An association has been found between receipt of harsh parenting in childhood and adult health problems. However, this research has been principally retrospective, has treated children as passive recipients of parental behavior, and has overlooked individual differences in youth responsivity to harsh parenting. In a 10-year multiple-wave prospective study of African American families, we addressed these issues by focusing on the influence of polymorphisms in the oxytocin receptor gene (OXTR), variants of which appear to buffer or amplify responses to environmental stress. The participants were 303 youths, with a mean age of 11.2 at the first assessment, and their parents, all of whom were genotyped for variations in the rs53576 (A/G) polymorphism. Teachers rated preadolescent (ages 11 to 13) emotionally intense and distractible temperaments, and adolescents (ages 15 and 16) reported receipt of harsh parenting. Allostatic load was assessed during young adulthood (ages 20 and 21). Difficult preadolescent temperament forecast elevated receipt of harsh parenting in adolescence, and adolescents who experienced harsh parenting evinced high allostatic load during young adulthood. However, these associations emerged only among children and parents who carried A alleles of the OXTR genotype. The results suggest the oxytocin system operates along with temperament and parenting to forecast young adults’ allostatic load.

Epigenetics processes may play a vital role in the biological embedding of early environmental adversity and the development of psychopathology. Accumulating evidence suggests that maltreatment is linked to methylation of the glucocorticoid receptor gene, nuclear receptor subfamily 3, group C, member 1 (NR3C1), which is a key regulator of the hypothalamus–pituitary–adrenal axis. However, prior work has been exclusively cross-sectional, greatly constraining our understanding of stress-related epigenetic processes over time. In the current study, we examined the effect of maltreatment and other adversity on change in NR3C1 methylation among at-risk preschoolers to begin to characterize within-child epigenetic changes during this sensitive developmental period. Participants were 260 preschoolers (3–5 years old, 53.8% female), including 51.5% with moderate to severe maltreatment in the past 6 months. Child protection records, semistructured interviews, and parent reports were used to assess child stress exposure. Methylation of exons 1D and 1F of NR3C1 via saliva DNA were measured at two time points approximately 6 months apart. Results indicate that maltreated children evidence higher baseline levels of NR3C1 methylation, significant decreases in methylation over time, and then at follow-up, lower levels of methylation, relative to nonmaltreated preschoolers. Findings from the current study highlight the complex nature of stress-related epigenetic processes during early development.

Previous studies demonstrate that boys' monoamine oxidase A (MAOA) genotype interacts with adverse rearing environments in early childhood, including punitive discipline, to predict later antisocial behavior. Yet the mechanisms by which MAOA and punitive parenting interact during childhood to amplify risk for antisocial behavior are not well understood. In the present study, hostile attributional bias and aggressive response generation during middle childhood, salient aspects of maladaptive social information processing, were tested as possible mediators of this relation in a sample of 187 low-income men followed prospectively from infancy into early adulthood. Given racial–ethnic variation in MAOA allele frequencies, analyses were conducted separately by race. In both African American and Caucasian men, those with the low-activity MAOA allele who experienced more punitive discipline at age 1.5 generated more aggressive responses to perceived threat at age 10 relative to men with the high-activity variant. In the African American subsample only, formal mediation analyses indicated a marginally significant indirect effect of maternal punitiveness on adult arrest records via aggressive response generation in middle childhood. The findings suggest that maladaptive social information processing may be an important mechanism underlying the association between MAOA × Parenting interactions and antisocial behavior in early adulthood. The present study extends previous work in the field by demonstrating that MAOA and harsh parenting assessed in early childhood interact to not only predict antisocial behavior in early adulthood, but also predict social information processing, a well-established social–cognitive correlate of antisocial behavior.

Research on attachment transmission has focused on variable-centered analyses, where hypotheses are tested by examining linear associations between variables. The purpose of this study was to apply a relationship-centered approach to data analysis, where adult states of mind, maternal sensitivity, and infant attachment were conceived as being three components of a single, intergenerational relationship. These variables were assessed in 90 adolescent and 99 adult mother–infant dyads when infants were 12 months old. Initial variable-centered analyses replicated the frequently observed associations between these three core attachment variables. Relationship-based, latent class analyses then revealed that the most common pattern among young mother dyads featured maternal unresolved trauma, insensitive interactive behavior, and disorganized infant attachment (61%), whereas the most prevalent adult mother dyad relationship pattern involved maternal autonomy, sensitive maternal behavior, and secure infant attachment (59%). Three less prevalent relationship patterns were also observed. Moderation analyses revealed that the adolescent–adult mother distinction differentiated between secure and disorganized intergenerational relationship patterns, whereas experience of traumatic events distinguished between disorganized and avoidant patterns. Finally, socioeconomic status distinguished between avoidant and secure patterns. Results emphasize the value of a relationship-based approach, adding an angle of understanding to the study of attachment transmission.

