation in offspring. Elevated cortisol in
children increases sensitivity to stress (Sanchez et al., 2001), which increases children’s
vulnerability to develop depression (Graham et al., 1999). Similarly, abnormal EEG patterns
and, particularly, a pattern of relative right frontal activation are associated with the tendency to
experience “withdrawal” emotions such as sadness or fear (Davidson & Fox, 1989), making
child vulnerable to depression (Ashman & Dawson, 2002). Thus, support for this criterion is
limited to evidence for the role of the mediator in the emergence of vulnerabilities to depression,
and not yet for depression or other disorders.
There is mounting evidence that the association between maternal depression and
children’s depression and other outcomes decreases significantly, when controlling for measures
of neuroregulation (EEG patterns or cortisol responses to stress). Dawson and colleagues’ have
found that 3-year olds’ frontal brain activation mediates the relation between maternal depression
and child behavior problems, supporting the idea that maternal depression affects children’s
patterns of brain activity, whether through genetics, or fetal or early postnatal experiences
(Dawson et al., 2003). Indeed, the frontal lobe develops rapidly the first two years of life,
suggesting that it may be sensitive to early adverse experiences (Chugani & Phelps, 1986).
Depression in Mothers 21
Dawson et al.’s (2003) findings are also consistent with increasing knowledge of the role of the
frontal lobe in the regulation of emotion and affect and, thus, in increasing children’s
vulnerability to the development of psychopathology. In particular, the pattern of right frontal
EEG asymmetry (left frontal activation), which characterizes depressed adults and adolescents,
has been found to be associated with the experience of “withdrawal” emotions in children
(Davidson et al., 1990; Dawson et al., 1999a; Dawson, Grofer Klinger, Panagiotides, Hill, &
Spieker, 1992a; Finman et al., 1989).
Mechanism 3: Exposure to Mother’s Negative or Maladaptive Cognitions, Behaviors, And Affect
The third mechanism refers to two processes: (a) the effects of adverse parenting on
children’s developing psychobiological systems and (b) the prospect that children may model or,
through other social learning processes, acquire their depressed mothers’ negative or maladaptive
cognitions, behaviors, and affect. The criteria to establish support for mediation through these
mechanisms are that (a) depression in mothers is associated with adverse parenting and to
children’s exposure to the cognitive, behavioral, and affective manifestations of the mother’s
depression; (b) these exposures are associated with the outcomes in children that have been
associated with maternal depression; and (c) controlling for measures of maternal parenting and
cognition, behavior, and affect, the association between maternal depression and children’s
depression and other outcomes decreases significantly.
The first criterion is well supported and extensively described in several reviews. In a
recent meta-analysis of 46 observational studies, a strong effect size was found for the
association between maternal depression and negative (hostile/coercive) parenting behavior, a
moderate effect size for the association with disengagement from the child, and, a small effect
size for the association with (less) positive behavior (Lovejoy et al., 2000). The effect size for
Depression in Mothers 22
the association between maternal depression and positive behavior was moderated by
socioeconomic status and age of child such that the effect size was moderate for economically
disadvantaged women and for women of infants and significantly smaller for nondisadvantaged
women and women with children between the ages of 1 and 5 years of age.
Researchers have also found that the negatively biased cognitions that are consistently
found to be associated with depression in adults (Gotlib, Gilboa, & Sommerfeld, 2000) extend to
their parenting. Depressed mothers, relative to those with no depression, endorse more negative
views of themselves as parents (Gelfand & Teti, 1990; Goodman, Sewell, Cooley, & Leavitt,
1993) and report less confidence in being able to positively influence their children (Kochanska,
Radke-Yarrow, Kuczynski, & Friedman, 1987).
