Prenatal adversity shapes child neurodevelopment and risk for later mental health problems. The quality of the early care environment can buffer some of the negative effects of prenatal adversity on child development. Retrospective studies, in adult samples, highlight epigenetic modifications as sentinel markers of the quality of the early care environment; however, comparable data from pediatric cohorts are lacking. Participants were drawn from the Maternal Adversity Vulnerability and Neurodevelopment (MAVAN) study, a longitudinal cohort with measures of infant attachment, infant development, and child mental health. Children provided buccal epithelial samples (mean age = 6.99, SD = 1.33 years, n = 226), which were used for analyses of genome-wide DNA methylation and genetic variation. We used a series of linear models to describe the association between infant attachment and (a) measures of child outcome and (b) DNA methylation across the genome. Paired genetic data was used to determine the genetic contribution to DNA methylation at attachment-associated sites. Infant attachment style was associated with infant cognitive development (Mental Development Index) and behavior (Behavior Rating Scale) assessed with the Bayley Scales of Infant Development at 36 months. Infant attachment style moderated the effects of prenatal adversity on Behavior Rating Scale scores at 36 months. Infant attachment was also significantly associated with a principal component that accounted for 11.9% of the variation in genome-wide DNA methylation. These effects were most apparent when comparing children with a secure versus a disorganized attachment style and most pronounced in females. The availability of paired genetic data revealed that DNA methylation at approximately half of all infant attachment-associated sites was best explained by considering both infant attachment and child genetic variation. This study provides further evidence that infant attachment can buffer some of the negative effects of early adversity on measures of infant behavior. We also highlight the interplay between infant attachment and child genotype in shaping variation in DNA methylation. Such findings provide preliminary evidence for a molecular signature of infant attachment and may help inform attachment-focused early intervention programs.

The fetal phase of life has long been recognized as a sensitive period of development. Here we posit that pregnancy represents a simultaneous sensitive period for the adult female with broad and persisting consequences for her health and development, including risk for psychopathology. In this review, we examine the transition to motherhood through the lens of developmental psychopathology. Specifically, we summarize the typical and atypical changes in brain and behavior that characterize the perinatal period. We highlight how the exceptional neuroplasticity exhibited by women during this life phase may account for increased vulnerability for psychopathology. Further, we discuss several modes of signaling that are available to the fetus to affect maternal phenotypes (hormones, motor activity, and gene transfer) and also illustrate how evolutionary perspectives can help explain how and why fetal functions may contribute to maternal psychopathology. The developmental psychopathology perspective has spurred advances in understanding risk and resilience for mental health in many domains. As such, it is surprising that this major epoch in the female life span has yet to benefit fully from similar applications.

This longitudinal study examined personal-accentuation and contextual-amplification models of pubertal timing. In these models, individual and contextual risk factors during childhood and adolescence can magnify the effects of early or late puberty on depression symptoms that occur years later. The moderating role of prepubertal individual factors (emotional problems in late childhood) and interpersonal factors (deviant peer affiliation, early dating, perceived peer popularity, and perceived parental rejection during adolescence) were tested. A representative sample of 1,431 Canadian adolescents between 10–11 and 16–17 years of age was followed biannually. In line with the personal-accentuation model, early puberty has been shown to be a predictor for depression in both girls and boys who presented emotional problems in childhood. This effect was also noted for late maturing boys. Consistent with the contextual-amplification model, early puberty predicted later depression in youth who perceived greater parental rejection. Interpersonal experiences such as early dating in girls and deviant peer affiliation in boys predicted depression in early maturers as well. For girls, early dating was also found to be amplified by childhood emotional problems. In line with biopsychosocial models, results indicate that the effect of pubertal timing on depressive symptoms must be conceptualized through complex interactions between characteristics of adolescents' interpersonal relationships and prepubertal vulnerabilities.

The uneven cognitive phenotype in the adult outcome of Williams syndrome has led some researchers to make strong claims about the modularity of the brain and the purported genetically determined, innate specification of cognitive modules. Such arguments have particularly been marshaled with respect to language. We challenge this direct generalization from adult phenotypic outcomes to genetic specification and consider instead how genetic disorders provide clues to the constraints on plasticity that shape the outcome of development. We specifically examine behavioral studies, brain imaging, and computational modeling of language in Williams syndrome but contend that our theoretical arguments apply equally to other cognitive domains and other developmental disorders. While acknowledging that selective deficits in normal adult patients might justify claims about cognitive modularity, we question whether similar, seemingly selective deficits found in genetic disorders can be used to argue that such cognitive modules are prespecified in infant brains. Cognitive modules are, in our view, the outcome of development, not its starting point. We note that most work on genetic disorders ignores one vital factor, the actual process of ontogenetic development, and argue that it is vital to view genetic disorders as proceeding under different neurocomputational constraints, not as demonstrations of static modularity.

