In recent years, translational research involving humans and animals has uncovered biological and physiological pathways that explain associations between early adverse circumstances and long-term mental and physical health outcomes. In this article, we summarize the human and animal literature demonstrating that epigenetic alterations in key biological systems, the hypothalamus–pituitary–adrenal axis and immune system, may underlie such disparities. We review evidence suggesting that changes in DNA methylation profiles of the genome may be responsible for the alterations in hypothalamus–pituitary–adrenal axis and immune system trajectories. Using some preliminary data, we demonstrate how explorations of genome-wide and candidate-gene DNA methylation profiles may inform hypotheses and guide future research efforts in these areas. We conclude our article by discussing the many important future directions, merging perspectives from developmental psychology, molecular genetics, neuroendocrinology, and immunology, that are essential for furthering our understanding of how early adverse circumstances may shape developmental trajectories, particularly in the areas of stress reactivity and physical or mental health.

Gene–environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N = 627, M age = 11.27). Variants in three genes were examined: tryptophan hydroxylase 1 (TPH1), serotonin transporter linked polymorphic region (5-HTTLPR), and monoamine oxidase A (MAOA) upstream variable number tandem repeat. In addition to child maltreatment status, we considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer, and adult counselor reports. In a series of analyses of covariance, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all report forms. Genetic effects operated primarily in the context of gene–environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms of TPH1, 5-HTTLPR, and MAOA were each related to heightened self-report of antisocial behavior; the interaction of 5-HTTLPR and developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype. TPH1 and 5-HTTLPR interacted with maltreatment subtype to predict peer reports of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. The TPH1 and 5-HTTLPR polymorphisms also moderated the effects of maltreatment subtype on adult reports of antisocial behavior; again, the genetic effects were strongest for children who were abused. In addition, TPH1 moderated the effect of developmental timing of maltreatment and chronicity on adult reports of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.

Since this journal's inception, the field of adolescent brain development has flourished, as researchers have investigated the underpinnings of adolescent risk-taking behaviors. Explanations based on translational models initially attributed such behaviors to executive control deficiencies and poor frontal lobe function. This conclusion was bolstered by evidence that the prefrontal cortex and its interconnections are among the last brain regions to structurally and functionally mature. As substantial heterogeneity of prefrontal function was revealed, applications of neuroeconomic theory to adolescent development led to dual systems models of behavior. Current epidemiological trends, behavioral observations, and functional magnetic resonance imaging based brain activity patterns suggest a quadratic increase in limbically mediated incentive motivation from childhood to adolescence and a decline thereafter. This elevation occurs in the context of immature prefrontal function, so motivational strivings may be difficult to regulate. Theoretical models explain this patterning through brain-based accounts of subcortical–cortical integration, puberty-based models of adolescent sensation seeking, and neurochemical dynamics. Empirically sound tests of these mechanisms, as well as investigations of biology–context interactions, represent the field's most challenging future goals, so that applications to psychopathology can be refined and so that developmental cascades that incorporate neurobiological variables can be modeled.

Although early-life adversity can undermine healthy development, children growing up in harsh environments may develop intact, or even enhanced, skills for solving problems in high-adversity contexts (i.e., “hidden talents”). Here we situate the hidden talents model within a larger interdisciplinary framework. Summarizing theory and research on hidden talents, we propose that stress-adapted skills represent a form of adaptive intelligence that enables individuals to function within the constraints of harsh, unpredictable environments. We discuss the alignment of the hidden talents model with current knowledge about human brain development following early adversity; examine potential applications of this perspective to multiple sectors concerned with youth from harsh environments, including education, social services, and juvenile justice; and compare the hidden talents model with contemporary developmental resilience models. We conclude that the hidden talents approach offers exciting new directions for research on developmental adaptations to childhood adversity, with translational implications for leveraging stress-adapted skills to more effectively tailor education, jobs, and interventions to fit the needs and potentials of individuals from a diverse range of life circumstances. This approach affords a well-rounded view of people who live with adversity that avoids stigma and communicates a novel, distinctive, and strength-based message.

