We examined associations between specific self-regulatory mechanisms and externalizing behavior patterns from ages 2 to 15 (N = 443). The relation between multiple self-regulatory indicators across multiple domains (i.e., physiological, attentional, emotional, and behavioral) at age 2 and at age 5 and group membership in four distinct externalizing trajectories was examined. By examining each of these self-regulatory processes in combination with one another, and therefore accounting for their shared variance, we aimed to better understand which specific self-regulatory skills were associated most strongly with externalizing behavioral patterns. Findings suggest that behavioral inhibitory control and emotion regulation are particularly important in distinguishing between children who show normative declines in externalizing behaviors across early childhood and those who demonstrate high levels through adolescence.

Ethnic–racial and socioeconomic residential segregation are endemic in the United States, representing societal-level sociocultural processes that likely shape development. Considered alongside communities’ abilities to respond to external forces, like stratification, in ways that promote youth adaptive functioning and mitigate maladaptive functioning, it is likely that residence in segregated neighborhoods during adolescence has both costs and benefits. We examined the influences that early adolescents’ neighborhood structural characteristics, including Latino concentration and concentrated poverty, had on a range of developmentally salient downstream outcomes (i.e., internalizing, externalizing, prosocial behaviors, and ethnic–racial identity resolution) via implications for intermediate aspects of adolescents’ community participation and engagement (i.e., ethnic–racial identity exploration, ethnic–racial discrimination from peers, and school attachment). These mediational mechanisms were tested prospectively across three waves (Mage w1-w3 = 12.79, 15.83, 17.37 years, respectively) in a sample of 733 Mexican-origin adolescents (48.8% female). We found higher neighborhood Latino concentration during early adolescence predicted greater school attachment and ethnic–racial identity exploration and lower discrimination from peers in middle adolescence. These benefits, in turn, were associated with lower externalizing and internalizing and higher ethnic–racial identity resolution and prosocial behaviors in late adolescence. Findings are discussed relative to major guidelines for integrating culture into development and psychopathology.

There is clear evidence that the mother's stress, anxiety, or depression during pregnancy can alter the development of her fetus and her child, with an increased risk for later psychopathology. We are starting to understand some of the underlying mechanisms including the role of the placenta, gene–environment interactions, epigenetics, and specific systems including the hypothalamic–pituitary–adrenal axis and cytokines. In this review we also consider how these effects may be different, and potentially exacerbated, in different parts of the world. There can be many reasons for elevated prenatal stress, as in communities at war. There may be raised pregnancy-specific anxiety with high levels of maternal and infant death. There can be raised interpersonal violence (in Afghanistan 90.2% of women thought that “wife beating” was justified compared with 2.0% in Argentina). There may be interactions with nutritional deficiencies or with extremes of temperature. Prenatal stress alters the microbiome, and this can differ in different countries. Genetic differences in different ethnic groups may make some more vulnerable or more resilient to the effects of prenatal stress on child neurodevelopment. Most research on these questions has been in predominantly Caucasian samples from high-income countries. It is now time to understand more about prenatal stress and psychopathology, and the role of both social and biological differences, in the rest of the world.

While the trajectory of self-esteem from adolescence to adulthood varies from person to person, little research has examined how differences in early developmental processes might affect these pathways. This study examined how early motor skill development interacted with preterm birth status to predict self-esteem from adolescence through the early 30s. We addressed this using the oldest known, prospectively followed cohort of extremely low birth weight (<1000 g) survivors (N = 179) and normal birth weight controls (N = 145) in the world, born between 1977 and 1982. Motor skills were measured using a performance-based assessment at age 8 and a retrospective self-report, and self-esteem was reported during three follow-up periods (age 12–16, age 22–26, and age 29–36). We found that birth weight status moderated the association between early motor skills and self-esteem. Stable over three decades, the self-esteem of normal birth weight participants was sensitive to early motor skills such that those with poorer motor functioning manifested lower self-esteem, while those with better motor skills manifested higher self-esteem. Conversely, differences in motor skill development did not affect the self-esteem from adolescence to adulthood in individuals born at extremely low birth weight. Early motor skill development may exert differential effects on self-esteem, depending on whether one is born at term or prematurely.