Relations between political violence and child adjustment are matters of international concern. Past research demonstrates the significance of community, family, and child psychological processes in child adjustment, supporting study of interrelations between multiple social ecological factors and child adjustment in contexts of political violence. Testing a social ecological model, 300 mothers and their children (M = 12.28 years, SD = 1.77) from Catholic and Protestant working class neighborhoods in Belfast, Northern Ireland, completed measures of community discord, family relations, and children's regulatory processes (i.e., emotional security) and outcomes. Historical political violence in neighborhoods based on objective records (i.e., politically motivated deaths) were related to family members' reports of current sectarian antisocial behavior and nonsectarian antisocial behavior. Interparental conflict and parental monitoring and children's emotional security about both the community and family contributed to explanatory pathways for relations between sectarian antisocial behavior in communities and children's adjustment problems. The discussion evaluates support for social ecological models for relations between political violence and child adjustment and its implications for understanding relations in other parts of the world.

In the coming years we can look forward to research that clarifies specific mechanisms that account for the interplay between genetic and environmental influences on psychological development. Certain misconceptions, arising from research traditions initiated by Francis Galton on the one hand and G. Stanley Hall on the other, may now be set aside in the light of new evidence. Three important findings promise a new synthesis. First, while each of us is born with about 100,000 genes that, under ordinary circumstances, do not change, the expression of these genes on behavior is dynamic. Some genetic influences are expressed early in development, but others are manifest many years later. Second, genetic factors often account not only for some of the individual differences in the measures of adjustments we typically use to monitor development but also for individual differences in environmental experiences that covary with those measures of adjustment. Indeed, genetic factors have been found to account for a surprising amount of covariance between measures of the social environment and of adjustment in young children, adolescents, and adults. Third, the expression of genetic influences are very malleable and responsive to the social environment. These new findings are revealing specific mechanisms for the interplay of genetic and social environmental factors in four domains. First, the social environment may play both a necessary and specific role in the expression of particular genetic influences on a range of behaviors from depression to social responsibility. Second, an understanding of the interplay between the social environment and genetics may lead to a clearer definition of the phenotypic manifestations of particular genetic influences. Third, we will—as a result of these studies—have a clearer fix on the timing of important events and their sequence in development. Fourth, this new genre of work promises to illumine more completely mechanisms by which the social environment influences development independent of genetic influence.

This report examines the predictive validity of sociometric status at age 9–10 to young adult (age 23–24) antisocial behavior, work and school engagement, and arrests using Oregon Youth Study males (N = 206). A variety of analytic strategies included (a) multivariate analyses to examine the variation in adult adaptation as a function of sociometric classification at age 9–10, (b) regression analyses to evaluate the relative contribution of “liked most” and “liked least” peer nominations, and (c) structural equation modeling to predict the young adult outcome constructs from social preference at age 9–10. Contrary to expectation, when controlling for early antisocial behavior and academic skills, boys' social preference scores still predicted young adult outcomes. Longitudinal findings are discussed with respect to the salience of male peer rejection in middle childhood and the social developmental processes that may account for the predictive validity of peer rejection.This project was supported by a grant (MH 37940) from the National Institute of Mental Health (NIH) to Deborah Capaldi, PhD, Oregon Social Learning Center, and by grants (DA 05304 and DA 16110) from the National Institute on Drug Abuse (NIH) to the second author (T.J.D.). Thanks to Ann Simas for editing and graphics preparation on this manuscript.

The course of severe depressive symptoms from pregnancy to 6 months postpartum, as well as the occurrence of severe paranoid symptoms prenatally, were examined by the Millon Clinical Multiaxial Inventory I and the Beck Depression Inventory, in 78 women who were heavy, chronic cocaine users and who retained custody of their children after birth. Six months postpartum, the quality of caregiving was observed and assessed in the home, and the children were assessed on the Bayley MDI Index in the laboratory. Mothers who were depressed and paranoid prenatally, regardless of whether the depression continued to 6 months postpartum, were less sensitive in caregiving than women without severe symptoms of paranoia or depression during pregnancy or those who reported only depression that lifted by 6 months postpartum. Mothers who were depressed prenatally and continued to be depressed by 6 months postpartum, regardless of the presence or absence of paranoia, had infants who earned lower Bayley MDI scores than the offspring of women without severe psychological symptoms or women whose depression had lifted. Severe depressive symptoms during pregnancy, if they did not continue to 6 months postpartum, did not appear to adversely influence either caregiving or infant functioning.