In utero exposure to maternal psychological distress is a risk factor for developmental psychopathology, and these effects are believed to partially occur via dysregulation of the maternal and fetal hypothalamus–adrenal–pituitary axes. Nevertheless, only a few human studies have directly assessed the effects of prenatal cortisol exposure on infant cortisol reactivity, and none have investigated sex differences or potential interactions between prenatal cortisol and psychological distress. Here we report on a prospective longitudinal investigation (N = 236) of in utero exposure to maternal cortisol and distress in a relatively high socioeconomic status and low-risk population to determine whether these exposures interact in their effects on infant (M age = 3.0 months, range = 2.3–5.0 months, 51.9% male) cortisol reactivity and whether there are sex differences in these effects. Results revealed both sexually dimorphic and interactive effects of prenatal cortisol and distress, even after controlling for postnatal distress. In general, blunted reactivity in females was associated with exposure to high maternal distress and flattened patterns of diurnal maternal cortisol, whereas blunted reactivity in males was associated with exposure to steeper morning increases and daytime decreases in maternal cortisol. The findings suggest that sex differences in the effects of prenatal cortisol and distress on infant cortisol reactivity are a plausible mechanism by which maternal experiences during pregnancy contribute to sex differences in the development of psychopathology.

Children who grow up in poverty are more likely to experience chronic stressors that generate “wear” on stress regulatory systems including the hypothalamus–pituitary–adrenal (HPA) axis. This can have long-term consequences for health and well-being. Prior research has examined the role of proximal family and home contributions to HPA axis functioning. However, there is evidence to suggest that more distal levels of context, including neighborhoods, also matter. Prior evidence has primarily focused on adolescents and adults, with little evidence linking the neighborhood context with HPA activity in infancy and toddlerhood. We tested whether neighborhood disadvantage (indexed by US Census data) was associated with basal salivary cortisol levels at 7, 15, and 24 months of child age in a large sample of families (N = 1,292) residing in predominately low-income and rural communities in the United States. Multilevel models indicated that neighborhood disadvantage was positively associated with salivary cortisol levels and that this effect emerged across time. This effect was moderated by the race/ethnicity of children such that the association was only observed in White children in our sample. Findings provide preliminary evidence that the neighborhood context is associated with stress regulation during toddlerhood, elucidating a need for future work to address possible mechanisms.

The methodological and epistemological challenges that research on ethnopolitical violence faces are examined. This research area is fundamentally important for political reasons and for understanding, as well as subsequent interventions to ameliorate, youths’ responses to ethnopolitical violence. Advances in methods are reviewed that can overcome the obstacles placed by the various challenges. These issues are discussed in the context of the articles that comprise this Special Section.

A considerable body of evidence suggests that early caregiving may affect the short-term functioning and longer term development of the hypothalamic–pituitary–adrenocortical axis. Despite this, most research to date has been cross-sectional in nature or restricted to relatively short-term longitudinal follow-ups. More important, there is a paucity of research on the role of caregiving in low- and middle-income countries, where the protective effects of high-quality care in buffering the child's developing stress regulation systems may be crucial. In this paper, we report findings from a longitudinal study (N = 232) conducted in an impoverished periurban settlement in Cape Town, South Africa. We measured caregiving sensitivity and security of attachment in infancy and followed children up at age 13 years, when we conducted assessments of hypothalamus–pituitary–adrenocortical axis reactivity, as indexed by salivary cortisol during the Trier Social Stress Test. The findings indicated that insecure attachment was predictive of reduced cortisol responses to social stress, particularly in boys, and that attachment status moderated the impact of contextual adversity on stress responses: secure children in highly adverse circumstances did not show the blunted cortisol response shown by their insecure counterparts. Some evidence was found that sensitivity of care in infancy was also associated with cortisol reactivity, but in this case, insensitivity was associated with heightened cortisol reactivity, and only for girls. The discussion focuses on the potentially important role of caregiving in the long-term calibration of the stress system and the need to better understand the social and biological mechanisms shaping the stress response across development in low- and middle-income countries.

The main objective of this prospective longitudinal study was to investigate bidirectional associations between adolescent cannabis use (CU) and neurocognitive performance in a community sample of 294 young men from ages 13 to 20 years. The results showed that in early adolescence, and prior to initiation to CU, poor short-term and working memory, but high verbal IQ, were associated with earlier age of onset of CU. In turn, age of CU onset and CU frequency across adolescence were associated with (a) specific neurocognitive decline in verbal IQ and executive function tasks tapping trial and error learning and reward processing by early adulthood and (b) lower rates of high-school graduation. The association between CU onset and change in neurocognitive function, however, was found to be accounted for by CU frequency. Whereas the link between CU frequency across adolescence and change in verbal IQ was explained (mediated) by high school graduation, the link between CU frequency and tasks tapping trial and error learning were independent from high school graduation, concurrent cannabis and other substance use, adolescent alcohol use, and externalizing behaviors. Findings support prevention efforts aimed at delaying onset and reducing frequency of CU.

