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Researchers have identified genetic and neural risk factors for externalizing behaviors. However, it has not yet been determined if genetic liability is conferred in part through associations with more proximal neurophysiological risk markers.
Participants from the Collaborative Study on the Genetics of Alcoholism, a large, family-based study of alcohol use disorders were genotyped and polygenic scores for externalizing (EXT PGS) were calculated. Associations with target P3 amplitude from a visual oddball task (P3) and broad endorsement of externalizing behaviors (indexed via self-report of alcohol and cannabis use, and antisocial behavior) were assessed in participants of European (EA; N = 2851) and African ancestry (AA; N = 1402). Analyses were also stratified by age (adolescents, age 12–17 and young adults, age 18–32).
The EXT PGS was significantly associated with higher levels of externalizing behaviors among EA adolescents and young adults as well as AA young adults. P3 was inversely associated with externalizing behaviors among EA young adults. EXT PGS was not significantly associated with P3 amplitude and therefore, there was no evidence that P3 amplitude indirectly accounted for the association between EXT PGS and externalizing behaviors.
Both the EXT PGS and P3 amplitude were significantly associated with externalizing behaviors among EA young adults. However, these associations with externalizing behaviors appear to be independent of each other, suggesting that they may index different facets of externalizing.
We studied the pattern of personality development in a longitudinal population-based sample of 752 American adolescents. Personality was assessed reliably with the Junior Temperament and Character Inventory at 12, 14, and 16 years of age. The rank-order stability of Junior Temperament and Character Inventory traits from age 12 to 16 was moderate (r = .35). Hierarchical linear modeling of between-group variance due to gender and within-group variance due to age indicated that harm avoidance and persistence decreased whereas self-directedness and cooperativeness increased from age 12 to 16. Novelty seeking, reward dependence, and self-transcendence increased from age 12 to 14 and then decreased. This biphasic pattern suggests that prior to age 14 teens became more emancipated from adult authorities while identifying more with the emergent norms of their peers, and after age 14 their created identity was internalized. Girls were more self-directed and cooperative than boys and maintained this advantage from age 12 to 16. Dependability of temperament at age 16 was mainly predicted by the same traits at earlier ages. In contrast, maturity of character at age 16 was predicted by both temperament and character at earlier ages. We conclude that character develops rapidly in adolescence to self-regulate temperament in accord with personally valued goals shaped by peers.
To investigate familial influences on the full range of variability in attention and activity across adolescence, we collected maternal ratings of 339 twin pairs at ages 12, 14, and 16, and estimated the transmitted and new familial influences on attention and activity as measured by the Strengths and Weaknesses of Attention-Deficit/Hyperactivity Disorder Symptoms and Normal Behavior Scale. Familial influences were substantial for both traits across adolescence: genetic influences accounted for 54%–73% (attention) and 31%–73% (activity) of the total variance, and shared environmental influences accounted for 0%–22% of the attention variance and 13%–57% of the activity variance. The longitudinal stability of individual differences in attention and activity was largely accounted for by familial influences transmitted from previous ages. Innovations over adolescence were also partially attributable to familial influences. Studying the full range of variability in attention and activity may facilitate our understanding of attention-deficit/hyperactivity disorder's etiology and intervention.
Adolescents are prone to risk-taking behaviors leading to adverse consequences such as substance abuse, accidents, violence, and victimization. However, little is known about the contribution of genetic and environmental factors to individual differences in the propensity for risk-taking. This study investigated developmental changes, longitudinal stability, and heritability of risk-taking using data from 752 adolescent twins including 169 MZ and 203 DZ pairs. The Balloon Analogue Risk Task (BART), an experimental behavioral measure of risk taking, was administered to the twins at age 12 and then re-administered to a part of this sample at age 14. Risk-taking increased with age, but individual differences showed a significant longitudinal stability. Genetic model fitting showed that at age 12, heritability of risk-taking was modest but significant in both sexes, whereas at age 14, heritability increased to 55% in males and became nonsignificant in females. The findings suggest that propensity for risk-taking as measured by BART can be a useful endophenotype for genetic studies of adolescent externalizing psychopathology, however, the utility of this measure may be limited by sex differences in heritability.
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