This article reviews and reflects on studies that have explored the effects of war on children around the world. Most are cross-sectional and based on self-reports. They describe a range of mental health problems, related to dose effects and to the negative impact of being a victim or witness of violent acts, threats to and loss of loved ones, prolonged parental absence, and forced displacement. The more recent the exposure to war, and the older the child, the higher was the likelihood of reported posttraumatic stress disorder symptoms. Especially vulnerable to long-term emotional distress were child soldiers, children who were raped, and children who had been forcibly displaced. In adulthood, war-traumatized children displayed significantly increased risks for a wide range of medical conditions, especially cardiovascular diseases. Among protective factors that moderated the impact of war-related adversities in children were a strong bond between the primary caregiver and the child, the social support of teachers and peers, and a shared sense of values. Among the few documented intervention studies for children of war, school-based interventions, implemented by teachers or locally trained paraprofessionals, proved to be a feasible and low-cost alternative to individual or group therapy. More longitudinal research with multiple informants is needed to document the trajectories of risk and resilience in war-affected children, to assess their long-term development and mental health, and to identify effective treatment approaches.

The focus of this article is to present current progress in understanding the interplay among adversity, physiological sensitivity to context, and adaptive functioning, with an emphasis on implications and future directions for resilience researchers. It includes a review of current literature that demonstrates (a) links between various levels of adversity exposure and variability in physiological reactivity, (b) how the interplay between children's physiological reactivity and different sources of risk and adversity relates to variability in adaptive functioning, and (c) various approaches for capturing a more dynamic nature of physiological reactivity and related processes. Throughout, important conceptual and empirical issues are highlighted.

Low resting respiratory sinus arrhythmia (RSA), and to a lesser extent excessive RSA reactivity to emotion evocation, are observed in many psychiatric disorders characterized by emotion dysregulation, including syndromes spanning the internalizing and externalizing spectra, and other conditions such as nonsuicidal self-injury. Nevertheless, some inconsistencies exist. For example, null outcomes in studies of RSA–emotion dysregulation relations are sometimes observed among younger participants. Such findings may derive from use of age inappropriate frequency bands in calculating RSA. We combine data from five published samples (N = 559) spanning ages 4 to 17 years, and reanalyze RSA data using age-appropriate respiratory frequencies. Misspecifying respiratory frequencies results in overestimates of resting RSA and underestimates of RSA reactivity, particularly among young children. Underestimates of developmental shifts in RSA and RSA reactivity from preschool to adolescence were also observed. Although correlational analyses revealed weak negative associations between resting RSA and aggression, those with clinical levels of externalizing exhibited lower resting RSA than their peers. No associations between RSA reactivity and externalizing were observed. Results confirm that age-corrected frequency bands should be used when estimating RSA, and that literature-wide overestimates of resting RSA, underestimates of RSA reactivity, and underestimates of developmental shifts in RSA and RSA reactivity may exist.

The current study investigated the relationship between previous, recent, or chronic maternal depressive symptoms and subtypes of child behavior problems rated by teachers and mothers among 64 low-income children aged 4–6 years. Sixty-nine percent of mothers with high depressive symptom levels at the preschool assessment had also reported high symptom levels during the child's infancy. Children whose mothers reported depressive symptoms at both ages exhibited significantly elevated rates of hostile behavior problems in the classroom and at home compared to children of never-depressed mothers. Children of mothers who were previously but not currently depressed showed significantly more anxious and withdrawn behavior at school and at home, while children of recently depressed mothers were more hyperactive and demanding. Child cognitive scores and father absence were also related to behavior problems, but these variables did not mediate the independent effects of chronicity and timing of maternal depressive symptoms on the types of child symptoms displayed.

We examined two hypotheses about the developmental relation between substance abuse and individual differences in desistance from antisocial behavior during young adulthood. The “snares” hypothesis posits that substance abuse should result in time-specific elevations in antisocial behavior relative to an individual's own developmental trajectory of antisocial behavior, whereas the “launch” hypothesis posits that substance abuse early in young adulthood slows an individual's overall pattern of crime desistance relative to the population norm during this developmental period. We conducted latent trajectory analyses to test these hypotheses using interview data about antisocial behaviors and substance abuse assessed at ages 18, 21, and 26 in men from the Dunedin Multidisciplinary Health and Development Study (N = 461). We found significant individual variability in initial levels and rates of change in antisocial behavior over time as well as support for both the snares hypothesis and the launch hypothesis as explanations for the developmental relation between substance abuse and crime desistance in young men.We thank the Dunedin Study members, Dunedin Unit Director Richie Poulton, Unit research staff, and Study founder Phil Silva. Research assistance was provided by HonaLee Harrington. The Dunedin Multidisciplinary Health and Development Research Unit is supported by the New Zealand Health Research Council. We also thank Alex Piquero for his helpful comments. This research received support from the NIDA (Grant DA15398 and DA13148), NIMH (Grants MH45070 and MH49414), William T. Grant Foundation, and Air New Zealand.