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.

Articles in this timely Special Section represent an important milestone in the developmental science on children and youth involved in political violence and armed conflict. With millions of children worldwide affected by past and present wars and conflicts, there is an urgent and growing need for research to inform efforts to understand, prevent, and mitigate the possible harm of such violence to individual children, families, communities, and societies, for present as well as future generations. The four programs of research highlighted in this Special Section illustrate key advances and challenges in contemporary development research on young people growing up in the midst or aftermath of political violence. These studies are longitudinal, methodologically sophisticated, and grounded in socioecological systems models that align well with current models of risk and resilience in developmental psychopathology. These studies collectively mark a critically important shift to process-focused research that holds great promise for translational applications. Nonetheless, given the scope of the international crisis of children and youth affected by political violence and its sequelae, there is an urgent global need for greater mobilization of resources to support translational science and effective evidence-based action.

Statistical tests of differential susceptibility have become standard in the empirical literature, and are routinely used to adjudicate between alternative developmental hypotheses. However, their performance and limitations have never been systematically investigated. In this paper I employ Monte Carlo simulations to explore the functioning of three commonly used tests proposed by Roisman et al. (2012). Simulations showed that critical tests of differential susceptibility require considerably larger samples than standard power calculations would suggest. The results also showed that existing criteria for differential susceptibility based on the proportion of interaction index (i.e., values between .40 and .60) are especially likely to produce false negatives and highly sensitive to assumptions about interaction symmetry. As an initial response to these problems, I propose a revised test based on a broader window of proportion of interaction index values (between .20 and .80). Additional simulations showed that the revised test outperforms existing tests of differential susceptibility, considerably improving detection with little effect on the rate of false positives. I conclude by noting the limitations of a purely statistical approach to differential susceptibility, and discussing the implications of the present results for the interpretation of published findings and the design of future studies in this area.

There is now ample evidence that the quality of early attachment experiences shapes expectations for supportive and responsive care and ultimately serves to scaffold adaptation to the salient tasks of development. Nonetheless, few studies have identified neural mechanisms that might give rise to these associations. Using a moderately large sample of low-income male participants recruited during infancy (N = 171), we studied the predictive significance of attachment insecurity and disorganization at age 18 months (as measured in the Strange Situation Procedure) for patterns of neural activation to reward and loss at age 20 years (assessed during a reward-based task as part of a functional magnetic resonance imaging scan). Results indicated that individuals with a history of insecure attachment showed hyperactivity in (a) reward- and emotion-related (e.g., basal ganglia and amygdala) structures and (b) emotion regulation and self-referential processing (cortical midline structures) in response to positive and negative outcomes (and anticipation of those outcomes). Further, the neural activation of individuals with a history of disorganized attachment suggested that they had greater emotional reactivity in anticipation of reward and employed greater cognitive control when negative outcomes were encountered. Overall, results suggest that the quality of early attachments has lasting impacts on brain function and reward processing.

Longitudinal investigations that have applied Moffitt's dual taxonomic framework to criminal offending have provided support for the existence of adolescent-limited and life-course persistent antisocial individuals, but have also identified additional trajectories. For instance, rather than a single persistent trajectory, studies have found both high-level and moderate-level persistent offenders. To inform theory and progress our understanding of chronic antisocial behavior, the present study used a sample of serious adolescent offenders (N =1,088) followed from middle adolescence to early adulthood (14–25 years), and examined how moderate-level persistent offenders differed from low-rate, desisting, and high-level persistent offenders. Results indicated that moderate-level persisters' etiology and criminal offense patterns were most similar to high-level persisters, but there were notable differences. Specifically, increasing levels of contextual adversity characterized both moderate-level and high-level persisting trajectories, but moderate-level persisters reported consistently lower levels of environmental risk. While both high- and moderate-level persisters committed more drug-related offenses in early adulthood compared to adolescence, moderate-level persisters engaged in lower levels of antisocial behavior across all types of criminal offenses. Taken cumulatively, the findings of this study suggest that sociocontextual interventions may be powerful in reducing both moderate- and high-level persistence in crime.