There is a strong evidence base supporting associations between these aspects of
parenting and the development of depression and other problems in children and adolescents
(Cicchetti & Toth, 1998; Cole & Rehm, 1986; Garber & Martin, 2002; Hetherington & Martin,
1986; Rubin & Mills, 1991; Sheeber, Hops, & Davis, 2001; Zahn-Waxler, Usher, & Goldman,
2003a). For example, depressed mothers have more negative, critical perceptions of their
children relative to other mothers, and this pattern has been associated with children’s tendency
to engage in self-blaming attributions for negative events and with lower perceived self-worth
(Goodman et al., 1994; Jaenicke et al., 1987; Kochanska et al., 1987; Radke-Yarrow, Belmont,
Nottelman, & Bottomly, 1990). These findings suggest that children are internalizing their
parents’ negative views into their own self-perceptions of being unworthy, which increases their
risk for the development of depression (Beck & Young, 1985). Researchers also find that family
environments of depressed children, and of children with high levels of internalizing problems,
relative to controls, are characterized by aversive social exchange, parents’ use of authoritative
Depression in Mothers 23
discipline and guilt-induction, less warmth and more criticism (Cicchetti & Toth, 1998; Cole &
Rehm, 1986; Davis, Sheeber, & Hops, 2002; Donenberg & Weisz, 1998; Gallimore & Kurdek,
1992; Hamilton, Asarnow, & Tompson, 1999; Hetherington & Martin, 1986; Hops, Lewinsohn,
Andrews, & Roberts, 1990; Rubin & Mills, 1991; Stark, Humphrey, Laurent, Livingston, &
Christopher, 1993; Zahn-Waxler et al., 2003a; Zahn-Waxler, Usher, & Goldman, 2003b).
The third criterion, that controlling for measures of maternal parenting and depression-
related cognition, behavior, and affect, the association between maternal depression and
children’s depression and other outcomes decreases significantly, has been submitted to
empirical test more often than has this criterion for the other mechanisms. Most of the studies
reported here relied on structural equation modeling to determine support for mediation. Table 1
summarizes the findings. In contrast to support for these mediators, mothers’ ability to maintain
stability and routines in their children’s activities failed to mediate the association between
maternal depression and either mother- or teacher-reported child adjustment (Roderick, 2002).
Similarly, family coercion failed to mediate the association between maternal depression during
the early school years and boys’ and girls’ later antisocial behavior or depression, suggesting that
other processes are more relevant (Compton, Snyder, Schrepferman, Bank, & Shortt, 2003). On
the other hand, consistent with support for mediation, in one of our studies we found the negative
attitudes mothers expressed toward their children moderated the association between maternal
depression and children’s lower global self-worth (Goodman et al., 1994).
Intervention studies are another potential source of support for mediation. Essentially,
interventions are experimental tests of the mechanisms or mediators. If interventions are
successful in reducing the aspects of parenting that are of concern in women with depression and
the intervention is associated with improvement in child functioning, they offer clear support for
Depression in Mothers 24
the mechanism. This is essentially what (Lyons-Ruth, Connell, Grunebaum, & Botein, 1990)
tested, but she and her colleagues failed to find support for the mechanism in an intervention
targeting women at high social risk (experiencing a combination of maternal depression, poverty,
and inadequate caretaking). Although the treatment (a home-visiting service with the goals of
helping families to meet basic needs and for the mother to interact positively and appropriately
with her infant), was associated with infants’ significant improvement in mental and physical
development and in attachment security, these changes were not associated with changes in
mothers’ increased involvement or decreased hostility/intrusiveness with their infants. In
contrast, other intervention studies yielded results that are consistent with the mechanisms in the
model. As reviewed recently, interventions designed to improve the quality of parenting and
parent-child relationships are demonstrating effectiveness in reducing levels of depression in
children, from infancy through adolescence (Gladstone & Beardslee, 2002).
Mechanism 4: Exposure to Stressful Environments
The fourth mechanism refers to the role of stressors in the association between maternal
depression and adverse child outcomes. The criteria to establish support for mediation through
exposure to stressful environments are that (a) depression in mothers is associated with
children’s exposure to stressful environments; (b) exposure to stressful environments is
associated with depression in children, as well as with the other disorders and the vulnerabilities
that have been associated with maternal depression; and (c) controlling for measures of stressful
environments, the association between maternal depression and children’s depression and other
outcomes decreases significantly.
Support is strong for the first criterion, that depression in mothers is associated with
children’s exposure to stressful environments. As reviewed recently, maternal depression
Depression in Mothers 25
increases children’s exposure to stress in several ways (Hammen, 2002). First, the mothers’
depression itself, by its symptoms, impairment, and episodic course, is stressful to children
(Compas, Langrock, Keller, Merchant, & Copeland, 2002). Second, depression in adults
typically occurs in the context of chronic and episodic stressors, including economic, work-
related, and marital- and other family conflicts. Third, depression has been found to increase the
likelihood of further stressful events. Thus, there is strong support for this criterion, making it all
the more compelling to determine how these stressors relate to the risk for the development of
psychopathology in children with depressed mothers.