The most stringent test of differential susceptibility theory is provided by randomized control trials examining the moderating role of genetic markers of differential susceptibility in experimental manipulations of the environment (Gene × Experimental Environment interactions), being at least 10 times more powerful than correlational Gene × Environment interaction studies. We identified 22 experiments involving 3,257 participants with various developmental outcomes (e.g., externalizing problems, internalizing behaviors, and cognitive development). Effect sizes contrasting experimental versus control group were computed both for subjects with the polymorphism considered indicative of heightened susceptibility (e.g., the dopamine receptor D4 gene seven-repeat allele and the serotonin transporter polymorphic region short allele) and others expected to be low in susceptibility (e.g., the dopamine receptor D4 gene four-repeat allele and the serotonin transporter polymorphic region short allele). Clear-cut experimental support for genetic differential susceptibility emerged: the combined effect size of the interventions for the susceptible genotypes amounted to r = .33 (95% confidence interval = 0.23, 0.42; p < .01) versus a nonsignificant r = .08 (95% confidence interval = −0.02, 0.17; p = .12) for the hypothesized nonsusceptible genotypes. Macrotrials showed more evidence of genetic differential susceptibility than microtrials, and differential susceptibility was more clearly observed in trials with externalizing and cognitive outcomes than with internalizing problems. This meta-analysis shows proof of principle for genetic differential susceptibility and indicates that it is time to explore its mechanisms and limits. The concept of differential susceptibility alters the idea of constitutional “risk” factors (reactive temperament and risk genotypes), and points to intervention efficacy hidden in Gene × Environment interactions.

In the wake of prominent theoreticians in developmental science, whose contributions we review in this article, many developmental psychologists came to endorse a systems approach to understanding how the individual, as it develops, establishes functional relationships to social ecological contexts that from birth to school entry rapidly increase in complexity. The concept of developmental cascade has been introduced in this context to describe lawful processes by which antecedent conditions may be related with varying probabilities to specified outcomes. These are understood as processes by which function at one level or in one domain of behavior affect the organization of competency in later developing domains of general adaptation. Here we propose a developmental sequence by which the developing child acquires regulative capacities that are key to adjustment to a society that demands considerable control of emotional and cognitive functions early in life. We report empirical evidence showing that the acquisition of regulative capacities may be understood as a cascade of shifts in control parameters induced by the progressive integration of biological, transactional, and socioaffective systems over development. We conclude by suggesting how the developmental process may be accessed for effective intervention in populations deemed “at risk” for later problems of psychosocial adjustment.

The field of developmental psychopathology is faced with a dual challenge. On the one hand, we must build interdisciplinary theoretical models that adequately reflect the complexity of normal and abnormal human development over time. On the other hand, to remain a viable empirical science, we must rigorously evaluate these theories using statistical methods that fully capture this complexity. The degree to which our statistical models fail to correspond to our theoretical models undermines our ability to validly test developmental theory. The broad class of random coefficient trajectory (or growth curve) models allow us to test our theories in ways not previously possible. Despite these advantages, there remain certain limits with regard to the types of questions these models can currently evaluate. We explore these issues through the pursuit of three goals. First, we provide an overview of a variety of trajectory models that can be used for rigorously testing many hypotheses in developmental psychopathology. Second, we highlight what types of research questions are well tested using these methods and what types of questions currently are not. Third, we describe areas for future statistical development and encourage the ongoing interchange between developmental theory and quantitative methodology.

