The genetic architecture of the association between psychopathic traits and reduced skin conductance responses (SCRs) is poorly understood. By using 752 twins aged 9–10 years, this study investigated the heritability of two SCR measures (anticipatory SCRs to impending aversive stimuli and unconditioned SCRs to the aversive stimuli themselves) in a countdown task. The study also investigated the genetic and environmental sources of the covariance between these SCR measures and two psychopathic personality traits: impulsive/disinhibited (reflecting impulsive–antisocial tendencies) and manipulative/deceitful (reflecting the affective–interpersonal features). For anticipatory SCRs, 27%, 14%, and 59% of the variation was due to genetic, shared environmental, and nonshared environmental effects, respectively, while the percentages for unconditioned SCRs were 44%, 2%, and 54%. The manipulative/deceitful (not impulsive/disinhibited) traits were negatively associated with both anticipatory SCRs (r = –.14, p < .05) and unconditioned SCRs (r = –.17, p < .05) in males only, with the former association significantly accounted for by genetic influences (rg = –.72). Reduced anticipatory SCRs represent a candidate endophenotype for the affective–interpersonal facets of psychopathic traits in males.

Identifying the mechanisms linking early experiences, genetic risk factors, and their interaction with later health consequences is central to the development of preventive interventions and identifying potential boundary conditions for their efficacy. In the current investigation of 412 African American adolescents followed across a 20-year period, we examined change in body mass index (BMI) across adolescence as one possible mechanism linking childhood adversity and adult health. We found associations of childhood adversity with objective indicators of young adult health, including a cardiometabolic risk index, a methylomic aging index, and a count of chronic health conditions. Childhood adversities were associated with objective indicators indirectly through their association with gains in BMI across adolescence and early adulthood. We also found evidence of an association of genetic risk with weight gain across adolescence and young adult health, as well as genetic moderation of childhood adversity's effect on gains in BMI, resulting in moderated mediation. These patterns indicated that genetic risk moderated the indirect pathways from childhood adversity to young adult health outcomes and childhood adversity moderated the indirect pathways from genetic risk to young adult health outcomes through effects on weight gain during adolescence and early adulthood.

Werner's orthogenetic principle states that human behavior proceeds from a state of global diffuseness to one of articulated complexity, and that as individuals develop, their responses to the environment become more specific and more differentiated. The present study evaluated this hypothesis, in relation to psychopathology in general and depression in particular. Child Behavior Checklist responses for 1, 345 outpatient and inpatient children and adolescents were compared along two developmental dimensions: age and clinical severity. Results failed to support the hypothesis that the psychopathology in general is more differentiated among older and more severely disturbed children. The findings did indicate, however, that depression was more distinct among the older, more severely disturbed subjects. Finally, little evidence of a categorical depression was found in any of the four age by severity groups.

Drawing on data from the Early Childhood Longitudinal Study-Birth Cohort (n = 10,700), we evaluate indirect effects − via parent negative psychology and harsh-inconsistent parenting − of income harshness, unpredictability, and their interaction on kindergarteners’ socioemotional development. Income harshness is operationalized as the typical level of family income-to-needs across four repeated measurements from 9 months to kindergarten and unpredictability as random variation across the same repeated measurements. Results indicate that the effects of greater income harshness and the harshness-X-unpredictability interaction (reflecting more predictable income harshness) on more “problematic” child behavior operated via both parent negative psychology (i.e., greater psychological stress) and harsh-inconsistent parenting. Results underscore the utility of simultaneously investigating effects of income harshness and unpredictability, as well as their interaction and mechanisms of influence.

