The prenatal and early postnatal periods constitute a time of rapid development when the brain is in a state of both heightened plasticity and vulnerability. Premature infants and infants of diabetic mothers represent two experiments of nature that allow researchers to observe how the developing brain responds to early biological challenge of either a global or regionally specific nature. We outline a set of organizing principles for conceptualizing the mechanisms by which early adverse experience may be encoded in the brain and subsequently expressed in behavior. We then review the available literature on developmental outcomes for infants born premature and infants of diabetic mothers. Research examining the relative influence of experience and maturation in the development of preterm infants indicates that advance experience does not accelerate the advent of specific cognitive capacities, but may enhance performance once the particular ability has emerged. Long-term follow-up of preterm infants also reveals evidence for plasticity and cognitive improvement into early adolescence for later maturing executive functions. Finally we offer an integrated model for investigating cognitive outcomes in infants of diabetic mothers that incorporates data from animal, electrophysiological, and behavioral measures.

Defining child maltreatment has never been easy. This is true irrespective of whether the focus is abuse or neglect, or whether the maltreatment in question is physical, emotional, and/or psychological in nature. Thus, McGee and Wolfe (1991) set for themselves no small task in generating an operational definition of psychological maltreatment that would be useful for research. In the main, I come away from their article believing that they have failed to advance the definitional state of the field, though admiring of their effort. In order to substantiate this point of view, I will begin by highlighting a series of concerns that I have with the definition they advance and end by raising broader questions about unstated assumptions that underlie their work.

Biometric analyses of variability in behavioral phenotypes have demonstrated that genotype plays a significant role in all behavioral development, but the developmental significance of the environment has remained obscure. Behavior genetic analyses typically show the effect of shared family environment to be very small, although considerable variability remains to be explained after genetic factors have been accounted for. Behavior geneticists have suggested, contrary to intuition, that almost all of the important effects of the environment serve to make family members more different from each other. Environmentalists of several persuasions have pointed to the crucial importance of the environment in the initiation and regulation of all developmental processes. In this article, we present a series of simulations to suggest that some of the difficulty of identifying environmental effects in biometric models is methodological. Adding simple dynamic parameters to models of development leads to systems in which environment produces substantial variability that can be detected in the context of a particular genotype, but vanishes when genotype is allowed to vary.

Prenatal exposure to maternal mood disturbances shapes children's cognitive development reflected in the critical construct of executive functions (EFs). Little is known, however, about underlying mechanisms. By examining cortisol responses in both everyday and lab challenge settings, we tested whether the child/offspring hypothalamic–pituitary–adrenal axis mediates effects of prenatal maternal mood on child EFs at age 6. In 107 Canadian children born to women with a wide range of anxious and depressive symptoms during pregnancy, we found that in boys but not girls, depressed and/or anxious prenatal maternal mood is associated with heightened diurnal cortisol levels in everyday settings, as well as heightened cortisol reactivity to a lab challenge and that this heightened reactivity was associated with poorer EFs. Among boys we also observed that cortisol reactivity but not diurnal cortisol mediated the association between depressed and/or anxious prenatal maternal mood and EFs. Depressed and/or anxious prenatal maternal mood was related to child EFs for both girls and boys. To our knowledge, this is the first study to demonstrate a mediating role for child stress regulation in the association between prenatal maternal stress-related mood disturbances and child EFs, providing evidence of a mechanism contributing to fetal programming of cognition.

The confluence model theorizes that dynamic transactions between peer rejection and deviant peer clustering amplify antisocial behavior (AB) within the school context during adolescence. Little is known about the links between peer rejection and AB as embedded in changing networks. Using longitudinal social network analysis, we investigated the interplay between rejection, deviant peer clustering, and AB in an ethnically diverse sample of students attending public middle schools (N = 997; 52.7% boys). Adolescents completed peer nomination reports of rejection and antisocial behavior in Grades 6–8. Results revealed that rejection status was associated with friendship selection, and adolescents became rejected if they were friends with others who were rejected. Youth befriended others with similar levels of AB. Significant patterns of peer influence were documented for AB and rejection. As hypothesized, rejected youth with low AB were more likely to affiliate with others with high AB instead of similarly low AB. In contrast, nonrejected youth preferred to befriend others with similarly high or low AB. Results support an updated confluence model of a joint interplay between rejection and AB as ecological conditions that lead to self-organization into deviant clusters in which peer contagion on problem behaviors operates.

