Several theoretical models of child development have posited the spread of conflict within families; however, few researchers have studied this process in association with relationships children have with teachers and peers at school. The present study examined the direct, additive, and interactive contributions of interparental, parent–child, and sibling conflict in relation to teacher–child and child–peer conflict in a sample of 117 low-income boys from ages 3.5 to 6 years. Overall, the results suggest that while conflict in any one dyadic family relationship is only modestly associated with later conflictual relationships at school, risk for conflict in relationships with teachers and peers increases when multiple forms of early family conflict are experienced. Results are discussed in terms of the development of conflict across early relationships.

Child maltreatment, peer victimization, and a polymorphism of the serotonin transporter gene (5-HTTLPR) were examined as predictors of depressive symptomatology. Children (M age = 11.26, SD = 1.65), including 156 maltreated and 145 nonmaltreated children from comparable low socioeconomic backgrounds, provided DNA samples and self-reports of relational peer victimization, overt peer victimization, and depressive symptoms. Path analysis showed that relational and overt victimization mediated the association between child maltreatment and depressive symptoms. Bootstrapping procedures were used to test moderated mediation and demonstrated that genotype moderated the indirect effects of relational and overt victimization on child depressive symptoms, such that victimized children with the long/long variation were at an increased risk for depressive symptoms compared to victimized children carrying a short allele. Results highlight the utility of examining process models that incorporate biological and psychological factors contributing to the development of depressive symptomatology and provide direction toward understanding and promoting resilience among high-risk youth from a multiple levels of analysis approach.

Age at menarche, a sentinel index of pubertal maturation, was examined in relation to early family relationships (conflict, cohesion) and polymorphic variation in the gene encoding estrogen receptor-α (ESR1) in a midlife sample of 455 European American women. Consistent with prior literature, women who reported being raised in families characterized by close interpersonal relationships and little conflict tended to reach menarche at a later age than participants reared in families lacking cohesion and prone to discord. Moreover, this association was moderated by ESR1 variation, such that quality of the family environment covaried positively with menarcheal age among participants homozygous for minor alleles of the two ESR1 polymorphisms studied here (rs9304799, rs2234693), but not among women of other ESR1 genotypes. In addition, (a) family relationship variables were unrelated to ESR1 variation, and (b) genotype-dependent effects of childhood environment on age at menarche could not be accounted for by personality traits elsewhere shown to explain heritable variation in reported family conflict and cohesion. These findings are consistent with theories of differential susceptibility to environmental influence, as well as the more specific hypothesis (by Belsky) that girls differ genetically in their sensitivity to rearing effects on pubertal maturation.

Adolescents' trajectories of impulsive and hostile behaviors provide a dynamic index of risk for the emergence of Cluster B (antisocial and borderline) personality disorders in early adulthood. In the current study, we tested the hypothesis that preoccupied states of mind in the Adult Attachment Interview would increase both the level and rate of growth in adolescents' trajectories of aggressive and sexual risk-taking behaviors measured at ages 13, 15, and 17. Overall, preoccupied states of mind predicted higher levels of sexual risk taking and aggressive behaviors across all three assessments as well as higher rates of growth in sexual-risk taking and caregiver-reported aggression over time. In addition, preoccupied females showed slower rates of decline in self-reported hostile emotions than did preoccupied males. The effects of gender as a moderator of the relations between preoccupied status and risk trajectories for personality disorders are discussed.

This longitudinal study investigated the relation between negative reactivity and attachment in children with Down syndrome (DS). Specifically, we examined whether extremely low negative reactivity is associated with the enactment and organization of attachment behaviors. To address this issue 30 infants with DS (13 female, 17 male) were observed in Ainsworth's Strange Situation at 19 and 27 months. The intensity and duration of distress reactions were coded in 15-s intervals throughout each Strange Situation episode. Children's distress intensity during separations from caregivers was used to place children into Low versus Moderate/High Negative Reactivity groups. In addition, ratings of infants' social interactive behaviors (contact maintenance, proximity seeking, distance interaction, resistance, and avoidance) were made for each episode and used to assess the quality of infants' attachment relationships. The data indicated that there are high rates of Type A and D insecure attachments within the DS population at each age studied. However, low negative reactivity was not consistently related to the activation of the attachment behavioral system, or associated with insecure attachment relationships. Alternative explanations for the high rate of insecure attachments are discussed.

