In the present study, we used separate measures of parental monitoring and parental knowledge and compared their associations with youths’ antisocial behavior during preadolescence, between the ages of 10 and 12. Parental monitoring and knowledge were reported by mothers, fathers, and youths taking part in the Environmental Risk (E-Risk) Longitudinal Twin Study that follows 1,116 families with twins. Information on youths’ antisocial behavior was obtained from mothers as well as teachers. We report two main findings. First, longitudinal cross-lagged models revealed that greater parental monitoring did not predict less antisocial behavior later, once family characteristics were taken into account. Second, greater youth antisocial behavior predicted less parental knowledge later. This effect of youths’ behavior on parents’ knowledge was consistent across mothers’, fathers’, youths’, and teachers’ reports, and robust to controls for family confounders. The association was partially genetically mediated according to a Cholesky decomposition twin model; youths’ genetically influenced antisocial behavior led to a decrease in parents’ knowledge of youths’ activities. These two findings question the assumption that greater parental monitoring can reduce preadolescents’ antisocial behavior. They also indicate that parents’ knowledge of their children's activities is influenced by youths’ behavior.

Parental depression is associated with disruptions in the parent–child relationship, exposure to stressful family life events, and offspring depressive symptoms. Evidence suggests that intergenerational transmission of depression involves environmental and inherited contributions. We sought to evaluate the role of passive gene–environment correlation (rGE) in relation to depression, family life events that were due to parental behavior, and parental positivity in a sample where children varied in genetic relatedness to their rearing parents. Our study included 865 families with children born through assisted conception (444 related to both parents, 210 related to the mother only, 175 related to the father only, and 36 related to neither parent). Consistent with previous studies, the intergenerational transmission of depressive symptoms was largely due to environmental factors, although parent and child gender influenced results. Maternal and paternal depressive symptoms were associated with reduced positivity and increased parentally imposed life events regardless of parent–child relatedness. Results of path analysis were consistent with passive rGE for both maternal and paternal positivity in that positivity partially mediated the link between maternal/paternal depression and child depression only in genetically related parent–child pairs. Results also suggested passive rGE involving parentally imposed life events for mothers and fathers although passive rGE effects were smaller than for positivity.

The current study examined the course of depressive symptoms of young men from early adolescence through young adulthood using a growth model approach and the influence of early parental (i.e., depressive symptoms, antisocial behaviors, substance use) and contextual (i.e., family income and parental marital transitions) risk factors on both the level of depressive symptoms in early adolescence and on changes over a 10-year period, controlling for young men's early antisocial behavior. On average, depressive symptoms of the youths tended to decrease slightly as they reached young adulthood. Among the parental and contextual risk factors, parent's marital transitions was the most significant predictor for the level of depressive symptoms in early adolescence. Parent's marital transitions and family income were also significantly related to changes in depressive symptoms. As hypothesized, there was a significant interaction effect of paternal and maternal depressive symptoms on depressive symptoms in early adolescence and on changes over time. Maternal depressive symptoms were related to the son's depressive symptoms only when the father's depressive symptoms were also high. The results also suggested that parenting practices did not mediate the effects of the parental and contextual risk factors on the development of depressive symptoms among young men.

Previous research suggests that mothers’ and fathers’ parenting may be differentially influenced by marital and child factors within the family. Some research indicates that marital stress is more influential in fathers’ than mothers’ parenting, whereas other research shows that children's difficult behavior preferentially affects mothers’ parenting. The present study examined marital stress and children's externalizing behavior in middle childhood as predictors of mothers’ versus fathers’ consistency, monitoring, and support and care in early adolescence, and the subsequent associations of these parenting behaviors with externalizing behavior 1.5 years later. Pathways were examined within a longitudinal mediation model testing for moderation by parent gender (N = 276 mothers, N = 229 fathers). Children's externalizing behavior in middle childhood was found to more strongly inversely predict mothers’ versus fathers’ monitoring in early adolescence. In contrast, marital stress more strongly predicted low monitoring for fathers than for mothers. Regardless of parent gender, marital stress predicted lower levels of parental consistency, and children's externalizing behavior predicted lower levels of parental support. Mothers’ monitoring and fathers’ support in early adolescence predicted lower levels of externalizing behavior 1.5 years later. The results are discussed with respect to family transactions relative to parent gender and implications for intervention.

