PRENATAL INTIMATE PARTNER VIOLENCE AND DEPRESSION DURING
CHILDHOOD: THE ROLE OF PHYSIOLOGICAL STRESS RESPONSE DYSREGULATION

By

Cecilia Martinez-Torteya

A DISSERTATION

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY

Psychology

2011

ABSTRACT
PRENATAL INTIMATE PARTNER VIOLENCE AND DEPRESSION DURING
CHILDHOOD: THE ROLE OF PHYSIOLOGICAL STRESS RESPONSE DYSREGULATION
By
Cecilia Martinez-Torteya
Objective: This study investigates the influence of exposure to intimate partner violence (IPV)
during pregnancy on offspring depressive problems during childhood, examining HPA axis
dysregulation (via stress-induced levels of salivary cortisol) as a mediating mechanism. This
research is guided by the ―fetal programming‖ theory, which proposes that the environmental
conditions during pregnancy can exert long-term neural adaptations and influence later
physiological and psychological functioning. In addition, trauma theory supports the role of IPV
as a particularly deleterious influence, due to its interpersonal and chronic nature, and wellestablished associated neuroregulatory deficits. Finally, consistent with developmental
psychopathology, a number of factors at the individual and family levels were examined, and
interactions between different levels of risk and protection were explored. Previous empirical
studies support the proposed pathway: prenatal stress predicts child temperamental difficulties,
internalizing symptoms, and HPA axis dysregulation. However, only one study to date has
reported a link between prenatal stress, HPA axis functioning, and depression. No study to date
has evaluated the distinct effect of prenatal IPV on long-term offspring neuroendocrine and
psychological outcomes. Method: Participants were 119 children followed longitudinally since
pregnancy, who were about 10 years old for the present assessment. Questionnaires assessed
IPV, maternal mental health, maternal early parenting, family history of depression, and income.
A coded laboratory task measured maternal warmth towards their child during infancy. HPA
axis dysregulation was assessed via salivary cortisol levels before, 20 minutes after and 40

minutes after the Trier Social Stress Task for Children. Child depressive symptoms were
assessed through maternal and child reports, using questionnaires and a semi-structured clinical
interview (K-SADS-PL). Results: Structural Equation Modeling, Latent Class Analysis,
Logistic Regression, and MANCOVA were used for hypothesis testing. Exposure to IPV during
pregnancy and current exposure to IPV predicted higher salivary cortisol output. Depression
during childhood was predicted by IPV during pregnancy, maternal mental health during
pregnancy, early parenting, current exposure to IPV, current maternal mental health, gender, and
cortisol levels; however, different predictors were significant for mother-reported and childreported depressive symptoms. Gender and family history of depression moderated the
relationships between child depressive symptoms and prenatal, postnatal, and familial risk.
Discussion: Findings support the ―programming hypothesis‖ and the role of prenatal IPV as a
unique risk factor associated with HPA axis functioning and childhood depression, over and
above the effects of other prenatal stressors and postnatal adversity. Results support the multidetermined nature of child depressive symptoms, as prenatal and postnatal factors at the
individual and family levels significantly influenced outcomes. This is the first study to link
prenatal IPV exposure with HPA axis dysregulation and depressive symptoms. Future research
should replicate the present findings, using multiple indices of HPA axis functioning and
examine whether this mechanism differentiates distinct subgroups of depressed children.

ACKNOWLEDGEMENTS

I would like to thank my Advisor, G. Anne Bogat, Ph.D., for her guidance,
encouragement, and support during the last 6 years. I am particularly grateful for her dedication
to this dissertation project; Dr. Bogat’s mentorship has been critical for my professional
development, and for this I am deeply indebted. I also thank the members of my committee,
Alytia Levendosky, Ph.D., Alexander von Eye, Ph.D., Joseph Lonstein, Ph.D., and Kathy
Stansbury, Ph.D., for their valuable advice and feedback on this dissertation.
I would like to acknowledge the funding sources for this project: Blue Cross Blue Shield
of Michigan Student Research Grant, American Psychological Association Dissertation Award,
Society for Research in Child Development Dissertation Award, International Society for
Traumatic Stress Studies Student Research Award, John Hurley Dissertation Award, and
Michigan State University’s Enrichment Fellowship. This research would not have been
possible without their support. I am also grateful to the undergraduate and graduate students
who worked on this research project. Their dedicated work was an invaluable contribution to
this study.
I am eternally grateful to my family and friends, as I could always count on their love and
support during the challenging moments of this process. I specially want to thank my father
Carlos E. Martinez Davila, Ph.D., who inspired my curiosity and love for knowledge, which has
motivated my research and clinical endeavors.
Lastly, I would like to thank the women and children who participated in this study over
the course of 10 years. By sharing their stories with this project they have allowed me to learn
from their strengths and struggles.

iv

TABLE OF CONTENTS

LIST OF TABLES ........................................................................................................... vii
LIST OF FIGURES ......................................................................................................... viii
INTRODUCTION ...............................................................................................................1
THE EFFECTS OF EXPOSURE TO IPV AND INCREASED STRESS DURING
PREGNANCY …………………………………………………………………………... 5
IPV Definition and Prevalence ...……………..…………………………………. 5
Consequences of IPV Exposure for Women and Children ...…………………… 6
Prenatal Stress and Offspring Outcomes ...……………………………………… 9
Traumatic Stress …..……………………………………….……………. 9
Chronic Stressors: Stressful Life Events, Maternal Perceived Distress,
Depression, and Anxiety …...…………………………………………... 10
PRENATAL STRESS EXPOSURE AND OFFSPRING STRESS RESPONSE .....….. 14
The Stress Response ..……………………………………………………….…. 14
The Programming Role of Cortisol ..…………………………………………... 16
CHILD HPA AXIS DYSREGULATION AND DEPRESSIVE SYMPTOMS ..……... 20
Definition and Epidemiology of Childhood Depression ...…………………….. 20
HPA-Axis Dysregulation and Childhood Depression .......…………………….. 21
INDIVIDUAL, FAMILIAL, AND ENVIRONMENTAL RISK AND PROTECTION
FOR DEPRESSION …………………………………………………………………... 24
Risk and Protection: Maternal Mental Health, Early Parenting, and Exposure
to IPV during Childhood ..……………………………………………………... 24
Maternal Mental Health and Early Parenting ...……………………...… 24
Intimate Partner Violence ...………………………………………….… 27
Familial Risk and Gender as Moderators of Environmental Risk ...…………… 29
Familial Risk ...……………………………………………………….… 29
Gender …...……………………………………………………………... 30
THE PRESENT STUDY ………………………………………………………………. 32
Hypotheses ...…………………………………………………………………… 35
METHODS .…………………………………………………………………………..... 36
Participants ...………………………………………………………………...… 36
Measures ...…………………………………………………………………...… 37
Dependent Variables: Maternal Report ...……………………………… 37
Dependent Variables: Child Report ...………………………………….. 38
Independent Variables: Maternal Report ...…………………………….. 39
Independent Variables: Child Report ...………………………………… 42
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Experimental Manipulation……………………………………………... 42
Salivary Cortisol Collection ...………………………………………….. 44
Procedures ...……………………………………………………………………. 45
Saliva Samples Storage and Analysis ...………………………………... 48
Data Storage ...………………………………………………………..… 48
Training ...………………………………………………………………. 48
RESULTS .……………………………………………………………………………... 49
Missing Data ...…………………………………………………………………. 49
Descriptive Statistics ...……………………………………………………….… 49
Data Analytic Plan ...…………………………………………………………… 50
Hypothesis Testing ...…………………………………………………………… 50
Hypothesis 1 ...………………………………………………………….. 50
Hypothesis 2 ...………………………………………………………….. 54
Hypothesis 3 ...……………………………………………………..…… 55
Hypothesis 4 ...………………………………………………………….. 58
Hypothesis 5 ...………………………………………………………….. 60
DISCUSSION ....……………………………………………………….………………. 63
Child Stress-Induced Cortisol Levels ...………………………………………... 64
Child Depression and Familial, Prenatal, and Postnatal Risk ...……………….. 70
Child Cortisol Levels and Depressive Symptoms ...………………………….... 73
Moderation by Gender and Family History ...………………………………….. 75
Limitations and Future Directions ...…………………………………………… 76
Clinical Implications ...……………………………………………………….… 79
Conclusions ...…………………………………………………………………... 80
APPENDICES .…………………………………………………………………………. 81
Appendix A: Tables …………………………………………………………….. 82
Appendix B: Figures ……………………………………………………………. 90
REFERENCES…………………………………………………………………………. 106

vi

LIST OF TABLES
Table 1. Demographics for Full and Reduced Samples With t-test Comparisons …………. 83
Table 2. Measures Across All Data Collection Periods ……………………………………. 84
Table 3. Correlations Between All Predictors and Outcomes ……………………………… 85
Table 4. Latent Profile Analysis Using Baseline, Peak, and Recovery Cortisol Levels ….… 86
Table 5. Logistic Regression Predicting Cortisol Latent Profile Membership ……………... 87
Table 6. Fit Indices for Models Predicting Childhood Depression …………………………. 88
Table 7. Hypothesis 3: MANCOVA for Differences on Maternal and Child Reports
Across 3 Latent Profiles of Cortisol ……………………………………………………….... 89

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LIST OF FIGURES

Figure 1. Hypothesis 1: Proposed Model Predicting Salivary Cortisol Levels Using
Prenatal and Postnatal Risk…………………………………………………………………… 91
Figure 2. Three-Latent Profiles of Cortisol Output …………………………………………... 92
Figure 3. Hypothesis 2: Estimated Model Predicting Child Depression Using Prenatal
and Postnatal Risk …………………………………………………………………………….. 93
Figure 4. Hypothesis 3: Estimated Model Predicting Child Depression Using Cortisol
Decrease, Prenatal and Postnatal Risk ……………………………………………………….... 94
Figure 5. Hypothesis 3: Estimated Model Predicting Child Depression Using Cortisol
AuCg, Prenatal and Postnatal Risk ……………………………………………………………. 95
Figure 6. Hypothesis 4: Mediation Model with Cortisol Decrease, Pregnancy, and
Postnatal Risk …………………………………………………………………………………. 96
Figure 7. Hypothesis 4: Mediation Model with Cortisol AuCg, Pregnancy, and Postnatal
Risk …………………………………………………………………………………………… 97
Figure 8. Hypothesis 5: Mediation Model for Self-Reported Child Depression via
Cortisol Decrease, by Gender ………………………………………………………………… 98
Figure 9. Hypothesis 5: Mediation Model for Self-Reported Child Depression via
Cortisol AuCg, by Gender ……………………………………………………………………. 100
Figure 10. Hypothesis 5: Mediation Model for Self-Reported Child Depression via
Cortisol Decrease, by Family History of Depression ………………………………………… 102
Figure 11. Hypothesis 5: Mediation Model for Self-Reported Child Depression via
Cortisol AuCg, by Family History of Depression ……………………………………………. 104

viii

PRENATAL INTIMATE PARTNER VIOLENCE AND DEPRESSION DURING
CHILDHOOD: THE ROLE OF PHYSIOLOGICAL STRESS RESPONSE DYSREGULATION
The present study examines prenatal exposure to intimate partner violence (IPV) as a risk
factor for children’s later psychological problems, examining the specific link between exposure
to IPV in utero and childhood depressive problems, mediated via neuroendocrine abnormalities
in children’s physiological response to stressors.
This research is guided by the ―fetal programming‖ theory (Barker, 1998; Beydoun &
Saftlas, 2008; Huizink, Mulder, & Buitelaar, 2004; O’Connor, Heron, Golding, Beveridge, &
Glover, 2002; Talge, Neal, & Glover, 2007), which posits that the prenatal conditions determine
fetal growth and development, producing long-term physiological adaptations. The relevance of
the prenatal environment can be understood using the concept of ―sensitive periods‖ or phases of
greater susceptibility (Bateson & Hinde, 1987), during which the fetus undergoes rapid changes
in the developing neural structures and is most responsive to environmental conditions. The
sensitive period begins in utero and, due to the plasticity of the young brain, extends into infancy
and beyond (Cushing & Kramer, 2005).
Fetal programming via retarded fetal growth has been associated with a number of
problems during adulthood, including diabetes, coronary heart disease, and hypertension (Barker,
1998). The Dutch Hunger Winter Study found that maternal malnutrition during pregnancy,
preceded and followed by adequate nutrition, was associated with increased risk for breast
cancer, coronary heart disease, glucose intolerance, stress sensitivity, and obesity (Roseboom, de
Rooij, & Painter, 2006). However, these adaptations are aimed to ensure offspring survival in
the short-term, and can promote long-term adaptation to similar adverse conditions in postnatal
life. For example, the Leningrad Siege Study found that maternal malnutrition during pregnancy
was not associated with glucose intolerance, dyslipidaemia, hypertension, or cardiovascular
1

disease in adulthood in the context of chronic poor nutrition prior to pregnancy and during the
first few years of life (Stanner & Yudkin, 2001).
A number of authors (Maccari et al., 2003; Talge et al., 2007) have proposed that
exposure to adversity during pregnancy also has important implications for psychological
outcomes; structural and functional changes in the central nervous system (CNS) can underlie
later behavioral and emotional regulation deficits and result in psychiatric symptoms. Boyce and
Ellis (2005) propose that the prenatal environment serves as a template for the environmental
conditions that the fetus will encounter after birth and influence the development of stress
reactivity: high reactivity is developed to promote offspring survival in a threatening
environment, with high levels of circulating stress hormone (i.e., cortisol) protecting against
immune, infectious, and inflammatory diseases (Kapcala, Chautard, & Eskay, 1995). However,
the frequent activation of the offspring stress response results in chronic tissue exposure to high
levels of cortisol, potentially conducive to deficits on brain structure and function, and
abnormalities in the physiological response to stressors.
An elevated response to stressors may be a marker for impaired threat signal detection or
inefficient regulation of pleasure/motivation systems among depressed children (Goodyer, 2008),
and a result of the interplay between a genetic vulnerability and chronic activation of the stress
response via frequent adversity. Importantly, addressing the earliest observable individual
differences that convey risk for psychopathology may promote competencies during early life
and provide the building blocks for subsequent adaptation, buffering the impact of later adversity
(Sroufe, Carlson, Levy, & Egeland, 1999). Research consistently identifies early precursors to
later internalizing symptoms (Bayer, Hiscock, Ukoumunne, Price, & Wake, 2008; Bayer &
Sanson, 2003; Gladstone & Parker, 2006) and have found that an abnormal physiological

2

response to stressors can precede the development of depressive symptoms (Young, Vazquez,
Jiang, & Pfeffer, 2006). Delineating specific pathways that lead from early (prenatal) risk to
depressive problems during childhood is essential for successful targeted prevention and
treatment efforts.
The present study is also guided by complex trauma theory, which posits that exposure to
trauma is qualitatively different from exposure to stress and results in developmental deficits
related to regulatory capacities, consistent with the multiple and non-specific symptoms
experienced after chronic traumatization (Cloitre et al., 2009). Specifically, complex trauma
theory proposes lasting changes in the victim’s central nervous system (CNS). This theory
supports the unique role of IPV during pregnancy on the victim’s neuroendocrine functioning,
given its interpersonal and chronic nature; the resulting stress regulation deficits are expected to
be above and beyond the victim’s psychiatric symptoms. Women’s neuroregulatory deficits
during pregnancy, in turn, influence fetal CNS development.
Importantly, mothers develop internal representations and attitudes towards their fetus
during pregnancy (Stern, 1995; Zeanah, Keener, & Anders, 1986). These representations are
largely influenced by exposure to IPV, as the violence occurs in the context of a significant
attachment relationship, influencing the women’s capacity for other healthy attachments
(including attachment to her baby). Research supports this notion: Huth-Bocks, Levendosky,
Theran, and Bogat (2004) found that women who experienced IPV during pregnancy had
significantly more negative prenatal representations of their infants and of themselves as mothers
than women who had not experienced violence during pregnancy. In addition, prenatal
representations predicted attachment relationships 1 year postpartum among this sample (HuthBocks, Levendosky, Bogat, & von Eye, 2004). Research has also demonstrated that these

3

internal representations during pregnancy predict maternal parenting behaviors, such that
negative representations are associated with more controlling and hostile behaviors towards the
infant among abused women (Dayton, Levendosky, Davidson, & Bogat, 2010).
Finally, developmental psychopathology theory also informs this research. This theory
proposes that children’s behavior is influenced by multiple determinants at the child, family and
societal levels, rather than being the result of a single precipitating factor (Finkelhor & KendallTackett, 1997). The basic principles of multifinality and equifinality (Cicchetti & Rogosch,
1996) suggest that a specific vulnerability may result in a number of different psychiatric
problems or resilient outcomes, while a specific psychiatric disorder may be caused by a variety
of different etiological pathways. Identification of specific psychiatric vulnerabilities at the
genetic, epigenetic, neurobiological, familial and social levels, as well as the mechanisms
through which these vulnerabilities evolve into specific psychiatric symptoms, is a major focus
of the field (Beauchaine, Neuhaus, Brenner, & Gatzke-Kopp, 2008).
The aim of this study is to evaluate the role of prenatal exposure to IPV as an early risk
factor for depressive problems during school age. In addition, abnormalities in one of the
physiological systems that regulate the response to stressors (Hypothalamic-Pituitary-Adrenal
axis- HPA), as indexed by basal and stress-induced levels of cortisol, are explored as a
mechanism that accompanies the expression of depressive symptoms in the context of early risk.
A model that integrates the early risk associated with exposure to IPV during the prenatal period
and a number of well established factors that convey vulnerability for childhood depression (i.e.,
family history of internalizing problems, maternal mental health, maternal early parenting, IPV
exposure during childhood, low income) was proposed and evaluated. In addition, abnormalities
in basal and stress-induced levels of cortisol, as well as empirically derived patterns of response

4

to a stressor were explored and associations with prenatal and lifetime risk and protective factors
were tested. Following the programming hypothesis, HPA axis function was examined as a
mediator for the negative effect of prenatal risk. Finally, gender and family history of depression
were examined as factors that may heighten or moderate the impact of early and lifetime
biological, familial, and environmental risk.
The Effects of Exposure to IPV and Increased Stress during Pregnancy
IPV Definition and Prevalence
Intimate partner violence (IPV) is defined by the Centers for Disease Control and
Prevention (2008) as physical, sexual, or psychological harm by a current or former partner or
spouse. Saltzman, Fanslow, McMahon, and Shelley (1999) describe four domains or types of
IPV, including physical violence, sexual violence, threats of physical and sexual violence, and
psychological violence. Physical violence refers to the intentional use of physical force with the
potential for causing harm, ranging from scratching and pushing to punching, burning, or using a
weapon. Sexual violence includes attempts at abusive sexual contact through the use of physical
force or coercion. Threats of physical or sexual violence include words, gestures, or weapons
that communicate threat of harm. Psychological violence involves harm to the victim via threats
or coercive tactics, including humiliating, controlling and isolating the victim (Saltzman et al.,
1999). For the purposes of this research, IPV will be defined as violent threats and physically
and sexually aggressive behaviors of a man towards his female romantic partner (e.g., pushing,
hitting, and threatening with a weapon).
IPV is a significant public health concern; national surveys and estimates based on
probability samples indicate that between 20% (Tjaden & Thoennes, 2000) and 34% (Frieze,
Knoble, Washburn, & Zomnir, 1980) of women experience physical abuse from a romantic

5

partner during their lifetime. Moreover, more than half of women experiencing IPV live with
children below age 12 (Fantuzzo, Boruch, Beriama, Atkins, & Marcus, 1997) and more than 10
million children in the U.S. are exposed to IPV (i.e., see, hear, are directly involved in, or
experience the aftermath of physical and sexual violence to their caregivers; Edleson, 1999).
Importantly, IPV during pregnancy appears to be highly prevalent with estimates that range from
1% to 20% when all types of abuse are included (i.e., physical, emotional, and sexual;
Gazmararian et al., 1996). Large variability between prevalence estimates may be due to
researchers using different definitions of abuse or different data collection methods.
Consequences of IPV Exposure for Women and Children
It is widely recognized that IPV results in a host of physical and psychological problems
for the female victims (Golding, 1999; Pico-Alfonso et al., 2006) and their children (Kitzman,
Gaylord, Holt, & Kenny, 2003). Women who experience IPV report higher levels of
psychopathology and distress and are more likely to display depression, posttraumatic stress
disorder (PTSD), anxiety disorders, and alcohol abuse (Dansky, Byrne, & Brady, 1999;
DeJonghe, Bogat, Levendosky, & von Eye, 2008; Laffaye, Kennedy, & Stein, 2003; Mourad,
Levendosky, Bogat, & von Eye, 2008; Tolman & Rosen, 2001). The amount of IPV experienced
and the victim’s perceptions of the abuse predict the degree of impairment she experiences
(Bogat, Levendosky, Theran, von Eye, & Davidson, 2003; Golding, 1999; Martinez-Torteya,
Bogat, Levendosky, von Eye & Davidson, 2009; Vogel & Marshall, 2001). Exposure to IPV
during pregnancy has been less well studied, but findings suggest increased risk for
psychological and physical problems for the pregnant woman, including injuries (Taggart &
Mattson, 1996), depression and PTSD (Varma, Chandra, Thomas, & Carey, 2007; Zareen,
Majid, Naqvi, Saboohi, & Fatima, 2009).