Psychobiological models of allostatic load have delineated the effects of multiple processes that contribute to risk for psychopathology. This approach has been fruitful, but the interactive contributions of allostatic and environmental load remain understudied in early childhood. Because this developmental period encompasses the emergence of internalizing problems and biological sensitivity to early experiences, this is an important time to examine this process. In two studies, we examined allostatic and environmental load and links to subsequent internalizing and externalizing problems. Study 1 examined relations between load indices and maladjustment, concurrently and at multiple times between age 2 and kindergarten; Study 2 added more comprehensive risk indices in a sample following a group of highly fearful toddlers from 2 to 3 years of age. Results from both studies showed that increased allostatic load related to internalizing problems as environmental risk also increased. Study 2, in addition, showed that fearfulness interacted with allostatic and environmental load indices to predict greater anxiety among the fearful children who had high levels of allostatic and environmental load. Taken together, the findings support a model of risk for internalizing characterized by the interaction of biological and environmental stressors, and demonstrate the importance of considering individual differences and environmental context in applying models of allostatic load to developmental change in early childhood.

Early adversities that are caregiving-related (crEAs) are associated with a significantly increased risk for mental health problems. Recent neuroscientific advances have revealed alterations in medial prefrontal cortex (mPFC)-subcortical circuitry following crEAs. While this work has identified alterations in affective operations (e.g., perceiving, reacting, controlling, learning) associated with mPFC–subcortical circuitry, this circuitry has a much broader function extending beyond operations. It plays a primary role in affective meaning making, involving conceptual-level, schematized knowledge to generate predictions about the current environment. This function of mPFC–subcortical circuitry motivates asking whether mPFC–subcortical phenotypes following crEAs support semanticized knowledge content (or the concept-level knowledge) and generate predictive models. I present a hypothesis motivated by research findings across four different lines of work that converge on mPFC–subcortical neuroanatomy, including (a) the neurobiology supporting emotion regulation processes in adulthood, (b) the neurobiology that is activated by caregiving cues during development, (c) the neurobiology that is altered by crEAs, and (d) the neurobiology of semantic-based meaning making. I hypothesize that the affective behaviors following crEAs result in part from affective semantic memory processes supported by mPFC–subcortical circuitry that over the course of development, construct affective schemas that generate meaning making and guide predictions. I use this opportunity to review some of the literature on mPFC–subcortical circuit development following crEAs to illustrate the motivation behind this hypothesis. Long recognized by clinical science and cognitive neuroscience, studying schema-based processes may be particularly helpful for understanding how affective meaning making arises from developmental trajectories of mPFC–subcortical circuitry.

This randomized controlled trial investigated the efficacy of Attachment and Biobehavioral Catch-up (ABC; Dozier, Bick, & Bernard, 2011) in reducing disrupted parenting behavior (affective communication errors, role/boundary confusion, fearful/disoriented, intrusive/negativity, and withdrawal) and its association with disorganized attachment. Participants were 105 mother–child dyads randomized to receive either ABC or a control intervention (a 10-session home-visiting intervention focused on improving children's cognitive abilities, gross and fine motor abilities, and language development). At the time of study enrollment, mothers were approximately 26.7 years old (SD = 7.8) and predominantly Black or African American (73.9%). At the first follow-up visit, children were approximately 20.7 months old (SD = 6.3) and most were identified as Black or African American (61.9%). Fifty-two percent of children were male (n = 55). Assessments of disrupted parenting behavior and child attachment quality were assessed approximately 7 months postintervention (SD = 5.8). A one-way analysis of variance revealed that parents who received ABC demonstrated lower levels of parental withdrawal than parents who received the control condition. A structural equation model revealed a significant indirect effect of intervention group on attachment quality through lower levels of parental withdrawal. Results add to the efficacy of the ABC intervention and identified parental withdrawal as a mediator of change.