In turn, exposure to stressful environments is associated with depression in children, as
well as with the other disorders and the vulnerabilities that have been associated with maternal
depression. In the classic stress-diathesis model, stress increases the likelihood that children will
develop depression and symptoms of other disorders in association with a range of
vulnerabilities, including genetic, neurobiological, cognitive, interpersonal, and contextual.
Qualitative and quantitative reviews of the literature reveal that, despite complications associated
with conceptualization and measurement of the key constructs, both chronic adversities and
episodic stressors are associated with depression symptoms and disorders and other internalizing
and externalizing disorders in children and adolescents (Compas, Grant, & Ey, 1994; Grant et al.,
2003). Stress is also implicated in the development of many of the proposed vulnerabilities, as in
Dawson’s premise that the stressfulness of infants’ interaction with an insensitive depressed
mother is associated with the development of the infants’ pattern of brain activity characterized
by reduced activity in the left frontal region (Dawson et al., 2003).
Studies designed to test the third criterion are emerging, with some support and some
mixed findings. For example, a high risk environment mediated the association between
Depression in Mothers 26
maternal depression and child behavior problems, although not the association with toddler’s
insecure attachment (Cicchetti, Rogosch, & Toth, 1998). In other studies, chronic family stress
was found to mediate the relationship between self-reported depression symptoms in a
community sample of mothers and adolescents’ depression symptoms (Brennan et al., 2002).
However, measures of social disadvantage did not explain the association between postnatal
depression and 11-year old children’s IQ scores (Hay & Pawlby, 2001). In other studies,
maternal depression was found to mediate the association between poverty in single-mother
families and 4- to 9-year old children’s socioemotional problems (Eamon & Zuehl, 2001).
Correspondingly, maternal depression symptoms mediated the relation between parents’
problematic drinking and 6- to 12-year old children’s internalizing problems (El-Sheikh &
Flanagan, 2001).
Given the common co-occurrence of women’s depression and marital discord, and the
known stressfulness for children of marital discord itself, it is important to understand whether
the effect of one is explained by the effect of the other, in predicting the development of
psychopathology in children. Several researchers have addressed this question. In one such
study, family discord, defined as marital discord, low family intimacy, and parenting
impairments, was found to be a significant mediator of the association between histories of
maternal depression symptoms and both conduct problems and depressive symptoms of children
in middle adolescence, but only in girls (Davies & Windle, 1997). However, in a later study
using a longitudinal design, (Davies & Dumenci, 1999) found that although marital distress
mediated the association between maternal depressive symptoms and externalizing symptoms in
adolescents, maternal depressive symptoms mediated the effects of marital distress on
adolescents’ depressive symptoms, supporting a pathway from marital distress through maternal
Depression in Mothers 27
depression to adolescents’ depression. Others find that the specific nature of the marital conflict
is what matters. For example, parents’ use of observable conflict strategies involving depressive
behaviors such as physical distress, withdrawal, sadness, and fear were found to mediate the
association between depressive symptoms in mothers and their children’s internalizing
symptoms whereas destructive and constructive marital conflict strategies did not serve as
mediators (Du Rocher Schudlich & Cummings, 2003). These latter studies suggest the need to
further consider the roles of maternal depression and marital discord in relation to each other and
the risk for the development of psychopathology in children. It will be important to also
consider the role of heritability in the model that best explains associations among maternal
depression, stressors, and the emergence of depression in children in that genetic factors are
significant in influencing individual differences in susceptibility to environmentally mediated
risk as well as risk for depression (Silberg & Rutter, 2001).