6

In addition to increased mental health problems, neuroendocrine dysregulation (as
indexed by levels of salivary or plasma cortisol) is also common among IPV victims and
suggests deficits within the stress-response systems. Lower levels of morning cortisol (Griffin,
Resick, & Yehuda, 2005; Seedat, Stein, Kennedy, & Hauger, 2003), higher levels of evening
cortisol (Pico-Alfonso, Garcia-Linares, Celda-Navarro, Herbert, & Martinez, 2004), and
increased daily cortisol output (Inslicht et al., 2006) have been reported among women exposed
to IPV. The resulting flattened daily cortisol pattern is different from the expected circadian
profile of gradual decrease from morning to evening, which may represent chronically high
levels of hormone output that are not effectively adapting to environmental changes (e.g., the
natural stressor of waking up). In addition, IPV victims display inefficient termination of the
stress response (i.e., slower return to baseline levels after stress; Griffin et al., 2005), which
results in longer brain exposure to high levels of cortisol. During pregnancy, IPV has been
associated with higher levels of afternoon resting salivary cortisol (Valladares, Pena, Ellsberg,
Persson, & Hogberg, 2009), suggesting abnormal response to stressors. Increased cortisol levels
and prolonged response are typically associated with depressive symptoms (Burke, Davis, Otte,
& Mohr, 2005); however, even when women’s depression levels are statistically controlled, the
relationship between IPV and neuroendocrine dysregulation is maintained, suggesting a direct
association between exposure to IPV during pregnancy and the victim’s physiological stress
response. Maternal biological and psychological functioning shape the environment that young
children are exposed to, contributing to the well-known detrimental impact of IPV exposure on
children.
Exposure to IPV negatively influences children’s psychological and neuroendocrine
development (Edleson, 1999; Wolfe, Crooks, Lee, McInthyre-Smith, & Jaffe, 2003). Increased

7

risk for internalizing (i.e., anxiety, depression, and trauma symptoms) and externalizing (i.e.,
aggression, defiance, inattention) problems during infancy and childhood (Bogat, DeJonghe,
Levendosky, Davidson, & von Eye, 2006; Grych, Jouriles, Swank, McDonald, & Norwood,
2000; Jarvis, Gordon, & Novaco, 2005; Martinez-Torteya, Bogat, von Eye, & Levendosky,
2009; Sternberg, Baradaran, Abbott, Lamb, & Guterman, 2006) have been reported, with
medium effect sizes found in meta-analyses (Evans, Davies, & DiLillo, 2008; Wolfe et al.,
2003). Exposure to IPV during childhood is also associated with HPA axis dysregulation;
Saltzman, Holden, and Holahan (2005) reported that school-age children exposed to IPV display
higher levels of resting salivary cortisol, as compared to non-exposed children. Children’s
adaptation to family violence is not only determined by the nature of the violent events (e.g.,
frequency and severity), but also by the individual and environmental resources available to offer
protection and support (Finkelhor & Kendall-Tackett, 1997; Martinez-Torteya et al., 2009).
Specifically, in the context of internalizing problems, children’s perceptions of threat and
negative affect in response to marital conflict (not specifically IPV) are predictive of increased
symptoms (Rhoades, 2008). Davies, Sturge-Apple, Cicchetti, and Cummings (2008) have
suggested that elevated levels of cortisol in response to stress are a marker for increased distress
when children are exposed to interparental conflict, suggesting that IPV may result in depressive
symptoms via the effects of heightened physiological and affective reactivity to adversity.
Although studies demonstrate that exposure to IPV results in deleterious outcomes as
early as infancy (Bogat et al., 2006), little research has examined the association between fetal
exposure to IPV and later offspring development. There is consistent evidence that prenatal IPV
results in a number of fetal insults (Saltzman, 1990), increasing risk for perinatal death, pre-term
delivery, and low birth weight (Coker, Sanderson, & Dong, 2004; Huth-Bocks, Levendosky, &

8

Bogat, 2002). The consequences of exposure to IPV during pregnancy extend after the pre- and
perinatal periods. For example, IPV during pregnancy is associated with more difficult infant
temperament (Quinlivan & Evans, 2005), as well as increased internalizing and externalizing
problems during infancy (Levendosky, Leahy, Bogat, Davidson, & von Eye, 2006; MartinezTorteya, Field, Bogat, Levendosky, Davidson, & von Eye, 2009). However, these findings are
solely based on maternal reports of IPV and children’s outcomes, and using multiple methods or
reporters may increase the external validity of results. In addition, studies that evaluate the longterm biopsychosocial impact of exposure to prenatal IPV are lacking. Research examining
maternal stress during pregnancy illustrates the mechanisms that may lead to psychological
problems via the physiological systems responsible for the stress response, over and above
exposure to environmental adversity after birth.
Prenatal Stress and Offspring Outcomes
A number of studies have explored the consequences of exposure to different types of
stress during pregnancy, including traumatic stress, chronic stress, and maternal distress.
Findings are reviewed in the following sections.
Traumatic Stress
Research exploring the impact of traumatic stress on pregnant women and their offspring
is sparse. Landrigan et al. (2008) reported that pregnant women exposed to the World Trade
Center attacks on 9/11/2001 had higher rates of intrauterine growth restriction, more infants with
low birth weight, and shorter gestation than unexposed mothers. Similarly, Xiong et al. (2008)
reported that pregnant women who endorsed more disaster-related experiences during hurricane
Katrina (e.g., walking through floodwaters, having a loved one die) had more frequent preterm
births and more low birth weight offspring compared to women with few or no disaster-related

9

experiences. Interestingly, these differences were not dependent on women’s concurrent mental
health symptoms, including PTSD or depression. Prenatal exposure to traumatic stress can
adversely impact the development of the offspring during early childhood; Laplante et al. (2004)
reported that exposure of pregnant women to a natural disaster (Quebec ice-storm) predicted
worse intellectual and language skills of offspring at age 2. However, research exploring the
psychological outcomes during childhood after exposure to traumatic stress in utero is still
needed. Only one study to date has examined the impact of traumatic stress during pregnancy on
offspring HPA axis regulation; Huizink et al. (2008) reported increased cortisol levels among
adolescents exposed to a man-made disaster in utero, suggesting HPA axis hyperactivity. Taken
together, findings indicate that traumatic stressors during pregnancy are associated with
important developmental and neurobiological deficits.
Chronic Stressors: Stressful Life Events, Maternal Perceived Distress, Depression, and Anxiety
Chronic stress during pregnancy, assessed via exposure to stressful events or maternal
stress-induced psychological symptoms, predicts numerous psychological difficulties early in
life. Stressful life events and maternal subjective report of perceived stress during pregnancy
predict infant temperamental difficulties (Bergman, Sarkar, O'Connor, Modi, & Glover, 2007;
Mohler, Parzer, Brunner, Wiebel, & Resch, 2006), while higher maternal distress during
pregnancy (i.e., more depression and/or anxiety) predicts multiple early deficits, such as attention
regulation problems (Austin, Hadzi-Pavlovic, Leader, Saint, & Parker, 2005; Huizink, de
Medina, Mulder, Visser, & Buitelaar, 2002), increased behavioral reactivity to novelty
(Brouwers, van Baar, & Pop, 2001; Davis et al., 2007), and increased negative affect (Huot,
Brennan, Stowe, Plotsky, & Walker, 2004). The effects of early behavioral and emotional

10

dysregulation are maintained during toddlerhood and associated with increased externalizing
problems (Gutteling et al., 2005).
The effects of stress during pregnancy are also apparent in the long-term. Prospective
reports of maternal pregnancy distress (i.e., depression and anxiety symptoms) predicted
negative emotionality and inhibition at age 5 (Martin, Noyes, Wisenbacker, & Huttunen, 1999),
emotional and conduct problems at age 4 (O'Connor et al., 2002) and age 7 (O’Connor et al.,
2005), as well as anxiety at age 8 (van den Bergh & Marcoen, 2004). In their prospective
longitudinal study, van den Bergh, van Calster, Smits, van Huffel, and Lagae (2008) reported an
association between maternal prenatal anxiety and offspring depressive symptoms during
adolescence. Studies using retrospective report have also found associations during adolescence;
for example, Allen, Lewinsohn, and Seeley, (1998), reported that a Major Depressive or
Dysthymic Disorder diagnosis before age 16 was associated with poor maternal emotional health
during pregnancy.
Prenatal stress is also associated with HPA axis abnormalities during infancy and
childhood, as measured via basal and stress-induced cortisol levels (for review see Glover,
O’Connor, & O’Donnell, 2010). Tollenaar, Beijers, Jansen, Riksen-Walraven, & de Weerth
(2011) found that pregnancy-specific anxiety predicted a dysregulated response to stressors
during infancy. However, this response depended on the age of evaluation and the stressinduction task used, with increased cortisol response after a bathing task with 5-week-old infants
and a blunted cortisol response after a vaccination task at 5 weeks and a separation task at 12
months. In contrast, most studies have replicated cortisol hypersecretion in the context of
prenatal stress, including higher baseline cortisol levels during infancy (Brennan et al., 2008),
heightened cortisol response to a ―still face‖ stress-induction task during infancy (Grant et al.,

11

2009), higher cortisol levels in reaction to the first day of school at age 5 (Gutteling, De Weerth,
& Buitelaar, 2005), and higher awakening cortisol levels at age 10 (i.e., natural stressor;
O’Connor et al., 2005). Prenatal stress continues to impact the offspring’s HPA axis functioning
in the long-term. Van den Bergh et al. (2008) reported an association between maternal anxiety
during pregnancy and adolescents’ afternoon cortisol levels, while Entringer, Kumsta,
Hellhammer, Wadhwa, and Wust (2009) showed that healthy young adults whose mothers
experienced stressful life events during pregnancy had a larger increase in stress-induced plasma
cortisol levels, as compared to controls.
Taken together, findings indicate that stressful life events, perceived stress, and stressinduced distress during pregnancy increase temperamental risk and behavioral/emotional
problems during infancy, childhood, and adolescence as well as HPA axis dysregulation. Many
of these findings were significant over and above the effects of demographic, obstetric, antenatal,
and postnatal factors, emphasizing the unique effect of prenatal stress. Results have been
replicated using different methods: some studies use cross-sectional designs, which allow
researchers to recruit more targeted populations (e.g., children experiencing a specific
vulnerability), although findings may be affected by recollection biases. Other studies used
prospective longitudinal designs, which allow for a potentially more accurate assessment of
stressors during pregnancy, but tend to follow participants for a relatively short period of time
(infancy or early childhood) and recruit large community samples with low rates of exposure to
traumatic stressors or psychiatric problems.
Studies have also used different conceptualizations for prenatal stress. Importantly,
Bergman et al. (2007) found that marital conflict during pregnancy (i.e., serious arguments with
partner, separated/divorced, partner was emotionally cruel) was the prenatal life event most

12

highly correlated with temperamental difficulties during infancy, whereas events such as serious
accident, illness, financial problems, and daily hassles did not predict infant outcomes. These
results suggest that some stressors are more likely to be associated with deleterious outcomes
than others and provide support for the relevance of partner conflict during pregnancy. Trauma
Theory suggests that IPV may be more deleterious than other stressful experiences, because it
occurs in the context of an intimate relationship, increasing the victim’s isolation, guilt, shame,
and negative self-cognitions (Calvete, Estevez, & Corral, 2007; Murphy & Hoover, 1999; Street,
Gibson, & Holohan, 2005; Walker, 1984). In addition, the chronic pattern of victimization
experienced by victims is likely to be associated with lasting biological neuroregulatory deficits
for women (Cloitre et al., 2009). Lastly, IPV during pregnancy influences the woman’s
relationship with the developing fetus through the influence of violence in maternal
representations of herself and her baby (Huth-Bocks, Levendosky, Theran, et al., 2004) which
will shape the mother-child attachment relationship (Huth-Bocks, Levendosky, Bogat, et al.,
2004) and maternal parenting behaviors (Dayton et al., 2010). Thus, exposure to IPV in utero is
hypothesized to increase risk for emotional and behavioral problems during childhood.
Most studies to date have focused on prenatal stress as a risk factor for general
temperamental difficulties or maladaptation, rather than delineating its relationship with specific
psychiatric disorders. Unfortunately, this perspective provides little information about
prevention efforts or mechanisms of risk for individual children. In contrast, a disorder-specific
or person-oriented perspective proposes that there may be specific mechanisms that result in
psychiatric symptoms for a subgroup of children. Aggregating all subjects in a single group may
misrepresent relationships between variables in significant ways, while identification of
empirically derived homogeneous subgroups may help clarify specific within-group patterns of

13

association (von Eye & Bergman, 2003). A disorder-specific model was proposed by van den
Bergh et al. (2008) who assessed the effect of prenatal maternal anxiety on adolescent depressive
symptoms. This model is consistent with the early behavioral characteristics reported by
prenatal stress research, including difficult temperament, high levels of negative affect, and high
levels of internalizing symptoms. In addition, these authors proposed mediation via HPA axis
dysregulation, which is consistent with the biological correlates found among both depressed
children and those exposed to stress in utero. The following sections will address the role of
offspring stress response and a specific pathway from pregnancy IPV to HPA axis abnormalities
and depressive problems during childhood.
Prenatal Stress Exposure and Offspring Stress Response
The Stress Response
Psychosocial stress involves 4 main elements: the stimulus (environmental or internal);
subjective appraisals of the stimulus; coping/adaptation responses; and consequences (Kaplan,
1996, pg. 7). The stimuli may vary in terms of their number, frequency, intensity, and duration,
and these characteristics will influence the individual’s appraisals and response. Subjective
appraisals or cognitive interpretations of a potential stressor are directly associated with the
individual’s emotional distress (Lazarus & Folkman, 1984). Primary appraisals refer to the
evaluation of the significance, relevance, or impact of a stimulus, while secondary appraisals
refer to an evaluation of the individual’s resources or ability to manage effectively a potentially
stressful situation, or coping resources (Lazarus & Folkman, 1984). Environmental stressors
elicit a physiological and psychological stress reaction only when they are interpreted as salient
to the individual’s well being and appraised as threatening, harmful, challenging, or surpassing
the individual’s resources. The appraisal of stressors initiates responses to reduce emotional

14

distress, but unsuccessful attempts can increase feelings of fatigue, hopelessness, and depressed
affect (Kaplan, 1996, pg. 10).
The stress response consists of a set of adaptive physiological and behavioral changes,
such as increased heart rate and blood pressure, inhibition of vegetative functions, and activation
of fight/flight responses that are designed to prepare the organism to face an environmental
challenge or threat (Boyce & Ellis, 2005; Meyer, Chrousos, & Gold, 2001). The physiological
stress response system is constituted by two interdependent systems: the Hypothalamic-PituitaryAdrenal (HPA) axis and the Sympathetic-Adrenomedullary (SA) system (Boyce & Ellis, 2005;
Gunnar & Quevedo, 2007). These systems are interrelated and communicate with the amygdala,
anterior cingulate cortex, medial prefrontal cortex, and the dopaminergic system, which are
implicated in regulation of fear, anxiety, emotional memory, reward and pleasure, as well as
behavioral and affective flexibility (Meyer et al., 2001).
The HPA axis consists of the hypothalamus, the anterior pituitary, and the adrenal cortex,
which secrete corticotropine releasing hormone (CRH), arginine vasopressin (AVP),
adrenocorticotropic hormone (ACTH), B-endorphin (B-E), and glucocorticoid hormones (i.e.,
cortisol in humans). The HPA axis initiates a stress response after receiving information from
the amygdala, hippocampus, and the autonomic nervous system by increasing the release of
CRH and AVP from the hypothalamic paraventricular nuclei into the pituitary (Gunnar &
Quevedo, 2007). CRH stimulates ACTH and B-E release from the pituitary gland into the
circulatory system, and onto the adrenal cortex, where secretion of cortisol is stimulated.
Cortisol is released into the body and the brain, inducing changes in blood pressure, glucose
metabolism, growth, and reproduction (Meyer et al., 2001), as well as cognition, memory, and
emotion (Cicchetti & Rogosch, 2001).

15

This stress-induced increase in blood cortisol levels is down-regulated through an
inhibitory negative-feedback loop. Cortisol binds to the hippocampal mineralocorticoid (MR) or
Type 1 receptors and glucocorticoid (GR) or Type 2 receptors; increased binding exerts an
inhibitory effect in production and release of CRH and ACTH, which results in a return to
baseline cortisol levels and termination of the HPA stress response (Gunnar & Quevedo, 2007).
An efficient HPA response to stressors is characterized by a rapid increase in release of CRH,
ACTH, and cortisol after stressful stimuli, and a rapid return to the baseline state of homeostasis
once the stressor is terminated, through the inhibitory effects of hippocampal receptors (Talge et
al., 2007; Herbert et al., 2006). Effective termination of CRH and ACTH secretion limits tissue
exposure to cortisol, minimizing its deleterious catabolic, lipogenic, antireproductive, and
immunosuppressive effects (Charmandari, Tsigos, & Chrousos, 2005). The HPA axis
functioning has a typical circadian rhythm of cortisol secretion, with highest levels during the
morning that gradually decrease throughout the day (Herbert et al., 2006).
The Programming Role of Cortisol
The development and regulation of the HPA axis is influenced by the individual’s genetic
make-up and environmental factors (Ellis, Jackson, & Boyce, 2006). The ―programming
hypothesis‖ proposes that fetal nervous system development is shaped by the uterine
environment, in order to match the prenatal environmental demands and increase the chance of
successful coping in the postnatal environment (Boyce & Ellis, 2005). In this manner, the
prenatal period, during which the fetus undergoes rapid brain development, can set the
foundation for the regulation of the stress response later on (Maccari et al., 2003; Huizink et al.,
2004; Talge et al., 2007).

16

Lupien, McEwen, Gunnar, and Heim (2009) propose that the impact of increased stress
during pregnancy is mediated via fetal exposure to high levels of cortisol in utero and
consequent dysregulation of the offspring’s HPA axis activity. Barbazanges, Piazza, LeMoal,
and Maccari (1996) have shown that the effects of prenatal stress on offspring’s depressive-like
behaviors and heightened HPA axis response to stressors are dependent on increased
glucocorticoid secretion from the mothers, as the behavioral and neuroendocrine effects of
prenatal stress are not observed among offspring of adrenalectomized rats, who cannot produce
higher levels of glucocorticoids after prenatal stressors. In addition, repeated administration of
glucocorticoids to undisturbed pregnant females results in HPA axis dysregulation of the
offspring among both rodents (Welberg, Seckl, & Holmes, 2001) and rhesus monkeys (Uno et
al., 1994). This research clearly demonstrates a direct relationship between exposure to
increased levels of cortisol in utero and behavioral or neuroendocrine deficits after birth.
Animal studies provide strong evidence for the ―programming‖ role of increased
glucocorticoid exposure in utero. However, important considerations should be noted when
extrapolating the results of animal studies to humans. The timing of physiological development
is different in animals and humans. Among primates, maximal brain growth and neuroendocrine
maturation occurs during gestation, while much of the rodent’s brain and neuroendocrine
development occurs after birth. For example, rat embryonic days 11-21 are comparable to
human embryonic weeks 4-16, while the rat neurodevelopment at postnatal day 7 to 13 is
equivalent to that of the human brain at birth (Clancy, Finlay, Darlington, & Anand, 2007). With
these caveats, animal studies can provide useful insights into specific mechanisms of risk
transmission, as laboratory manipulations can help isolate specific risk processes from
confounding factors that are commonly present in human studies.