Identifying prenatal environmental factors that have genuinely causal effects on psychopathology is an important research priority, but it is crucial to select an appropriate research design. In this review we explain why and what sorts of designs are preferable and focus on genetically informed/sensitive designs. In the field of developmental psychopathology, causal inferences about prenatal risks have not always been based on evidence generated from appropriate designs. We focus on reported links between maternal smoking during pregnancy and offspring attention-deficit/hyperactivity disorder or conduct problems. Undertaking a systematic review of findings from genetically informed designs and “triangulating” evidence from studies with different patterns of bias, we conclude that at present findings suggest it is unlikely that there is a substantial causal effect of maternal smoking in pregnancy on either attention-deficit/hyperactivity disorder or conduct problems. In contrast, for offspring birth weight (which serves as a positive control) findings strongly support a negative causal effect of maternal smoking in pregnancy. For maternal pregnancy stress, too few studies use genetically sensitive designs to draw firm conclusions, but continuity with postnatal stress seems important. We highlight the importance of moving beyond observational designs, for systematic evaluation of the breadth of available evidence and choosing innovative designs. We conclude that a broader set of prenatal risk factors should be examined, including those relevant in low- and middle-income contexts. Future directions include a greater use of molecular genetically informed designs such as Mendelian randomization to test causal hypotheses about prenatal exposure and offspring outcome.

Research has shown a developmental process of “maturing out” of alcohol involvement beginning in young adulthood, but the precise nature of changes characterizing maturing out is unclear. We used latent transition analysis to investigate these changes in a high-risk sample from a longitudinal study of familial alcoholism (N = 844; 51% children of alcoholics; 53% male, 71% non-Hispanic Caucasian, 27% Hispanic). Analyses classified participants into latent drinking statuses during late adolescence (ages 17–22), young adulthood (ages 23–28), and adulthood (ages 29–40), and characterized transitions among these statuses over time. The resulting four statuses were abstainers, low-risk drinkers who typically drank less than weekly and rarely binged or showed drinking problems, moderate-risk drinkers who typically binged less than weekly and showed moderate risk for drinking problems, and high-risk drinkers who typically binged at least weekly and showed high risk for drinking problems. Maturing out between late adolescence and young adulthood was most common among initial high-risk drinkers, but they typically declined to moderate-risk drinking rather than to nonrisky drinking statuses. This suggests that the developmental phenomenon of maturing out pertains primarily to relatively high-risk initial drinkers and that many high-risk drinkers who mature out merely reduce rather than eliminate their risky drinking.

This paper reports on a randomized control trial involving children less than 3 years old and their mothers who were regarded at risk of maltreating their children by referral agencies. Mothers’ risk status derived from a heavy trauma burden (average exposure over the first 18 years of their lives to 10 possible adverse childhood experiences [ACEs] was >5), mental health challenges (15%–28% had experienced a prior psychiatric hospitalization), and prior removal of a child to foster care (20%). Mothers were randomly assigned to either a widely used parenting class known as Systematic Training for Effective Parenting (STEP) or the Group Attachment-Based Intervention (GABI), a multifamily 26-week treatment. The resulting mother–child pairs available for consideration in this baseline versus end-of-treatment report were 35 families in the STEP arm and 43 families in the GABI arm. The focus of this paper is the outcome measure of observed parent–child relationship assessed with the Coding of Interactive Behavior (Feldman, 1998) collected at baseline and end of treatment. In comparison to STEP, results indicated that GABI was linked to significant improvements in maternal supportive presence and dyadic reciprocity, and significant declines in maternal hostility and dyadic constriction (proxies for risk of child maltreatment). These medium-to large-sized effects remained significant even after controlling for mothers’ prior ACEs in analysis of covariance procedures. In addition, two small interaction effects of ACEs by treatment type were found, underlining the need for, and value of, treatments that are sensitive to parents’ traumatic histories.