Despite the commonly held belief that there is a high degree of intergenerational continuity in maltreatment, studies to date suggest a mixed pattern of findings. One reason for the variance in findings may be related to the measurement approach used, which includes a range of self-report and official indicators of maltreatment and both cross-sectional and longitudinal designs. This study attempted to shed light on the phenomenon of intergenerational continuity of maltreatment by examining multiple indicators of perpetration of maltreatment in young adults and multiple risk factors across different levels within an individual's social ecology. The sample included 166 women who had been placed in out-of-home care as adolescents (>85% had a substantiated maltreatment incident) and followed into young adulthood, and included three waves of adolescent data and six waves of young adult data collected across 10 years. The participants were originally recruited during adolescence as part of a randomized controlled trial examining the efficacy of the Treatment Foster Care Oregon intervention. Analyses revealed weak to modest associations among the three indicators of perpetration of maltreatment in young adulthood, that is, official child welfare records, self-reported child welfare system involvement, and self-reported maltreatment (r = .03–.51). Further, different patterns of prediction emerged as a function of the measurement approach. Adolescent delinquency was a significant predictor of subsequent self-reported child welfare contact, and young adult partner risk was a significant predictor of perpetration of maltreatment as indexed by both official child welfare records and self-reported child welfare contact. In addition, women who were originally assigned to the intervention condition reported perpetrating less maltreatment during young adulthood. Implications for measurement and interventions related to reducing the risk for intergenerational transmission of risk are discussed.

Differential susceptibility theory stipulates that some children are more susceptible than others to both supportive and adverse developmental experiences/exposures. What remains unclear is whether the same individuals are most affected by different exposures (i.e., domain general vs. specific). We address this issue empirically for the first time using, for illustrative and proof-of-principle purposes, a novel influence-statistics’ method with data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care. Results indicated that previously documented effects of greater quality of care on enhanced pre-academic skills and greater quantity of care on more behavior problems apply mostly to different children. Analyses validating the new method indicated, as predicted, that (a) the quantity-of-care effect applied principally to children from more socioeconomically advantaged families and that (b) being highly susceptible to both, one or neither childcare effect varied as a function of a three-gene, polygenic-plasticity score (serotonin transporter linked polymorphic region [5-HTTLPR], dopamine receptor D4 [DRD4], brain-derived neurotrophic factor [BDNF]) in a dose–response manner (i.e., 2>1>0). While domain-specific findings involving child-care effects cannot be generalized to other environmental influences, the influence-statistics’ approach appears well suited for investigating the generality–specificity of environment effects, that is, of “differential, differential susceptibility.”

Rigorously evaluated interventions that target protective factors and positive resources rather than ameliorating negative outcomes in child refugees are rare. To address this, we developed and evaluated a short, group-based resilience-building intervention called Strengths for the Journey (SFJ), which was designed for war-affected children. We conducted a quasi-randomized pilot study of the SFJ intervention with 72 7- to 14-year-old forcibly displaced children (Mage = 10.76, 64.8% female) in three refugee camps in Lesvos, Greece. Intervention effectiveness was assessed by measuring pre-post changes in well-being, self-esteem, optimism, and depressive symptoms from before (T1) to immediately after the intervention/wait-list task (T2). Four focus group interviews were conducted with 31 of the participants to discuss their views on the effects of the intervention and the continued use of the skills that were learned. Using repeated-measures ANOVAs, we found improvements in well-being, F (1, 46) = 42.99, ηp2 = .48, self-esteem, F (1, 56) = 29.11, ηp2 = .40, optimism, F (1, 53) = 27.16, ηp2 = .34, and depressive symptoms, F (1, 31) = 62.14, ηp2 = .67, in the intervention group compared with the wait-listed group (p < .05). Focus group participants highlighted the importance of SFJ in developing a sense of togetherness and building their strengths. Child refugees in low-resource settings may benefit from brief, first-line interventions that target protective factors such as well-being, hope, self-esteem, and belonging.

How do clinical observations of repression square with experimental evidence suggesting that emotionally arousing memories are especially enduring? This discrepancy can be understood by examining three kinds of memory distortions that give the impression in a clinical context, of repression. Potentially traumatic events such as childhood sexual abuse (CSA) may be subject to ordinary forgetting. Recent research suggests people who fail to understand the sexual nature of CSA report that they remember it less well. In other words, the event occurred and it was forgotten, but not “repressed.” In addition, people may be wrong about experiencing a period of forgetting, i.e. the event occurred but was never forgotten. Finally, people may believe that a particular traumatic event occurred and was repressed when, in fact, it did not happen in the first place. Under certain circumstances, some combination of these distortions could lead to situations that are mistakenly interpreted as repression.