Children exposed to maternal smoking during pregnancy (MSDP) exhibit difficulties in executive function (EF) from infancy through adolescence. Due to the developmental significance of EF as a predictor of adaptive functioning throughout the life span, the MSDP–EF relation has clear public health implications. In this paper, we provide a comprehensive review of the literature on the relationship between MSDP and offspring EF across development; consider brain-based assessments, animal models, and genetically informed studies in an effort to elucidate plausible pathways of effects; discuss implications for prevention and intervention; and make calls to action for future research.

Several studies have suggested that the neuropeptide oxytocin may enhance aspects of social communication in autism. Little is known, however, about its effects on nonsocial manifestations, such as restricted interests and repetitive behaviors. In the empathizing–systemizing theory of autism, social deficits are described along the continuum of empathizing ability, whereas nonsocial aspects are characterized in terms of an increased preference for patterned or rule-based systems, called systemizing. We therefore developed an automated eye-tracking task to test whether children and adolescents with autism spectrum disorder (ASD) compared to matched controls display a visual preference for more highly organized and structured (systemized) real-life images. Then, as part of a randomized, double-blind, placebo-controlled crossover study, we examined the effect of intranasal oxytocin on systemizing preferences in 16 male children with ASD, compared with 16 matched controls. Participants viewed 14 slides, each containing four related pictures (e.g., of people, animals, scenes, or objects) that differed primarily on the degree of systemizing. Visual systemizing preference was defined in terms of the fixation time and count for each image. Unlike control subjects who showed no gaze preference, individuals with ASD preferred to fixate on more highly systemized pictures. Intranasal oxytocin eliminated this preference in ASD participants, who now showed a similar response to control subjects on placebo. In contrast, control participants increased their visual preference for more systemized images after receiving oxytocin versus placebo. These results suggest that, in addition to its effects on social communication, oxytocin may play a role in some of the nonsocial manifestations of autism.

The links between low socioeconomic status and poor health are well established, yet despite adversity, some individuals with low socioeconomic status appear to avoid these negative consequences through adaptive coping. Previous research found a set of strategies, called shift-and-persist (shifting the self to stressors while persisting by finding meaning), to be particularly adaptive for individuals with low socioeconomic status, who typically face more uncontrollable stressors. This study tested (a) whether perceived social status, similar to objective socioeconomic status, would moderate the link between shift-and-persist and health, and (b) whether a specific uncontrollable stressor, unfair treatment, would similarly moderate the health correlates of shift-and-persist. A sample of 308 youth (Meanage = 13.0, range 8–17), physician diagnosed with asthma, completed measures of shift-and-persist, unfair treatment, asthma control, and quality of life in the lab, and 2 weeks of daily diaries about their asthma symptoms. Parents reported on perceived family social status. Results indicated that shift-and-persist was associated with better asthma profiles, only among youth from families with lower (vs. higher) parent-reported perceived social status. Shift-and-persist was also associated with better asthma profiles, only among youth who experienced more (vs. less) unfair treatment. These findings suggest that the adaptive values of coping strategies for youth with asthma depend on the family's perceived social status and on the stressor experienced.

This study examined the mediated effect of early adolescence familial context on early adulthood problematic substance use through effortful control in late adolescence. The sample consisted of a community sample of 311 adolescents and their families comprising the control group within a randomized trial intervention. Parental monitoring and parent–child relationship quality (P-C RQ) were measured annually from ages 11 to 13. Effortful control was measured by self-reports and parent and teacher reports at ages 16 to 17. Self-reports of problematic tobacco, alcohol, and marijuana use were measured at ages 18 to 19, 21 to 22, 23 to 24, and 26 to 27. Structural equation modeling was employed to test hypothesized models. Only P-C RQ was found to be significantly associated with adolescent effortful control. As expected, higher levels of adolescent effortful control were associated with lower problematic substance use through early adulthood, controlling for previous substance use levels. Mediation analyses showed that effortful control significantly mediated the relationship between P-C RQ and problematic substance use. Higher relationship quality between youth and parents in early adolescence is associated with higher effortful control, which in turn relates to a lower level of problematic substance use in early adulthood.

