Emerging research in epigenetics has shown that there is variability in how environmental exposures “get under the skin” through mechanisms like DNA methylation to influence gene expression that may lead to differential adaptations to stress. This is the first study to examine prospectively the relationship between DNA methylation at birth and resilience to prenatal environmental stressors in several domains (conduct, hyperactivity, emotional problems, and global symptomatology) in middle childhood. We focused on DNA methylation in the vicinity of the oxytocin receptor (OXTR) gene as it has been previously associated with impairments in social–cognitive processes that may underlie a wide range of childhood psychopathology. Participants were 91 youth exposed to pre- and postnatal adversity with established conduct problem trajectories drawn from the Avon Longitudinal Study of Parents and Children. Consistent with our hypothesis, OXTR DNA methylation was predictive of resilience in the conduct problems domain in middle childhood. DNA methylation profiles did not predict resilience in domains of emotional, hyperactivity, and global symptomatology, suggesting a potential role for OXTR in the development of conduct problems in particular. However, individuals who were resilient to conduct problems were also broadly resilient across multiple domains. Therefore, future research should elucidate the biological pathways between OXTR DNA methylation and gene expression and its relation to impairments in social behavior.

Researchers have identified cross-sectional links between interpersonal stress and inflammation. Little is known, however, about how these dynamics unfold over time, what underlying immune pathways might exist, or whether moderators such as race could alter the strength of the connection between interpersonal stress and inflammatory processes. We examined whether adolescent girls whose relationship trajectories were characterized by chronic stress would exhibit a proinflammatory phenotype marked by systemic inflammation, heightened cytokine responses to bacterial challenges, and resistance to the anti-inflammatory properties of cortisol. Significant Stress × Race interactions revealed that family stress trajectories predicted glucocorticoid sensitivity and peer stress trajectories predicted cytokine production for White but not Asian girls. Relationship stress trajectories were not associated with systemic inflammation, however. These findings suggest that particular subgroups of adolescent girls who face chronic and elevated stress in their close relationships may be at risk for disruptions to the immune system.

This study used four waves of data from a longitudinal study of 749 Mexican origin youths to test a developmental cascades model linking contextual adversity in the family and peer domains in late childhood to a sequence of unfolding processes hypothesized to predict problem substance use and risky sexual activity (greater number of sex partners) in late adolescence. Externalizing and internalizing problems were tested as divergent pathways, with youth-reported and mother-reported symptoms examined in separate models. Youth gender, nativity, and cultural orientation were tested as moderators. Family risk, peer social rejection, and their interaction were prospectively related to externalizing symptoms and deviant peer involvement, although family risk showed stronger effects on parent-reported externalizing and peer social rejection showed stronger effects on youth-reported externalizing. Externalizing symptoms and deviant peers were related, in turn, to risk taking in late adolescence, including problem alcohol–substance use and number of sexual partners. Peer social rejection predicted youth-reported internalizing symptoms, and internalizing was related, in turn, to problem alcohol and substance use in late adolescence. Tests of moderation showed some of these developmental cascades were stronger for adolescents who were female, less oriented to mainstream cultural values, and more oriented to Mexican American cultural values.

Behavioral Inhibition (BI) is a temperament type that predicts social withdrawal in childhood and anxiety disorders later in life. However, not all BI children develop anxiety. Attention bias (AB) may enhance the vulnerability for anxiety in BI children, and interfere with their development of effective emotion regulation. In order to fully probe attention patterns, we used traditional measures of reaction time (RT), stationary eye-tracking, and recently emerging mobile eye-tracking measures of attention in a sample of 5- to 7-year-olds characterized as BI (N = 23) or non-BI (N = 58) using parent reports. There were no BI-related differences in RT or stationary eye-tracking indices of AB in a dot-probe task. However, findings in a subsample from whom eye-tracking data were collected during a live social interaction indicated that BI children (N = 12) directed fewer gaze shifts to the stranger than non-BI children (N = 25). Moreover, the frequency of gazes toward the stranger was positively associated with stationary AB only in BI, but not in non-BI, children. Hence, BI was characterized by a consistent pattern of attention across stationary and ambulatory measures. We demonstrate the utility of mobile eye-tracking as an effective tool to extend the assessment of attention and regulation to social interactive contexts.

Childhood maltreatment can disturb brain development and subsequently lead to adverse socioemotional and mental health problems across the life span. The long-term association between childhood maltreatment and resting–wake brain activity during adulthood is unknown and was examined in the current study. Forty-one medically stable and medication-free military veterans (M = 29.31 ± 6.01 years, 78% male) completed a battery of clinical assessments and had [18F]-fluorodeoxyglucose positron emission tomography neuroimaging scans during quiet wakefulness. After statistically adjusting for later-life trauma and mental health problems, childhood maltreatment was negatively associated with brain activity within a priori defined regions that included the left orbital frontal cortex and left hippocampus. Childhood maltreatment was significantly associated with increased and decreased brain activity within six additional whole-brain clusters that included the frontal, parietal–temporal, cerebellar, limbic, and midbrain regions. Childhood maltreatment is associated with altered neural activity in adulthood within regions that are involved in executive functioning and cognitive control, socioemotional processes, autonomic functions, and sleep/wake regulation. This study provides support for taking a life span developmental approach to understanding the effects of early-life maltreatment on later-life neurobiology, socioemotional functioning, and mental health.

