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Social skills are traditionally viewed as acquired through social environments including parenting. However, biopsychosocial models highlight the importance of genetic influences and gene-environment interactions (G×Es) in child development. Extant G×E investigations often fail to account for developmental changes in the phenotype or rigorously assess the social environment using observational measures. The present study prospectively assessed 110 children (44.5% female) and their parents to explore biologically plausible independent and interactive associations of the serotonin transporter-linked polymorphic region (5-HTTLPR) and observed positive and negative parenting in prediction of (a) initial levels of social skills at school entry (age 6 years) and (b) developmental changes in social skills across the early school years (ages 6-9 years). Overall, the SS (vs. SL/LL) 5-HTTLPR genotype inversely predicted social skills across all domains, although parenting behavior moderated these associations wherein putative G×E effects differed by developmental timing and social skills domain. Positive parenting positively predicted concurrent (age 6) overall social skills for children with SL/LL genotypes, but not the SS genotype. However, for the SS group only, age 6 positive parenting positively predicted prospective growth in social responsibility, although negative parenting positively predicted growth in social cooperation. Findings suggest that 5-HTTLPR may signal differential sensitivities to parenting styles and patterns of social development, which may help to inform targeted intervention approaches to enhance person-environment fit. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Although parenting behavior and friendship quality predict adolescent externalizing behaviors (EBs), individual differences in temperament may differentially affect susceptibility to these factors over time. In a multi-method and multi-informant study of 141 children followed prospectively from toddlerhood to adolescence, we tested the independent and interactive associations of age 3 reactive temperament (e.g., negative emotionality) and age 13 observed parenting (i.e., positive and negative behavior) and friendship (i.e., conflict and warmth), with multi-informant ratings of age 15 aggression and rule-breaking behavior. Negative parenting predicted growth in parent-rated EB, but only for adolescents with early reactive temperament. Temperament did not affect sensitivity to positive parenting or friendship. Results are discussed in the context of differential susceptibility theory and intervention implications for adolescents.

Individual differences in emotion regulation are central to social, academic, occupational, and psychological development, and emotion dysregulation (ED) in childhood is a risk factor for numerous developmental outcomes. The present study aimed to (a) describe the developmental trajectory of ED across early childhood (3-6 years) and (b) examine its sensitivity to youth serotonin transporter genotype, positive and negative parenting behaviors, and their interaction. Participants were 99 families in the Collaborative Family Study, a longitudinal study of children with or without developmental delays. Child ED and early parenting were coded from parent-child interactions. To examine serotonin transporter genotype as a moderator between parenting and child emotion dysregulation (ED), children with the homozygous short (SS) genotype were compared to children with the homozygous long (LL) or heterozygous (SL) genotype. We used latent growth curve modeling (LGCM) to model yearly change in ED from child age 3 to 6 years. LGCM revealed that ED decreased overall across early childhood. In addition, we observed separate Genotype × Positive and Genotype × Negative parenting behavior interactions in predictions of ED growth curves. Children with the SL/LL genotype had ED trajectories that were minimally related to positive and negative parenting behavior, whereas ED decreased more precipitously among children with the SS genotype when exposed to low negative parenting or high positive parenting. These findings provide evidence for Gene × Environment interactions (G×Es) in the development of ED in a manner that is conceptually consistent with vantage sensitivity, and they improve inferences afforded by prospective designs.

Although gene × environment interactions contribute to youth attention-deficit/hyperactivity disorder (ADHD) symptoms, the pathways mediating these influences are unknown. We tested genetic moderation of indirect effects from parenting behavior to youth ADHD symptoms through multiple neurocognitive factors. Two hundred and twenty-nine youth with and without ADHD were assessed at baseline (Wave 1; ages 5-10) and at a 2-year follow-up (Wave 2; ages 7-13). At Wave 1, youth completed a neurocognitive battery including measures of response inhibition, visuospatial working memory, and fluid reasoning, and a standardized parent-child interaction task yielding observational measures of positive and negative parenting. At Wave 2, youth psychopathology was rated by parents and teachers using multiple methods (i.e., structured interview, rating scale). We employed moderated multiple mediation and compared conditional indirect effects across youth genotypes at two biologically plausible genetic loci. Controlling for parent ADHD symptoms as well as youth demographic factors and co-occurring externalizing symptoms, these genetic factors moderated the indirect effect from Wave 1 parenting to multi-method/informant Wave 2 ADHD symptoms through Wave 1 neurocognitive functioning. This preliminary study is the first to identify genetic moderation of mediated effects underlying ADHD symptoms and suggests that specific gene × parenting interactions may underlie neurocognitive functioning deficits and subsequent ADHD.

Cumulative risk research has increased understanding of how multiple risk factors impact various socioemotional and interpersonal outcomes across the life span. However, little is known about risk factors for parent-child conflict early in development, where identifying predictors of change could be highly salient for intervention. Given their established association with parent-child conflict, child developmental delay (DD) and emotion dysregulation were examined as predictors of change in conflict across early to middle childhood (ages 3 to 7 years). Participants (n = 211) were part of a longitudinal study examining the development of psychopathology in children with or without DD. Level of parent-child conflict was derived from naturalistic home observations, whereas child dysregulation was measured using an adapted CBCL-Emotion Dysregulation Index. PROCESS was used to examine the conditional interactive effects of delay status (typically developing, DD) and dysregulation on change in conflict from child ages 3 to 5 and 5 to 7 years. Across both of these timeframes, parent-child conflict increased only for families of children with both DD and high dysregulation, providing support for an interactive risk model of parent-child conflict. Findings are considered in the context of developmental transitions, and implications for intervention are discussed. (PsycINFO Database Record

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]