17

Although glucocorticoid manipulations are not possible among human populations,
correlational research provides support for the link between maternal HPA axis functioning
during pregnancy and offspring behavioral outcomes. High baseline and awakening levels of
maternal cortisol during late pregnancy have been associated with heightened reactivity, more
irritability, more negative affect, and difficult temperament during infancy (Davis et al., 2007;
De Weerth, van Hees, & Buitelaar, 2003). The effects of high levels of maternal cortisol during
pregnancy seem to be maintained during early childhood. Wadhwa, Sandman, and Garite (2001)
reported an association between high maternal baseline cortisol levels during late pregnancy and
infant difficult temperament at 3 years of age.
Two potential mechanisms of risk transmission have been proposed. One is maternal
stress-induced dysregulation of the HPA axis during pregnancy, resulting in higher levels of
maternal cortisol output. Consistent with this hypothesis, elevated cortisol levels have been
found in women exhibiting psychological distress during pregnancy (Diego et al., 2006; Field et
al., 2004; Field, Hernandez-Reif, Diego, Figueiredo, & Schanberg 2006). Importantly, HPA axis
dysregulation in the context of traumatic stress during pregnancy also has been demonstrated
among IPV victims (Valladares et al., 2009). Correlations between maternal levels of cortisol
during pregnancy and fetal or newborn cortisol levels also provide support for the role of
maternal glucocorticoid levels as a ―programming‖ mechanism (Field et al., 2004; Gitau,
Cameron, Fisk, & Glover, 1998). However, not all studies have found evidence for the
relationship between maternal cortisol levels during pregnancy and infant temperament:
Rothenberger, Resch, Dospod, and Moehler (2011) found that maternal perceived levels of stress
were associated with infant affective reactivity to stressors, but cortisol levels during each
trimester were not associated with infant outcomes.

18

The second proposed mechanism consists of enzyme deficits in the maternal placenta,
which leads to increased fetal exposure to cortisol in utero, regardless of increases in maternal
overall cortisol output during pregnancy. Glover, Bergman, Sarkar, and O'Connor (2009) have
proposed that prenatal stress is associated with reduced activity of the enzyme 11-betahydroxysteroid dehydrogenase 2 (11b-HSD2), which metabolizes cortisol to its inactive form
(cortisone) once it reaches the placenta, in order to regulate the transmission of glucocorticoids
from mother to fetus. There is some evidence for their hypothesis; Glover et al. (2009) found
that the correlation between maternal plasma cortisol levels and cortisol levels in the amniotic
fluid is much greater for those mothers who report higher levels of trait anxiety during their
pregnancies, suggesting increased passing of maternal cortisol through the placenta in the
context of high levels of stress during pregnancy. Although there is no direct evidence for this
proposed pathway among humans, two animal studies have shown that the 11b-HSD2 enzyme is
downregulated in pregnant rats that undergo stress during pregnancy (Mairesse et al., 2007;
Welberg, Thrivikraman, & Plotsky, 2005).
In summary, there is evidence that maternal HPA axis functioning during pregnancy
exerts an important influence on offspring behavioral and physiological responses to stress
during infancy and perhaps childhood, but studies have not followed subjects into middle
childhood or adolescence, when many psychiatric symptoms become more prevalent. Animal
studies provide convincing evidence for the causal role of glucocorticoids in offspring increased
reactivity to stress during childhood and adulthood. Two mechanisms involving increased in
utero exposure to cortisol have been proposed in the context of prenatal stress and offspring
maladaptation. Importantly, early offspring dysregulated response to stressors may be a marker

19

for later internalizing or depressive problems (Essex, Klei, Cho, & Kalin, 2002; Smider et al.,
2002); this association will be reviewed in the following section.
Child HPA Axis Dysregulation and Depressive Symptoms
Definition and Epidemiology of Childhood Depression
Depressive problems refer to a number of symptoms that accompany sad mood and can
constitute a syndrome (dimensional approach) or be classified as a diagnosis (categorical
approach). The internalizing or anxious/depressed cluster (Achenbach, 1991) includes
symptoms such as ―lonely,‖ ―cries a lot,‖ ―perfectionistic,‖ ―feels unloved,‖ ―nervous,‖ ―selfconscious,‖ and ―worries.‖ On the other hand, Major Depressive Disorder (MDD), as defined in
the Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition (DSM-IV-TR;
American Psychological Association-APA, 2000), includes sad, depressed, or irritable mood,
anhedonia (i.e., inability to experience pleasure) or diminished interest in most activities, poor
appetite or overeating, diminished or excessive sleep, psychomotor agitation or retardation,
feelings of worthlessness or excessive guilt, problems with concentration and decision making,
and recurrent thoughts of death. A diagnosis of MDD requires experiencing at least five
symptoms (including sad/irritable mood and/or anhedonia) nearly every day during a 2-week
period.
Rates of MDD ranging from 2% to 6% among children and 4% to 16% for adolescents
have been reported in large epidemiological studies (Birmaher, Ryan, et al., 1996). Moreover,
many more children experience subsyndromal or moderate depressive symptoms, which are
associated with increased risk for developing MDD during later childhood, adolescence and
adulthood (Gotlib, Lewinsohn, & Seeley, 1995). Depression is relatively rare among young
children and preschoolers (less than 1%), but becomes more frequent by school-age, with age of

20

onset typically around 11 years old (Kovacs, Feinberg, Crouse-Novak, Paulauskas, &
Finkelstein, 1984). Developmental differences in symptoms have been reported: young
depressed children are less likely to report feelings of sadness and hopelessness (Carlson &
Kashani, 1988), hypersomnia, weight loss or gain, anhedonia, melancholic symptoms, and
concentration problems (Kovacs, 1996; Sorensen, Nissen, Mors, & Thomsen, 2005; Weiss &
Garber, 2003), as compared to adults. In contrast, children show more thoughts of
worthlessness, somatic complaints, and psychomotor agitation (Sorensen, Nissen, Mors, &
Thomsen, 2005; Ryan et al., 1987).
HPA Axis Dysregulation and Childhood Depression
HPA axis abnormalities have been proposed as a core mechanism of dysfunction for the
development of depressive problems. As reviewed previously, the HPA axis is one of the main
components of the body’s response to environmental threats to the organism’s state of
homeostasis. Thus, dysregulation of this system may reflect increased sensitivity to stressors and
depressive symptoms can emerge as alostatic load; that is, the associated cost of attempting to
maintain homeostasis and associated chronic activation of the physiological stress response
(McEwen, 2000). Goodyer (2008) has proposed that abnormal HPA axis functioning is
associated with atypical early neurogenesis and acquired neuroendangerment. Abnormally high
or low levels of cortisol are linked with dysregulation of the amygdala and associated ventral
prefrontal areas, which are essential to threat signal detection. This may result in a greater and
more rapid activation of emotion to incoming stimuli and intense negative reactions to potential
stressors. In addition, adversity can result in cortisol hypersecretion, exposing the hippocampus
to excessive cortisol, and evoking a decline in communication with associated structures (i.e.,
acquired neuroendangerment). Inefficient communication with the nucleus accumbens and

21

ventral tegmental area, which regulate pleasure and motivation, may be associated with the low
positive emotionality that characterizes depressive problems (Caspi, Moffitt, Newman, & Silva,
1996).
Depressed adults display a well-established pattern of heightened HPA axis activity,
reflected by abnormal basal and stress-challenged cortisol levels (Birmaher, Dahl, et al., 1996;
Burke et al., 2005). Research examining HPA axis functioning among depressed children and
adolescents also provides evidence for abnormal responses. In a recent meta-analysis, LopezDuran, Kovaks, and George (2009) found that depressed youth (ages 9 to 15) were characterized
by an overactive response to stress and higher baseline cortisol levels. Evening basal cortisol
levels have been found to be higher than those of non-depressed children and adolescents (ages 8
to 16; Goodyer et al., 1996), especially for those with co-morbid dysthymia (Herbert et al., 1996)
and chronic depression (i.e., over a 1 year period; Goodyer, Park, & Herbert, 2001). In addition,
Luby et al. (2003) provided evidence of outcome specificity, reporting higher cortisol secretion
post-stressor among depressed preschoolers, as compared to children diagnosed with other
psychiatric disorders. Importantly, studies with community (non-clinical) samples also suggest
an early association between elevated cortisol levels and internalizing symptoms, suggesting that
HPA axis hyperactivity is a precursor and not a consequence of depressive symptoms: high
levels of afternoon resting cortisol predict high levels of mother-rated and teacher-rated
internalizing symptoms among preschoolers (Essex et al., 2002; Smider et al., 2002). Supporting
the role of elevated cortisol as a marker for later depressive problems, children at high-risk for
depression due to familial predisposition also display a profile of HPA axis hyperactivity,
characterized by high baseline levels of cortisol output (Ashman, Dawson, Panagiotides,
Yamada, & Wilkinson, 2006; Young et al., 2006).

22

The pattern of HPA axis dysregulation that is associated with depressive symptoms in
adults is not consistent across all studies with children and youth. For example, Birmaher, Dahl,
et al. (1996) did not find differences in overall diurnal secretion levels among 6 to 13-year-old
children, while DeBellis et al. (1996) found decreased cortisol secretion when measured during
the first 4 hours after sleep onset. Hankin, Badanes, Abela, and Watamura (2010) have
suggested that HPA axis response to stressors among depressed children and adolescents can
vary as a function of their developmental stage: in their study, depressed toddlers had a blunted
stress-induced cortisol response, while depressed teenagers showed an elevated peak, as
compared to non-depressed peers. Importantly, results are also likely influenced by the existence
of other co-morbid disorders or traumatic experiences. For example, DeBellis et al. (1996)
included a large number of sexually abused children in their study (who potentially experienced
PTSD symptoms), and these children had the lowest levels of cortisol. Finally, extant research
has not examined the prolonged post-stressor cortisol response (i.e., slower return to baseline
levels) characteristic of adults (Burke et al., 2005) among children, which can result in chronic
brain exposure to cortisol and amplification of its negative impact on brain structures.
In summary, research provides evidence for HPA axis dysregulation among depressed
children, non-depressed children with high levels of internalizing problems, and non-depressed
children with familial predisposition for depression. The specific pattern of dysregulation is not
consistent across all studies, although a recent meta-analysis suggests high cortisol baseline
levels and overactive response to stressors (Lopez-Duran et al., 2009). Given the heterogeneity
of clinical presentation among depressed children, characterizing all children within one generic
profile of HPA axis dysregulation may not be accurate. Person-oriented methods (von Eye &

23

Bergman, 2003) can aid identification of more homogeneous profiles of neuroendocrine risk
associated with depression and specific risk/protective influences.
Individual, Familial, and Environmental Risk and Protection for Depression
Risk and Protection: Maternal Mental Health, Early Parenting, SES, and Exposure to IPV
during Childhood
The etiology and clinical manifestation of depression is heterogeneous. Multiple
characteristics at the individual, family, and societal levels have been identified as risk factors for
the development of depressive symptoms during childhood and a number of models that
emphasize one or more of these domains have been proposed, including family models, life
stress models, and biological models (Hammen & Rudolph, 2003). Most contemporary models
propose contributions from different systems, including biological, psychological, and social
levels, and the relative influence of each domain varies across individuals and across different
stages of development (Cicchetti & Toth, 1998). In this section, the negative or protective
impact of early maternal parenting, maternal mental health, low income, and intimate partner
violence will be reviewed.
Maternal Mental Health and Early Parenting
Family models of depression have focused on the effects of early maternal parenting on
the mother-child relationship and on children’s development. Maternal mental health has been
associated with internalizing symptoms among children of female victims of abuse or IPV
(Kaslow et al., 2004; Morrel, Dubowitz, Kerr, & Black, 2003). Research consistently identifies a
strong relationship between maternal depression and anxiety and offspring internalizing
problems (Connell & Goodman, 2002), and having a parent with MDD is one of the strongest
predictors for childhood depression (Beardslee, Versage, & Gladstone, 1998). Goodman and

24

Gotlib (1999) proposed four mechanisms of risk transmission, including (a) genetic, (b) offspring
dysfunctional neuroregulatory mechanisms, (c) exposure to the mother’s maladaptive affect,
behavior, and cognitions, and (d) additional stressors associated with maternal mental health
problems.
There is consistent evidence for the familial transmission of childhood depression, which
will be discussed in the following section. In terms of neuroregulatory deficits, maternal
depression and anxiety symptoms during pregnancy, infancy, and childhood are associated with
abnormal HPA axis regulation among offspring, suggesting an impaired physiological response
to stressors (Dougherty, Klein, Olino, Dyson, & Rose, 2009; Feldman et al., 2009). Maternal
depression may also influence children’s adaptation by providing a model of maladaptive coping
strategies, negative emotionality and withdrawn behaviors. For example, Kliewer et al. (2004)
found that, among children exposed to community violence, a mother’s inability to regulate her
sadness is a significant predictor of her child’s internalizing problems. Lastly, maternal
depression has a strong influence on maternal parenting, increasing negative maternal behaviors
and disengagement, and decreasing positive parenting (Lovejoy, Graczyk, O’Hare, & Neuman,
2000). Importantly, both maternal depression and maternal behaviors are associated with
childhood outcomes (NICHD Early Child Care research Network, 1999), providing evidence that
maternal depression influences children’s behaviors through multiple pathways.
The timing of maternal mental health problems influences the mechanisms through which
it impacts children’s adaptation. As described previously, mental health during pregnancy is
most closely associated with neuroregulatory deficits, reflected by cortisol hypersecretion among
children born to prenatally depressed and anxious mothers (Brennan et al., 2008; Grant et al.,
2009; Gutteling et al., 2005; O’Connor et al., 2005). On the other hand, mothers who are only

25

depressed during the postnatal period are likely to shape their children’s adaptation through
modeling maladaptive affect regulation strategies and ineffective parenting.
Maternal parenting predicts childhood depressive symptoms (McLeod, Wiesz, & Wood,
2007). Specifically, low levels of parental warmth and high levels of parental aversive behavior
are strongly related to children’s depression. One mechanism of risk transmission is based on
attachment theory. Bowlby (1982) proposed that infants who were unable to establish a secure
attachment with a trusted caregiver would construct maladaptive ―working models‖ or schemas
of relationships, developing increased risk for depressive problems. Importantly, a meta-analysis
demonstrated that maternal sensitivity during early childhood has a moderate effect on
attachment (De Wolff & van IJzendoor, 1997), and numerous studies support the link between
early attachment and later depressive symptoms (for a review, see Brumariu & Kerns, 2010).
Maternal involvement and warmth can also influence children’s neuroendocrine
functioning and sensitivity to stressors; Grant et al. (2009) found that depressed mothers with
lower levels of sensitivity had infants with increased salivary cortisol levels in response to
stressors, while Pendry and Adam (2007) reported abnormal diurnal cortisol rhythms among
young children of mother’s with low levels of warmth. These effects appear to be sustained in
the long-term: Murray, Halligan, Goodyer, and Herbert (2010) reported that maternal levels of
withdrawal during infancy were associated with higher cortisol secretion during adolescence.
In contrast, maternal warmth early in life can moderate the impact of early adversity
(Fish et al., 2004) as it promotes the development of basic abilities necessary for later adaptation,
including self-regulation (Jennings et al., 2008). Animal studies have consistently shown that
early maternal behavior has a long-term stable influence on offspring’s behavioral and endocrine
response to stressors (Fish et al., 2004). Specifically, early maternal parenting can buffer the

26

impact of early adversity, including prenatal stress. Studies with rodents exposed to stressful
manipulations in utero show that offspring endocrine and behavioral reactivity to stress can be
decreased via early postnatal handling (Bogoch, Biala, Linial, & Weinstock, 2007; Wakshlak &
Weinstock, 1990; Vallee et al., 1997) or high levels of maternal attention and stimulation after
adoption (Maccari et al., 1995). Among humans, Kaplan, Evans and Monk (2008) found that
observed high maternal sensitivity was associated with low levels of baseline salivary cortisol
among infants of women with anxiety or depression problems during pregnancy, which were not
different from cortisol levels of infants of healthy women, but were significantly lower than
those of infants of anxious/depressed women with low sensitivity.
Intimate Partner Violence
The life stress model highlights the importance of cumulative adversity in the etiology of
childhood depression, including poverty, family violence and high levels of stressful life events
(Cicchetti & Toth, 1998; Luby, Belden, & Spitznagel, 2006; Sternberg et al., 1993). This
perspective emphasizes the role of chronic stress as a vulnerability or trigger for depressive
problems during childhood, particularly interpersonal stress and loss (Eley & Stevenson, 2000).
In addition, this model also posits that individual stressors rarely occur in isolation, and
environmental adversity impacts the family and individual systems (Sameroff, 2000).
Socioeconomic status (SES) has been widely recognized as a risk factor for psychiatric
problems (Bradley & Corwyn, 2002; McLeod & Shanahan, 1996). Consistent with the life stress
model, the stressors associated with lower SES, such as economic strain, family conflict or IPV,
trauma, or discrimination, can influence the development of psychopathology (Wadsworth et al.,
2008). In addition, children living in poverty have less social support and experience less
adequate parenting (more authoritarian, less responsive; Evans, 2004). Parental mental illness

27

may also influence their ability to find and keep employment, resulting in family poverty; thus,
poor children may be more likely to face genetic and environmental vulnerabilities (South &
Krueger, 2011). Importantly, research shows that low SES is also associated with higher levels
of salivary cortisol during childhood (Lupien, King, Meaney, & McEwen, 2001).
IPV may be particularly deleterious to women and their children, as it often occurs in the
context of a pattern of chronic domination. Broad conceptualizations of IPV highlight the
elements of isolation, threats and degradation, and coercive control (Walker, 1984), such that
victims experience chronic fear, increased dependency on the abuser, and negative selfcognitions (Murphy & Hoover, 1999). For children, exposure to IPV may include unpredictable
acute traumatic incidents in the context of chronic interparental conflict, resulting in constant
fear and activation of the stress response. Consistent with the life stress model, IPV is associated
with additional adversity, including more life stressors, difficult child temperament, maternal
depression, and ineffective parenting (Eby, 2004; Graham-Bermann, Gruber, Girz, & Howell,
2009; Huang, Wang, & Warrener, 2010; Levendosky et al., 2006; Martinez-Torteya, Bogat, von
Eye, & Levendosky, 2009). Notably, children exposed to chronic IPV are less likely to have
additional individual and family strengths, such as positive temperament or maternal mental well
being, and show a pattern of early maladaptation (Martinez-Torteya, Bogat, von Eye, &
Levendosky, 2009)
Empirical evidence supports the link between IPV exposure and depressive problems
among children (Perks & Jameson, 1999; Sternberg et al., 2006). Grych et al. (2000) explored
different outcome patterns among children exposed to IPV. Their results showed a highinternalizing group, which was distinguished from a high-externalizing group by higher levels of
male-to-female IPV, more aggression from parents, and higher perceptions of threat and self-

28

blame. Jouriles, Spiller, Stephens, McDonald, and Swank (2000) also reported that appraisals of
threat were associated with child depression, but not with externalizing symptoms. These studies
suggest that increased sensitivity to marital conflict is distinctively associated with internalizing
symptoms; this pattern of hyper-sensitivity to conflict is consistent with the increased
physiological reactivity to stressors found among children who witness IPV and those
experiencing or at high-risk for depression (Luby et al., 2003; Saltzman et al., 2005).
Familial Risk and Gender as Moderators of Environmental Risk
Familial Risk
Biological models emphasize the role of genetic vulnerabilities and heritability. During
childhood, depressive symptoms appear to have a high familial component, with 35% to 70%
first-degree relatives and 10% to 25% second-degree relatives of depressed children reportedly
diagnosed with a mood disorder (Kovacs, Devlin, Pollock, Richards, & Mukerji, 1997). Twin
studies have addressed potential confounding factors, including the increased environmental
adversity that offspring of depressed mothers experience, and have found moderate to high
effects for genetic vulnerability (as compared to shared environmental or non-shared
environmental influences; Eaves et al., 1997; Kendler, Gardner, & Lichtenstein, 2008). In terms
of specific genetic markers, it has been demonstrated that the short allele of the serotonin
transporter gene (5-HTTLPR) increases vulnerability for depression (Kaufman et al., 2006)
through reduction in serotonin expression and uptake (Lesch et al., 1996). Current etiological
models of childhood depression include interactions between genetic and environmental factors
(Downey and Coyne, 1990; Eley et al., 2004; Rice, Harold, & Thapar, 2002). Specifically,
children with genetic predisposition for depressive disorders are more likely to develop