Individuals who have experienced high levels of childhood stress are at increased risk for a wide range of behavioral problems that persist into adulthood, yet the neurobiological and molecular mechanisms underlying these associations remain poorly understood. Many of the difficulties observed in stress-exposed children involve problems with learning and inhibitory control. This experiment was designed to test individuals' ability to learn to inhibit responding during a laboratory task. To do so, we measured stress exposure among a community sample of school-aged children, and then followed these children for a decade. Those from the highest and lowest quintiles of childhood stress exposure were invited to return to our laboratory as young adults. At that time, we reassessed their life stress exposure, acquired functional magnetic resonance imaging data during an inhibitory control task, and assayed these individuals' levels of methylation in the FK506 binding protein 5 (FKBP5) gene. We found that individuals who experienced high levels of stress in childhood showed less differentiation in the dorsolateral prefrontal cortex between error and correct trials during inhibition. This effect was associated only with childhood stress exposure and not by current levels of stress in adulthood. In addition, FKBP5 methylation mediated the association between early life stress and inhibition-related prefrontal activity. These findings are discussed in terms of using multiple levels of analyses to understand the ways in which adversity in early development may affect adult behavioral adaptation.

Changes in conduct problems from middle school through early adulthood were examined in a sample of 1191 African American and White males and females. Predictors were selected from a number of ecological contexts to examine the relative contribution of family, peer, school, and neighborhood factors to conduct problems during the 7th, 8th, and 11th grade and across transitions in middle school, into high school, and into young adulthood. Almost all contexts made a unique contribution to conduct problems except for the neighborhood setting. The variables that had the most regular influences during each of these periods were Family Consistent Control, Family Discipline Harshness, and Negative Peers. Positive family and positive peer variables had less consistent relations to outcomes. School variables were more influential in middle school than later. Few gender or race differences were found in the patterning of predictors across time. Studies using only one or two settings as predictors of conduct problems, may provide a misleading picture of their impact by excluding other contextual influences.The authors acknowledge the Russell Sage Foundation, the National Institute of Child Health and Human Development, the National Institute of Mental Health, and the following individuals (listed alphabetically) for support during the preparation of this article: Elaine Belansky, Todd Bartko, Heather Bouchey, Nick Butler, Celina Chatman, Diane Early, Kari Fraser, Leslie Gutman, Katie Jodl, Ariel Kalil, Linda Kuhn, Sarah Lord, Karen McCarthy, Oksana Malanchuk, Alice Michael, Melanie Overby, Robert Roeser, Sherri Steele, Erika Taylor, Janice Templeton, Cindy Winston, and Carol Wong.

The World Health Organization recently reported that maternal mental health is a major public health concern. As many as one in four women suffer from psychiatric disorders at some point during pregnancy or the first postpartum year. Furthermore, self-injurious thoughts and behaviors (SITBs) represent one of the leading causes of death among women during this time. Thus, efforts to identify women at risk for serious forms of psychopathology and especially for SITBs are of utmost importance. Despite this urgency, current single-diagnostic approaches fail to recognize a significant subset of women who are vulnerable to perinatal stress and distress. The current study was among the first to investigate emotion dysregulation—a multilevel, transdiagnostic risk factor for psychopathology—and its associations with stress, distress, and SITBs in a sample of pregnant women (26–40 weeks gestation) recruited to reflect a range of emotion dysregulation. Both self-reported emotion dysregulation and respiratory sinus arrhythmia, a biomarker of emotion dysregulation, demonstrated expected associations with measures of mental health, including depression, anxiety, borderline personality pathology, and SITBs. In addition, self-reported emotion dysregulation was associated with blunted respiratory sinus arrhythmia responsivity to an ecologically valid infant cry task. Findings add to the literature considering transdiagnostic risk during pregnancy using a multiple-levels-of-analysis approach.