The present study examined the specificity of autobiographical memory in adolescents and adults with versus without child sexual abuse (CSA) histories. Eighty-five participants, approximately half of whom per age group had experienced CSA, were tested on the Autobiographical Memory Interview. Individual difference measures, including those for trauma-related psychopathology, were also administered. Findings revealed developmental differences in the relation between autobiographical memory specificity and CSA. Even with depression statistically controlled, reduced memory specificity in CSA victims relative to controls was observed among adolescents but not among adults. A higher number of posttraumatic stress disorder criteria met predicted more specific childhood memories in participants who reported CSA as their most traumatic life event. These findings contribute to the scientific understanding of childhood trauma and autobiographical memory functioning and underscore the importance of considering the role of age and degree of traumatization within the study of autobiographical memory.

Early identification of problems with psychosocial stress regulation is important for supporting mental and physical health. However, we currently lack knowledge about when reliable individual differences in stress-responsive physiology emerge and which aspects of maternal behavior determine the unfolding of infants' stress responses. Knowledge of these processes is further limited by analytic approaches that do not account for multiple levels of within- and between-family effects. In a low-risk sample (n = 100 dyads), we observed infant cortisol and mother/infant behavior during regular play and stress sessions longitudinally from age 1 to 3, and used a three-level model to separately examine variability in infant cortisol trajectories within sessions, across years, and across infants. Stable individual differences in hypothalamus–pituitary–adrenal axis regulation were observed in the first 3 years of life. Infants of less sensitive and more intrusive mothers manifested stress sensitization, that is, elevated cortisol levels during and following stress exposure, a profile related to behavioral distress. These findings have important practical implications, suggesting that children at risk for long-term stress dysregulation may be identified in the earliest years of life.

The natural history and course of borderline personality disorder (BPD) has long been the focus of speculation, typically guided by impressions from clinical work with BPD-affected individuals. Not unlike the other personality disorders (PDs), it has long been assumed that BPD is relatively stable, traitlike, and enduring in nature. The extent to which BPD is or is not a plastic construct has implications not only for understanding its longitudinal course, but also for understanding its development and, ultimately, its treatment and/or prevention. This paper consists of two parts. The first part reviews the longitudinal research corpus that bears directly upon the issue of stability of BPD in both adolescents and adults. The consistent trend in very nearly all studies, whether using a categorical or dimensional approach to assessment, is one of considerable change over time. This literature presents complexities, however, because most of the extant studies examine BPD-affected individuals who have been exposed to treatment. However, at least two large-scale longitudinal studies, which include both treated and untreated persons, also provide support for viewing BPD as a malleable disorder that declines in severity over time. The second part presents original data from the Longitudinal Study of Personality Disorders that specifically examine the predictors of change in BPD using a neurobehavioral model of personality within an individual growth curve (IGC) analytical framework. This IGC analysis revealed important predictors of both overall level of BPD features as well as rate of change in BPD features, with particularly important roles played by the agentic positive emotion (i.e., incentive motivation) and anxiety (negative emotion) systems. The benefits of the IGC approach for understanding the developmental psychopathology of BPD is also stressed.This research was supported in part by NIMH Grant MH 45448 to Mark F. Lenzenweger for the Longitudinal Study of Personality Disorders.

Social-communication skills emerge within the context of rich social interactions, facilitated by an infant's capacity to attend to people and objects in the environment. Disruption in this early neurobehavioral process may decrease the frequency and quality of social interactions and learning opportunities, potentially leading to downstream deleterious effects on social development. This study examined early attention in infant siblings of children with autism spectrum disorder (ASD) who are at risk for social and communication delays. Visual and auditory attention was mapped from age 1 week to 5 months in infants at familial risk for ASD (high risk; N = 41) and low-risk typically developing infants (low risk; N = 39). At 12 months, a subset of participants (N = 40) was administered assessments of social communication and nonverbal cognitive skills. Results revealed that high-risk infants performed lower on attention tasks at 2 and 3 months of age compared to low-risk infants. A significant association between overall attention at 3 months and developmental outcome at 12 months was observed for both groups. These results provide evidence for early vulnerabilities in visual attention for infants at risk for ASD during a period of important neurodevelopmental transition (between 2 and 3 months) when attention has significant implications for social communication and cognitive development.