29

symptoms as a response to environmental stress or adversity (Kaufman et al., 2006; Rice,
Harold, Shelton, & Thapar, 2006).
Goodyer (2008) has proposed that the prenatal environment can have inhibiting or
promoting effects on the genes that regulate the HPA system, modifying offspring reactivity to
stress. In the context of prenatal stress, animal research suggests a significant interaction
between genetic risk and exposure to stress in utero. For example, in a study with prenatally
stressed rodents, the offspring only displayed an increased and prolonged glucocorticoid
response to stressors during adulthood if they had a biological predisposition for high sensitivity
to stress, but had a normal response to stressors when the genetic vulnerability was absent
(Clinton, Miller, Watson, & Akil, 2008). Similarly, Lucassen et al. (2009) reported that only
prenatally stressed rodents with biological predisposition to high stress sensitivity failed to
increase placental levels of the 11BHSD2 enzyme (which transforms glucocorticoids to its
inactive form in the placenta), resulting in increased fetal exposure to glucocorticoids. One
recent study provides evidence that the relationship between prenatal stress and offspring
temperament may be moderated by a genetic vulnerability among humans. Pluess et al. (2011)
reported an association between maternal anxiety during pregnancy and offspring negative
emotionality in early infancy only among infants carrying the 5-HTTLPR short allele, but no
associations for those homozygous for the long allele. These studies suggest that prenatal stress
may be a potential epigenetic process in the etiology of HPA axis dysregulation and depressive
problems during childhood.
Gender
Research has consistently documented gender differences in the prevalence of depression
during adolescence and adulthood (Costello, Egger, & Angold, 2005; Angold & Rutter, 1992)

30

but these differences do not appear to be present during childhood (Birmaher, Ryan, et al., 1996).
However, gender may impact children’s responses to specific risk factors. For example,
Jacobvitz, Hazen, Curran and Hitchens (2004) reported that boys responded to a pattern of
enmeshed parenting with increased ADHD symptoms, while girls with this family interaction
style showed higher levels of depressive symptoms. In a similar study, Garai et al. (2009) found
that girls’ internalizing symptoms were predicted by maternal levels of depression and low
parenting sensitivity, while these maternal characteristics were not associated with internalizing
symptoms for boys. Importantly, Sternberg et al. (2006) reported gender differences in
children’s outcomes in the context of exposure to IPV. Girls exposed to family violence had
higher levels of internalizing and externalizing symptoms, while IPV exposed boys were not
significantly different from controls. The mechanisms that explain these gender differences are
still unknown, but emotion regulation strategies have been proposed as a potential link; Silk,
Shaw, Skuban, Oland, and Kovacs (2006) reported that daughters of depressed mothers used
more passive emotion regulation strategies while boys were not different from controls, which
may explain some of their higher risk for psychopathology in the context of adversity.
Gender differences may also play an important role in the ―programming effect‖ of
prenatal IPV. De Bruijn, van Bakel, Wijnen, Pop, and van Baar (2009) examined stress-induced
responses after a mother-child interaction and a frustration task among toddlers and preschoolers.
Maternal emotional complaints during pregnancy were associated with HPA axis reactivity
among females only: Girls exposed to prenatal stress had higher stress-induced cortisol levels
than non-exposed girls, while there were no differences between exposed and non-exposed boys.
Notably, Van den Bergh et al. (2008) tested a mediation model for the effect of prenatal maternal
anxiety on adolescent depressive symptoms, as mediated via baseline cortisol levels, and found

31

that this model predicted depressive symptoms among girls only; stress in utero was associated
with a flattened diurnal profile of cortisol output among boys also, but neither prenatal anxiety or
cortisol levels were associated with depression for boys.
The Present Study
The present study proposes a model that integrates the early risk associated with
exposure to IPV during the prenatal period with a number of well established factors that convey
vulnerability for childhood depression (i.e., family history of internalizing problems, maternal
mental health, maternal early parenting, exposure to IPV during childhood), including the child’s
physiological response to stressors as a mediating mechanism. This research is guided by the
―fetal programming‖ theory, which posits that prenatal adversity results in structural and
functional neural changes that are associated with offspring neurodevelopmental deficits (e.g.,
Maccari et al., 2003), suggesting that pregnancy is a ―sensitive period‖ for later adaptation to
environmental stress due to the rapid fetal brain development. Secondly, the unique impact of
IPV is supported by complex trauma theory, which proposes that chronic traumatic stress results
in a number of lasting neurobiological deficits for the victim and thus hinders the developing
fetus when it occurs during pregnancy. In particular, IPV is associated with high levels of shame
and guilt due to its interpersonal and chronic nature (Calvete et al., 2007; Street et al., 2005) and
impacts maternal representations of the developing fetus, which translate into early attachment
and caregiving deficits (Dayton et al., 2010; Huth-Bocks, Levendosky, Bogat, & von Eye, 2004).
Finally, consistent with a developmental psychopathology framework, multiple influences at the
child, family and societal levels are included in the proposed model, and identification of the
specific mechanisms that can translate early risk into distinct psychological symptoms is sought.

32

Addressing the earliest manifestations of specific psychiatric risk can promote the development
of the basic competencies that will enhance later adaptation.
The present study builds on previous research examining the effects of prenatal
adversity. One prospective longitudinal study reported associations between increased stress in
utero and depressive problems during adolescence, as mediated via HPA axis functioning (Van
den Bergh et al., 2008); however, these authors did not examine the impact of specific types of
stressors, including traumatic stress, despite evidence of distinct outcomes associated with
different stressors (Wheaton, 1996). In contrast, studies that specifically examine the effects of
exposure to IPV during pregnancy have found links with negative offspring health and
psychological outcomes during the perinatal and infancy periods (e.g., Coker et al., 2004; HuthBocks et al., 2002; Levendosky et al., 2006; Martinez-Torteya, Field, et al., 2009; Quinlivan &
Evans, 2005), but have relied solely on maternal reports, have not used a disorder-specific or
mechanistic perspective, and have not examined long-term offspring outcomes following
exposure to IPV in utero.
This research addresses some of the limitations of the extant literature. First, its
prospective longitudinal nature allows examination of the influence of risk and protection at
different developmental periods on children’s depressive problems. Second, results are based on
different reporters (mother and child) and different methods of assessment (biological samples,
questionnaires, semi-structured interview, and coded laboratory observations). In addition, the
current research includes both variable- and person-oriented approaches to hypothesis testing to
address the conflicting findings reported by previous research; aggregating all subjects in a
single group may misrepresent relationships between variables in significant ways, while
identification of homogeneous profiles of HPA axis dysregulation or subgroups of children with

33

specific individual or familial risk may help clarify specific within-group patterns of association
(von Eye & Bergman, 2003).
In addition, most studies to date with prenatally stressed samples have failed to propose
etiological pathways that are specific to one psychiatric outcome and have instead focused on
general associations between stress during pregnancy and maladaptation (e.g., O’Connor et al.,
2002). Unfortunately, this perspective provides little information for targeted intervention and
prevention efforts. In contrast, the present research uses a disorder-specific perspective, based
on findings of increased difficult temperament, inhibition, high levels of negative affect, high
levels of internalizing symptoms, and HPA axis dysregulation among prenatally stressed
children, which are consistent with behavioral and neuroendocrine precursors to depressive
symptoms.
The current study examined the contribution of exposure to IPV in utero to the
development of depressive symptoms during childhood, as reported by both the child and the
mother, as well as mediation via children’s cortisol levels in response to a laboratory stressinduction task. Mediation is proposed, although interpretation of causality is limited, as cortisol
levels were assessed concurrently with depressive symptoms, rather than during a prior
assessment. However, previous studies document that HPA axis dysregulation is a precursor of
depressive symptoms (Essex et al., 2002; Smider et al., 2002), and no studies to date have
documented the opposite relationship among children (HPA abnormalities that developed as a
consequence of depression). To assess for individual differences in stress reactivity, the
relationships between empirically derived profiles of stress-induced responses and depressive
symptoms will be examined in the present research. The influence of other individual and
environmental risk experienced during the prenatal and postnatal periods was also examined,

34

including prenatal maternal mental health, current maternal mental health, IPV exposure,
income, and maternal early parenting. Based on previous research, familial risk and gender will
be explored as moderators, as they may enhance or buffer the impact of other adversity.
Hypotheses
1. Prenatal exposure to IPV predicts HPA axis dysregulation (as indexed by salivary cortisol
levels) after controlling for familial (family history of depression) prenatal (maternal
mental health), and postnatal risk (gender, early maternal parenting, maternal mental
health, lifetime exposure to IPV, and income). Analyses using both variable- and personoriented approaches will be pursued to test this hypothesis.
2. Prenatal exposure to IPV predicts childhood depressive symptoms after controlling for
familial (family history of depression) prenatal (maternal mental health), and postnatal
risk (gender, early maternal parenting, maternal mental health, lifetime exposure to IPV,
and income).
3. HPA axis dysregulation (as indexed by salivary cortisol levels) is associated with higher
levels of depressive symptoms, after controlling for familial (family history of
depression) prenatal (maternal mental health), and postnatal risk (gender, early maternal
parenting, maternal mental health, lifetime exposure to IPV, and income).
4. The effect of prenatal IPV on childhood depressive symptoms is partially mediated
through a dysregulated HPA axis stress response (as indexed by salivary cortisol levels).
5. The effect of prenatal IPV is moderated by gender and family history of depression. It is
predicted that girls will be more susceptible to the impact of prenatal stress than boys. In
addition, those with genetic predisposition (as indexed by family history of depression)

35

will also be more susceptible to the impact of prenatal stress. Analyses using both
variable- and person-oriented approaches will be pursued to test this hypothesis.
Methods
Participants
Participants were a subset of mother-child dyads recruited through a larger longitudinal
domestic violence study (www.msu.edu/~mis), who completed up to 9 waves of data collection
and were assessed for the 10th time, around children’s age 10. Participants of the larger
longitudinal study were 206 pregnant women recruited throughout the Clinton, Eaton, Ingham,
and Shiawassee counties of Michigan, through fliers posted at Obstetric/Gynecologic or
women’s health clinics (39%), libraries, laundromats, stores, and similar public places (27%),
social service programs such as FIA, WIC, Head Start, Jump Start, and Maternal Infant Outreach
Program (26%), childbirth classes (5%), the county prosecutor’s office (2%), and a local
domestic violence shelter (1%). Inclusion criteria for the longitudinal study was: 1) being in the
last trimester of pregnancy at the time of the initial interview, 2) 18 to 40 years of age, 3)
involvement in a romantic relationship for at least 6 weeks during the pregnancy, and 4)
understanding English well enough to complete questionnaires and interviews. The average age
of women was 25 years (SD = 5). Forty-five percent of the women had a high school diploma or
some high school education; 35% had some college education; 15% had an Associate or
Bachelor’s Degree, and 5% had a graduate degree. The mean monthly family income was
$1,823 (SD = $1,507), ranging from $0 to $9,500. Half of the women were single, never
married, 40% were married, and 10% were separated, divorced, or widowed. Children were
51% boys and 49% girls. Forty-six percent of the children were identified by their mothers as

36

White/Caucasian, 24% Black/African American, 23% Multiracial, 2% Latino, 2% Native
American, and 1% Asian American.
The final sample for the present study consisted of 119 mother-child dyads (65 boys and
54 girls). Ethnicity was 50% white, 23% Black/African-American, 23% multiracial, 2% Latino,
1% Native American and 1% Asian American. The mean monthly family income was $2,002
(SD = $1,652). Eleven percent of the women did not complete High School, 28% completed HS,
42% completed some college or trade school, 11% had a BA/BS, and 6% had some graduate
school or a graduate degree. Those who were not included in the present study had similar
demographics to those who completed this wave of data collection; however, those who did not
participate in the current study had significantly lower monthly family income during pregnancy
(See Table 1).
Measures
Prenatal levels of IPV (maternal report), maternal depression, and maternal anxiety were
collected during the first wave of data collection (M = 33 weeks gestation) using the same
questionnaires that were used in the present assessment. Exposure to IPV was measured via
maternal report during interviews around child’s age 1, 2, 3, 4, 5, 6, and 7. Maternal parenting
was assessed via observational and self-report measures around ages 1, 2, and 3. Family history
rd

of depression was assessed around the child’s 3 birthday. All other measures included in this
study were collected during the present (age 10) assessment (See Table 2).
Dependent Variables: Maternal Report
Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and
Lifetime Version (K-SADS-PL; Kaufman, Birmaher, Brent, Rao, & Ryan, 1996). Parent report of
Major Depressive Disorder was used to assess children's current and past depressive symptoms.
37

This semi-structured clinical interview is based on DSM-IV criteria and provides reliable and
valid psychiatric diagnoses for children 6 to 18 years old. Percent agreement for all diagnoses
ranges from 93% to 100%, test-retest reliability ranges from .63 to .90, and diagnostic categories
are consistent with scores in the Child Behavioral Checklist (CBCL) subscales (Kaufman et al.,
1997). In the present sample, 8% of children met lifetime diagnostic criteria for MDD, while 6%
had a lifetime subthreshold diagnosis. Current symptoms are rated as not present (0),
subthreshold (1), and present (2). Scores for all depression items were summed into a current
symptoms score. Mean score for current symptoms (range = 0 to 20) was 1.34 (SD = 1.86).
Child Behavioral Checklist for ages 6-18 (CBCL/6-18; Achenbach & Rescorla, 2001).
This 113-item questionnaire assesses maternal report of behavioral and emotional problems,
yielding 2 broadband internalizing and externalizing scales and 8 empirically derived subscales.
This checklist has good reliability; internal consistency ranges from α = .72 to α = .94 and testretest reliability ranges from r = .82 to r = .92. Validity is supported through correlations with
the Behavior Assessment System for Children (BASC) Scales (r = .38 to r = .88) and a high
percentage of correct classification of referred vs. non-referred children (80% to 85%;
Achenbach & Reschorla, 2001). The age-normed T-score (range = 30 to 100) for the
Depressed/Withdrawn scale was used to assess child depressive symptoms; higher scores
indicate higher levels of depression as compared to other children of the same age. For the
present sample, α = .82, M = 53.11, SD = 6.61. Thirteen percent of children had depression
levels above the borderline cut-off score (T-score >= 60).
Dependent Variables: Child Report
Children's Depression Inventory (CDI; Kovacs, 1992). This 27-item questionnaire
assesses depressive symptoms among 6 to 17 year-old children, yielding 5 subscales: Negative

38

Mood, Interpersonal Difficulties, Negative Self-Esteem, Ineffectiveness, and Anhedonia.
Children are asked to select one out of three statements that best describes their feelings during
the past two weeks. This is a reliable and well-validated measure; internal consistency
coefficients range from α = .71 to α = .89, test-retest coefficients range from r = .74 to r = .83,
and discrimination of depression vs. other psychiatric problems is adequate (Kovacs, 1992). The
Total age-normed T-score (range = 0 to 54) was used; higher scores reflect higher levels of
depression. For the current sample α = .83, M = 44.90, SD = 7.68. Six percent of children had
depression levels above the borderline cut-off score (T-score >= 60).
Behavioral Assessment System for Children- Self-report of personality (Reynolds &
Kamphaus, 2002). This 131-item self-report measure assesses behavioral and emotional
problems among 8 to 11 year-old children. The 13-item depression subscale was used to
evaluate children’s depressive symptoms. Children are asked to rate items as ―true‖ or ―false‖ or
in a 4-point frequency scale. The depression score (range = 0 to 20) was used; higher scores
reflect higher levels of depression. Good reliability and validity have been reported (Reynolds &
Kamphaus, 2002). For the current sample, depression subscale α = .71, M = 3.38, SD = 2.78.
Independent Variables: Maternal Report
Severity of Violence against Women Scales (SVAWS; Marshall, 1992). This 46-item
questionnaire assesses violent behaviors and threats that the woman has experienced from her
partner during the past year. Examples of items include ―Destroyed something belonging to
you,‖ and ―Punched you.‖ Women rate their experiences on a 4-point frequency scale. High
internal consistency (α = .97) has been reported for the full scale (Huth-Bocks, Levendosky, &
Semel, 2001). For the present study, ratings for items 9 to 46 were added to create a battering
score (range = 0 to 114); higher scores represent more frequent abuse. Violence during

39

rd

pregnancy was measured during the mother's 3 trimester (M = 33 weeks gestation). For the
present sample, α = .93, M = 2.8, SD = 6.94. Thirty-one percent of women experienced IPV
during pregnancy. An IPV score was obtained for each time period and α ranged from .91 to 1.0.
Correlations between different time periods ranged from .03 to .67, and the average for all
correlations was .35. To account for total exposure to IPV throughout childhood, a lifetime
exposure to IPV variable was created by summing the scores at ages 1, 2, 3, 4, 5, 6, 7, and 10. In
the present sample, lifetime IPV M = 17.45, SD = 35.63, and 61% of children were exposed to
IPV by age 10.
Maternal Mental Health. Scores for the Beck Depression Inventory (BDI; Beck,
Mendelson, Mock, & Erbaugh, 1961) and the Brief Symptom Inventory (BSI; Derogatis &
Melisaratos, 1983) were combined to obtain an index of maternal mental health. The BDI is a
21-item self-report questionnaire measuring symptoms of depression. Women select the best
evaluative statement out of 4 options, which describe their feelings and behaviors during the last
two weeks, with values from 0 to 3 (e.g., ―I have no appetite at all anymore‖ = 3). Good internal
consistency has been reported (α = .86; Beck, Steer, & Garbin, 1988). The total score (range = 0
to 63) was be used; higher scores reflect more severe symptoms. For this sample, α = .86, M =
10.10, SD = 6.91 during pregnancy. During the present assessment, α = .89, M = 2.68, SD =
3.84. The 6-item BSI anxiety scale measures symptoms of anxiety. Participants rated how much
each symptom affected them during the past two weeks using a 5-point scale, ranging from ―Not
at all‖ to ―Extremely.‖ Examples of items include ―Feeling easily annoyed or irritated,‖ ―Feeling
fearful,‖ and ―Feeling that you are watched or talked about by others.‖ Derogatis and
Melisaratos (1983) report good internal consistency (α = .81) and adequate test-retest reliability
(r = .79). The total score (range = 0 to 24) was used; higher scores indicate more severe anxiety.
40

For this sample, α = .83, M = 4.52, SD = 4.38 during pregnancy. During the present wave of
data collection, α = .85, M = 5.98, SD = 6.56. Correlations between concurrent maternal
depression and anxiety were strong (r = .70 and .57), supporting an aggregate score to avoid
multicollinearity. For the maternal mental health composite, M = 14.53, SD = 10.45 during
pregnancy and M = 8.66, SD = 9.31 during the present assessment.
Maternal Early Parenting. Parenting was measured via maternal self-report and
laboratory observation. The 20-item Nurturing scale from the Parent Behavior Checklist (PBC;
Fox, 1994) was completed by mothers when their children were 1, 2, and 3 years old. Items are
scored on a 4-point scale (e.g., ―I read to my child at bedtime,‖) and higher total scores (range =
20 to 80) reflect more nurturing parenting. High internal consistency has been reported for the
nurturing scale (α = .82; Fox, 1994). Scores ranged from 31 to 75 (Age 1 M = 56.98, SD = 8.56;
Age 2 M = 62.08, SD = 9.42; Age 3 M = 62.49, SD = 9.51). In addition, a mother-infant
interaction (MII) also assessed maternal parenting at age 1. Mother and infant were videotaped
in a 30-minute free-play situation. Following Ainsworth, Bell, and Stayton (1971) maternal
sensitivity was coded from 1 to 5. Higher sensitivity scores suggest that the mother perceives
and accurately interprets the infant’s signals and responds to them appropriately and promptly.
Scores ranged from 1 to 5 for Sensitivity (M = 2.86, SD = 1.10). Correlations between all
parenting indices were moderate to strong (r = .29 to r = .66).
Family History (Klump, 2001– unpublished). Near the child's third birthday, mothers
were asked to indicate whether any family members (including the mother herself) have had
major psychological problems with depression, and if so, which family members (e.g., sister,
cousin, in relation to mother). A sheet with the definitions of the disorder was presented to the
woman in case she had any questions about the diagnostic terms. The mother also completed the

