Impulsivity is a multifaceted personality construct that plays an important role throughout the lifespan in psychopathological disorders involving self-regulated behaviors. Its genetic and environmental etiology, however, is not clearly understood during the important developmental period of adolescence. This study investigated the relative influence of genes and environment on self-reported impulsive traits in adolescent twins measured on two separate occasions (waves) between the ages of 11 and 16. An adolescent version of the Barratt Impulsiveness Scale (BIS) developed for this study was factored into subscales reflecting inattention, motor impulsivity, and non-planning. Genetic analyses of these BIS subscales showed moderate heritability, ranging from 33–56% at the early wave (age 11–13 years) and 19–44% at the later wave (age 14–16 years). Moreover, genetic influences explained half or more of the variance of a single latent factor common to these subscales within each wave. Genetic effects specific to each subscale also emerged as significant, with the exception of motor impulsivity. Shared twin environment was not significant for either the latent or specific impulsivity factors at either wave. Phenotypic correlations between waves ranged from r = 0.25 to 0.42 for subscales. The stability correlation between the two latent impulsivity factors was r = 0.43, of which 76% was attributable to shared genetic effects, suggesting strong genetic continuity from mid to late adolescence. These results contribute to our understanding of the nature of impulsivity by demonstrating both multidimensionality and genetic specificity to different facets of this complex construct, as well as highlighting the importance of stable genetic influences across adolescence.
Atypical eletrodermal and cardiovascular response patterns in psychopathic individuals are thought to be biological indicators of fearless and disinhibition. This study investigated the relationship between psychopathic traits and these autonomic response patterns using a count-down task in 843 children (aged 9–10 years). Heart rate (HR) and non-specific skin conductance responses (NS-SCRs) were recorded while participants anticipated and reacted to 105 dB signaled or unsignaled white-noise bursts. Using multilevel regression models, both larger HR acceleration and fewer NS-SCR were found to be significantly associated with psychopathic traits during anticipation of signaled white-noise bursts. However, two divergent patterns appeared for HR and SCR: (1) larger HR acceleration was specific to the callousness-disinhibition factor of psychopathic traits while reduced NS-SCR was only associated with the manipulative-deceitfulness factor; (2) the negative association between the manipulative-deceitfulness factor and NS-SCR was only found in boys but not in girls. These findings replicated what has been found in psychopathic adults, suggesting that autonomic deficits present in children at risk may predispose them to later psychopathy. The divergent findings across psychopathic facets and sexes raised the possibility of different etiologies underlying psychopathy, which may in turn suggest multiple treatment strategies for boys and girls.
The Southern California Twin Register at the University of Southern California (USC) was initiated in 1984 and continues to provide an important resource for studies investigating genetic and environmental influences on human behavior. This article provides an update on the current register and its potential for future twin studies using recruitment through school district databases and voter records. An overview is also provided for an ongoing longitudinal twin study investigating the development of externalizing psychopathology from childhood to young adulthood, the USC Study of Risk Factors for Antisocial Behavior. Characteristics of the twins and their families are presented, including recruitment and participation rates, as well as attrition analyses and a summary of key findings to date.
In the present study, we investigated genetic and environmental effects on motor impulsivity from childhood to late adolescence using a longitudinal sample of twins from ages 9 to 18 years. Motor impulsivity was assessed using errors of commission (no-go errors) in a visual go/no-go task at 4 time points: ages 9–10, 11–13, 14–15, and 16–18 years. Significant genetic and nonshared environmental effects on motor impulsivity were found at each of the 4 waves of assessment with genetic factors explaining 22%–41% of the variance within each of the 4 waves. Phenotypically, children’s average performance improved across age (i.e., fewer no-go errors during later assessments). Multivariate biometric analyses revealed that common genetic factors influenced 12%–40% of the variance in motor impulsivity across development, whereas nonshared environmental factors common to all time points contributed to 2%–52% of the variance. Nonshared environmental influences specific to each time point also significantly influenced motor impulsivity. Overall, results demonstrated that although genetic factors were critical to motor impulsivity across development, both common and specific nonshared environmental factors played a strong role in the development of motor impulsivity across age.
Mounting evidence indicates that early-life exposure to particulate air pollutants pose threats to children’s cognitive development, but studies about the neurotoxic effects associated with exposures during adolescence remain unclear. We examined whether exposure to ambient fine particles (PM2.5) at residential locations affects intelligence quotient (IQ) during pre-/early- adolescence (ages 9–11) and emerging adulthood (ages 18–20) in a demographically-diverse population (N = 1,360) residing in Southern California. Increased ambient PM2.5 levels were associated with decreased IQ scores. This association was more evident for Performance IQ (PIQ), but less for Verbal IQ, assessed by the Wechsler Abbreviated Scale of Intelligence. For each inter-quartile (7.73 μg/m3) increase in one-year PM2.5 preceding each assessment, the average PIQ score decreased by 3.08 points (95% confidence interval = [-6.04, -0.12]) accounting for within-family/within-individual correlations, demographic characteristics, family socioeconomic status (SES), parents’ cognitive abilities, neighborhood characteristics, and other spatial confounders. The adverse effect was 150% greater in low SES families and 89% stronger in males, compared to their counterparts. Better understanding of the social disparities and sexual dimorphism in the adverse PM2.5–IQ effects may help elucidate the underlying mechanisms and shed light on prevention strategies.
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