The aim of the current research was to disentangle four theoretically sound models of externalizing behavior etiology (i.e., attachment, language, inhibition, and parenting) by testing their relation with behavioral trajectories from early childhood to adolescence. The aim was achieved through a 10-year prospective longitudinal study conducted over five waves with 111 referred children aged 3 to 5 years at the onset of the study. Clinical referral was primarily based on externalizing behavior. A multimethod (questionnaires, testing, and observations) approach was used to estimate the four predictors in early childhood. In line with previous studies, the results show a significant decrease of externalizing behavior from early childhood to adolescence. The decline was negatively related to mothers’ coercive parenting and positively related to attachment security in early childhood, but not related to inhibition and language. The study has implications for research into externalizing behavior etiology recommending to gather hypotheses from various theoretically sound models to put them into competition with one another. The study also has implications for clinical practice by providing clear indications for prevention and early intervention.

The aim of this study was to examine if family system dynamics (e.g., parent mental health, marriage quality, conflict, and cohesion) that have often been overlooked when studying Latino families play a more important role in predicting adolescent internalizing symptoms than acculturation processes. Data comes from the Latino Acculturation and Health Project, a longitudinal investigation of acculturation in Latino families in North Carolina and Arizona (Smokowski & Bacallao, 2006, 2010). Researchers conducted in-depth, community-based interviews with 258 Latino adolescents and 258 of their parents in metropolitan, small-town, and rural areas. Interviews were conducted at four time points at intervals of approximately 6 months. Parent and adolescent ratings of the adolescent's internalizing symptoms were used as the dependent variable in a longitudinal hierarchical linear model with a rater effects structure. Results showed that parent–adolescent conflict and parent mental health (fear/avoidance of social situations and humiliation sensitivity) were significant predictors of adolescent internalizing symptoms. Acculturation scales were not significant predictors; however, internalizing symptoms decreased with time spent in the United States. Females and adolescents from lower socioeconomic status families reported more internalizing symptoms, while participants who had been in the United States longer reported fewer internalizing symptoms. Implications were discussed.

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.

Children who spend their early lives in institutions experience profound psychosocial deprivation that is associated with altered stress response system development. Here, we used data from a longitudinal randomized controlled trial of foster care for institutionally reared children to examine whether caregiving quality and stressful life events (SLEs) in early adolescence (age 12) influence patterns of hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS) reactivity. Controlling for the effect of institutional care, higher caregiving quality at age 12 was associated with heightened cortisol and SNS reactivity. However, moderation analysis revealed that the latter effect was only observed among never-institutionalized children, whereas ever-institutionalized children demonstrated a persistently blunted SNS response regardless of recent caregiving quality. Among institutionally reared children, SLEs interacted with prior random assignment to foster care, such that those placed in foster care early in development had a SNS response that approximated never-institutionalized children when SLEs at age 12 were low. In contrast, SNS reactivity was persistently blunted among those with prolonged deprivation, regardless of recent SLEs. Early-life deprivation is associated with persistent blunting of stress response systems, but normalization may be achievable if SLEs are limited following placement into enriched family-based care.

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.

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.

Questions concerning the long-term effects of early experience on psychological development in humans continue to stir up controversy. There are, at present, great diversity and contradictions among extant conceptual models and inadequate data to resolve these differences. Limited opportunities to use experimental approaches and the inherent restrictions of observational approaches in research on humans implies that alternative research designs are needed. This article examines the use of “natural experiments” as a method for testing hypotheses concerning the effects of early experience on psychological development. The benefits and limitations of using natural experiments are reviewed and several case illustrations are considered.

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.

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.

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.

The codevelopment of symptoms of depression and socially prescribed perfectionism across adolescence (age 12–17) and non–age-overlapping childhood predictors (age 10–11) of joint trajectory group membership were examined in a sample of 700 Canadian youth. Results indicated that most adolescents (75.8%) followed a trajectory of low depression symptoms (low stable), whereas 15.7% followed an increasing trajectory (increasing), and 8.5% followed a trajectory that began high and decreased over time (high decreasing). More girls than boys were found in the increasing and high decreasing depression trajectories. Adolescents followed three distinct trajectories of socially prescribed perfectionism: 41.6% were in a low stable group, 40.5% in a moderate increasing group, and 17.9% in a high increasing group. Eight percent followed a high-risk dual trajectory of increasing depression and high increasing socially prescribed perfectionism. This joint trajectory was predicted by being bullied, anxious, and relationally aggressive (compared to the low-risk trajectory of low stable depression and perfectionism) at ages 10 and 11. These same predictors, along with poorer family functioning and lower family income, differentiated the joint high decreasing depression/high increasing perfectionism group from the low/low joint group, which comprised of 3.8% of the sample. The developmental progression was best characterized as depression leading to socially prescribed perfectionism. Implications for clinical practice are discussed.

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.

Research consistently demonstrates that common polymorphic variation in monoamine oxidase A (MAOA) moderates the influence of childhood maltreatment on later antisocial behavior, with growing evidence that the “risk” allele (high vs. low activity) differs for females. However, little is known about how this Gene × Environment interaction functions to increase risk, or if this risk pathway is specific to antisocial behavior. Using a prospectively assessed, longitudinal sample of females (n = 2,004), we examined whether changes in emotional reactivity (ER) during adolescence mediated associations between this Gene × Environment and antisocial personality disorder in early adulthood. In addition, we assessed whether this putative risk pathway also conferred risk for borderline personality disorder, a related disorder characterized by high ER. While direct associations between early maltreatment and later personality pathology did not vary by genotype, there was a significant difference in the indirect path via ER during adolescence. Consistent with hypotheses, females with high-activity MAOA genotype who experienced early maltreatment had greater increases in ER during adolescence, and higher levels of ER predicted both antisocial personality disorder and borderline personality disorder symptom severity. Taken together, findings suggest that the interaction between MAOA and early maltreatment places women at risk for a broader range of personality pathology via effects on ER.