The error-related negativity (ERN) is a negative deflection in the event-related potential occurring when individuals make mistakes, and is increased in children with internalizing psychopathology. We recently found that harsh parenting predicts a larger ERN in children, and recent work has suggested that variation in the brain-derived neurotrophic factor (BDNF) gene may moderate the impact of early life adversity. Parents and children completed measures of parenting when children were 3 years old (N = 201); 3 years later, the ERN was measured and diagnostic interviews as well as dimensional symptom measures were completed. We found that harsh parenting predicted an increased ERN only among children with a methionine allele of the BDNF genotype, and evidence of moderated mediation: the ERN mediated the relationship between parenting and internalizing diagnoses and dimensional symptoms only if children had a methionine allele. We tested this model with externalizing disorders, and found that harsh parenting predicted externalizing outcomes, but the ERN did not mediate this association. These findings suggest that harsh parenting predicts both externalizing and internalizing outcomes in children; however, this occurs through different pathways that uniquely implicate error-related brain activity in the development of internalizing disorders.

There remains little debate that the period before birth sets the stage for subsequent development, yet scant evidence exists showing continuity from characteristics of the individual fetus to characteristics of the child. This report examines, in two studies, whether baseline and evoked fetal neurobehavioral functioning are predictive of features of child temperament and behavior as reported by mothers when offspring were between 7 and 14 years old (M = 10.1 years). Study 1 utilizes data generated from 333 maternal–fetal pairs collected during an undisturbed condition during the second half of gestation in relation to the child temperament dimensions of behavioral inhibition and exuberance. Associations at 32 weeks gestation were detected between all features of fetal neurobehavior and behavioral inhibition. In adjusted models, slower fetal heart rate and less fetal movement were associated with significant unique variance in predicting higher levels of childhood behavioral inhibition. No associations were detected for exuberance. Study 2 focuses on the association of evoked fetal reactivity and recovery to induced maternal arousal with subsequent child behavioral difficulties in a subset of the full sample (n = 130). Greater recovery in fetal heart rate following maternal stimulation was predictive of fewer behavioral difficulties and more prosocial behavior in childhood. Results from both studies provide support for gestational origins of core individual differences that portend childhood outcomes with foundational reactivity and regulatory components.

Prenatal experience is both a formative and a regulatory force in the process of development. As a result, birth is not an adequate starting point for explanations of behavioral development. However, surprisingly little is currently known regarding the role of prenatal experience in the emergence and facilitation of perceptual, cognitive, or social development. Our lack of knowledge in this area is due in part to the very restricted experimental manipulations possible with human fetuses. A comparative approach utilizing animal models provides an essential step in addressing this gap in our knowledge and providing testable predictions for studies with human fetuses, infants, and children. Further, animal-based comparative research serves to minimize the amount of exploratory research undertaken with human subjects and hone in on issues and research directions worthy of further research investment. In this article, I review selected animal-based research exploring how developmental influences during the prenatal period can guide and constrain subsequent behavioral and social development. I then discuss the importance of linking the prenatal environment to postnatal outcomes in terms of how psychologists conceptualize “innate” biases, preferences, and skills in the study of human development.

This study examined whether executive functions (EFs) might be common features of internalizing and externalizing behavior problems across development. We examined relations between three EF latent variables (a common EF factor and factors specific to updating working memory and shifting sets), constructed from nine laboratory tasks administered at age 17, to latent growth intercept (capturing stability) and slope (capturing change) factors of teacher- and parent-reported internalizing and externalizing behaviors in 885 individual twins aged 7 to 16 years. We then estimated the proportion of intercept–intercept and slope–slope correlations predicted by EF as well as the association between EFs and a common psychopathology factor (P factor) estimated from all 9 years of internalizing and externalizing measures. Common EF was negatively associated with the intercepts of teacher-rated internalizing and externalizing behavior in males, and explained 32% of their covariance; in the P factor model, common EF was associated with the P factor in males. Shifting-specific was positively associated with the externalizing slope across sex. EFs did not explain covariation between parent-rated behaviors. These results suggest that EFs are associated with stable problem behavior variation, explain small proportions of covariance, and are a risk factor that that may depend on gender.