A representative community sample of primiparous depressed women and a nondepressed control group were assessed while in interaction with their infants at 2 months postpartum. At 3 months, infants were assessed on the Still-face perturbation of face to face interaction, and a subsample completed an Instrumental Learning paradigm. Compared to nondepressed women, depressed mothers' interactions were both less contingent and less affectively attuned to infant behavior. Postnatal depression did not adversely affect the infant's performance in either the Still-face perturbation or the Instrumental Learning assessment. Maternal responsiveness in interactions at 2 months predicted the infant's performance in the Instrumental Learning assessment but not in the Still-face perturbation. The implications of these findings for theories of infant cognitive and emotional development are discussed.This research was supported by the award of a Medical Research Council Training Fellowship to Charles Stanley. Lynne Murray was supported by a Medical Research Council Senior Research Fellowship. Alan Stein was supported by the Tedworth Trust and the Wellcome Trust. The authors would like to thank Anji West and Agnese Fiori\NCowley for their help with the coding of the assessments, Robbie Paterson for administrative assistance, Richard Hooper for assistance with the statistical analyses and Peter Cooper for collaboration in the planning of the study.

In this study, we evaluated predictors of resilience among 8- to 12-year-old children recruited from primarily low socioeconomic status neighborhoods, 117 of whom suffered from clinical levels of conduct problems and/or depression, and 63 of whom suffered from no significant symptoms. Tests of interactions were conducted between (a) paternal antisocial behavior and maternal depression and (b) several physiological indices of child temperament and emotionality in predicting (c) children's conduct problems and depression. Both internalizing and externalizing outcomes among children were associated specifically with maternal melancholic depression, and not with nonmelancholic depression. In addition, low levels of respiratory sinus arrhythmia (RSA) among children conferred significant risk for depression, regardless of maternal melancholia, whereas high RSA offered partial protection. Furthermore, high levels of maternal melancholia conferred significant risk for child depression, regardless of paternal antisocial behavior, whereas low levels of maternal melancholia offered partial protection. Finally, low levels of electrodermal responding (EDR) conferred significant risk for conduct problems, regardless of paternal antisocial behavior, whereas high EDR offered partial protection. None of the identified protective factors offered complete immunity from psychopathology. These findings underscore the complexity of resilience and resilience-related processes, and suggest several potential avenues for future longitudinal research.

Within the framework of a cumulation/nesting theory for the emergence of adult psychopathology, a typing structure for alcoholism based upon variations in life course continuity of antisocial behavior over childhood and adulthood was examined for its ability to differentiate symptomatic and life history variations among alcoholic and nonalcoholic men accessed by way of a population-based recruitment strategy. Results supported the theory and identified two alcoholic types, one high on lifetime antisociality (antisocial alcoholic = AAL), the other low (nonantisocial alcoholic = NAAL), and a third nonalcoholic type with low lifetime antisociality. Types differed in age of onset, severity, number, and life course of alcohol problems, measures of social adaptation, amount and severity of other psychopathology, and salience of family history load of alcoholism. Antisociality and alcoholism tended to be nested characteristics.

The principal aim of this study was to assess personal relatedness and attachment patterns in 12-month-old infants of mothers with borderline personality disorder (BPD). We also evaluated maternal intrusive insensitivity toward the infants in semistructured play. We videotaped 10 mother–infant dyads with borderline mothers and 22 dyads where the mothers were free from psychopathology, in three different settings: a modification of Winnicott's Set Situation in which infants faced an initially unresponsive (“still-face”) stranger, who subsequently tried to engage the infant in a game of give and take; the Strange Situation of Ainsworth and Wittig; and a situation in which mothers were requested to teach their infants to play with miniature figures and a toy train. In relation to a set of a priori predictions, the results revealed significant group differences as follows: (a) compared with control infants, toward the stranger the infants of mothers with BPD showed lower levels of “availability for positive engagement,” lower ratings of “behavior organization and mood state,” and a lower proportion of interpersonally directed looks that were positive; (b) in the Strange Situation, a higher proportion (8 out of 10) of infants of borderline mothers were categorized as Disorganized; and (c) in play, mothers with BPD were rated as more “intrusively insensitive” toward their infants. The results are discussed in relation to hypotheses concerning the interpersonal relations of women with BPD, and possible implications for their infants' development.This research was generously supported by grants from the Winnicott Trust, the Hayward Foundation, and the Baily Thomas Charitable Fund, as well as by a Wellcome Fellowship to Matthew Patrick and an NIH Fellowship to Lisa Crandell. We also received support from the UK National Health R&D Budget. We are indebted to the mothers and infants who agreed to take part, Lynne Murray for inspiration and guidance, Lucy Chiemielski and Leezah Hertzmann for their help with ratings of videotapes, Betty Carlson and Alan Sroufe for their invaluable and very generous input, and Jessica Meyer for her helpful comments and suggestions.