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.

While many studies focus on the association between early life adversity and the later risk for psychopathology, few simultaneously explore diverse forms of environmental adversity. Moreover, those studies that examined the cumulative impact of early life adversity focus uniquely on postnatal influences. The objective of this study was to focus on the fetal period of development to construct and validate a cumulative prenatal adversity score in relation to a wide range of neurodevelopmental outcomes. We also examined the interaction of this adversity score with a biologically informed genetic score based on the serotonin transporter gene. Prenatal adversities were computed in two community birth cohorts using information on health during pregnancy, birth weight, gestational age, income, domestic violence/sexual abuse, marital strain, as well as maternal smoking, anxiety, and depression. A genetic score based on genes coexpressed with the serotonin transporter in the amygdala, hippocampus, and prefrontal cortex during prenatal life was constructed with an emphasis on functionally relevant single nucleotide polymorphisms, that is, expression quantitative trait loci. Prenatal adversities predicted a wide range of developmental and behavioral alterations in children as young as 2 years of age in both cohorts. There were interactions between the genetic score and adversities for several domains of the Child Behavior Checklist (CBCL), with pervasive developmental problems remaining significant adjustment for multiple comparisons. Scores combining different prenatal adverse exposures predict childhood behavior and interact with the genetic background to influence the risk for psychopathology.

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.

The effects of psychoactive substance abuse are not limited to the user, but extend to the entire family system, with children of substance abusers being particularly at risk. This meta-analysis attempted to quantify the longitudinal relationship between parental alcohol, tobacco, and drug use and child well-being, investigating variation across a range of substance and well-being indices and other potential moderators. We performed a literature search of peer-reviewed, English language, longitudinal observational studies that reported outcomes for children aged 0 to 18 years. In total, 56 studies, yielding 220 dependent effect sizes, met inclusion criteria. A multilevel random-effects model revealed a statistically significant, small detriment to child well-being for parental substance abuse over time (r = .15). Moderator analyses demonstrated that the effect was more pronounced for parental drug use (r = .25), compared with alcohol use (r = .13), tobacco use (r = .13), and alcohol use disorder (r = .14). Results highlight a need for future studies that better capture the effect of parental psychoactive substance abuse on the full breadth of childhood well-being outcomes and to integrate substance abuse into models that specify the precise conditions under which parental behavior determines child well-being.

Registration: PROSPERO CRD42017076088

This study examined individual differences in how mothers' depressive symptoms affect children's early adjustment. It tested whether problematic development among children high in negative emotionality is accentuated by (a) maternal reactivity, the negative reactivity of mothers with depressive symptoms to difficult child characteristics; and (b) child vulnerability, the susceptibility of negatively emotional children to the negative parenting of mothers with depressive symptoms. Based on 1,364 participants from the NICHD Study of Early Child Care, results showed that mothers' depressive symptoms predicted greater risk for adjustment problems at age 3 among children who as infants were high rather than low in negative emotionality. Increased risk was evident for behavior problems, low responsiveness, high separation distress, and low social competence. Mediational tests suggested that increased risk reflected maternal reactivity: the stronger mothers' depressive symptoms, the more they responded with negative parenting to children high in negative emotionality. The proposal that child vulnerability mediates the greater impact of mothers' depressive symptoms on negatively emotional children was verified only for separation distress. The results support the proposal that, when mothers are high in depressive symptoms, aversive characteristics of children and their behavior increasingly influence early adjustment and do so because they elicit negative parent behavior.

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.

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.

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.

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.

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.

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.