Poor family cohesion and elevated adolescent aggression are associated with greater alcohol use in adolescence and early adulthood. In addition, evocative gene–environment correlations (rGEs) can underlie the interplay between offspring characteristics and negative family functioning, contributing to substance use. Gene–environment interplay has rarely been examined in racial/ethnic minority populations. The current study examined adolescents’ polygenic risk scores for aggression in evocative rGEs underlying aggression and family cohesion during adolescence, their contributions to alcohol use in early adulthood (n = 479), and differences between Mexican American and European American subsamples. Results suggest an evocative rGE between polygenic risk scores, aggression, and low family cohesion, with aggression contributing to low family cohesion over time. Greater family cohesion was associated with lower levels of alcohol use in early adulthood and this association was stronger for Mexican American adolescents compared to European American adolescents. Results are discussed with respect to integration of culture and racial/ethnic minority samples into genetic research and implications for alcohol use.

We present a developmental cascade model of the longitudinal relationships between internalizing symptoms, externalizing problems, and academic performance in middle childhood, utilizing a large sample (N = 1,771) from the United Kingdom in a 3-year, cross-lag design. Three hypotheses were tested: adjustment erosion, academic incompetence, and (cumulative) shared risk. In addition, we sought to examine whether developmental cascade pathways varied across gender, while also statistically exploring indirect, mediation pathways. Structural equation models that accounted for within-time covariance, data nesting, and temporal stability provided evidence of gender-specific effects as follows: externalizing-attainment adjustment erosion pathways were found only in boys, while attainment-internalizing/externalizing academic incompetence pathways were found only in girls. Analysis of mediation pathways provided further support for these gender-specific longitudinal profiles. Protective longitudinal internalizing-externalizing and externalizing-internalizing pathways were found for both boys and girls. Finally, while it improved model fit for both genders, the influence of cumulative shared risk on the aforementioned pathways was relatively meager, substantively affecting only one (externalizing-attainment adjustment erosion pathway in boys). The implications of these findings are discussed, and study limitations noted.

Liability to substance use disorder (SUD) is largely nonspecific to particular drugs and is related to behavior dysregulation, including reduced cognitive control. Recent data suggest that cognitive mechanisms may be influenced by exposure to neurotropic infections, such as human herpesviruses. In this study, serological evidence of exposure to human herpesvirus Herpes simplex virus Type 1 (HSV-1), cytomegalovirus (CMV), and Epstein–Barr virus (EBV) as well as Toxoplasma gondii was determined in childhood (age ~11 years) in 395 sons and 174 daughters of fathers with or without SUD. Its relationships with a cognitive characteristic (IQ) in childhood and with risk for SUD in adulthood were examined using correlation, regression, survival, and path analyses. Exposure to HSV-1, EBV, and T. gondii in males and females, and CMV in males, was associated with lower IQ. Independent of that relationship, EBV in females and possibly in males, and CMV and possibly HSV-1 in females were associated with elevated risk for SUD. Therefore, childhood neurotropic infections may influence cognitive development and risk for behavior disorders such as SUD. The results may point to new avenues for alleviating cognitive impairment and SUD risk.

Growing evidence from developmental psychology and social neuroscience emphasizes the importance of third-party harm aversion for constructing morality. A sensitivity to interpersonal harm emerges very early in ontogeny, as reflected in both the capacity for implicit social evaluation and an aversion for antisocial agents. Yet it does not necessarily entail avoidance toward inflicting pain to others. Later, an understanding that harmful actions cause suffering emerges, followed by an integration of rules that can depend on social contexts and cultures. These developmental findings build on a burgeoning literature, which suggests that the fundamental nature of moral and social cognition, including their motivational and hedonic value, lies in general computational processes such as attention, approach–avoidance, social valuation, and decision making rather than in fully distinct, dedicated neural regions for morality. Bridging the gap between cognition and behaviors and the requisite affective, motivational, and cognitive mechanisms, a developmental neuroscience approach enriches our understanding of the emergence of morality.