African American youths are overrepresented in the American juvenile justice system relative to Caucasians. Yet, research on antisocial behaviors (ASB) has focused on predominantly Caucasian populations. Furthermore, relatively little is known about how environmental factors, such as supportive parenting (e.g., how close adolescents feel to their parent) and school connectedness (e.g., how supported adolescents feel at school), affect trajectories of ASB in Caucasians versus African Americans. This study mapped developmental trajectories of ASB in Caucasians (n = 10,764) and African Americans (n = 4,091) separately, using four waves of data from the National Longitudinal Study of Adolescent to Adult Health. We then examined supportive parenting and school connectedness on the trajectories of ASB. Four trajectories of ASB were identified for both Caucasians and African Americans: negligible, adolescence-peaked, low-persistence, and high-persistence ASB, although prevalence rates differed by racial-ethnic status. Supportive parenting reduced the risk of membership into the adolescence-peaked trajectory for both Caucasians and African Americans. However, school connectedness was less protective for African Americans than for Caucasians because it only predicted a lower risk of adolescence-peaked membership for African Americans. Findings may reflect the complex social dynamics between race and schools in the development of ASB.

Externalizing behavior in early adolescence is associated with alcohol use in adolescence and early adulthood and these behaviors often emerge as part of a developmental sequence. This pattern can be the result of heterotypic continuity, in which different behaviors emerge over time based on an underlying shared etiology. In particular, there is largely a shared genetic etiology underlying externalizing and substance use behaviors. We examined whether polygenic risk for alcohol use disorder predicted (1) externalizing behavior in early adolescence and alcohol use in adolescence in the Early Steps Multisite sample and (2) externalizing behavior in adolescence and alcohol use in early adulthood in the Project Alliance 1 (PAL1) sample. We examined associations separately for African Americans and European Americans. When examining European Americans in the Early Steps sample, greater polygenic risk was associated with externalizing behavior in early adolescence. In European Americans in PAL1, we found greater polygenic risk was associated with alcohol use in early adulthood. Effects were largely absent in African Americans in both samples. Results imply that genetic predisposition for alcohol use disorder may increase risk for externalizing and alcohol use as these behaviors emerge developmentally.

While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: nbirth = 804, nage 7 = 877) and trajectories of social communication deficits at age 8–17 years. Methylomic variation at three loci across the genome (false discovery rate = 0.048) differentiated children following high (n = 80) versus low (n = 724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at 7 years of age. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from childhood to adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated.

The current investigation utilized a developmental psychopathology approach to test the hypothesis that multigenic (i.e., dopaminergic and serotonergic genes) and multienvironmental factors interactively contribute to developmental pathways of antisocial behavior (ASB). A sample of 8,834 Caucasian individuals from the National Longitudinal Study of Adolescent to Adult Health (Add Health) were used to (a) examine the developmental pathways of ASB from age 13 to 32 using growth mixture modeling, (b) compute weighted multigenic risk scores (Add Health MRS) for ASB from six well-characterized polymorphisms in dopamine and serotonin genes, and (c) test the interaction between the Add Health MRS and a measures of support (incorporating indicators of both positive and negative support from parents and schools). Four pathways of adolescent to adult ASB emerged from the growth mixture models: low, adolescence-peaked, high decline, and persistent. Add Health MRS predicted the persistent ASB pathway, but not other ASB pathways. Males with high Add Health MRS, but not low MRS, had significantly greater odds of being in the adolescence-peaked pathway relative to the low pathway at low levels of school connectedness. Nonfamilial environmental influences during adolescence may have a cumulative impact on the development of ASB, particularly among males with greater underlying genetic risks.

Studies using the Emotional Availability Scales have burgeoned in the past decade. The collection of papers included in this Special Section represents the latest innovations in research with this paradigm. Consistent with a developmental psychopathology perspective, these papers evaluate emotional availability in a variety of typical, at-risk, international, and intergenerational samples of children and caregivers, with many utilizing longitudinal designs or employing measures from multiple levels of analysis. One study begins to translate findings from this body of research into a promising intervention program. Although further growth and refinement in research with this paradigm is needed, the results to date begin to place the construct of emotional availability into a complex, dynamic biopsychosocial context, and promise to inspire a new generation of studies. In this commentary, some of the key contributions and challenges of this collection of studies are highlighted using a developmental psychopathology framework.

