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Adolescence is a time of increasing engagement in a variety of problem behaviors, including substance use and delinquency. Genetic risk for problem behavior increases over adolescence, is mediated partially by individual differences in sensation seeking, and is exacerbated by involvement with deviant peers. In this article, we describe how findings from behavioral genetic research on problem behavior intersect with research from developmental neuroscience. In particular, the incentive-processing system, including the ventral striatum, responds increasingly to rewards in adolescence, particularly in peer contexts. This developmental shift may be influenced by hormonal changes at puberty. Individual differences in the structure and function of reward-responsive brain regions may be intermediary phenotypes that mediate adolescents' genetic risk for problem behavior. The study of problem behavior can be enriched by interdisciplinary research that integrates measures of brain structure and function into genetically informed studies. [ABSTRACT FROM AUTHOR]

Background: Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. Method: Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (≤12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. Results: Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. Conclusions: Future research should discriminate between alternative possible mechanisms underlying gene 9 puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression. [ABSTRACT FROM AUTHOR]

Callous-unemotional (CU) traits, such as lacking empathy and emotional insensitivity, predict the onset, severity, and persistence of antisocial behavior. CU traits are heritable, and genetic influences on CU traits contribute to antisocial behavior. This study examines genetic overlap between CU traits and general domains of personality. We measured CU traits using the Inventory of Callous-Unemotional Traits (ICU) and Big Five personality using the Big Five Inventory in a sample of adolescent twins from the Texas Twin Project. Genetic influences on the Big Five personality dimensions could account for the entirety of genetic influences on CU traits. Item Response Theory results indicate that the Inventory of Callous and Unemotional Traits is better at detecting clinically relevant personality variation at lower extremes of personality trait continua, particularly low agreeableness and low conscientiousness. The proximate biological mechanisms that mediate genetic liabilities for CU traits remain an open question. The results of the current study suggest that understanding the development of normal personality may inform understanding of the genetic underpinnings of callous and unemotional behavior. [ABSTRACT FROM AUTHOR]

Adolescents whose parents are affectionate, maintain consistent rules, and are knowledgeable about their whereabouts tend to exhibit more adaptive levels of psychological functioning across multiple domains. Behavioral genetic research has documented the sensitivity of parenting to genetically influenced child characteristics and behaviors. Yet, the question of whether the correlations between parenting behaviors are driven by overlapping parent effects, overlapping child effects, or some combination of the two remains open. In a sample of N = 542 twins, ages 13.6 to 20.1 years, from the Texas Twin Project, we evaluated the extent to which adolescents' genetically influenced traits broadly affect multiple dimensions of parenting (maternal and paternal warmth and control, and parental monitoring). We found that shared environmental factors primarily accounted for the covariation among parental warmth, control, and monitoring. Child-driven genetic effects were primarily detected in parenting variance unique to fathers. These results indicate that adolescents' family-wide environmental contexts are general across multiple domains of parenting, whereas genetically influenced adolescent-driven effects are specific to particular aspects of parenting and to particular relationships. (PsycINFO Database Record [ABSTRACT FROM AUTHOR]

Individual differences in children’s executive functions (EFs) are relevant for a wide range of normal and atypical psychological outcomes across the life span, but the origins of variation in children’s EFs are not well understood. We used data from a racially and socioeconomically diverse sample of 505 third- through eighth-grade twins and triplets from the Texas Twin Project to estimate genetic and environmental influences on a Common EF factor and on variance unique to four core EF domains: inhibition, switching, working memory, and updating. As has been previously demonstrated in young adults, the Common EF factor was 100% heritable, which indicates that correlations among the four EF domains are entirely attributable to shared genetic etiology. Nonshared environmental influences were evident for variance unique to individual domains. General EF may thus serve as an early life marker of genetic propensity for a range of functions and pathologies later in life. [ABSTRACT FROM AUTHOR]