Experiencing maltreatment during childhood can have long-lasting consequences for both mental and physical health. Immune cell telomere length (TL) shortening might be one link between child maltreatment (CM) experiences and adverse health outcomes later in life. While the stress hormone cortisol has been associated with TL attrition, the attachment-related hormone oxytocin may promote resilience. In 15 mothers with and 15 age- and body mass index-matched mothers without CM, we assessed TL in peripheral blood mononuclear cells and selected immune cell subsets (monocytes, naive, and memory cytotoxic T cells) by quantitative fluorescence in situ hybridization, as well as peripheral cortisol and oxytocin levels. Memory cytotoxic T cells showed significantly shorter TL in association with CM, whereas TL in monocytes and naive cytotoxic T cells did not significantly differ between the two groups. Across both groups, cortisol was negatively associated with TL, while oxytocin was positively associated with TL in memory cytotoxic T cells. These results indicate that long-lived memory cytotoxic T cells are most affected by the increased biological stress state associated with CM. Keeping in mind the correlational and preliminary nature of the results, the data suggest that cortisol may have a damaging and oxytocin a protective function on TL.

Adolescence is a critical period for the development of self-regulation, and peer interactions are thought to strongly influence regulation ability. Simple exposure to peers has been found to alter decisions about risky behaviors and increase sensitivity to rewards. The link between peer exposure and self-regulation is likely to vary as a function of the type and quality of peer interaction (e.g., rejection or acceptance). Little is known about how the nature of interactions with peers influences different dimensions of self-regulation. We examined how randomization to acceptance or rejection by online “virtual” peers influenced multiple dimensions of self-regulation in a multisite community sample of 273 adolescents aged 16–17 years. Compared to a neutral condition, exposure to peers produced increases in cold cognitive control, but decreased hot cognitive control. Relative to peer acceptance, peer rejection reduced distress tolerance and increased sensitivity to losses. These findings suggest that different dimensions of adolescent self-regulation are influenced by the nature of the peer context: basic cognitive functions are altered by mere exposure to peers, whereas more complex decision making and emotion regulation processes are influenced primarily by the quality of that exposure.

Development involves synergistic interplay among genotypes and the physical and cultural environments, and integrating genetics into experimental designs that manipulate the environment can improve understanding of developmental psychopathology and intervention efficacy. Consistent with differential susceptibility theory, individuals can vary in their sensitivity to environmental conditions including intervention for reasons including their genotype. As a consequence, understanding genetic influences on intervention response is critical. Empirically, we tested an interaction between a genetic index representing sensitivity to the environment and the Family Check-Up intervention. Participants were drawn from the Early Steps Multisite randomized prevention trial that included a low-income and racially/ethnically diverse sample of children and their families followed longitudinally (n = 515). As hypothesized, polygenic sensitivity to the environment moderated the effects of the intervention on 10-year-old children's symptoms of internalizing psychopathology, such that children who were genetically sensitive and were randomly assigned to the intervention had fewer symptoms of child psychopathology than genetically sensitive children assigned to the control condition. A significant difference in internalizing symptoms assessed with a clinical interview emerged between the intervention and control groups for those 0.493 SD above the mean on polygenic sensitivity, or 25% of the sample. Similar to personalized medicine, it is time to understand individual and sociocultural differences in treatment response and individualize psychosocial interventions to reduce the burden of child psychopathology and maximize well-being for children growing up in a wide range of physical environments and cultures.

Following recent advances in behavioral and psychiatric epigenetics, researchers are increasingly using epigenetic methods to study prenatal exposure to maternal mood disorder and its effects on fetal and newborn neurobehavior. Despite notable progress, various methodological limitations continue to obscure our understanding of the epigenetic mechanisms underpinning prenatal exposure to maternal mood disorder on newborn neurobehavioral development. Here we detail this problem, discussing limitations of the currently dominant analytical approaches (i.e., candidate epigenetic and epigenome-wide association studies), then present a solution that retains many benefits of existing methods while minimizing their shortcomings: epigenetic pathway analysis. We argue that the application of pathway-based epigenetic approaches that target DNA methylation at transcription factor binding sites could substantially deepen our mechanistic understanding of how prenatal exposures influence newborn neurobehavior.