This study examined the independent and interactive contributions of maternal depression and youth stress responses to trajectories of youth depression in adolescence. Youths (n = 165, M age = 12.43, SD = 1.18) and their maternal caregivers participated in a 4-year longitudinal study. Mothers and youths were administered diagnostic interviews assessing depression, and youths provided reports of their responses to peer stress. Consistent with an interactive model, adaptive responses to stress (high effortful engagement and low involuntary disengagement) buffered the effect of maternal depression on initial levels and trajectories of youth depression, with gender differences emerging. Consistent with a dual-risk model, maternal depression and maladaptive responses to stress (high effortful disengagement and involuntary engagement) contributed additive risks such that youths displayed the highest levels of depression when they were exposed to maternal depression and showed maladaptive stress responses. This research provides novel evidence that responses to stress contribute to individual differences in depression among offspring of depressed mothers, and suggests that responses to stress are an important target for efforts to promote resilience in at-risk youth.

This longitudinal study examined the joint role of pubertal timing and temperament variables (emotional reactivity and self-regulation) in predicting adolescents' internalizing symptoms. The multiethnic sample included 1,025 adolescent girls and boys followed from age 11 to age 15 (M age = 11.03 years at Time 1). In structural equation models, age 11 measures of pubertal timing, emotional reactivity, and self-regulation and their interactions were used to predict adolescents' internalizing behavior concurrently and at age 15. Results indicated that, among girls, early pubertal timing, higher emotional reactivity, and lower self-regulation predicted increased internalizing behavior. In addition, self-regulation moderated the effect of pubertal timing such that effects of earlier timing on subsequent internalizing were seen primarily among girls with relatively poor self-regulation. Among boys, higher levels of emotional reactivity and lower self-regulation predicted increased internalizing, but there were no effects of pubertal timing. After controlling for Time 1 internalizing symptoms, only self-regulation predicted change in internalizing symptoms. Discussion focuses on the possible interplay of temperament and pubertal development in predicting internalizing problems during adolescence.

The present study utilizes longitudinal data from a high-risk community sample to examine the unique effects of genetic risk, parental knowledge about the daily activities of adolescents, and peer substance use on emerging adult substance use disorders (SUDs). These effects are examined over and above a polygenic risk score. In addition, this polygenic risk score is used to examine gene–environment correlation and interaction. The results show that during older adolescence, higher adolescent genetic risk for SUDs predicts less parental knowledge, but this relation is nonsignificant in younger adolescence. Parental knowledge (using mother report) mediates the effects of parental alcohol use disorder (AUD) and adolescent genetic risk on risk for SUD, and peer substance use mediates the effect of parent AUD on offspring SUD. Finally, there are significant gene–environment interactions such that, for those at the highest levels of genetic risk, less parental knowledge and more peer substance use confers greater risk for SUDs. However, for those at medium and low genetic risk, these effects are attenuated. These findings suggest that the evocative effects of adolescent genetic risk on parenting increase with age across adolescence. They also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.