41

form for the child’s father, to the extent that she knew the history. The measure is scored
positive or negative for history of that particular illness. A dichotomous measure was used;
children with family history of depression on either the maternal or paternal side will receive a
positive score. Forty-three percent of children had a positive family history of depression.
Income. Mothers reported on their average monthly family income throughout the last
year. Last year’s income was used in all analysis, rather than income during pregnancy, given
evidence that recent SES has more influence on internalizing symptoms during childhood than
does early income (Ackerman, Brown, & Izard, 2004).
Independent Variables: Child Report
Conflict Tactics Scale—Child Report (CTS; Straus, 1979). The modified 19-item
verbal/symbolic and physical aggression scales from the Conflict Tactics Scale—Form N
measure children's report of the frequency with which their mother and her male partner use
aggression to resolve conflict, using a 4-point scale, ranging from 0 (never) to 6 (more than 20
times during the past year). Item examples include "Father insulted or swore at mother" and
―Father pushed or shoved mother.‖ Internal consistency for this adapted measure is high (α =
.87; O'Brien, Bahadur, Gee, Balto, & Erber, 1997). The total score for male-to-female
aggression (range = 0 to 76) will be used; higher scores indicate higher levels of IPV. For the
present sample, α = .80, M = 4.95, SD = 6.71. Sixty-four percent of the children reported
witnessing some verbal and physical aggression towards their mother during the past year.
Experimental Manipulation
Trier Social Stress Test for Children (TSST-C; Buske-Kirschbaum et al., 1997). After a
brief period of non-stressful interactions, the experimenter told the child that he/she had to create
a very exciting 5-minute ending for a story and his/her response would be videotaped and

42

reviewed by a judge. The story read was: "Yesterday my best friend Robert and I went home
from school. Suddenly, we had the idea to visit Mr. Greg who lived in the big old house located
in the dark forest near our town. Mr. Greg was a crazy old man and our parents didn't like the
idea that we sometimes went visiting him. There was a rumor in town that there was a mystery
about the old house. When we arrived at the house we were surprised that the door was open.
Suddenly we heard a strange noise and cautiously, we entered the dark hall. . ." After a 5-minute
preparation period, a second experimenter, unknown to the child, entered the room and asked the
child to stand by the camera and finish the story, so that his/her performance could be video
recorded and reviewed by the ―judge.‖ The experimenter maintained a serious stance while
listening to the child’s story, and if the child finished the story in less than 5 minutes, the
experimenter asked the child to elaborate on his/her story.
Mathematical Calculation Task (Buske-Kirschbaum et al., 1997). Children were asked to
serially subtract the number 7 from 758 as fast and as accurately as possible, and were told their
performance would be compared to other children's. On every failure, the experimenter said
"Stop, please start again" and the child had to restart at 758. After four mistakes the task was
discontinued.
Children completed a 5-point manipulation check of how stressful they found the speech
and arithmetic tasks. These combined tasks are adapted from a standardized adult stress
paradigm and have been reported to elicit a reliable physiological stress response among children
9 to 14 years of age (Buske-Kirschbaum et al., 1997). In the present sample, children found this
task to be somewhat stressful (M = 3.24), with 37% of children giving a rating of ―quite
stressful‖ or higher and only 5% of children providing a rating of ―not stressful at all.‖ Children
were debriefed and received a certificate for their participation.

43

Salivary Cortisol Collection
Saliva samples were obtained using the passive drool method before the stressful task, as
well as 20 and 40 minutes after the stress manipulation. Children were asked to gently pass
saliva into a 2 mL tube using a straw, following the procedures outlined by Salimetrics, LLC and
recommendations of Douglas Granger, PhD. (2009, personal communication). Children
imagined eating their favorite food and were offered a citric scent to stimulate saliva production.
Immediately after collection, saliva was placed in a cooler, and samples were stored at -70°C
after the interview was completed. Samples were shipped to Salimetrics, LLC following best
practice guidelines and assayed in duplicate for salivary cortisol levels. Scores for each time
period were M = .088 ug/dl for baseline, M = .076 ug/dl for peak and M = .053 ug/dl for
recovery. Four different scores were calculated as indices of HPA axis activity, following the
recommendations of Fekedulegn et al. (2007): (1) area under the curve with respect to ground
(AuCg; total area under all measurements), (2) area under the curve with respect to increase
(AuCi; area under measurements with reference to baseline levels), (3) cortisol increase (peak –
baseline), and (4) cortisol decrease (peak – recovery).
The AuC indexes were calculated using the formula from Pruessner, Kirschbaumb,
Meinlschmide, and Hellhammer (2003), as follows:
AuCg = [(baseline + peak)/2 * (time between sample 1 and 2 = 40 min)] + [(peak +
recovery)/2) * (time between sample 2 and 3 = 20 min)]
AuCi = [(baseline + peak)/2 * (time between sample 1 and 2 = 40 min)] + [(peak +
recovery)/2) *(time between sample 2 and 3 = 20 min)] – [baseline * (time between sample 1
and 3 = 60 min)]

44

Procedures
For the larger longitudinal study, pregnant women contacted the research office if they
were interested in participating in the study, at which time a research assistant conducted a brief
screening to determine eligibility and provided a description of the assessment protocol. To
oversample for women who experienced domestic violence during pregnancy, items 9-19 from
the Conflict Tactics Scale (Straus, 1979) began to be administered over the telephone after
approximately half the sample had been recruited and interviewed (n = 96). Overall, 161 women
who were screened were ineligible because they did not meet age, relationship status, or
battering experience criteria. However, there were no other demographic differences between
excluded women and participants.
Eight undergraduate and five graduate research assistants conducted the pregnancy
assessment. They were trained to administer the questionnaires and conducted two to five
supervised interviews until they reached 95% reliability for standard administration of measures.
The interviews lasted about 3 hours and were conducted in the woman’s home or the project
office. Interviewers were blind to the women's battering status, administering the violence
questionnaires last.
During the data collection when children were age 7, mothers were asked if they would
like to be contacted for future assessments and indicated if they wished to be contacted directly
or though an ―alternative contact.‖ For the present wave of data collection, participants who
consented future contact were approached. If they asked to be contacted directly, participants
were telephoned according to any preferences indicated (e.g., blocking caller ID). A research
assistant invited the woman to participate in an interview with her child, providing a brief
description of the present study. If the woman was interested in participating, she was scheduled

45

to come in for an interview to the project's office. A number of options for future contact were
offered to ensure the woman’s safety, including blocking caller ID, not leaving messages on the
answering machine, not leaving messages if someone other than the participant picked up the
phone, and not identifying ourselves as the MSU Mother-Infant Study. If unable to contact the
woman over the phone, and if the woman had agreed, a letter inviting the woman to call the
project office was sent to her home address.
When staff was unable to contact the woman directly the friend/relative recontact
information provided by the woman during her last interview was used. During the 7 year old
assessment, women provided the address and telephone numbers of up to 3 friends or family
members, and signed letters that were sent to these ―recontact‖ individuals, explaining that the
woman participated in the Mother-Infant Study and had given permission for the research staff to
communicate with them if the staff was unable to locate the participant. When telephoning the
re-contact individuals, research assistants left a message to be passed along to the participant. If
we were unable to reach the ―recontact‖ individuals by telephone, a letter was sent to their
address.
For the present wave of data collection, the mother and her 10-year-old child came to
MSU for the assessment. Because levels of salivary cortisol naturally rise and decrease with the
circadian rhythm, all interviews were started between 4 and 5 pm to restrict the potential impact
of time of saliva collection. Upon arrival, mother and child completed the informed consent and
informed assent procedures, and then completed the rest of the assessment in separate rooms.
The mother completed questionnaires and interviews with a Master's level clinician
(Interviewer), while the child completed questionnaires and a challenging task in a separate room
with an advanced undergraduate research assistant (Child Tester). Child outcomes were assessed
46

using both maternal and child report, in order to increase the external validity of the information
gathered, and consistent with the children's cognitive capacities.
The challenge task was selected to test children’s increased/decreased sensitivity to mild
stressors. Salivary cortisol was used as a measure of HPA axis because it is a minimally invasive
procedure and salivary cortisol levels are highly correlated with blood serum cortisol levels
(Schwartz, Granger, Susman, Gunnar, & Laird, 1998). Saliva was collected during resting
condition upon arrival to the interview, 20 minutes after the challenging task (to capture peak
levels), and 40 minutes after the challenging task (to capture return to baseline/resting levels).
After the challenging task (before the second and third saliva collections), children spent 20
minutes engaged in age-apropriate free play, aimed at facilitating return to a positive mood and
baseline levels of stress.
If the mother or the child indicated suicidal ideation during the interview, a suicide
protocol was completed by the master's level clinician to assess the degree of risk. None of the
participants assessed were actively suicidal, and clinicians provided referrals for mental health
services to all families. At the end of the interview, women provided recontact information for
potential future assessments, received a list of resources of support and counseling services, and
received financial compensation for their participation.
Nineteen participants were unable to come to the project office for the assessment
because they lived out of state. These women completed all mother-report questionnaires over
the telephone with a Master’s level clinician. Child’s report of depressive symptoms and IPV, as
well as saliva samples, were not obtained from these families.

47

Saliva Samples Storage and Analysis
At the end of the interview, saliva samples were stored in a locked laboratory freezer at 70 F. Upon completion of data collection, all samples were sent to Salimetrics, LLC for
assaying in duplicate. The assay (25 ul test volume) is 510K cleared (US FDA) as a diagnostic
measure of adrenal function: range of detection is from 0.003 to 3.0 µg/dl, inter and intra-assay
coefficients of variation are less than 10 and 15%. The correlation between plasma and saliva
cortisol levels is 0.91. The assay is highly specific to cortisol, with less than 0.5% crossreactivity for other steroids. Saliva samples were destroyed 30 days after assays were completed.
Data Storage
To protect confidentiality to the highest extent possible, participant code numbers, not
participant names, were placed on the questionnaires and videotapes. All data, including
videotapes, were stored in locked file cabinets. The information linking ID’s with participant
names (i.e., consent form, participation voucher, contact information sheet) was separated from
the rest of the data and placed in a separate file.
Training
The author was previously trained to administer and code the semi-structured interview
(K-SADS-PL) and to assess victims of domestic violence. Six undergraduate research assistants
were trained as child testers, observing the first author administering questionnaires and
collecting saliva samples, and being evaluated while administering the protocol, to assess
reliability of administration. In addition, six additional Master's level clinicians were trained to
administer and code the semi-structured interview and questionnaires with the mother, as well as
the challenging task with the children. All undergraduate research assistants were trained as data

48

enterers and schedulers, using the procedures developed to protect women’s safety and
confidentiality. All interviewers and child testers were trained to be sensitive to the special
challenges that working with this population involves.
Results
Missing Data
Missing data were imputed using the Expectation-Maximization algorithm of SPSS 17.0
(SPSS: An IBM Company, 2010). Overall, only 7% of all data points were imputed. To identify
any possible differences between participants with missing data and the rest of the sample, the
pattern of missingness was examined. Participants were categorized into those with missing data
and those with complete data; t-test comparisons for all variables were estimated. Results
showed non-significant differences on all variables used for analysis. In addition, the MCAR
2

statistic indicates that data was missing at random (χ = 816.20, df = 1008, p = .98)
Descriptive Statistics
Overall, variables showed the expected associations. Maternal mental health during
pregnancy had a large correlation with current mental health (r = .39). Similarly, pregnancy IPV
had a large correlation with lifetime exposure to IPV (r = .42). In terms of cross-informant
correlations, maternal ratings of lifetime IPV had a large correlation with child’s report of
current IPV (r = .39). For depression indices, maternal ratings on the structured interview were
highly associated with mother-reported Withdrawn/Depressed scores on the CBCL (r = .50).
Similarly, child reported levels of depression were highly correlated using both questionnaires
(CDI and BASC, r = .63). However, KSAD-MDD current symptoms were not associated with
child’s report of depressive symptoms, while maternal responses to the CBCL had small to
medium associations with child’s report (CDI r = .25; BASC r = .19). Pregnancy risk (IPV and
49

maternal mental health) showed small to medium associations with depression scores (r = .21 to
.29), while postnatal risk (lifetime IPV, current IPV, current maternal mental health, and income)
had small to large associations with outcomes (r = .21 to .39). Lower income was associated
with higher levels of pregnancy and lifetime risk (r = -.25 to -.32), as well as higher childreported depression (r = -.19 to -.23). Family history of depression was correlated with maternal
current mental health (r = .30) and maternal reports of child depression (r = .20 to .27). In
addition, measures of HPA axis functioning were highly associated among themselves (r = .44 to
.80) and were associated with maternal reports of child depression (r = .22 to .30; See Table 3).
Data Analytic Plan
Statistical analyses were completed using Mplus 4.2 (Muthen & Muthen, 2007) and SPSS
17.0 (SPSS: An IBM Company, 2010). For all structural equation models (SEM), global fit was
2

evaluated using the overall χ test of model fit (p > .05), the root mean square error of
approximation (RMSEA < .08; Browne & Cudeck, 1993), the comparative fit index (CFI > .95),
and the standardized root mean square residual (SRMR < .07). Additional absolute model fit
indices are also reported for comparisons between models, including the Akaike’s information
criterion (AIC) and the Bayesian information criterion (BIC). Lower values for the AIC and BIC
indicate improved fit.
Hypothesis Testing
Hypothesis 1
Prenatal exposure to IPV was expected to predict HPA axis dysregulation (as indexed by
salivary cortisol levels) after controlling for familial (family history of depression) prenatal
(maternal mental health), and postnatal risk (gender, early maternal parenting, maternal mental
health, lifetime exposure to IPV, and income). Models predicting each of the cortisol outcomes
50

were estimated, using pregnancy exposure to IPV, pregnancy maternal mental health, lifetime
exposure to IPV, child report of current IPV, current maternal mental health, family history of
depression, and child’s gender as manifest variables predicting outcomes. An early maternal
sensitivity latent variable was estimated using observed maternal sensitivity at age 1, as well as
maternal report of nurturance at ages 1, 2, and 3 (See Figure 1). Due to the lack of association
between cortisol levels and income, models were estimated with and without income as a
predictor; since results remained mostly unchanged, results are reported for the most
parsimonious model (i.e., model without income).
The first model explained 5% of the variance of increase in cortisol levels and was a
2

good fit for the data, χ = 29.99, df = 26, p = .27; CFI = .98, RMSEA = .04, SRMR = .04. Child
report of current IPV predicted higher increase from baseline to peak, standardized b = .21, p =
.03. The second model predicted decrease in cortisol levels using the same familial, prenatal,
and postnatal risk. This model explained 11% of the variance in decrease and was an excellent
2

fit for the data, χ = 24.76, df = 26, p = .53; CFI = 1.00, RMSEA = .00, SRMR = .04; IPV during
pregnancy, standardized b = .26, p = .01, and current levels of IPV (child report), standardized b
= .27, p = .00, predicted a larger decrease from peak to recovery. The third model (using the
2

same predictors) explained 5% of the variance of AuCg and it was an excellent fit for the data, χ
= 22.92, df = 26, p = .64; CFI = 1.00, RMSEA = .00, SRMR = .03. IPV during pregnancy
predicted cortisol levels respective to ground, standardized b = .21, p = .05. Finally, the fourth

model (using the same predictors) explained 4% of the variance of AuCi and provided a good fit
2

for the data, χ = 28.61, df = 26, p = .33; CFI = .99, RMSEA = .03, SRMR = .04. However,
none of the predictors were significantly associated with cortisol levels respective to increase.
51

Overall, exposure to IPV during pregnancy and child report of current IPV were associated with
cortisol levels (AuCg, increase, and decrease).
Mean cortisol levels at baseline, peak, and recovery did not follow the expected invertedU shape within the present sample. However, aggregating all subjects in a single group can
misrepresent the individuals within the group in many important aspects (von Eye & Bergman,
2003). Alternatively, a person-oriented approach assumes that individuals are unique and
relatively homogeneous subgroups can be identified based on predictable patterns that occur
across the dependent and independent variables (Bogat, Levendosky, & von Eye, 2005). For
example, Cicchetti, Rogosch, Gunnar, and Toth (2010) reported that depressed children
displayed a flattened pattern of daily cortisol output only when also exposed to early trauma,
while depressed non-traumatized and controls displayed different profiles. Latent Profile
Analysis (McCutcheon, 1987) was conducted using baseline, peak, and recovery cortisol scores
to identify subgroups of children with distinct profiles of stress-induced cortisol output. Model
fit was evaluated using log-likelihood, BIC, AIC, and entropy, as suggested by Grant et al.
(2009). Lower log-likelihood, BIC and AIC suggest increased external validity or
generalizability, while higher entropy reflects maximal distinction between the groups (Kline,
2005).
Models with one through four latent profiles were estimated. Fit indices (See Table 4)
suggest that AIC and BIC improve as the number of profiles increase, with a significant
improvement on both indices from the 1-profile model to the 2-profile model, and from the 2profile model to the 3-profile model. AIC and BIC difference was moderate between the 3profile model and the 4-profile model. In addition, entropy is best for the model with 3 profiles;
thus, this model was chosen as the best fitting one. Means for the 3 latent profiles suggested a

52

group (n = 88) with consistently low levels of cortisol at baseline, peak and recovery (See Figure
2). The second profile was comprised of a small group of children (n = 10) who displayed
consistently high levels of cortisol, with an increase from baseline to peak, and a large decrease
from peak to recovery. Children in the third profile displayed a decreasing trajectory of cortisol
levels, with overall medium levels of cortisol (n = 21).
Multinomial logistic regression (Hosmer & Lemeshow, 1989) was utilized to predict
profile membership (high, medium, or low cortisol). Pregnancy exposure to IPV, pregnancy
maternal mental health, lifetime exposure to IPV, child report of current IPV, current maternal
mental health, early maternal sensitivity, family history of depression, and gender were entered
as predictors in this model. The factor score for early maternal sensitivity estimated in the
previous models was saved and used as a manifest variable in the regression models. All
predictors were entered into the first step of the model. Because high levels of cortisol have been
consistently linked with risk for internalizing problems, the high cortisol class was used as the
reference group.
2

The proposed model showed significantly better fit than the null model, LR- χ (16, N =
2

119) = 33.12, p = .01, and the overall model fit was good, LR- χ (220, N = 119) = 194.88, p =
2

.89; Pearson χ (220, N = 119) = 142.38, p = 1.00. Taken together, all predictors explained a
2

2

medium amount of variance in group membership (Nagelkerke r = .32). Pregnancy IPV, LR- χ
2

(2, N = 119) = 11.23, p = .00, child’s report of current IPV, LR- χ (2, N = 119) = 14.85, p = .00,
2

and early maternal sensitivity, LR- χ (2, N = 119) = 8.90, p = .01, emerged as significant
predictors (See Table 5). Predictors had small effect sizes. Children with higher levels of