Gender Specificity
Of particular relevance to addressing prevention, treatment, and social policy of
depression in women who are mothers are mechanisms through which depression is maintained
in families through intergenerational transmission of risk from depressed mothers to daughters,
who may themselves become depressed mothers. Adolescent girls are at particularly high risk
for depression. While there are no consistent gender differences in rates of depression in
preadolescent children (Angold, 1988), females are about twice as likely as males to be
depressed during adolescence (Nolen-Hoeksema & Girgus, 1994). Gender differences in
depressive symptoms appear to emerge around age thirteen at which time girls’ depressive
symptoms continue to increase and boys’ symptom levels remain relatively stable (Ge, Conger,
& Elder, 2001; Ge, Lorenz, Conger, Elder, & Simons, 1994). Although girls’ relatively elevated
Depression in Mothers 28
rates of depression do not emerge until adolescence, gender differences in vulnerabilities for the
development of psychopathology and early signs of depression likely develop earlier in life
(Zahn-Waxler et al., 2003a). With respect to Goodman and Gotlib’s model, it is important to
explore gender of the child as a moderating variable that affects the associations between
mothers’ depression and children’s depression and other disorders and vulnerabilities.
Although researchers have suggested that the greatest risk for depression posed by
maternal depression may be to adolescent girls, relatively little research exists to support gender
differences in the risk for psychopathology among offspring of depressed mothers (Cummings &
Davies, 1994; Hops, 1992). The limited research on greater risk for girls relative to boys has
shown that adolescent daughters of depressed mothers have more dysphoric and less happy
affect than adolescent daughters of nondepressed mothers, though no significant difference in
affect was found for adolescent boys of depressed mothers compared to sons of nondepressed
mothers (Hops, Sherman et al., 1990). Additionally, depressed mothers and their daughters, but
not depressed mothers and their sons, have been shown to have synchronous bouts of depression
(Radke-Yarrow, Nottelman, Belmont, & Welsch, 1993). Moreover, in community samples,
mothers’ depressive symptoms are associated with adolescent daughters’, but not sons’,
depressive symptoms (Davies & Windle, 1997; Fergusson, Horwood, & Lynskey, 1995; Hops,
1992, 1996). However, while maternal depression seems to affect mood in girls more than in
boys, maternal depression appears to affect intellectual functioning more in boys than in girls
(Hay & Pawlby, 2001).
Several mechanisms have been proposed to help explain the gender difference in the
prevalence of depression in general samples of adolescents who are not necessarily children of
depressed mothers. These mechanisms include gender-related changes in biological and
Depression in Mothers 29
hormonal functioning, cognitive styles and coping patterns, amount and type of stress
encountered, and socialization practices (Nolen-Hoeksema & Girgus, 1994; Peterson, Sarigiani,
& Kennedy, 1991). The role of girls’ changing body morphology in the development of
depression during puberty has been supported in many studies over the last two decades (e.g.,
(Angold & Rutter, 1992; Ge, Conger, & Elder, 1996). Recently, however, Angold and
colleagues (1999) have found that associations between levels of testosterone and estradiol and
diagnoses of depression in girls eliminate the effect of changes in body morphology on the
probability of becoming depressed (Angold et al., 1999). Thus, increased levels of depression in
adolescent girls appear to be related to hormonal changes, rather than the morphological changes
in puberty. However, this study did not address whether these associations between hormone
levels and depression are different for girls and boys, and thus do not necessarily support
hormone levels as a mediator responsible for gender differences in rates of depression.
Somewhat more, though still limited, evidence supports the etiological role of socialization of
affective and cognitive vulnerabilities in girls (Hankin & Abramson, 1999). For example,
studies provide empirical evidence that girls’ identification with feminine stereotypes (e.g.,
needing to appear thin and becoming dissatisfied with body shape and appearance) increase
during adolescence and gender-role identification is associated with increases in depression
(Nolen-Hoeksema & Girgus, 1994). This socialization pattern may be related to greater
rumination, more negative inferential styles, and lower self-worth as well as and with greater
perceived impact of negative events in girls relative to boys (Ge et al., 1994; Hankin &
Abramson, 1999).
Furthermore, Sheeber and colleagues (2002) (Sheeber, Davis, & Hops, 2002) suggest
several familial socialization processes that indirectly increase the risk of depression in girls. For
Depression in Mothers 30
example, girls’ expressions of depressive-like behaviors are often normalized and even
encouraged, and parents may provide differential reinforcement for gender-typic behaviors
related to risk for depression, such as less instrumental and more relationship-focused behaviors.