Marvin and Stewart and Byng–Hall proposed that effective family collaboration requires family members to construct “shared family working models,” and that the renegotiation of these working models during family transitions is facilitated by family members' “interactional awareness” (ability to be perceptive observers of family relationships). We apply these constructs to data collected from 71 mothers and their 4.5- to 5.0-year-old preschool children, 2 years after parental divorce. Maternal representations of the father as coparent and ex-spouse, and of father– and mother–child relationships were assessed via two interviews. A family story completion task captured child representations of mother–child and father–child, coparental and ex-spousal interactions. Maternal accounts of mother–child conversations illustrated the negotiation of shared working models. Primarily qualitative analyses contrasting maternal and child perspectives are presented in the first section. Then we use regression analyses to predict children's story themes from maternal representations of flexible, sensitive, and effective discipline-related interactions; maternal depressive symptoms; and perception of the child's father. Finally, we identify gender differences in children's enactments of divorce-related and child-empathy themes. We conclude by considering how our findings could be used to assist postdivorce families in constructing shared rather than conflicting working models of family relations.This research was funded by Grant R01 HD267766 awarded to the first author by the NICHD. Additional support was received from the University of Wisconsin Graduate School Research Committee, the Waisman Center, and the Vilas Trust. We express our deep appreciation to the mothers and children who participated in this study. We also thank Barbara Golby, Angel Gullon–Rivera, Patti Herman, Chris Halvorsen, Vicky Lenzlinger, Kristine Munholland, Reghan Walsh, and Laura Winn for assisting with data collection and analysis and acknowledge helpful advice from John Byng–Hall, Robert Emery, Paul Amato, and Daniel Veroff.

By 18 months children demonstrate a range of social–cognitive skills that can be considered important precursors to more advanced forms of social understanding such as theory of mind. Although individual differences in social cognition have been linked to neurocognitive maturation, sociocultural models of development suggest that environmental influences operate in the development of children's social–cognitive outcomes. In the current study of 501 children and their mothers, we tested and found support for a model in which distal environmental risk, assessed when children were newborns, was indirectly associated with children's social–cognitive competency at 18 months through mothers' responsivity at 18 months. Part of this effect also operated through children's concomitant language skills, suggesting both a language-mediated and a language-independent mechanism of social–cognitive development. These findings are discussed with respect to the Vygotskian themes of internalization and semiotic mediation.

Late adolescence and emerging adulthood (specifically ages 15–24) represent a period of heightened sexual risk taking resulting in the greatest annual rates of sexually transmitted infections and unplanned pregnancies in the US population. Ongoing efforts to prevent such negative consequences are likely to benefit from a deepening of our understanding of biological mechanisms through which sexual risk taking emerges and biases decision making during this critical window. Here we present a neuroscience framework from which a mechanistic examination of sexual risk taking can be advanced. Specifically, we adapt the neurodevelopmental triadic model, which outlines how motivated behavior is governed by three systems: approach, avoidance, and regulation, to sexual decision making and subsequent risk behavior. We further propose a testable hypothesis of the triadic model, wherein relatively decreased threat-related amygdala reactivity and increased reward-related ventral striatum reactivity leads to sexual risk taking, which is particularly exaggerated during adolescence and young adulthood when there is an overexpression of dopaminergic neurons coupled with immature top-down prefrontal cortex regulation. We conclude by discussing how future research based on our adapted triadic model can inform ongoing efforts to improve intervention and prevention efforts.

Growing evidence suggests that maltreatment is reproduced across generations as victims of maltreatment are at an increased risk for maltreatment perpetration. Unfortunately, little information about mediating pathways exists to provide an explanation for why maltreatment begets maltreatment. We use the number of types of maltreatment experienced to predict later maltreatment perpetration and then examine two developmental pathways that may serve as bridges between maltreatment victimization and perpetration: adolescent problem behaviors and precocious transitions to adulthood. With prospective, longitudinal data from the Rochester Youth Development Study, we assess the relevance of these pathways for the number of maltreatment experiences as well as the number of maltreatment victimization experiences by developmental period (i.e., childhood and adolescence). Our results demonstrate a significant relationship between maltreatment victimization and maltreatment perpetration. Adolescent delinquency and two precocious transitions, dropping out of school and independent living, as well as the accumulation of precocious transitions and problem behaviors, serve as mediators of this intergenerational relationship. Furthermore, the relationship between the number of types of maltreatment and subsequent perpetration is primarily driven by experiences of maltreatment during adolescence. We discuss the implications of these results and set an agenda for the development of programs and policies to interrupt the cycle of maltreatment.