53

pregnancy IPV were more likely to be in the high cortisol group, as compared to the low cortisol
group (1.20 times; OR = .84, CI.95 = .73, .96) and the medium cortisol group (OR = 1.35 times,
OR = .74, CI.95 = .58, .85). Children who reported higher levels of current IPV were also more
likely to be in the high cortisol group as compared to the medium (1.36 times; OR = .73, CI.95 =
.61, .89) and low cortisol groups (1.16 times; OR = .86, CI.95 = .77, .96). Interestingly, more
early maternal sensitivity predicted membership in the high cortisol group (1.35 times; OR = .74,
CI.95 = .59, .93), as compared to the medium cortisol group. Multinomial regression also
supports the association between exposure to IPV during pregnancy and current IPV exposure
with a profile of neuroendocrine risk.
Hypothesis 2
Prenatal exposure to IPV was expected to childhood depressive symptoms after
controlling for familial (family history of depression), prenatal (maternal mental health), and
postnatal risk (gender, early maternal parenting, maternal mental health, lifetime exposure to
IPV, and income). Discrepancies between child and mother reports on child’s behavior have
been consistently reported, especially for internalizing symptoms (De los Reyes & Kazdin,
2005). Epidemiological studies have shown that child self-report yields higher levels of
depressive symptoms as compared to maternal reports (Braaten et al., 2001). In contrast,
depressed mothers tend to report more internalizing symptoms for their children, as compared to
the children’s self-reports (van der Toorn et al., 2010). Since both informants convey important
information about the child’s emotional outcomes, the impact of prenatal IPV was evaluated
estimating two child depression latent variables, one as reported by mother and the other based
on child reports. Manifest variables for pregnancy exposure to IPV, pregnancy maternal mental
54

health, lifetime exposure to IPV, child report of current IPV, current maternal mental health,
family history of depression and gender were included as predictors. Income was included in
this model due to its association with child reports of depression. The early maternal sensitivity
latent variable was also used as a predictor.
This model explained 37% of the variance of maternal reports of child depression (latent
2

variable) and 34% of child’s self-reported depression (latent variable). Model fit was good, χ =
72.68, df = 57, p = .08; CFI = .96, RMSEA = .05, SRMR = .04, and indicators significantly
loaded on latent variables in the expected direction (See Figure 3). Maternal reports of child
depression were positively associated with child reports, r = .19, p = .03. Maternal reports of
child depression were predicted by early maternal parenting, standardized b = .36, p = .02,
maternal mental health during pregnancy, standardized b = .27, p = .01, current maternal mental
health, standardized b = .23, p = .03, and child’s report of current IPV, standardized b = .22, p =
.03. Children’s reports of depressive symptoms were predicted by IPV exposure during
pregnancy, standardized b = .21, p = .05, and children’s report of current exposure to IPV,
standardized b = .38, p = .00. In addition, male gender predicted higher levels of child-reported
depression, standardized b = -.28, p = .00. All other predictors had non-significant associations
with the depression latent variables.
Hypothesis 3
HPA axis dysregulation (as indexed by salivary cortisol levels) was expected to predict
higher levels of depressive symptoms, after controlling for familial (family history of
depression), prenatal (maternal mental health), and postnatal risk (gender, early maternal
parenting, maternal mental health, lifetime exposure to IPV, and income). Independent models
were estimated using each of the indices of HPA axis functioning as predictors (i.e., decrease,
55

AuCg), to prevent multicollinearity problems due to high associations among the cortisol scores.
Increase from baseline to peak and AuCi were not included in the models, as they failed to show
correlations with child outcomes (See Table 3). Prenatal risk (pregnancy IPV and maternal
mental health), postnatal risk (lifetime IPV, current IPV- child report, current maternal mental
health, income), family history of depression, early maternal sensitivity, and gender were also
included as predictors in all models.
The model including cortisol decrease explained 51% of the variance of maternal reports
2

and 34% of the variance of self-reported child depression. This model had good fit indices, χ =
76.87, df = 62, p = .10; CFI = .96, RMSEA = .05, SRMR = .04 (See Table 6), and all indicators
loaded significantly on the latent variables in the expected direction (See Figure 4). Motherreported child depression was again significantly correlated with child self-reports, r = .19, p =
.02. Maternal reports of child depression were predicted by cortisol decrease, standardized b =
.36, p = .00, maternal mental health during pregnancy, standardized b = .26, p = .01, early
parenting, standardized b = .35, p = .02, maternal report of current mental health, standardized b
= 30, p = .00, and family history of depression, standardized b = .18, p = .04. Child reports of
depression symptoms were predicted by IPV exposure during pregnancy, standardized b = .21, p
= .05, and child’s report of current exposure to IPV, standardized b = .39, p = .00, predicted
increased self-reported depression. In addition, male gender predicted higher levels of
depression, standardized b = -.29, p = .00. All other predictors were non-significant.
The model including cortisol AuCg explained 47% of the variance of maternal reports of
child depression and 34% of the variance of child reports of depressive symptoms. This model
2

had good fit indices, χ = 76.38, df = 62, p = .10; CFI = .96, RMSEA = .04, SRMR = .04 (See
Table 6), and again, all indicators loaded significantly on the latent variables in the expected
56

direction. Cortisol AuCg was a significant predictor of mother-reported child depression,
standardized b = .28, p = .00, as well as maternal mental health during pregnancy, standardized
b = .28, p = .01, maternal early parenting, standardized b = .38, p = .01, maternal current mental
health, standardized b = .27, p = .01, and income, standardized b = -.25, p = .03. Child reports
of depression were predicted by child’s report of current exposure to IPV, standardized b = .38,
p = .00, and male gender, standardized b = -.28, p = .00. Pregnancy exposure to IPV displayed a
trend to significance, standardized b = .21, p = .06 (See Figure 5). In sum, higher levels of
cortisol AuCg and steeper decrease from peak to recovery were associated with higher levels of
child depression as reported by mother. However, child reports of their own depressive
symptoms were not associated with cortisol levels.
To test for differences in child depressive symptoms associated with different cortisol
profiles (low, medium, or high cortisol), a MANCOVA using child reports and maternal reports
of depression as dependent variables was used. Prenatal (pregnancy IPV and maternal mental
health) and postnatal risk (lifetime IPV, current IPV- child report, current maternal mental
health, and income) were also included as covariates. The model was significant for each of the
outcomes, including levels of depression/withdrawal using the CBCL-maternal report, F(8,110)
= 4.50, p = .00; the clinical interview–maternal report, F(8,110) = 2.61, p = .01; child report on
the CDI F(8,110) = 2.72, p = .01; and child report on the BASC Depression Scale, F(8,110) =
3.18, p = .00.
To correct for the unequal variances of each depression score across the three groups, the
White estimator (1980) was used and univariate ANCOVAs were conducted using the
unstandardized residuals as weights. When maternal report on the CBCL was used as the
2

independent variable, income, F(1,110) = 5.26, p = .02, Partial η = .05; IPV during pregnancy,

57

2

F(1,110) = 16.69, p = .01, Partial η = 06; maternal mental health during pregnancy, F(1,110) =
2

6.29, p = .01, Partial η = .05; and latent profile membership, F(1,110) = 11.23, p = .00, Partial
2

η = .17, were all associated with differences in levels of depressive symptoms (See Table 7).
Specifically, those in the high cortisol profile had higher levels of depression/withdrawal as
compared to those in the low and medium cortisol profiles. Latent profile membership, F(1,110)
2

= 5.64, p = .01, Partial η = .09, was also associated with higher levels of depression based on
the KSADS-MDD-maternal report of current symptoms. Again, those in the high cortisol class
had higher levels of depression/withdrawal as compared to those in the low and medium cortisol
classes. Only child’s report of current IPV was associated with child’s report of depressive
2

symptoms (BASC), F(1,110) = 11.06, p = .01, Partial η = .09. In sum, membership in the highrisk cortisol latent profile was associated with higher levels of mother-reported child depressive
symptoms, after controlling for pregnancy and postnatal risk.
Hypothesis 4
The effect of prenatal IPV on childhood depressive symptoms is expected to be partially
mediated through a dysregulated HPA axis stress response (as indexed by salivary cortisol
levels). Models predicting both child depressive symptoms as reported by mother and child were
estimated. Again, independent models were estimated for cortisol decrease and AuCg, which
were the only cortisol scores associated with both risk and depression levels. These models
included prenatal (pregnancy IPV and maternal mental health) and postnatal risk (lifetime IPV,
current IPV-child report, current maternal mental health), as well as family history of depression,
early parenting, and gender as predictors of both cortisol levels and depressive symptoms. In
addition, cortisol levels were included as a predictor for both depression latent variables.
58

Finally, the indirect effects from the pregnancy risk to outcomes via cortisol levels were
calculated using the Sobel test. Due to inconsistent associations with outcomes in the previous
models, income was not used as a predictor in these models.
Figure 6 displays the mediation model using cortisol decrease. This model predicted 50% of
the variance of the maternal report latent variable and 34% of the self-report child depression
2

latent variable. Model fit was good, χ = 63.16, df = 57, p = .27; CFI = .98, RMSEA = .03,
SRMR = .04 (See Table 6). Cortisol decrease was predicted by IPV exposure during pregnancy,
standardized b = .26, p = .01, and child report of current IPV exposure, standardized b = .27, p =
.00. Maternal report of child depression was predicted by cortisol decrease, standardized b =
.36, p = .00, maternal early parenting, standardized b = .25, p = .04, maternal mental health
during pregnancy, standardized b = .26, p = .01, and current maternal mental health,
standardized b = .33, p = .00. Child report of depressive symptoms was predicted by male
gender, standardized b = .29, p = .00, pregnancy exposure to IPV, standardized b = .22, p = .04,
and child report of current IPV exposure, standardized b = .40, p = .00. The only significant
indirect pathway was pregnancy IPV  cortisol decrease  maternal report of child depression,
standardized b = .09, p = .04.
The mediation model using cortisol AuCg predicted 44% of the variance of the maternal
report latent variable and 34% of the child report depression latent variable (See Figure 7).
2

Model fit was good, χ = 62.43, df = 57, p = .29; CFI = .99, RMSEA = .03, SRMR = .04.
Cortisol AuCg was only predicted by IPV exposure during pregnancy, standardized b = .22, p =
.05. Maternal report of child depression was predicted by cortisol AuCg, standardized b = .25, p
= .01, maternal early parenting, standardized b = .25, p = .04, maternal mental health during
pregnancy, standardized b = .28, p = .01, current maternal mental health, standardized b = .31, p
59

= .00, and current child report of exposure to IPV, standardized b = .23, p = .02. Child report of
depressive symptoms was predicted by male gender, standardized b = .28, p = .00, pregnancy
exposure to IPV, standardized b = .21, p = .05, and child report of current IPV exposure,
standardized b = .39, p = .00. None of the indirect pathways was significant. In sum, cortisol
decrease mediated the association between prenatal IPV exposure and maternal report of child
depression.
To test for qualitative differences in associations between risk and outcomes across
children in the three different latent profiles, the models were also estimated without the 10
children in the high cortisol profile. Model fit was good for the model using AuCg, but fit
indices worsened for the model using the decrease score. When the children in the high cortisol
group were removed, the relationship between risk and cortisol output and the relationship
between cortisol levels and depressive symptoms became non-significant. This preliminary
analysis suggests that those with a profile of neuroendocrine risk may have a distinct profile of
environmental risk and depressive symptoms.
Hypothesis 5
The effect of prenatal IPV may be moderated by gender and family history of depression.
It was predicted that girls are more susceptible to the impact of prenatal stress than boys. In
addition, those children with genetic predisposition (as indexed by family history of depression)
are expected to be more susceptible to the impact of prenatal stress. Both variable- and personoriented approaches were used to test this hypothesis. Differences between boys and girls as
well as those with and without a history of depression were explored using t-test comparisons.
Boys and girls were similar in all predictors, cortisol indices, and most depression scores;
however, boys had more depressive symptoms as reported on the BASC Depression Scale.

60

Those with and without a family history of depression were also similar in most respects, but
children with a family history of depression had higher levels of depressive symptoms as
reported by mothers, and their mothers had higher levels of current depression. The groups were
not different in any of the indices of salivary cortisol.
To assess the moderating role of gender, a 2-group model was proposed, which estimated
different parameters for boys (n = 65) and girls (n = 54). Prenatal risk, postnatal risk, and family
history of depression were used as predictors, while cortisol levels (i.e., decrease or AuCg) were
included as a mediator. Model estimation revealed difficulties with the mother-report child
depression latent variable; thus, the models were estimated only for the child-reported depression
latent variable.
The model using cortisol decrease (See Figure 8) explained 39% of boys’ and 36% of
2

girls’ variance on child-reported levels of childhood depression. Model fit was good, χ = 82.15,
df = 76, p = .29, CFI = .98, RMSEA = .04, RMSR = .07 (See Table 6). For boys, depression was
only predicted by current levels of IPV, standardized b = .31, p = .03, while cortisol decrease
was also only predicted by current levels of IPV, standardized b = .31, p = .02. For girls, less
cortisol decrease, standardized b = -.28, p = .03, more pregnancy IPV, standardized b = .48, p =
.00, and higher levels of current IPV, standardized b = .48, p = .00, were associated with
depressive symptoms. Cortisol decrease was associated with IPV exposure during pregnancy,
standardized b = .35, p = .02, and lifetime exposure to IPV, standardized b = -.33, p = .04.
Based on the Sobel test, standardized b = .02, p = ns for boys and standardized b = -.10, p = ns
for girls, there was no evidence of mediation.
The model using cortisol AuCg (See Figure 9) explained 40% of boys’ and 36% of girls’
2

variance on self-reported childhood depression. Model fit was good, χ = 78.68, df = 76, p = .39,
61

CFI = .99, RMSEA = .02, RMSR = .07 (See Table 6). For boys, depression was only predicted
by current levels of IPV, standardized b = .30, p = .02, while cortisol decrease was not predicted
by any of the variables included in the model. For girls, less cortisol AuCg, standardized b = .26, p = .04, more pregnancy IPV, standardized b = .47, p = .00, and higher levels of current
IPV, standardized b = .43, p = .00, were associated with depressive symptoms. Cortisol AuCg
was associated with IPV exposure during pregnancy, standardized b = .37, p = .02, and lifetime
exposure to IPV, standardized b = .48, p = .00. Based on the Sobel test, standardized b = .02, p
= ns for boys, and standardized b = -.10, p = ns for girls, there was no evidence of mediation.
To assess the moderating role of family history of depression, a 2-group model was
estimated, which provided different parameters for those with (n = 50) and without (n = 69)
family history of depression. Again, model estimation revealed difficulties with the motherreport child depression latent variable; thus, the models were estimated only for the childreported depression latent variable. The model using cortisol decrease (See Figure 10) explained
27% of the variance of self-reported levels of childhood depression for those without a family
2

history of depression, and 38% for those with a family history. Model fit was good, χ = 81.85,
df = 76, p = .30, CFI = .98, RMSEA = .04, RMSR = .06 (See Table 6). For those without family
history of depression, child depression was predicted by male gender, standardized b = -.32, p =
.00, and higher levels of current IPV, standardized b = .34, p = .01. Cortisol decrease was not
predicted by any of the variables included in the model. For those with a family history of
depression, male gender, standardized b = -.28, p = .04, more pregnancy IPV, standardized b =
.34, p = .04, and higher levels of current IPV, standardized b = .52, p = .00, were associated with
depressive symptoms. Cortisol decrease was associated with more current IPV exposure,
standardized b = .39, p = .00, and less maternal current mental health problems, standardized b =
62

-.28, p = .04. Based on the Sobel test, there was no evidence of mediation for those without a
family history of depression standardized b = .02, p = ns, or for children with a family history of
depression, standardized b = -.10, p = ns.
The model using cortisol AuCg (See Figure 11) also explained 27% of the variance of
self-reported levels of childhood depression for those without a family history, and 38% for
2

those with a family history of depression. Model fit was good, χ = 80.41, df = 76, p = .34, CFI
= .99, RMSEA = .03, RMSR = .06. Similar to the previous model, for those without family
history of depression, depression was predicted by male gender, standardized b = -.32, p = .00,
and higher levels of current IPV, standardized b = .33, p = .01. Cortisol decrease was not
predicted by any of the variables included in the model. For those with a family history of
depression, male gender, standardized b = -.29, p = .03, more pregnancy IPV, standardized b =
.36, p = .03, and higher levels of current IPV, standardized b = .52, p = .00, were associated with
depressive symptoms. Cortisol decrease was associated with more pregnancy IPV exposure,
standardized b = .36, p = .03, and less maternal current mental health problems, standardized b =
-.28, p = .05. Based on the Sobel test, there was no evidence of mediation for children without a
family history, standardized b = .00, p = ns, and those with a family history of depression,
standardized b = -.03, p = ns.
DISCUSSION
The aim of this prospective longitudinal study was to evaluate the influence of prenatal
exposure to IPV on the development of depressive problems during middle childhood (i.e., 10year-old children), examining HPA axis functioning as a mechanism of risk transmission. The
present study tested a model that integrates the early risk associated with exposure to IPV during
pregnancy with a number of well established factors that convey vulnerability for childhood
63

depression including family history of internalizing problems, maternal mental health, maternal
early parenting, and exposure to adversity during childhood. In addition, based on the ―fetal
programming‖ theory, the effect of IPV during pregnancy was expected to be mediated via
changes in the offspring’s neuroendocrine response to stressors, given the rapid development of
the central nervous system in utero.
Results indicate that exposure to IPV during pregnancy predicted increased cortisol
output and higher levels of child-reported depressive symptoms. Child report of recent exposure
to IPV also was a significant predictor of higher levels of cortisol output and child depressive
problems, as reported by both informants. In turn, increased cortisol output was associated with
maternal reports of child depressive symptoms. Gender and family history of depression also
emerged as moderating factors, such that exposure to IPV in utero was especially deleterious for
girls and for those with a family history of depression. In the following sections, findings for
each of the hypotheses will be discussed in detail. Limitations, future directions, and potential
clinical implications are also delineated.
Child Stress-Induced Cortisol Levels
Average levels for the three indices of HPA axis functioning collected in the present
study (baseline, peak, and recovery salivary cortisol) were consistent with those generally
reported by previous research examining childhood depression and HPA axis response to a
psychosocial stress manipulation (Hankin et al., 2010; Rao, Hammen, Ortiz, Chen, & Poland
2008; Spinrad et al., 2009). In contrast, cortisol levels in the present sample are higher than
those reported among 9-14 year old children by Buske-Kirschbaum et al. (1997) using the same
stress paradigm. Differences may be due to the high-risk nature and the potentially higher

64

percentage of children showing a hyperactive HPA axis response to stressors in the present
sample.
As a group, children in the present study did not display the expected pattern of poststressor cortisol increase. Other research studies have reported similar difficulties obtaining a
reliable post-stressor increase (Dougherty et al., 2009; Spinrad et al., 2009). One possible
explanation is that the manipulation task was not stressful enough to mobilize the HPA system
among participants. However, children in this sample rated the stress-induction task as
somewhat stressful (M = 3.24), with 37% of children giving a rating of ―quite stressful‖ or higher
and only 5% of children providing a rating of ―not stressful at all.‖ A second alternative is that
participation in the assessment and arrival to the project office was an unfamiliar and stressful
situation on its own for many children, mobilizing the stress response and making it difficult to
obtain a ―true‖ baseline measure. This is consistent with the initially high levels that decline
when measured 40 minutes after the stress-induction task. However, current findings are
difficult to interpret, as it is unclear if they reflect baseline levels or reactivity to stressors
(laboratory visit and challenge task).
Although mean levels of cortisol were not consistent with HPA axis activation, some
children did show the expected increase after the challenging task and return to baseline 40
minutes post-stressor. Person-oriented Latent Profile Analysis yielded three empirically derived
profiles of stress-induced cortisol output, which were characterized by consistently low levels of
cortisol, consistently medium levels of cortisol, and consistently high levels of cortisol. This
third ―high cortisol‖ profile also displayed increased levels 20 minutes post-stressor (peak), and
an efficient return to low levels during the recovery period. One previous study found a similar
pattern of results, such that the mean for the full sample failed to display the expected post-

65

stressor increase in cortisol levels, but a subgroup of children, with increased temperamental and
familial risk, displayed the expected increase after the stress-inducing task (Dougherty et al.,
2008). The pattern of HPA axis activation shown by this group is also consistent with the results
of Zimmermann and Stansbury (2004) who found that temperamental reactivity was associated
with elevations in the initial response to stress, but found no evidence of ineffective return to
baseline or recovery after the threat was discontinued. This research, using a high-risk sample, is
particularly relevant, as the ability to effectively regulate cortisol levels in response to
environmental changes has been posited as an essential aspect of self-regulation and coping in
the face of challenging stimuli (Gunnar & Donzella, 2002). In contrast, chronic HPA axis
hyperactivity has been consistently linked to maladaptation; diverse deficits in basic
mechanisms, such as arousal, attention, or memory (Erickson, Drevets, & Schulkin, 2003) result
in maladaptive or inefficient coping responses.
Membership in the ―high cortisol‖ group was predicted by pregnancy exposure to IPV,
over and above prenatal, postnatal, and familial risk, providing support for the role of pregnancy
as a sensitive period. Prenatal IPV was associated with higher overall and peak levels of cortisol
output, suggesting that stress during gestation, during which the fetus undergoes rapid brain
development, sets the foundation for the regulation of the stress response during childhood
(Maccari et al., 2003; Huizink et al., 2004; Talge et al., 2007). IPV exposure during pregnancy
can increase fetal exposure to cortisol, via chronically elevated cortisol levels among mothers
(Field et al., 2004) and/or decreased levels of placental 11b-HSD2 enzyme (Glover et al., 2009),
which metabolizes cortisol to its inactive form, reducing hormone levels in the placenta. Results
are consistent with previous studies that provide evidence of a link between prenatal stress