Empirical evidence to support Sheeber’s hypothesized socialization processes comes largely
from observational studies earlier in development. It is important to keep in mind that the
studies do not provide insight into the direction of influence (i.e., whether differential
socialization occurs before or subsequent to gender differences in behavior). Parents have been
observed to respond to emotional displays’ in girls through feeling-focused, passive interventions
and to boys’ through problem-focused, active interventions (Dino, Barnett, & Howard, 1984;
Eisenberg, Cumberland, & Spinrad, 1998; Nolen-Hoeksema, 1998). Moreover, girls are
encouraged to display dependency and affectionate behavior (Hops, Sherman et al., 1990;
Maccoby, 1990) and nurturing and caring behavior (Radke-Yarrow, Zahn-Waxler, Richardson,
& Susman, 1994; Zahn-Waxler, Cole, & Barrett, 1991; Zahn-Waxler & Robinson, 1995; Zahn-
Waxler & Smith, 1992). Girls also receive more encouragement for being concerned about the
feelings of others and having a sense of responsibility for others (Hops, 1996; Keenan & Shaw,
1997; Maccoby, 1990). Later, during adolescence, when there is greater pressure to conform to
sex-role stereotypes (Hill & Lynch, 1983; Nolen-Hoeksema & Girgus, 1994), girls’ engagement
in feminine-type activities is related to self-reported depression (Nolen-Hoeksema & Girgus,
1994). Given the lack of teaching and encouragement to use problem-solving strategies earlier
in life, adolescent girls are less equipped to effectively deal with the challenges of adolescence
(Allgood-Merten, Lewinsohn, & Hops, 1990).
In terms of mechanisms explaining gender specificity, some researchers report that
heritability estimates for depression are higher for girls than boys (Eley & Stevenson, 1999;
Depression in Mothers 31
Murray & Sines, 1996). Regarding the third mechanism, girls may be particularly vulnerable to
modeling their mothers’ depressive affect, cognitions and behaviors given the greater salience of
the same gender parent. Depressed mothers display depressive interpersonal behaviors and poor
problem-solving and coping skills to deal with depression, which increase susceptibility to
depression (Compas, Malcarne, & Fondacaro, 1988; Garber, Braafladt, & Zeman, 1991;
Kashani, Burbach, & Rosenberg, 1988). Children of depressed mothers have been shown to
demonstrate less active strategies for responding to negative affect (Garber et al., 1991; Nolen-
Hoeksema, Wolfson, Mumme, & Guskin, 1995), and modeling of these behavioral
vulnerabilities may be particularly salient to daughters of depressed mothers (Bandura, 1986).
Additionally, maternal depression is associated with poor parenting, which may be a specific risk
to girls through: 1) impaired mother-daughter relationships, which are already characterized by
high levels of conflict during adolescence (Hill, Holmbeck, Marlow, Green, & Lynch, 1985;
Steinberg, 1987, 1988), and 2) adolescent girls developing a sense of responsibility for the
family and taking on the role of parenting other children and caring for the depressed mother, a
burden that increases risk for depression (McGrath, Keita, Strickland, & Russo, 1990; Stephens,
Hokanson, & Welker, 1987). Finally, concerning the fourth mechanism, girls may be more
sensitive than boys to heightened levels of stress, and maternal depression is a nonspecific
stressor that may exacerbate the risk already posed to girls. Girls have been found to respond to
stressors, like marital discord and economic hardship, with internalizing symptoms (Conger,
Conger, Matthews, & Elder, 1999; Cummings & Davies, 1994) and likely may respond to the
stress of having a depressed mother with similar internalizing problems (Compas et al., 2002).
Therefore, accumulating evidence supports the moderating role of gender in three of the four
mechanisms proposed by Goodman and Gotlib’s model, suggesting the importance of
Depression in Mothers 32
considering gender of the children when studying the transmission of risk from depressed
mothers to their children.