This research tested the hypothesis that information-processing deficits associated with hyperactivity implicate a self-regulatory dysfunction. Hyperactive and control children were compared on nonspeeded classification tasks. In Studies 1 and 2, children classified sets of either three (triads) or four (tetrads) stimuli. The stimuli varied simultaneously on size and brightness or on length and density. They could be classified analytically (separably) on the basis of identical values for one dimension and holistically (integrally) on the basis of overall similarity. Control children made an equal number of dimensional classifications for triads and for tetrads. As predicted, however, hyperactive children made fewer dimensional classifications for tetrads, suggesting that they apparently resorted to less effortful holistic responding under the increased processing load. In an unexpected finding in Study 1, older hyperactive children appeared to behave like younger controls, making more dimensional classifications when size, rather than brightness, was the shared dimension. Study 3 explored the possibility that hyperactive children lagged behind the controls in their responding to the shared dimensions. Three age groups of normal children (mean ages: 5, 8, and 11 years) and adults were asked to classify stimuli that varied on size and brightness. Consistent with the lag hypothesis, normal preschoolers behaved like the young hyperactive children in Study 1, classifying equally on the basis of size and brightness. The discussion focuses on the contribution of processing load and stimulus salience to the cognitive deficits of hyperactive children.

Based on attachment theory, the construct of emotional availability and its assessment goes beyond attachment in important ways. Its origins in clinical experience and emotions research are discussed as well as the prospects for continuing advances in knowledge stimulated by the contributions in the Special Section. This is especially so in terms of developmental variations and the biological underpinnings of emotional availability. A major need and opportunity also exists concerning research related to psychopathology, clinical interventions, and training.

Impaired facial emotion recognition is a transdiagnostic risk factor for a range of psychiatric disorders. Childhood behavioral difficulties and parental emotional environment have been independently associated with impaired emotion recognition; however, no study has examined the contribution of these factors in conjunction. We measured recognition of negative (sad, fear, anger), neutral, and happy facial expressions in 135 children aged 5–7 years referred by their teachers for behavioral problems. Parental emotional environment was assessed for parental expressed emotion (EE) – characterized by negative comments, reduced positive comments, low warmth, and negativity towards their child – using the 5-minute speech sample. Child behavioral problems were measured using the teacher-informant Strengths and Difficulties Questionnaire (SDQ). Child behavioral problems and parental EE were independently associated with impaired recognition of negative facial expressions specifically. An interactive effect revealed that the combination of both factors was associated with the greatest risk for impaired recognition of negative faces, and in particular sad facial expressions. No relationships emerged for the identification of happy facial expressions. This study furthers our understanding of multidimensional processes associated with the development of facial emotion recognition and supports the importance of early interventions that target this domain.

Childhood adversity is thought to undermine youth socioemotional development via altered neural function within regions that support emotion processing. These effects are hypothesized to be developmentally specific, with adversity in early childhood sculpting subcortical structures (e.g., amygdala) and adversity during adolescence impacting later-developing structures (e.g., prefrontal cortex; PFC). However, little work has tested these theories directly in humans. Using prospectively collected longitudinal data from the Fragile Families and Child Wellbeing Study (FFCWS) (N = 4,144) and neuroimaging data from a subsample of families recruited in adolescence (N = 162), the current study investigated the trajectory of harsh parenting across childhood (i.e., ages 3 to 9) and how initial levels versus changes in harsh parenting across childhood were associated with corticolimbic activation and connectivity during socioemotional processing. Harsh parenting in early childhood (indexed by the intercept term from a linear growth curve model) was associated with less amygdala, but not PFC, reactivity to angry facial expressions. In contrast, change in harsh parenting across childhood (indexed by the slope term) was associated with less PFC, but not amygdala, activation to angry faces. Increases in, but not initial levels of, harsh parenting were also associated with stronger positive amygdala–PFC connectivity during angry face processing.