66

exposure and offspring HPA axis regulation deficits (Grant et al., 2009; Gutteling et al., 2005;
O’Connor et al., 2005).
In addition, prenatal IPV predicted child cortisol levels, whereas other prenatal factors
(i.e., maternal prenatal mental health) were not associated with HPA axis functioning. The
chronic and interpersonal nature of IPV results in high levels of shame, guilt, and negative selfcognitions among victims (Calvete et al., 2007; Street et al., 2005), exacerbating the
neurobiological deficits that are associated with other stressors or depression and anxiety
symptoms. The unique impact of IPV during pregnancy can also be understood given its
influence on maternal representations of the infant (Huth-Bocks, Levendosky, Theran, et al.,
2004), which are developed during pregnancy and are created in the context of other attachment
relationships (including the relationship with the abuser). Maternal representations of the infant
impact the emerging mother-child attachment (Huth-Bocks, Levendosky, Bogat, et al., 2004) and
maternal parenting (Dayton et al., 2010), shaping the young child’s ability to regulate cortisol
levels to meet environmental and internal challenges.
The results of our study are consistent with the distinctive association reported by
Bergman and colleagues (2007) between partner-specific stress and infant temperamental
dysregulation, which was not significant for other stressful life events. IPV may be specifically
associated with maternal HPA axis dysregulation and offspring in utero exposure to high levels
of cortisol because of its chronic and interpersonal nature, increasing the victim’s guilt, shame,
and negative self-cognitions (Calvete et al., 2007; Street et al., 2005). Although this is the first
study to examine the programming effects of IPV during pregnancy on offspring neuroendocrine
functioning, results are consistent with multiple studies that provide evidence of the impact of
IPV on women’s cortisol output (Inslicht et al., 2006; Pico-Alfonso et al., 2004), and research

67

that has established a link between prenatal stress and offspring HPA axis dysregulation (Grant
et al., 2009; Gutteling et al., 2005; O’Connor et al., 2005).
Membership in the ―high cortisol‖ group was also associated with child reports of
witnessing IPV, highlighting the influence of ongoing stressors on biological and behavioral
functioning, as a result of the continued plasticity of the brain during childhood (Cushing &
Kramer, 2005). IPV exposure may result in more frequent activation via the development of a
lower threshold to mobilize the stress response. Cohen, Perel, DeBellis, Friedman, and Putnam
(2002) have proposed that children exposed to traumatic events may have more frequent
activation of the HPA axis (even in response to relatively mild stressors) due to an over-reactive
amygdala, assigning threatening or stressful meaning to events more often than non-exposed
children. Specific to IPV, research has also shown that very young children who have
experienced interparental violence display heightened sensitivity to adult verbal conflict
(DeJonghe, Bogat, Levendosky, von Eye, & Davidson, 2005), such that social stimuli that may
not mobilize a stress response among control children, can result in chronic activation for those
who have witnessed IPV.
Familial risk, income, gender, and maternal mental health (pre- and postnatal) were not
significantly associated with group membership. These results are not entirely consistent with
previous research, which has documented that elevated cortisol output is associated with
maternal depression and low maternal sensitivity (Grant et al. 2009). However, previous studies
have not controlled for prenatal exposure to traumatic stress, which is also associated with
maternal depression and parenting, and may be uniquely contributing to the development of
depressive symptoms among the present sample.

68

Structural equation models (SEM) were used to test for linear associations among the full
sample. Area under the Curve with respect to Ground (AuCg) was used as an indicator of total
cortisol output during the laboratory visit. Similar results were obtained: prenatal exposure to
IPV was the only predictor of AuCg. Again, IPV during pregnancy had an important effect over
and above levels of prenatal maternal depression and anxiety, emphasizing the unique influence
of intimate partner abuse. Cortisol decrease (peak – recovery) was proposed as an indicator of
inefficient termination of the stress response (i.e., smaller decrease results in prolonged CNS
exposure to high cortisol levels). Cortisol decrease was predicted by pregnancy IPV, as well as
child report of current IPV (at age 10). However, the associations were opposite to expectations:
exposure to IPV predicted a steeper decrease from peak to recovery. Previous studies have failed
to document an association between prolonged HPA axis activation and adversity or depressive
symptoms during childhood. Thus, the reason for the pattern of association observed in this
study is unclear. Possibly, within the present sample, a larger decrease score reflects higher peak
levels, rather than more efficient termination. This alternative is consistent with the strong
correlation between AuCg and cortisol decrease (r = .80). Notably, the prenatal, posnatal, and
familial factors only accounted for about 5% of the variability in cortisol scores, which is
consistent with previous reports of significant individual differences in HPA axis activation
(Gunnar, Sebanc, Tout, Donzella, & van Dulmen, 2003).
Although results of the SEM models are difficult to interpret due to the lack of
mobilization of the HPA axis response after the stress-induction task, results consistently point to
an association between higher levels of cortisol output and pregnancy IPV as well as current
reports of IPV. Although high levels of circulating cortisol can be protective against immune,
infectious, and inflammatory diseases (Kapcala et al., 1995), frequent exposure to cortisol,

69

resulting from higher baseline levels or increased reactivity to stressors, can lead to brain
function abnormalities, including impaired threat signal detection or inefficient regulation of
pleasure and motivation systems (Goodyer, 2008).
Child Depression and Familial, Prenatal, and Postnatal Risk
Consistent with a developmental psychopathology framework, child depressive
symptoms were predicted by multiple individual and family risk and protection. Among this
high-risk sample of school-age children, 21% experienced borderline or clinical levels of
depressive problems, as reported by either the child or his/her mother. Maternal and child
reports of current depressive symptoms displayed non-significant to small associations (r = .19
to r = .21 for latent factors). Although this level of agreement is somewhat low, it is similar to
that reported by most studies, including Achenbach, McConaughy, and Howell’s (1987)
comprehensive meta-analysis (r = .25).
Discrepancies between parent and child report of internalizing symptoms are well
documented (Briggs-Gowan, Carter, & Schwab-Stone, 1996). Some studies have found that
children tend to report more internalizing symptoms than their parents (Edelbrock, Costello,
Dulcan, Conover, & Kala, 1986; Hodges, Gordon, & Lennon, 1990), whereas other studies
report that depressed mothers tend to over-report their children’s internalizing problems (Kiss et
al., 2007; Renouf & Kovacs, 1994). Consistency across reporters may also be influenced by
individual and familial risk; for example, maternal psychopathology can influence child-mother
symptom agreement (Morrel et al., 2003; Youngstrom, Loeber, & Stouthamer-Loeber, 2000).
Because mother and child reports may provide distinct information about children’s functioning
in different settings, information from both reporters was included simultaneously in the models.

70

To tease apart the influence of maternal psychopathology, maternal current depression and
anxiety symptoms were statistically controlled for in all models.
Structural equation models including prenatal, postnatal, and family risk provided a good
fit for the data. However, different risk factors had specific associations with maternal and child
reports of depression. Notably, child report of IPV exposure during the previous year was the
only risk factor that significantly predicted depressive symptoms as reported by both mother and
child, with similar effect sizes as those reported for internalizing symptoms in two meta-analyses
(Wolfe et al., 2003; Kitzmann et al., 2003). The effect of exposure to IPV on depressive levels
during childhood is consistent with the life stress theory (Cicchetti & Toth, 1998), such that
exposure to traumatic stress both hinders the development of regulatory and coping capacities
that are needed for facing environmental challenges and may trigger pre-existent vulnerabilities.
Witnessing IPV exposes the child to maladaptive models for modulation of emotional arousal
and poor behavioral regulation, which the child may utilize within interpersonal relationships
with poor outcomes, potentially reinforcing negative self-cognitions and reducing social
supports. In addition, exposure to IPV can increase the risk for depression as it increases the
likelihood of additional life stressors, such as difficult child temperament, maternal depression,
and ineffective parenting (Martinez-Torteya, Bogat, von Eye, & Levendosky 2009; Eby, 2004;
Levendosky et al., 2006), which may overwhelm the already vulnerable regulatory capacities of
the child exposed to IPV.
Similar to the findings with HPA axis regulation, evidence supports the role of the
prenatal environment on the development of depression during childhood. Child-reported levels
of depression were predicted by pregnancy IPV, while maternal reports of child depression were
associated with maternal mental health during pregnancy. These findings do provide support for

71

pregnancy as a sensitive period for emotional adaptation during childhood, as the prenatal
environment was a significant predictor over and above the impact of more recent stressors.
Results are similar to those reported by O’Connor and colleagues (2002, 2005) who found higher
levels of internalizing symptoms at ages 4 and 7 among children of mothers with high levels of
anxiety during pregnancy. Results are also consistent with those of Van den Bergh et al. (2008),
who found that maternal stress during pregnancy predicted adolescent depressive symptoms. In
contrast with the findings for HPA axis regulation, depression during childhood was not uniquely
associated with pregnancy IPV. Consistent with the principle of equifinality, children develop
depressive symptoms as a result of multiple pathways, including general adversity during
pregnancy as well as traumatic interpersonal stress. Specific clinical presentations across
children that develop depression via different pathways require further exploration.
Consistent with extant research, current maternal mental health was associated with
mother reports of child depression (Connell & Goodman, 2002; McLeod et al., 2007). Mothers
who experience depressive or anxiety symptoms model maladaptive coping strategies, as well as
poor affect and behavior regulation (Goodman & Gottlieb, 1999). In addition, depressed and
anxious mothers display less effective parenting, including poor monitoring and less sensitivity
(Lovejoy et al., 2000).
In contrast, the significant relationship between early parenting and mother reports of
child depression was in the opposite direction from expectations. Maternal sensitive early
parenting was hypothesized to promote the development of self-regulation (Jennings et al., 2008)
and protect against the development of depression. Maternal sensitivity has been linked to
positive child outcomes, particularly in the context of maternal depression, buffering its negative
impact on child adaptation. However, maternal sensitivity may also be associated with a more

72

accurate perception of childhood depressive symptoms. Some studies indicate that parents may
under-report their children’s depressive symptoms (Edelbrock et al., 1986; Hodges et al., 1990),
but mother-child agreement is also influenced by individual and relational factors, such as
maternal mental health (Morrel et al., 2003) and perhaps maternal sensitivity. The relationship
between maternal sensitivity and childhood depression may also be an artifact of reporter bias
and needs further evaluation and replication before conclusions can be drawn.
Child Cortisol Levels and Depressive Symptoms
Goodyer (2008) has proposed high levels of cortisol as a biomarker for deficits in threat
signal detection, which result in rapid and intense negative emotionality in response to incoming
stimuli, as well as inefficient regulation of pleasure and motivation, which result in low positive
emotionality (Caspi et al., 1996). Results revealed that overall cortisol output during the
laboratory visit (AuCg) and larger decrease from peak to recovery levels predicted more motherreported levels of child depression. Similarly, maternal reports of child depression were also
higher for those in the ―high cortisol‖ profile, such that depression was associated with
mobilization of the stress response after the stress-induction task (peak), in addition to overall
high levels of cortisol. Group membership accounted for 6% to 8% of the variance of mother
reports of childhood depression, using multiple methods (clinical interview and questionnaire).
Hyper-reactivity to stressors or high baseline cortisol levels perhaps result in continued tissue
exposure to the deleterious catabolic effects of cortisol. Cortisol-induced disruptions in the
threat signal detection system (amygdala and associated ventral prefrontal areas) and
pleasure/motivation regulation system (hippocampus, nucleus accumbens and ventral tegmental
area) can then result in the increased negative affect and anhedonia that characterize depression.

73

Self-reported levels of childhood depression were not associated with baseline, peak,
recovery levels, or total cortisol output. These negative findings are consistent with those of
Birmaher, Dahl, et al. (1996), suggesting that the HPA axis regulation deficits observed in adult
depressed samples do not emerge until puberty or adolescence. However, negative findings in
the present sample may also be a function of the variable-oriented approach used in modeling, as
parameters were estimated for the complete sample, aggregating all subjects in one group. In
contrast, the moderation models described in the following section may provide a more nuanced
characterization of subgroups of children.
Results partially support the mediating role of HPA axis dysregulation, as increased
reactivity and total cortisol output predicted increased risk for child depressive symptoms.
However, pregnancy IPV, maternal mental health during pregnancy, maternal early parenting,
current IPV exposure, maternal current mental health, and cortisol levels all independently
predicted increased depressive symptoms for children and specific mediation tests evaluating the
indirect effect were not significant. Results suggest that the coping disruptions associated with
ineffective regulation of cortisol output may not be distinctively linked with depressive
symptoms, and require the influence of other environmental and familial risk to be expressed as
depressive problems. Alternatively, capturing the stress regulation deficits that are specifically
linked to depression may require measuring complex interactions within the CNS and
sympathetic nervous system (SNS) response. For example, the ratio between cortisol and the
adrenal steroid dehydroepiandrosterone (DHEA) has been proposed as a better index of risk for
depression (Young, Gallagher, & Porter, 2002), while levels of salivary alpha-amylase (sAA)
reflect SNS activation and are more sensitive to psychological stressors (van Stegeren, Wolf, &
Kindt, 2008). In addition, the ―programming‖ impact of IPV likely disrupts other biological and

74

psychosocial processes that were not assessed in the present study, such as hippocampal
functioning, which may be closely linked to the information processing pleasure regulation
deficits characteristic of depressed children (McKinnon, Yucel, Nazarov, & MacQueen, 2009),
or maternal representations of the infant (Huth-Bocks, Levendosky, Theran, et al., 2004), which
disrupt secure mother-child attachment (Huth Bocks, Levendosky, Bogat, et al., 2004) and
effective maternal parenting (Dayton et al., 2010), increasing risk for depressive problems.
Moderation by Gender and Family History
It is well established that the etiology of childhood depression is multifactorial and results
from interactions among genetic, individual and environmental factors (Downey & Coyne, 1990;
Eley et al., 2004; Kaufman et al., 2006; Rice et al., 2006). Preliminary analyses supported an
interaction between family history of depression and exposure to IPV in utero, predicting both
total cortisol output and depressive symptoms. This finding suggests that prenatal IPV may act
as an epigenetic mechanism (Goodyer, 2008), activating children’s familial vulnerability and
resulting in increased cortisol secretion and depressive problems. Additional environmental
stressors, such as current levels of IPV and maternal distress also contributed to the development
of HPA axis regulation deficits and depressive symptoms in the context of familial vulnerability,
supporting a gene-environment interaction that is consistent with multiple previous studies of
depressed youth (Kaufman et al., 2006; Rice et al., 2006). However, findings should be
interpreted with caution due to small group sizes.
Moderation by gender was also supported. Different risk mechanisms may be involved
in the development of depressive symptoms as reported by boys and girls. Boys’ depressive
symptoms were only predicted by their report of current IPV exposure. In contrast, girls’
depressive symptoms were predicted by exposure to IPV during pregnancy, current exposure to

75

IPV, and cortisol output. Results are consistent with previous studies that suggest that females
are more susceptible to express the ―programming effects‖ of stress during pregnancy through
dysregulation of the stress response and depressed or anxious behavior (Weinstock, 2007).
Specifically, results partially replicate those of Van den Bergh et al. (2008), who reported that
antenatal maternal anxiety was only associated with depressed mood among female adolescents,
and this effect was partially mediated via a flattened diurnal cortisol profile and overall higher
daily cortisol secretion. Contrary to the pattern that emerged for maternal reports of childhood
depression, higher levels of lifetime IPV predicted a smaller cortisol decrease from peak to
recovery and lower total cortisol output, which in turn predicted higher self-reported depressive
problems among girls.
Although results are preliminary due to the small sample size for each group, they may
represent important distinctions between cortisol reactivity and specific depressive symptoms,
which may be more or less likely to be reported by mothers vs. children or boys vs. girls. For
example, Luby et al. (2003) reported that anhedonic depressed preschoolers (i.e., those who
endorsed inability to experience pleasure or had markedly diminished interest in most activities)
showed a decrease in cortisol from baseline to post-stress levels, while the levels among hedonic
depressed preschoolers were not different from the control group or children with other
psychiatric problems. Different profiles of risk may also be associated with psychiatric comorbidity. For example, DeBellis and colleagues (1996) reported that depressed traumatized
children exhibited a characteristic pattern of low cortisol output.
Limitations and Future Directions
The present prospective longitudinal study is the first to explore the long-term
programming effect of prenatal IPV on children’s psychological outcomes, adopting a disorder-

76

specific perspective and evaluating HPA axis functioning as a neuroendocrine mechanism of risk
transmission in the context of well-established familial, prenatal, and postnatal risk factors. This
study utilized a multi-method, multi-informant approach, enhancing external validity and
potential generalization of the present results. Moreover, data analyses were conducted using
both variable- and person-oriented approaches, such that conclusions can be derived about mean
levels of depressive symptoms, as well as relationships that may be specific to homogeneous
subgroups of children. In addition, this study retained during 10 years of data collection more
than 57% of the women who were originally recruited, and participants of the present study were
very similar to the original high-risk sample. However, the limitations of this study should be
noted and considered when evaluating the results obtained.
First, this study assessed HPA axis response to stressors using a social and performance
stress-induced manipulation. However, other studies with depressed children have reported
more consistent associations between cortisol levels and depressive symptoms using a biological
challenge (i.e., dexamethasone suppression test) or evaluating the daily profile of resting cortisol
output (i.e., flattened profile is associated with risk; Lopez-Duran et al., 2009). Future studies
would benefit from specifying the differential impact of prenatal IPV on these different indices
of HPA axis functioning, as well as potential developmental or temporal effects. For example, in
their cross-sectional study, Hankin and colleagues (2010) reported that depression is correlated
with a blunted cortisol response among toddlers and a heightened response among teenagers, but
no study to date has characterized children’s HPA axis functioning over time, to determine
fluctuations in children’s HPA system and its associations with depressive symptoms at different
developmental periods.

77

Second, this study provides evidence for the programming role of prenatal IPV on longterm HPA axis reactivity to stressors and the development of depressive symptoms, but does not
address the specific etiology of this programming effect. Animal research suggests that
increased levels of maternal cortisol and/or decreased levels of maternal placental enzyme 11bHSD2 may be directly responsible for the long-term organizational effects of stress during
pregnancy. However, maternal cortisol or enzyme levels during pregnancy were not available in
the present research. Future studies can provide a comprehensive understanding of the
neurobiological deficits associated with prenatal IPV by assessing cortisol and enzyme levels
among pregnant women.
In addition, some measurement and modeling issues should be noted. Family history of
depression was assessed solely by maternal report in the present study, which may have resulted
in inaccurate reports of risk on the paternal side. Given the nature of this research and potential
safety concerns, the child’s father was not invited to participate in the study, preventing the
research team from gathering more precise family history data. Results based on this measure
should be interpreted with caution. Future research would benefit from integrating father reports
when studying depressive problems among children exposed to prenatal IPV. In addition, the
sample size prevented examination of more complex interactions between different risk and
protective factors. For example, moderation by gender and family history could not be explored
using the 3 empirically-derived latent profiles, given the small size of two of these groups.
Similarly, differences in the relationship between cortisol levels and depression among different
groups of girls (e.g., with co-morbid psychiatric problems or traumatized) could not be explored
due to small sample size for each gender. Future research, using larger samples, would benefit

78

from examination of potentially different subgroups of children exposed to IPV in utero who
develop depressive symptoms.
Clinical Implications
Research investigating the mechanisms through which prenatal exposure to IPV may
result in depressive problems during childhood has the potential to reveal avenues for early
prevention and intervention efforts, including psychoeducation, skills-based, or pharmacological
approaches. Although factors that predict individual differences in response to IPV exposure in
utero remain to be examined, the present study suggests that IPV exposure during pregnancy is
associated with increased offspring HPA axis reactivity, as indexed by higher levels of cortisol
output in response to a mild stressor, as well as higher levels of depressive symptoms. Increased
risk among this group of children highlights the importance of identifying women who are
victimized during pregnancy. Research suggests that a large number of women who experience
IPV do not seek services to cope with the abuse experienced (Fugate, Landis, Riordan,
Naureckas, & Engel, 2005); thus, routine IPV screenings during prenatal care visits may be the
most effective way to link abused pregnant women with appropriate services. Psychoeducation
for prenatal care providers may improve identification of women exposed to IPV during
pregnancy and facilitate early intervention.
The impact of IPV exposure during pregnancy on levels of childhood depression and
associated dysregulation of the physiological response to stressors appeared to be most
pronounced for girls. Although the reason for this increased risk is unclear, prevention and
intervention efforts that focus on stress reactivity and emotion regulation may be particularly
effective among young girls exposed to IPV in utero. Finally, the present study also suggests

79

maternal early parenting as a fruitful avenue for intervention among women exposed to IPV
during pregnancy.
Conclusion
The present study underscores the interplay of multiple factors at the biological,
individual, and family levels that contribute to increased risk for depression. This is the first
prospective longitudinal study to examine the long-term biological and psychological impact of
exposure to IPV in utero, while accounting for relevant familial, prenatal and postnatal risk as
evaluated via multiple methods and informants. Exposure to IPV during pregnancy was directly
associated with increased cortisol output in response to psychosocial stress, as well as child
reports of depressive symptoms. Cortisol levels were also associated with concurrent exposure
to IPV (at age 10), highlighting the plasticity of the HPA system throughout childhood. In turn,
increased cortisol output was associated with maternal reports of child depressive symptoms, but
most models did not support mediation between IPV during pregnancy and depressive symptoms
during childhood. Gender and family history of depression emerged as moderating factors.
Consistent with previous research on prenatal stress, exposure to IPV in utero was especially
deleterious for girls. In addition, pregnancy IPV was only associated with increased risk for
HPA axis dysregulation and depression among those with a family history of depression,
suggesting that prenatal IPV may act as an epigenetic mechanism that amplifies familial risk.