Conclusion
Although researchers are beginning to design studies that test the processes by which
maternal depression is associated with the development of psychopathology in the children, this
line of research is new and many questions remain unanswered. The Goodman and Gotlib model
provides theoretical bases for the design of prevention and treatment of disorders in the offspring
of mothers with depression as well as for social policy. With this chapter, we took the further
steps of summarizing the published findings in support of empirical tests of mediation and
providing guides to the directions needed for future research to further test mediation. The
longer-term goals of these lines of research are to be able to provide empirical support for the
design of prevention and treatment studies and for policy recommendations. In particular,
support for any of the four mechanisms provides information essential to identify targets of
change for intervention and treatment. These suggestions are made in light of awareness that
knowledge of risk for psychopathology in children of depressed mothers has not, in itself, been
sufficiently compelling to drive a public health campaign to identify and treat depression in
women who are mothers. Thus even though it may be that treating women’s depression may
minimize risk for psychopathology in the children (although, see Goodman et al., in press),
research on mechanisms becomes necessary in that our best hope for preventing depression from
being passed onto other generations is to learn to prevent it by intervening in the mechanisms.
Among the research findings, the research on genetic mechanisms suggests the need for
interventions designed to minimize children’s exposure to high-risk environments in order to
reduce the role of environmental risks that are known to interact with genetic risk (Silberg &
Depression in Mothers 33
Rutter, 2002). Further, if research emerges for neuroregulatory mechanisms as mediators of the
association between maternal depression and the development of psychopathology in the
children, then it may be important to test age-appropriate interventions designed to improve
children’s stress reactivity and other aspects of emotion regulation and their coping skills (Clarke
et al., 1995; Compas et al., 2002).
Research on the effects of adverse parenting on children’s developing psychobiological
systems and other processes (e.g., socio-emotional regulation) through which children are
adversely affected by depressed mothers’ affect, cognitions, and behavior supports what may
have seemed to be an obvious and compelling next step: to intervene to improve the quality of
parenting provided by mothers suffering from depression. Research is needed to determine
whether the best approach is early intervention to treat the depression, with the implication that
the poor qualities of parenting that have been found to be associated with depression in mothers
would improve simultaneously or, alternatively, to target the intervention directly to improve
qualities of parenting. In one recent small-scale study, we found preliminary support for the
contention that parenting would improve as a secondary benefit of treatment for postpartum
depression (Goodman, Broth, Hall, & Stowe, 2003). It is also important to consider that
depression is known to be vastly under recognized and untreated, partly due to attitudinal and
other barriers to seeking treatment (Goodman & Tully, 2003). Research is needed to determine
if women with depression are more receptive to interventions designed to improve quality of
parenting relative to treatment for depression. Related questions include whether improving
quality of parenting itself can be effective in the context of maternal depression. Others have
found that depression and stress in mothers interferes with the effectiveness of parenting
interventions designed to treat children with aggressive and antisocial behavior (Kazdin &
Depression in Mothers 34
Whitley, 2003). Alternatively, researchers may find that effective parenting interventions have
the secondary benefit of alleviating at least mild symptoms of depression as women begin to
experience more behavioral successes and more positive affect in their interactions with their
children and alter their cognitions to perceive themselves as effective in their parenting.
Researchers also need to determine the role of timing of interventions that would
effectively interrupt the pathway from maternal depression to the development of
psychopathology in the children. In particular, we are concerned about children who are exposed
prenatally who may or may not be subject to later exposures, either in the postpartum period or
later. It is essential to test the extent to which prenatal depression predicts not only infant
outcomes but also outcomes at later, critical points in development such as at age 4 (e.g.,
development of emotion-regulation abilities and social development as their social worlds
become more complex with peers and teachers). In some of our current and planned studies on
this question, we extend findings from animal models, which show that prenatal challenges
influence reactivity of the offspring’s stress response system later in life (Newport, Stowe, &
Nemeroff, 2002; Sanchez et al., 2001). Overall, the interventions need to be shown to provide
children with the environmental supports that are known to be needed to facilitate healthy
development, such as appropriate levels of stimulation for infants (Ashman & Dawson, 2002;
Field, 2002), responsive and warm care giving (Lyons-Ruth, Lyubchik, Wolfe, & Bronfman,
2002), and models of healthy affective, behavioral, and cognitive functioning (Garber & Martin,
2002). These interventions should be sensitive to the children’s developmental level as well as
to their gender, and targets of the interventions may vary accordingly.