Perceived threat in youth’s environments can elevate risk for mental health, social, and neurocognitive difficulties throughout the lifespan. However, few studies examine variability in youth’s perceptions of threat across multiple contexts or evaluate outcomes across multiple domains, ultimately limiting our understanding of specific risks associated with perceived threats in different contexts. This study examined associations between perceived threat in youth’s neighborhood, school, and family contexts at ages 9–10 and mental health, social, and neurocognitive outcomes at ages 11–12 within a large US cohort (N = 5525) enrolled in the Adolescent Brain Cognitive DevelopmentSM Study (ABCD Study®). Latent profile analysis revealed four distinct profiles: Low Threat in all contexts, Elevated Family Threat, Elevated Neighborhood Threat, and Elevated Threat in all contexts. Mixed-effect models and post hoc pairwise comparisons showed that youth in Elevated Threat profile had poorer mental health and social outcomes 2 years later. Youth in the Elevated Family Threat profile uniquely showed increased disruptive behavior symptoms, whereas youth in the Elevated Neighborhood Threat profile predominantly displayed increased sleep problems and worse neurocognitive outcomes 2 years later. Together, findings highlight the importance of considering perceptions of threat across multiple contexts to achieve a more nuanced developmental picture.

This study examined how youth aggressive and delinquent externalizing problem behaviors across childhood and adolescence are connected to consequential psychosocial life outcomes in adulthood. Using data from a longitudinal, high-risk sample (N = 1069) that assessed children and their parents regularly from early childhood (ages 3–5) through adulthood, multilevel growth factors of externalizing behaviors were used to predict adult outcomes (age 24–31), providing a sense of how externalizing problems across development were related to these outcomes via maternal, paternal, teacher, and child report. Findings indicated strong support for the lasting connections between youth externalizing problems with later educational attainment and legal difficulties, spanning informants and enduring beyond other meaningful contributors (i.e., child sex, cognitive ability, parental income and education, parental mental health and relationship quality). Some support was also found, although less consistently, linking externalizing problems and later alcohol use as well as romantic relationship quality. Delinquent/rule-breaking behaviors were often stronger predictors of later outcomes than aggressive behaviors. Taken together, these results indicate the importance of the role youth externalizing behaviors have in adult psychosocial functioning one to two decades later.

The aim of this study was to use longitudinal population-based data to examine the associations between childhood sexual abuse (CSA) and risk for adverse outcomes in multiple life domains across adulthood. In 937 individuals followed from birth to age 45y, we assessed associations between CSA (retrospectively reported at age 26y) and the experience of 22 adverse outcomes in seven domains (physical, mental, sexual, interpersonal, economic, antisocial, multi-domain) from young adulthood to midlife (26 to 45y). Analyses controlled for sex, socioeconomic status, prospectively reported child harm and household dysfunction adverse childhood experiences, and adult sexual assault, and considered different definitions of CSA. After adjusting for confounders, CSA survivors were more likely than their peers to experience internalizing, externalizing, and thought disorders, suicide attempts, health risk behaviors, systemic inflammation, poor oral health, sexually transmitted diseases, high-conflict relationships, benefit use, financial difficulties, antisocial behavior, and cumulative problems across multiple domains in adulthood. In sum, CSA was associated with multiple persistent problems across adulthood, even after adjusting for confounding life stressors, and the risk for particular problems incremented with CSA severity. The higher risk for most specific problems was small to moderate, but the cumulative long-term effects across multiple domains reflect considerable individual and societal burden.

This study examined struggles to establish autonomy and relatedness with peers in adolescence and early adulthood as predictors of advanced epigenetic aging assessed at age 30. Participants (N = 154; 67 male and 87 female) were observed repeatedly, along with close friends and romantic partners, from ages 13 through 29. Observed difficulty establishing close friendships characterized by mutual autonomy and relatedness from ages 13 to 18, an interview-assessed attachment state of mind lacking autonomy and valuing of attachment at 24, and self-reported difficulties in social integration across adolescence and adulthood were all linked to greater epigenetic age at 30, after accounting for chronological age, gender, race, and income. Analyses assessing the unique and combined effects of these factors, along with lifetime history of cigarette smoking, indicated that each of these factors, except for adult social integration, contributed uniquely to explaining epigenetic age acceleration. Results are interpreted as evidence that the adolescent preoccupation with peer relationships may be highly functional given the relevance of such relationships to long-term physical outcomes.