Childhood abuse and neglect (CAN) is considered as a risk factor for substance use disorder (SUD). Based on the drinking to cope model, this study investigated the association of two trauma-relevant emotions (shame and sadness) and substance use. Using ecological momentary assessment we compared real-time emotion regulation in situations with high and low intensity of shame and sadness in currently abstinent patients with CAN and lifetime SUD (traumaSUD group), healthy controls with CAN (traumaHC group), and without CAN (nontraumaHC group). Multilevel analysis showed a positive linear relationship between high intensity of both emotions and substance use for all groups. The traumaSUD group showed heightened substance use in low, as well as in high, intensity of shame and sadness. In addition, we found an interaction between type of emotion, intensity, and group: the traumaHC group exhibited a fourfold increased risk for substance use in high intense shame situations relative to the traumaSUD group. Our findings provide evidence for the drinking to cope model. The traumaSUD group showed a reduced distress tolerance for variable intensity of negative emotions. The differential effect of intense shame for the traumaHC group emphazises its potential role in the development of SUD following CAN. In addition, shame can be considered a relevant focus for therapeutic preinterventions and interventions for SUD after CAN.

The parent–child attachment relationship plays an important role in the development of the infant's stress regulation system. However, genetic and epigenetic factors such as FK506 binding protein 51 (FKBP5) genotype and DNA methylation have also been associated with hypothalamus–pituitary–adrenal axis functioning. In the current study, we examined how parent–child dyadic regulation works in concert with genetic and epigenetic aspects of stress regulation. We study the associations of attachment, extreme maternal insensitivity, FKBP5 single nucleotide polymorphism 1360780, and FKBP5 methylation, with cortisol reactivity to the Strange Situation Procedure in 298 14-month-old infants. The results indicate that FKBP5 methylation moderates the associations of FKBP5 genotype and resistant attachment with cortisol reactivity. We conclude that the inclusion of epigenetics in the field of developmental psychopathology may lead to a more precise picture of the interplay between genetic makeup and parenting in shaping stress reactivity.

Prenatal cocaine exposure may affect developing stress response systems in youth, potentially creating risk for substance use in adolescence. Further, pathways from prenatal risk to future substance use may differ for girls versus boys. The present longitudinal study examined multiple biobehavioral measures, including heart rate, blood pressure, emotion, and salivary cortisol and salivary alpha amylase (sAA), in response to a stressor in 193 low-income 14- to 17-year-olds, half of whom were prenatally cocaine exposed (PCE). Youth's lifetime substance use was assessed with self-report, interview, and urine toxicology/breathalyzer at Time 1 and at Time 2 (6–12 months later). PCE × Gender interactions were found predicting anxiety, anger, and sadness responses to the stressor, with PCE girls showing heightened responses as compared to PCE boys on these indicators. Stress Response × Gender interactions were found predicting Time 2 substance use in youth (controlling for Time 1 use) for sAA and sadness; for girls, heightened sadness responses predicted substance use, but for boys, dampened sAA responses predicted substance use. Findings suggest distinct biobehavioral stress response risk profiles for boys and girls, with heightened arousal for girls and blunted arousal for boys associated with prenatal risk and future substance use outcomes.

Psychosocial acceleration theory suggests that pubertal maturation is accelerated in response to adversity. In addition, suboptimal caregiving accelerates development of the amygdala–medial prefrontal cortex circuit. These findings may be related. Here, we assess whether associations between family environment and measures of the amygdala–medial prefrontal cortex circuit are mediated by pubertal development in more than 2000 9- and 10-year-old children from the Adolescent Brain Cognitive Development Study (http://dx.doi.org/10.15154/1412097). Using structural equation modeling, demographic, child-reported, and parent-reported data on family dynamics were compiled into a higher level family environment latent variable. Magnetic resonance imaging preprocessing and compilations were performed by the Adolescent Brain Cognitive Development Study's data analysis core. Anterior cingulate cortex (ACC) thickness, area, white matter fractional anisotropy, amygdala volume, and cingulo-opercular network–amygdala resting-state functional connectivity were assessed. For ACC cortical thickness and ACC fractional anisotropy, significant indirect effects indicated that a stressful family environment relates to more advanced pubertal stage and more mature brain structure. For cingulo-opercular network–amygdala functional connectivity, results indicated a trend in the expected direction. For ACC area, evidence for quadratic mediation by pubertal stage was found. Sex-stratified analyses suggest stronger results for girls. Despite small effect sizes, structural measures of circuits important for emotional behavior are associated with family environment and show initial evidence of accelerated pubertal development.