Altered functioning of the hypothalamic–pituitary–adrenal (HPA) axis is a robust correlate of major depression in adults, and to a lesser extent, in adolescents. Premorbid differences in HPA axis function have been found to prospectively predict the onset of adolescent depression. To what extent might our knowledge of HPA axis function in adolescents with, or at risk for, depression, help guide efforts to prevent depression in this age group? We review evidence regarding the role of the HPA axis in the development of adolescent depression, and examine whether and which HPA axis measures might be useful in guiding prevention efforts as (a) as a criterion by which to select youth at risk for depression, (b) as a predictor of which youth will be most responsive to prevention efforts, and (c) as an indicator of whether prevention/intervention efforts are working. We conclude that our current understanding of the HPA axis, and its measurement, in adolescent depression are not sufficiently precise to be of immediate practical use in improving prevention efforts. Incorporating HPA axis measures into prevention studies, however, would be immensely useful in clarifying the role of the HPA axis in adolescent depression, such that future prevention efforts might more confidently rely on HPA axis information.

Little is known about the long-term neural consequences of adverse life events for healthy adolescents, and this is particularly the case for events that occur after a putative stress-sensitive period in early childhood. In this functional magnetic resonance imaging study of healthy adolescents, we found that prior exposure to severe adverse life events was associated with current anxiety and with increased amygdala reactivity to standardized emotional stimuli (viewing of fearful faces relative to calm ones). Conjunction analyses identified multiple regions, including the amygdala, insula, and prefrontal cortex, in which reactivity to emotional faces covaried with life events as well as with current anxiety. Our morphometric analyses suggest systemic alterations in structural brain development with an association between anxiety symptoms and global gray matter volume. No life events were reported for the period before 4 years of age, suggesting that these results were not driven by exposure to stress during an early sensitive period in development. Overall, these data suggest systemic effects of traumatic events on the dynamically developing brain that are present even in a nonclinical sample of adolescents.

This research examined personal-accentuation and contextual-amplification models of pubertal timing, wherein personal and contextual risks magnify the effects of earlier pubertal maturation on youth depression. A sample of 167 youths (M age = 12.41 years, SD = 1.19) and their maternal caregivers completed semistructured interviews and questionnaires at two waves. Consistent with a personal-accentuation model, earlier pubertal maturation more strongly predicted subsequent depression in youths with prior depression, certain personality traits, and maladaptive stress responses than in youths without these personal risks. Several of these effects were specific to earlier-maturing girls. Consistent with a contextual-amplification model, earlier pubertal maturation more strongly predicted subsequent depression in youths exposed to recent maternal depression and family stress than in youths without these contextual risks. These findings identify key characteristics of youths and their family context that help to explain individual variation in depressive reactions to earlier pubertal maturation. More broadly, this research contributes to integrative models of depression that consider the interplay among personal vulnerability, contextual risk, and developmental transitions.

A multidimensional study examined individual differences in observed behavior of 59 depressed mothers interacting with their 3–13-month-old infants in relation to selected demographic and psychosocial variables. Maternal competence–defined as sensitive, affectively appropriate maternal behavior, was positively related to maternal education, family income, and the number of hours mothers worked outside the home. Maternal competence was inversely related to life stress, marital discord, poor social support, and infant difficulty; all of these relations appeared to be mediated by the women's feelings of self-efficacy in the maternal role. A “risk index,” composed of noncorrelated variables (family income, hours per week mother worked outside the home, and maternal self-efficacy), was strongly related to maternal parenting competence. These results suggest that the quality of depressed mothers' behavior with their babies is related to self-evaluations and contextual risk or protective factors. The findings also highlight the heterogeneity in life circumstances and functioning of depressed women and the probable resulting variability in the level of functioning of their children.

The significance of genotype–environment interplay is its focus on how causal factors, whether environmental or genetic, have their effects. It is difficult to establish causality in observational research because of the potential for reverse causation and confounding. Most environmental measures are heritable, which means that their effects on the risk for psychopathology are potentially confounded by genotype. In contrast, genetic influences on psychopathology may be mediated by their effect on environmental exposures. The existence of genetic influences on putative environmental risk factors offers both possibilities and pitfalls for research into environmental epidemiology. We use the example of parenting and its influence on childhood externalizing problems to review how genotype–environment correlations can be exploited to demonstrate causal processes in pyschopathology.