80

APPENDICES

81

APPENDIX A

Tables

82

Table 1
Demographics for Full and Reduced Samples With t-test Comparisons
Original Sample N = 206

Study Sample N = 119

P

Gender

51% Boys
49% Girls

55% Boys
45% Girls

.26

Ethnicity

46% White/Caucasian
24% Black
23% Multiracial
2% Latino
2% Native American
1% Asian American

50% White/Caucasian
23% Black
23% Multiracial
2% Latino
1% Native American
1% Asian American

.55

Maternal Education

45% some HS
35% some college
15% BA/BS
5% graduate education

39% some HS
42% some college
11% BA/BS
6% graduate education

.09

Maternal Marital
Status

50% single/never married
40% married
10% separated/divorced/
widowed

45% single/never married
44% married
11% separated/divorced/
widowed

.19

Family Income

M = $1,823
SD = $1,507

M = $2,002
SD = $1,652

.04

Maternal Age

M = 25
SD = 5

M = 26
SD = 5

.31

83

Table 2
Measures Across All Data Collection Periods
Preg
IPV- Mother
Report
Maternal
Depression
Maternal
Anxiety
Maternal
Parenting
Family History
of Depression
Income
IPV- Child
Report
Child
Depression
Salivary
Cortisol

X

Age
1
X

Age
2
X

Age
3
X

Age
4
X

Age
5
X

Age
6
X

Age
7
X

Age
10
X

X

X

X

X
X

X

X
X
X
X
X
X

84

Table 3
Correlations Between All Predictors and Outcomes

1.Family Hist
MDD
2.Preg Mom
Mental Health
3.Preg IPV
4.Sensit Age 1
5.Nurt Age 1
6.Nurt Age 2
7.Nurt Age 3
8.Lifetime
IPV
9.Current
IPV- Child
10.Curr Mom
Mental Health
11.Current
Income
12.CBCL
With/ Dep
13.KSADS
MDD
14.BASC
Depression
15.CDI Total
16.Cort Incr
17.Cort Decr
18.Cort AuCg
19.Cortl AuCi
* p < .05

3
.13

4
.13

5
.09

6
.06

7
-.01

8
-.01

9
.08

10
.01

11
.30

12
-.01

13
.27

14
.20

15
-.01

16
-.13

17
-.04

18
.04

19
.07

20
-.07

.37

-.11

-.18

-.27

-.28

.25

.07

.39

-.26

.29

.18

.09

.12

-.09

.02

-.04

-.08

-.08

-.16

-.24

-.32
.43
.35
.29

.42
-.12
-.27
-.34
-.43

.11
-.08
-.17
-.11
-.20
.39

.29
-.04
-.13
-.16
-.24
.21

-.27
.31
.50
.41
.53
-.27

.12
.09
.09
.11
.01
.14

.11
-.07
-.05
-.03
-.03
.07

.21
.02
-.02
-.13
-.23
.22

.21
-.02
-.15
-.21
-.30
.33

-.05
-.03
.13
.11
-.04
-.03

.15
-.03
.03
.05
-.05
-.02

.11
.00
.06
.04
.01
-.05

-.03
-.03
.12
.10
-.04
-.03

.16

-.25

.24

.15

.39

.28

.16

.19

.05

.12

-.32

.35

.30

.06

.04

-.08

-.06

-.07

-.06

-.16

-.13

-.19

-.23

.10

-.04

.13

.10

.50

.19

.25

-.03

.30

.17

-.09

.14

.16

.04

.27

.22

-.01

.63

.00

.08

.03

.00

.06

.09
.44

-.02
.14
.80

.07
.97
.26
-.04

85

Table 4
Latent Profile Analysis Using Baseline, Peak, and Recovery Cortisol Levels

1 Latent
Profile

Free
param
6

N
N = 119

Loglikelihood
564.87

AIC

BIC

Adj BIC

-1117.74

-1101.07

Entropy

-1120.04

2 Latent
Profiles

10

LP1 =93
LP2 =26

674.43

-1328.85

-1301.06

-1332.68

.94

3 Latent
Profiles

14

LP1 = 88
LP2 = 20
LP3 = 11

710.76

-1393.53

-1354.62

-1398.88

.97

4 Latent
Profiles

18

LP1 = 87
LP2 = 11
LP3 = 14
LP4 = 7

723.57

-1411.14

-1361.12

-1418.03

.95

86

Table 5
Logistic Regression Predicting Cortisol Latent Profile Membership
Low Cortisol (n = 88)
Gender
Family History of MDD
Pregnancy IPV
Pregnancy Maternal Mental
Health
Lifetime IPV
Current IPV- Child Report
Current Maternal Mental
Health
Maternal Early Parenting

Medium Cortisol (n = 20)

B
-1.25
.00
-.18
.03

OR (CI95)
.29 (.05-1.71)
.99 (.19-5.22)
.84 (.73-.96)
1.03 (.93-1.14)

B
-1.90
-.12
-.30
.02

OR (CI95)
.15 (.02-1.15)
.89 (.13-6.12)
.74 (.58-.95)
1.02 (.91-1.14)

.01
-.15
.05

1.01 (.99-1.03)
.86 (.77-.96)
1.05 (.95-1.17)

.01
-.31
.02

1.01 (.97-1.04)
.73 (.61-.89)
1.02 (.91-1.14)

-.19

.82 (.67-1.01)

-.30

.74 (.59-.93)

2

2

Note. LR- χ (220, N = 119) = 194.88, p = .89; Pearson χ (220, N = 119) = 142.38, p = 1.00
2

Nagelkerke r = .32. Reference group = High Cortisol (n = 10)

87

Table 6
Fit Indices for Models Predicting Childhood Depression

Predictors
Prenatal and Postnatal Risk
Decrease, Prenatal and Postnatal
Risk
AuCg, Prenatal and Postnatal
Risk
Mediation: Decrease, Prenatal
and Postnatal Risk
Mediation: AuCg, Prenatal and
Postnatal Risk
Mediation by Gender: Decrease,
Prenatal and Postnatal Risk
Mediation by Gender: AuCg,
Prenatal and Postnatal Risk
Mediation by Family History of
MDD: Decrease, Prenatal and
Postnatal Risk
Mediation by Family History of
MDD: AuCg, Prenatal and
Postnatal Risk

2

CFI

RMSEA

SRMR

AIC

Adj BIC

56

72.68

0.96

0.05

0.04

12376.44

12360.00

62

76.87

0.96

0.05

0.04

11915.01

11897.42

62

76.38

0.96

0.04

0.04

12974.12

12956.54

57

63.16

0.99

0.03

0.04

9753.23

9733.74

57

62.43

0.99

0.03

0.04

10816.42

10796.93

76

82.15

0.98

0.04

0.07

8218.01

8193.55

76

78.68

0.99

0.02

0.07

9281.74

9257.28

76

81.85

0.98

0.04

0.06

8235.31

8210.85

76

80.41

0.99

0.03

0.06

9286.99

9262.52

df

χ

88

r

2

M = .37
C = .34
M = .51
C = .34
M = .47
C = .34
M = .50
C = .34
M = .44
C = .34
B = 39
G = 36
B = .40
G = .36
FH+ = .38
FH- = .27
FH+ = .38
FH- = .27

Table 7
Hypothesis 3: MANCOVA for Differences on Maternal and Child Reports Across 3 Latent
Profiles of Cortisol
Source
CBCL With/Dep – Mother
Model
Pregnancy IPV
Pregnancy Maternal Mental Health
Lifetime IPV
Current IPV- Child Report
Current Maternal Mental Health
Income
Latent Profile (3)
Error
KSADS-MDD Current - Mother
Model
Pregnancy IPV
Pregnancy Maternal Mental Health
Lifetime IPV
Current IPV- Child Report
Current Maternal Mental Health
Income
Latent Profile (3)
Error
CDI Total Tscore – Child
Model
Pregnancy IPV
Pregnancy Maternal Mental Health
Lifetime IPV
Current IPV- Child Report
Current Maternal Mental Health
Income
Latent Profile (3)
Error
BASC Depression Scale - Child
Model
Pregnancy IPV
Pregnancy Maternal Mental Health
Lifetime IPV
Current IPV- Child Report
Current Maternal Mental Health
Income
Latent Profile (3)
Error

2

p

4.50
1.20
4.54
.04
1.31
7.75
.12
4.52
35.29

.25
.01
.04
.00
.01
.07
.00
.08

.00
.28
.04
.85
.25
.01
.73
.01

8
1
1
1
1
1
1
2
110

2.61
.00
.55
.20
1.17
7.38
.21
3.43
7.35

.16
.00
.01
.66
.01
.06
.00
.06

.01
.95
.46
.00
.28
.01
.65
.04

8
1
1
1
1
1
1
2
110

2.72
.78
.18
3.59
3.15
1.47
1.63
.13
52.85

.17
.01
.00
.03
.03
.01
.02
.00

.01
.38
.67
.06
.08
.23
.20
.88

8
1
1
1
1
1
1
2
110

3.18
2.37
.00
.00
13.01
.41
.59
.01
6.75

.19
.02
.00
.00
.11
.00
.01
.00

.00
.13
.96
.95
.00
.52
.44
.99

df

F

9
1
1
1
1
1
1
2
110

89

Partial η

APPENDIX B

Figures

90

Figure 1
Hypothesis 1: Proposed Model Predicting Salivary Cortisol Levels Using Prenatal and
Postnatal Risk
__________________________________________________________________________
Gender
Pregnancy IPV
Pregnancy Maternal
Mental Health

Cortisol

Lifetime IPV
Current IPV
Current Maternal
Mental Health
Early Maternal
Parenting

Sensitivity
Nurture
Nurture
Nurture
age 1
age 1
age 2
age 3
____________________________________________________________________________

91

Figure 2
Three-Latent Profiles of Cortisol Output
_____________________________________________________________________________

.250000
.200518

.234178

.200000
.150000

.140176
.126788

.116936

.100000
.062376
.050000

.045356

Low cortisol
High cortisol
Med cortisol

.088749
.036646

.000000
baseline

challenge

recovery

______________________________________________________________________________

92

Figure 3
Hypothesis 2: Estimated Model Predicting Child Depression Using Prenatal and Postnatal Risk
______________________________________________________________________________
Income
Gender
FH of Depression
Pregnancy IPV

-.28

.21

.27

Pregnancy Maternal
Mental Health

.22

KSADSMDD
Current Sx

Child Depressive
Symptoms- Self-Report

Early Maternal
Parenting
Nurture
age 1

.57

.38

Current Maternal
Mental Health

Sensit
age 1

.89
CBCL
Withdrawn/
Depressed

.23

Current IPV

.73

.18
.37

Lifetime IPV

.42

Child Depressive
Symptoms- Mother
Report

.87

.84

Nurture
age 2

.75
Nurture
age 3

CDI Total
T-score

.84
BASC
Depression
Score

______________________________________________________________________________

93

Figure 4
Hypothesis 3: Estimated Model Predicting Child Depression Using Cortisol Decrease, Prenatal
and Postnatal Risk
______________________________________________________________________________
Cortisol
Decrease

Income
Gender

-.29

FH of Depression
Pregnancy IPV

.28

.30

Current IPV

KSADSMDD
Current Sx

Child Depressive
Symptoms- Self-Report

Early Maternal
Parenting

Nurture
age 1

CBCL
Withdrawn/
Depressed

.86

.75

Nurture
age 2

Nurture
age 3

94

.84

CDI Total
T-score

.84

.19

.60

.39

Current Maternal
Mental Health

Sensit
age 1

.84
.35

Lifetime IPV

.73

Child Depressive
Symptoms- Mother
Report

.26

.21

Pregnancy Maternal
Mental Health

.42

.36

BASC
Depression
Score

Figure 5
Hypothesis 3: Estimated Model Predicting Child Depression Using Cortisol AuCg, Prenatal and
Postnatal Risk
______________________________________________________________________________

Income

Cortisol
AuCg

-.25

.28

Gender

-.29

FH of Depression
Pregnancy IPV

.17
.21

Pregnancy Maternal
Mental Health

.27

Current IPV

Nurture
age 1

.86

.77

.84

Nurture
age 2

CDI Total
T-score

Nurture
age 3

95

.20

KSADSMDD
Current Sx

Child Depressive
Symptoms- Self-Report

Early Maternal
Parenting
Sensit age
1

CBCL
Withdrawn/
Depressed

.60

.38

Current Maternal
Mental Health

.73

.84
.38

Lifetime IPV

.42

Child Depressive
Symptoms- Mother
Report

.28

.82
BASC
Depression
Score

Figure 6
Hypothesis 4: Mediation Model with Cortisol Decrease, Pregnancy, and Postnatal Risk
______________________________________________________________________________
Cortisol
Decrease

Gender
.26

.36

.27

FH of Depression
Pregnancy IPV

Child Depressive
Symptoms- Mother
Report

.26
-.29

Pregnancy Maternal
Mental Health

.33

.22

Lifetime IPV

.25

.83
CBCL
Withdrawn/
Depressed

.60

.20

KSADSMDD
Current Sx

Current IPV
.40

Current Maternal
Mental Health

Child Depressive
Symptoms- Self-Report

Early Maternal
Parenting
.40

.71

Sensit
age 1

Nurture
age 1

.90

.74

Nurture
age 2

Nurture
age 3

.84

CDI Total
T-score

.82

BASC
Depression
Score

______________________________________________________________________________

96

Figure 7
Hypothesis 4: Mediation Model with Cortisol AuCg, Pregnancy, and Postnatal Risk
______________________________________________________________________________
Cortisol
AuCg

Gender

.25

.21
FH of Depression
Pregnancy IPV

Child Depressive
Symptoms- Mother
Report

.28
-.28 .23

Pregnancy Maternal
Mental Health

.83
.25
CBCL
Withdrawn
/Depressed

Lifetime IPV
.31

Current IPV

Child Depressive
Symptoms- Self-Report

Early Maternal
Parenting
.82
.40
.90
.71
Sensit
age 1

Nurture
age 1

Nurture
age 2

.76
CDI Total
T-score

Nurture
age 3

97

.21

KSADSMDD
Current Sx

.21

.39

Current Maternal
Mental Health

.60

.82
BASC
Depression
Score

Figure 8
Hypothesis 5: Mediation Model for Self-Reported Child Depression via Cortisol Decrease, by
Gender
______________________________________________________________________________
Boys
Cortisol
Decrease
FH of Depression

.31

Pregnancy
IPV
Pregnancy Maternal
Mental Health

Child Depressive
Symptoms- Self-Report

Lifetime IPV

.31
.66

Current IPV

CDI Total
T-score

Current Maternal
Mental Health

.90
BASC
Depression
Score

Early Maternal
Parenting
.77
.40
.91
.67
Sensit
age 1

Nurture
age 1

Nurture
age 2

Nurture
age 3

_____________________________________________________________________________

98

Figure 8 (cont’d)
______________________________________________________________________________
Girls

.35

Cortisol
Decrease

FH of Depression

-.28

Pregnancy IPV
.48

-.33
Pregnancy Maternal
Mental Health

Child Depressive
Symptoms- Self-Report

Lifetime IPV

.48
.72

Current IPV

CDI Total
T-score

Current Maternal
Mental Health

.42
Sensit
age 1

Early Maternal
Parenting
.89 .87
.77
Nurture
age 1

Nurture
age 2

Nurture
age 3

__

99

.96
BASC
Depression
Score

Figure 9
Hypothesis 5: Mediation Model for Self-Reported Child Depression via Cortisol AuCg, by
Gender
___________________________________________________________________________
Boys
Cortisol
AuCg
FH of Depression
Pregnancy IPV
Pregnancy Maternal
Mental Health

Child Depressive
Symptoms- Self-Report

Lifetime IPV

.30
.68

Current IPV

CDI Total
T-score

Current Maternal
Mental Health

.40
Sensit
age 1

Early Maternal
Parenting
.91
.67
Nurture
age 1

Nurture
age 2

.89
BASC
Depression
Score

.77
Nurture
age 3

______________________________________________________________________________

100

Figure 9 (cont’d)
______________________________________________________________________________
Girls
Cortisol
AuCg

.37
FH of Depression

-.26

Pregnancy IPV
.47

Pregnancy Maternal
Mental Health

Child Depressive
Symptoms- Self-Report

Lifetime IPV

.43
.73

Current IPV

CDI Total
T-score

Current Maternal
Mental Health

.42
Sensit
age 1

Early Maternal
Parenting
.89
.77
Nurture
age 1

.94
BASC
Depression
Score

.87

Nurture
age 2

Nurture
age 3

______________________________________________________________________________

101

Figure 10
Hypothesis 5: Mediation Model for Self-Reported Child Depression via Cortisol Decrease, by
Family History of Depression
_____________________________________________________________________________

Without MDD Family History
Cortisol
Decrease
Gender
Pregnancy IPV

-.32

Pregnancy Maternal
Mental Health

Child Depressive
Symptoms- Self-Report

Lifetime IPV

.34
.64

Current IPV

CDI Total
T-score

Current Maternal
Mental Health

.98
BASC
Depression
Score

Early Maternal
Parenting
.48
.80
.92
.71
Sensit
age 1

Nurture
age 1

Nurture
age 2

Nurture
age 3

______________________________________________________________________________

102

Figure 10 (cont’d)
______________________________________________________________________________
With MDD Family History
Cortisol
Decrease
Gender
Pregnancy IPV
Pregnancy Maternal
Mental Health

.34

-.28
Child Depressive
Symptoms- Self-Report

.39

Lifetime IPV

.52
.68

Current IPV
-.28

CDI Total
T-score

Current Maternal
Mental Health

.36
Sensit
age 1

.92
BASC
Depression
Score

Early Maternal
Parenting
.73
Nurture
age 1

.86
.87
Nurture Nurture
age 2
age 3

______________________________________________________________________________

103

Figure 11
Hypothesis 5: Mediation Model for Self-Reported Child Depression via Cortisol AuCg, by
Family History of Depression
______________________________________________________________________________
Without MDD Family History
Cortisol
AuCg
Gender
Pregnancy IPV

-.32

Pregnancy
Maternal Mental
Health
Lifetime IPV

Child Depressive
Symptoms- Self-Report
.33
.64

Current IPV

CDI Total
T-score

Current Maternal
Mental Health

.98
BASC
Depression
Score

Early Maternal
Parenting
.80
.48
.93
.71
Sensit
age 1

Nurture
age 1

Nurture
age 2

Nurture
age 3

_____________________________________________________________________________

104

Figure 11 (cont’d)
______________________________________________________________________________
With MDD Family History
Cortisol
AuCg
.36
Gender
Pregnancy IPV
.35

-.29

Pregnancy Maternal
Mental Health

Child Depressive
Symptoms- Self-Report

-.28
Lifetime IPV

.52
.68

Current IPV

CDI Total
T-score

Current Maternal
Mental Health

.92
BASC
Depression
Score

Early Maternal
Parenting
.85
.36
.87
.74
Sensit
age 1

Nurture
age 1

Nurture
age 2

Nurture
age 3

______________________________________________________________________________

105

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