Cognitive ability, externalizing symptoms, and internalizing symptoms are correlated in children. However, it is not known why they combine in the general child population over time. To address this, we used data on 17,318 children participating in the UK Millennium Cohort Study and followed-up five times between ages 3 and 14 years. We fitted three parallel-process latent growth curve models to identify the parallel unfolding of children's trajectories of internalizing symptoms, externalizing symptoms, and cognitive ability across this period. We also examined the effects of time-invariant (ethnicity, birth weight, maternal education and age at birth, and breastfeeding status) and time-varying covariates (maternal psychological distress and socioeconomic disadvantage) on the growth parameters of the trajectories. The results showed that the intercepts of the trajectories of cognitive ability and, particularly, externalizing symptoms were inversely correlated. Their linear slopes were also inversely correlated, suggesting parallel development. Internalizing symptoms were correlated positively with externalizing symptoms and inversely (and more modestly) with cognitive ability at baseline, but the slope of internalizing symptoms correlated (positively) only with the slope of externalizing symptoms. The covariates predicted 9% to 41% of the variance in the intercepts and slopes of all domains, suggesting they are important common risk factors. Overall, it appears that externalizing symptoms develop in parallel with both cognitive ability and internalizing symptoms from early childhood through to middle adolescence. Children on an increasing trajectory of externalizing symptoms are likely both increasing in internalizing symptoms and decreasing in cognitive skills as well, and are thus an important group to target for intervention.

Previous research suggests that the experience of abuse and neglect in childhood has negative implications for physical health in adulthood. Using data from the Minnesota Longitudinal Study of Risk and Adaptation (N = 115), the present research examined the predictive significance of childhood physical abuse, sexual abuse, and physical/cognitive neglect for multilevel assessments of physical health at midlife (age 37–39 years), including biomarkers of cardiometabolic risk, self-reports of quality of health, and a number of health problems. Analyses revealed that childhood physical/cognitive neglect, but not physical or sexual abuse, predicted all three health outcomes in middle adulthood, even when controlling for demographic risk factors and adult health maintenance behaviors. We discuss possible explanations for the unique significance of neglect in this study and suggest future research that could clarify previous findings regarding the differential impact of different types of abuse and neglect on adult health.

A wealth of evidence documents associations between various aspects of the rearing environment and later development. Two evolutionary-inspired models advance explanations for why and how such early experiences shape later functioning: (a) the external-prediction model, which highlights the role of the early environment (e.g., parenting) in regulating children's development, and (b) the internal-prediction model, which emphasizes internal state (i.e., health) as the critical regulator. Thus, by using data from the NICHD Study of Early Child Care and Youth Development, the current project draws from both models by investigating whether the effect of the early environment on later adolescent functioning is subject to an indirect effect by internal-health variables. Results showed a significant indirect effect of internal health on the relation between the early environment and adolescent behavior. Specifically, early environmental adversity during the first 5 years of life predicted lower quality health during childhood, which then led to problematic adolescent functioning and earlier age of menarche for girls. In addition, for girls, early adversity predicted lower quality health that forecasted earlier age of menarche leading to increased adolescent risk taking. The discussion highlights the importance of integrating both internal and external models to further understand the developmental processes that effect adolescent behavior.

Corticotropin-releasing hormone (CRH) is distributed throughout the brain and in peripheral sites but primarily is localized in the paraventricular nucleus of the hypothalamus. It is a “master” stress hormone that is responsible for the synthesis of proopiomelanocortin (POMC) in the anterior pituitary gland. Behaviorally active peptide hormones, including adrenocorticotropin hormone (ACTH) and B-endorphin, are liberated from POMC by enzymes to activate critical processes during stress. CRH is not detectable in the circulation even during extreme stress. However, during human pregnancy, the human placenta expresses the gene for CRH (pCRH) resulting in detectable levels in maternal plasma that increases 20- to 40-fold over the course of gestation. Placental CRH is identical to CRH of hypothalamic origin in size, structure, immunoreactivity, and bioactivity. However, unlike the negative feedback between adrenal cortisol and hypothalamic CRH, cortisol stimulates the synthesis and release of pCRH. The bidirectional release of pCRH into maternal and fetal compartments is associated with regulating the timing of delivery, remodeling the fetal nervous system, and influencing developmental trajectories. Fetal exposure to pCRH during early and late gestation is associated with unique patterns of cortical thinning in school-age children. Placental CRH is elevated in response to physical and behavioral stress and may be an integrative marker of early adversity.