This replication study examined protective effects of positive childhood memories with caregivers (“angels in the nursery”) against lifespan and intergenerational transmission of trauma. More positive, elaborated angel memories were hypothesized to buffer associations between mothers’ childhood maltreatment and their adulthood posttraumatic stress disorder (PTSD) and depression symptoms, comorbid psychopathology, and children's trauma exposure. Participants were 185 mothers (M age = 30.67 years, SD = 6.44, range = 17–46 years, 54.6% Latina, 17.8% White, 10.3% African American, 17.3% other; 24% Spanish speaking) and children (M age = 42.51 months; SD = 15.95, range = 3–72 months; 51.4% male). Mothers completed the Angels in the Nursery Interview (Van Horn, Lieberman, & Harris, 2008), and assessments of childhood maltreatment, adulthood psychopathology, children's trauma exposure, and demographics. Angel memories significantly moderated associations between maltreatment and PTSD (but not depression) symptoms, comorbid psychopathology, and children's trauma exposure. For mothers with less positive, elaborated angel memories, higher levels of maltreatment predicted higher levels of psychopathology and children's trauma exposure. For mothers with more positive, elaborated memories, however, predictive associations were not significant, reflecting protective effects. Furthermore, protective effects against children's trauma exposure were significant only for female children, suggesting that angel memories may specifically buffer against intergenerational trauma from mothers to daughters.

Past research highlights the importance of considering the sequelae of physical abuse in the context of other risk factors and possible exacerbating circumstances. The present research examines the relative, unique, and interactive effects of physical abuse, sociocultural disadvantage, and cumulative negative life events. Multiple measures and data sources were used to assess the socioeconomic circumstances, exposure to recent negative events, and social, cognitive, and affective adjustment of 19 physically abused and 49 nonabused elementary school-age children. Results indicated that abuse strongly independently predicted problems in children's adjustment with peers, self-perceptions, and depression. Abuse was also related to increased behavioral problems at home and at school, though this relation abated and even reversed itself as social disadvantage increased. Cumulative negative events independently predicted negative self-perceptions and, for girls, increased depression. Socioeconomic hardship was independently related to children's cognitive maturity. In addition, socioeconomic disadvantage qualified the relation between negative events and children's adjustment to peers, such that increased negative events were related to lower peer adjustment among less disadvantaged children but increased peer adjustment of children with more disadvantage. These results support calls for a more contextualized approach to examining the developmental outcomes of physical abuse, one that considers multiple risk factors simultaneously.

The goal of this study was to examine whether growth delay can serve as an index of allostatic load during early development, as it is well known that the activity of stress-mediating systems inhibits growth. The participants were children adopted internationally from institutional care (n = 36), children adopted internationally from foster care (n = 26), and nonadopted children (n = 35). For the adopted children, height for age and weight for height were assessed at adoption; for all children, disinhibited social approach (DSA; termed elsewhere as “indiscriminate friendliness”) and diurnal cortisol were assessed at 6–8 years (M = 6.9 years). For internationally adopted children in general, and postinstitutionalized children specifically, linear growth delay assessed at the time of adoption was associated with more dysregulated behavior in response to an unfamiliar adult (i.e., greater DSA) and a more dysregulated diurnal cortisol rhythm (i.e., higher late afternoon and evening values). Further, among the most growth-delayed children, higher cortisol levels later in the day were correlated with DSA. The potential for using growth delay as an allostatic load indicator and the possible problems and limitations in its use in child populations are discussed.

This article reviews past research on the parenting characteristics of childhood sexual abuse survivors and presents the results of a qualitative study exploring the women's perspectives on mothering as a survivor. Grounded theory was used in the collection and analysis of the data. Data sources included the narrative responses of 79 women (mean age = 38.2 years) and in-depth interviews of a purposive sample of 15 women (mean age = 39 years). They had an average of 2.2 children, ranging in age from 5 months to young adulthood. The theoretical model identified through analysis of data using the constant comparison method was entitled “The Hard Work of Mothering as a Survivor.” Processes emerged that described the ways participants managed the work of mothering in light of memories of the abuse and attempts to heal from this earlier trauma. The conditions for committing to the work included becoming aware of and accepting the reality of the abuse and how it affected one's life, and taking on the hard work of developing a mothering self. This included expanding awareness, developing and evaluating a personal model of mothering, navigating typical and abuse salient parenting challenges, mothering through the pain of recovery, and battling for balance. The findings highlighted the dynamic, multifaceted nature of recovery and resilience for these mothers and the need for an increased focus on parenting in counseling with childhood sexual abuse survivors. Provision of anticipatory guidance regarding commonly experienced stressors at varying stages of the child's development and the mother's stage of recovery and methods for coping with these challenges, would benefit these mothers and promote parenting competence. Specific implications for psychotherapy and directions for future research are discussed.