This study addressed the basis for the intergenerational transmission of psychosocial risk associated with maternal childhood abuse in relation to offspring adjustment. The study tested how far group differences in individual change in adjustment over time were explained by differences in exposure to specific environmental risk experiences. Data are drawn from the Avon Longitudinal Study of Parents and Children. Information on mothers' own experience of childhood abuse, offspring adjustment at ages 4 and 7 years, and hypothesized mediators was available for 5,619 families. A residuals scores analysis was used to track children's adjustment over time. Maternal childhood abuse was associated with poorer behavioral trajectories between ages 4 and 7 years. Children of abused mothers were more likely to experience a range of negative life events between ages 4 and 7 years, including changes in family composition, separations from parents, “shocks and frights” and physical assaults. Interim life events, together with antecedent psychosocial risk (maternal antenatal affective symptoms, age 4 parental hostility, age 4 family type) fully mediated the association between maternal childhood abuse and offspring prognosis.The authors express their gratitude to the families who participated in the study. Support for these analyses was provided by a grant from the Medical Research Council. The Avon Longitudinal Study of Parents and Children (ALSPAC) is part of the World Health Organisation initiated European Study of Pregnancy and Childhood, and is supported, among others, by the Wellcome Trust, The Department of Health, The Department of the Environment, and the Medical Research Council. The ALSPAC study team comprises interviewers, computer technicians, laboratory technicians, clerical workers, research scientists, volunteers, and managers who continue to make the study possible.

Improvements in temperance, perspective, and responsibility are a part of typical development of psychosocial maturity during adolescence. The existing literature suggests that the developmental course of psychosocial maturity is influenced by normative variations in social context, but little is known about how atypical contexts, such as incarceration, influence its development. The study investigates how the development of psychosocial maturity is affected by incarceration, using data from a 7-year longitudinal study of 1,171 adolescent males. We compared the effects of confinement in juvenile facilities with varying degrees of focus on incarceration versus rehabilitation (i.e., secure vs. residential treatment facilities) and tested whether facility quality and age at incarceration moderate the effect of incarceration on psychosocial maturity. The results indicate that incarceration in a secure setting, but not a residential treatment facility, is associated with a short-term decline in temperance and responsibility. The total amount of time incarcerated in a residential treatment facility, but not a secure setting, had a negative effect on the developmental trajectory of psychosocial maturity. Age at incarceration, but not the facility quality, moderated the effect of recent incarceration: older youths were more susceptible to short-term negative effects of recent incarceration in a secure setting, but they also benefited more than younger participants from short-term positive effects of incarceration in a residential treatment setting. Furthermore, youths who perceived their incarceration setting as unsafe evinced a decline in temperance. Future research and policy implications are discussed.

In the psychological tradition, desistance from antisocial behavior is viewed as the product of psychosocial maturation, including increases in the ability to control impulses, consider the implications of one's actions on others, delay gratification in the service of longer term goals, and resist the influences of peers. The present study investigates how individual variability in the development of psychosocial maturity is associated with desistance from antisocial behavior in a sample of 1,088 serious juvenile offenders followed from adolescence to early adulthood (ages 14–25). We find that psychosocial maturity continues to develop to the midtwenties and that different developmental patterns of maturation are found among those who desist and those who persist in antisocial behavior. Compared to individuals who desisted from antisocial behavior, youths who persisted exhibited diminished development of psychosocial maturity. Moreover, earlier desistance compared to later desistance is linked to greater psychosocial maturity, suggesting that there is an association between desistance from antisocial behavior and normative increases in psychosocial maturity.

In this paper, I propose a roadmap for the integration of culture in developmental psychopathology. This integration is pressing because culture continues to be somewhat disconnected from theory, research, training, and interventions in developmental psychopathology, thus limiting our understanding of the epigenesis of mental health. I argue that in order to successfully integrate culture into developmental psychopathology, it is crucial to (a) study cultural development, (b) consider both individual-level and social-level cultural processes, (c) examine the interplay between culture and biology, and (d) promote improved and direct cultural assessment. I provide evidence in support of each of these guidelines, present alternative conceptual frameworks, and suggest new lines of research. Hopefully, that these directions will contribute to the emerging field of cultural development and psychopathology, which focuses on the elucidation of the cultural processes that initiate, maintain, or derail trajectories of normal and abnormal behavior.