Research on the fourth mechanism, exposure to stressful environments, shows clear
support for the role of stressors in a model of the associations between maternal depression and
Depression in Mothers 35
the development of psychopathology in the children. However, the exact role of stressors is still
unclear, leaving up to future research to determine whether interventions would more effectively
target the stressors or the depression. Research on the associations between marital distress and
depression is informative on this matter: models that best account for the research findings are
bi-directional, including the effects of marital distress and depression on each other, and take into
account that the direction of influence may differ for men and women (Fincham, Beach, Harold,
& Osborne, 1997). As we reviewed recently (Goodman & Tully, 2003), for women more than
men, marital satisfaction is likely to lead to depression and marital therapy has been found to be
effective in treating depression (Beach, Fincham, & Katz, 1998; Beach & Jones, 2002). Other
research indicates that stress itself interferes with effective parenting (Lyons-Ruth et al., 2002;
Radke-Yarrow & Klimes-Dougan, 2002), thereby lending further support for interventions to
improve quality of parenting. Whether those interventions would be more effective if they target
the quality of parenting or aim to reduce the level of stress itself needs to be the subject of future
research.
The accumulated evidence of gender as a moderator of the proposed mechanisms for risk
of psychopathology in children of depressed mothers suggests that it is very important to
consider gender of the offspring when developing prevention and intervention strategies for
depression and other disorders in children of depressed mothers. Future research endeavors
should focus on developing models of risk for depression specific to daughters of depressed
mothers who not only have heightened risk for depression themselves but also pose the threat of
continuing the intergenerational pattern of transmission of psychopathology from mother to
child, passing the risk to their offspring.
Depression in Mothers 36
Table 1. Empirically supported mediators of the association between maternal depression and
outcomes in children
Citation Children’s Age Mediator Outcome
Lundy, 2002
6 months
Synchrony in mother-
infant interactions
Quality of mother-infant
attachment
Dawson et al.,
2003
14 months
Insensitivity
Reduced left frontal brain
activity
Snyder, 1991
4- to 5-years
Harsh, inconsistent, or
ineffective discipline
Conduct problems
Ghodsian,
Zayicek, &
Wolkind, 1984
Infant through
age 4
Frequency of physical
punishment
Child behavior problems
Murray &
Kempton, 1993
2 month old
Maternal speech
characterized by negative
affect and not infant
focused
Cognitive development at 18
months
Kam, 2001
2nd grade
Warmth
Emotion regulation skills
Harnish et al.,
1995
1st grade
Mother-child interaction
quality
Externalizing problems (but
not in African-Americans)
McCarty &
McMahon,
2003
11-12 years old
Cold, hostile, or difficult
mother-child relationship
Disruptive behavior problems
McCarty &
McMahon,
2003
11-12 years old
Less maternal social
support
Internalizing problems
Hammen,
Burge, &
Stansbury,
1990
8 – 16 years old
Dysfunctional
communication
Negative self-concept
Nelson, 2001
15 years old
Critical attitudes toward
the child
Externalizing problems
Hilsman, 2001
12-14 years old
Parental criticism
Depressive disorder
Prinstein &
LaGreca, 1999
5-6 years old
Maternal social skills
Social competence (girls only)
Depression in Mothers 37
Figure 1. Integrative model for the transmission of risk to children of depressed mothers
(Goodman & Gotlib, 1999)
Depressed
Mother
Heritability of
Depression
Innate
Dysfunctional
Neuroregulatory
Mechanisms
Exposure to
Mother’s
Negative and/or
Maladaptive
Cognitions,
Behaviors, and
Affect
Exposure to
Stressful
Environment
Other Factors
Father
Availab ility
Mental health
Timing/ Course of
Mother’s
Depression
Child
characteristics
Temperament
Gender
Intellectual,
Social-
Cognitive
Skills
Vulnerabilities
Psychological Dysfunction
Skills Deficits or Maladaptive
Styles or Behavioral Tendencies
Cognitive
Affective
Behavioral or Interpersonal
Outcome
Mechanisms
Risk
Childhood or
Adolescent
Depression
Other Disorders
Depression in Mothers 38
Figure 2. A mediated effects model for the associations between depression in mothers and
children’s psychological functioning
A
Mothers’
Depression
B
C
Mediators
Heritability of Depression
Innate Neuroregulatory Mechanisms
Exposure to Mothers’ Cognitions,
Affect, and Behavior
Exposure to Stressful Environment
Child’s
Psychological
Functioning
1
3
2
Depression in Mothers 39
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