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Early institutional rearing is associated with increased risk for subsequent peer relationship difficulties, but the underlying mechanisms have not been identified. Friendship characteristics, social behaviors with peers, normed assessments of social problems, and social cue use were assessed in 142 children (mean age = 10.06, SD = 2.02; range 7–13 years), of whom 67 were previously institutionalized (PI), and 75 were raised by their biological families. Anxiety and attention-deficit/hyperactivity disorder (ADHD) symptoms, often elevated among PI children, were examined as potential mediators of PI status and baseline social functioning and longitudinal follow-ups (2 and 4 years later). Twenty-seven percent of PI children fell above the Child Behavior Checklist Social Problems cutoff. An examination of specific social behaviors with peers indicated that PI and comparison children did not differ in empathic concern or peer social approach, though parents were more likely to endorse aggression/overarousal as a reason that PI children might struggle with friendships. Comparison children outperformed PI children in computerized testing of social cue use learning. Finally, across these measures, social difficulties exhibited in the PI group were mediated by ADHD symptoms with predicted social problems assessed 4 years later. These findings show that, when PI children struggle with friendships, mechanisms involving attention and behavior regulation are likely contributors. [ABSTRACT FROM AUTHOR]

Childhood maltreatment robustly predicts adolescent externalizing behaviors (EB; e.g., violence, delinquency, substance use) and may crystalize patterns of EB by influencing sensitivity to the social environment (e.g., parenting, friendships). In a nationally representative sample of 9,421 adolescents, we modeled latent growth curves of EB from age 13 to 32 years. Next, we explored whether maltreated youth differed from nonmaltreated youth in their sensitivity to parental closeness, friendship involvement, and polymorphisms from dopamine genes linked to EB (dopamine receptors D2 and D4, dopamine transporter). Overall, maltreated youth had significantly higher levels of EB across adolescence and adulthood; however, maltreated and nonmaltreated youth showed similar patterns of EB change over time: violent behavior decreased in adolescence before stabilizing in adulthood, whereas nonviolent delinquency and substance use increased in adolescence before decreasing in the transition to adulthood. Maltreatment reduced sensitivity to parental closeness and friendship involvement, although patterns varied based on type of EB outcome. Finally, none of the environmental effects on EB were significantly moderated by the dopamine polygenic risk score after accounting for multiple testing. These findings underline the enduring effects of early maltreatment and implicate that maltreatment may contribute to long-term risk for EB by influencing children's sensitivity to social relationship factors in adolescence. [ABSTRACT FROM AUTHOR]

Although prevailing theories of antisocial behavior (ASB) emphasize distinct developmental trajectories, few studies have explored gene–environment interplay underlying membership in empirically derived trajectories. To improve knowledge about the development of overt (e.g., aggression) and covert (e.g., delinquency) ASB, we tested the association of the 44-base pair promoter polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR), perceived parental support (e.g., closeness and warmth), and their interaction with ASB trajectories derived using latent class growth analysis in 2,558 adolescents followed prospectively into adulthood from the National Longitudinal Study of Adolescent Health. Three distinct trajectories emerged for overt (low desisting, adolescent peak, and late onset) and covert ASB (high stable, low stable, and nonoffending). Controlling for sex, parental support inversely predicted membership in the adolescent-peak overt ASB trajectory (vs. low desisting), but was unrelated to class membership for covert ASB. Furthermore, the 5-HTTLPR genotype significantly moderated the association of parental support on overt ASB trajectory membership. It is interesting that the pattern of Gene × Environment interaction differed by trajectory class: whereas short allele carriers were more sensitive to parental support in predicting the late-onset trajectory, the long/long genotype functioned as a potential “plasticity genotype” for the adolescent-peak trajectory group. We discuss these preliminary findings in the context of the differential susceptibility hypothesis and discuss the need for future studies to integrate gene–environment interplay and prospective longitudinal designs. [ABSTRACT FROM AUTHOR]

Although family support reliably predicts the development of adolescent depression and suicidal behaviors, relatively little is known about the interplay of family support with potential genetic factors. We tested the association of the 44 base pair polymorphism in the serotonin transporter linked promoter region gene (5-HTTLPR), family support (i.e., cohesion, communication, and warmth), and their interaction with self-reported depression symptoms and risk for suicide in 1,030 Caucasian adolescents and young adults from the National Longitudinal Study of Adolescent Health. High-quality family support predicted fewer symptoms of depression and reduced risk for suicidality. There was also a significant interaction between 5-HTTLPR and family support for boys and a marginally significant interaction for girls. Among boys with poor family support, youth with at least one short allele had more symptoms of depression and a higher risk for suicide attempts relative to boys homozygous for the long allele. However, in the presence of high family support, boys with the short allele had the fewest depression symptoms (but not suicide attempts). Results suggest that the short allele may increase reactivity to both negative and positive family influences in the development of depression. We discuss the potential role of interactive exchanges between family support and offspring genotype in the development of adolescent depression and suicidal behaviors. [ABSTRACT FROM PUBLISHER]

Although prevailing theories of antisocial behavior (ASB) emphasize distinct developmental trajectories, few studies have explored gene-environment interplay underlying membership in empirically derived trajectories. To improve knowledge about the development of overt (e.g., aggression) and covert (e.g., delinquency) ASB, we tested the association of the 44-base pair promoter polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR), perceived parental support (e.g., closeness and warmth), and their interaction with ASB trajectories derived using latent class growth analysis in 2,558 adolescents followed prospectively into adulthood from the National Longitudinal Study of Adolescent Health. Three distinct trajectories emerged for overt (low desisting, adolescent peak, and late onset) and covert ASB (high stable, low stable, and nonoffending). Controlling for sex, parental support inversely predicted membership in the adolescent-peak overt ASB trajectory (vs. low desisting), but was unrelated to class membership for covert ASB. Furthermore, the 5-HTTLPR genotype significantly moderated the association of parental support on overt ASB trajectory membership. It is interesting that the pattern of Gene × Environment interaction differed by trajectory class: whereas short allele carriers were more sensitive to parental support in predicting the late-onset trajectory, the long/long genotype functioned as a potential "plasticity genotype" for the adolescent-peak trajectory group. We discuss these preliminary findings in the context of the differential susceptibility hypothesis and discuss the need for future studies to integrate gene-environment interplay and prospective longitudinal designs.