Negative experiences with a caregiver during infancy can result in long-term changes in brain function and behavior, but underlying mechanisms are not well understood. It is our central hypothesis that brain and behavior changes are conferred by early childhood adversity through epigenetic changes involving DNA methylation. Using a rodent model of early-life caregiver maltreatment (involving exposure to an adverse caregiving environment for postnatal days 1–7), we have previously demonstrated abnormal methylation of DNA associated with the brain-derived neurotrophic factor (Bdnf) gene in the medial prefrontal cortex (mPFC) of adult rats. The aim of the current study was to characterize Bdnf DNA methylation in specific cell populations within the mPFC. In the prefrontal cortex, there is approximately twice as many neurons as glia, and studies have recently shown differential and distinctive DNA methylation patterns in neurons versus nonneurons. Here, we extracted nuclei from the mPFC of adult animals that had experienced maltreatment and used fluorescence-activated cell sorting to isolate cell types before performing bisulfite sequencing to estimate methylation of cytosine–guanine sites. Our data indicate that early-life stress induced methylation of DNA associated with Bdnf IV in a cell-type and sex-specific manner. Specifically, females that experienced early-life maltreatment exhibited greater neuronal cytosine–guanine methylation compared to controls, while no changes were detected in Bdnf methylation in males regardless of cell type. These changes localize the specificity of our previous findings to mPFC neurons and highlight the capacity of maltreatment to cause methylation changes that are likely to have functional consequences for neuronal function.

The reader might get the impression that the four projects described in this Special Section proceeded in a systematic and predictable way. Of course, those of us engaged in each research project encountered pitfalls and challenges along the way. A main goal of this Special Section is to provide pathways and encouragement for those who may be interested in advancing high-quality research on this topic. In this paper, we describe a set of practical and ethical challenges that we encountered in conducting our longitudinal, process-oriented, and translational research with conflict-affected youth, and we illustrate how problems can be solved with the goal of maintaining the internal and external validity of the research designs. We are hopeful that by describing the challenges of our work, and how we overcame them, which are seldom treated in this or any other literature on research on child development in high-risk contexts, we can offer a realistic and encouraging picture of conducting methodologically sound research in conflict-affected contexts.

Harsh, abusive, and rejecting behavior by parents toward their children is associated with increased risk for many developmental problems for youth. Children raised by harsh parents are also more likely to treat their own children harshly. The present study addresses conditions that would break this intergenerational cycle of harsh parenting. Data come from a three-generation study of a cohort of 290 adolescents (Generation 2 [G2], 52% female) grown to adulthood and their parents (Generation 1 [G1]). During adolescence, observers rated G1 harsh parenting to G2. Several years later observers rated G2 harsh parenting toward their oldest child (Generation 3 [G3]). Several adaptive systems fundamental to human resilience attenuate intergenerational continuity in harshness. G2 parents were relatively less harsh to G3 children (notwithstanding a history of harshness from G1) when G2's romantic partner (a) communicated positively with G2 and (b) had a good relationship with G3, and (c) when G2 was high on self-control. Interventions that target all of these protective factors may not only break but also reverse the intergenerational cycle of child maltreatment.

Using data from 1,177 families in eight countries (Colombia, Italy, Jordan, Kenya, the Philippines, Sweden, Thailand, and the United States), we tested a conceptual model of direct effects of childhood family adversity on subsequent externalizing behaviors as well as indirect effects through psychological mediators. When children were 9 years old, mothers and fathers reported on financial difficulties and their use of corporal punishment, and children reported perceptions of their parents’ rejection. When children were 10 years old, they completed a computerized battery of tasks assessing reward sensitivity and impulse control and responded to questions about hypothetical social provocations to assess their hostile attributions and proclivity for aggressive responding. When children were 12 years old, they reported on their externalizing behavior. Multigroup structural equation models revealed that across all eight countries, childhood family adversity had direct effects on externalizing behaviors 3 years later, and childhood family adversity had indirect effects on externalizing behavior through psychological mediators. The findings suggest ways in which family-level adversity poses risk for children's subsequent development of problems at psychological and behavioral levels, situated within diverse cultural contexts.

Extremely low birth weight (ELBW; <1000 g) infants have been exposed to stressful intrauterine and early postnatal environments. Even greater early adversity has been experienced by ELBW survivors who were also born small for gestational age (SGA; <10th percentile for GA) compared to those born appropriate for GA (AGA). ELBW survivors, particularly those born SGA, face increased risk for internalizing problems compared to normal BW (NBW; ≥2500 g) controls. Internalizing problems are related to allelic variations in the promoter region of the serotonin transporter linked polymorphic region gene (5-HTTLPR). We followed the oldest longitudinal cohort of ELBW survivors to adulthood. Participants provided buccal cells and reported on internalizing problems, using the Young Adult Self-Report when they were in their mid-20s (ELBW/SGA, N = 28; ELBW/AGA, N = 60; NBW, N = 81) and mid-30s (ELBW/SGA, N = 27; ELBW/AGA, N = 58; NBW, N = 76). The findings indicate that ELBW/SGAs carrying the 5-HTTLPR short allele reported increased internalizing problems, particularly depression, during the third and fourth decades of life. This is the first known report on gene–environment interactions predicting psychopathology among ELBW survivors. Our findings elucidate putative neurobiological pathways that underlie risk for psychopathology.