Chronic health conditions are hypothesized to disrupt the typical trajectory of child and adolescent development, and subsequently lead to increased levels of mental illness. However, due to methodological limitations in existing studies, this theory remains to be fully substantiated by empirical research. This study aimed to more thoroughly test hypotheses in the field. This study used data from the Avon Longitudinal Study of Parents and Children to examine the co-occurrence of mental illness among children with chronic illness in late childhood into early adolescence and explore mediating factors in these outcomes. Children with chronic health problems presented with a disproportionate rate of psychiatric illness at 10 years, and these chronic health problems continued to be associated with poor mental health outcomes at 13 years and 15 years. These outcomes were mediated by high levels of peer victimization and health-related school absenteeism. This study suggests that chronic illness may impact on functioning and social development in early adolescence, and consequently lead to increased rates of mental illness. Examining rates of school absenteeism and peer victimization may be key to identifying children at risk over time.

Associations between infants' frontal EEG asymmetry and temperamental negative affectivity (NA) across infants' first year of life and the potential moderating role of maternal prenatal depressive symptoms were examined prospectively in infants (n = 242) of mothers at elevated risk for perinatal depression. In predicting EEG, in the context of high prenatal depressive symptoms, infant NA and frontal EEG asymmetry were negatively associated at 3 months of age and positively associated by 12 months of age. By contrast, for low depression mothers, infant NA and EEG were not significantly associated at any age. Postnatal depressive symptoms did not add significantly to the models. Dose of infants' exposure to maternal depression mattered: infants exposed either pre- or postnatally shifted from a positive association at 3 months to a negative association at 12 months; those exposed both pre- and postnatally shifted from a negative association at 3 months to a positive association at 12 months. Prenatal relative to postnatal exposure did not matter for patterns of association between NA and EEG. The findings highlight the importance of exploring how vulnerabilities at two levels of analysis, behavioral and psychophysiological, co-occur over the course of infancy and in the context of mothers' depressive symptomatology.

The present study tested the role of FKBP5 binding protein 5 (FKBP5) genetic variation in an internalizing pathway from child maltreatment to emerging adult problem drinking among a sample of African American youth (N = 280) followed prospectively from ages 11 to 20. Specifically, whether childhood internalizing symptoms and emerging adult tension reduction alcohol expectancies sequentially mediate the effect of child maltreatment on emerging adult problem drinking and whether FKBP5 moderates these associations were investigated. The results indicate that individuals with at least one copy of the FKBP5 CATT haplotype (minor alleles) are more vulnerable to traversing the hypothesized internalizing pathway of risk than individuals without this genotypic profile. Taken together our findings highlight the importance of FKBP5 genetic variation in the context of early adversity; support the role of two prospective sequential mediators of an internalizing pathway to problematic drinking, namely, childhood internalizing symptoms and emerging adult tension reduction alcohol expectancies; and identify a subgroup of maltreated children most susceptible to progressing along this less common pathway of risk.

Mexican-origin adolescent mothers face numerous social challenges during dual-cultural adaptation that are theorized to contribute to greater depressive symptoms. Alongside challenges, there are familial resources that may offer protection. As such, the current study examined the trajectories of depressive symptoms among 204 Mexican-origin adolescent mothers (Mage = 16.80, SD = 1.00) across a 4-year period (third trimester of pregnancy, and 10, 24, and 36 months postpartum). Further, we examined the within-person relations of two unique sources of stress experienced during dual-cultural adaptation, acculturative and enculturative stress, and youths' depressive symptoms; we also tested whether adolescent mothers' perceptions of warmth from their own mothers emerged as protective. Adolescent mothers reported a decline in depressive symptoms after the transition to parenthood. Acculturative and enculturative stress emerged as significant positive within-person predictors of depressive symptoms. Maternal warmth emerged as a protective factor in the relation between enculturative stressors and depressive symptoms; however, for acculturative stressors, the protective effect of maternal warmth only emerged for US-born youth. Findings illustrate the multidimensionality of stress experienced during the cultural adaptation process and a potential mechanism for resilience among Mexican-origin adolescent mothers.