Sharon Niv

Heritability and Longitudinal Stability of Impulsivity in Adolescence

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.

Aggression and rule-breaking: Heritability and stability of antisocial behavior problems in childhood and adolescence

PURPOSE This twin study examined the structure of genetic and environmental influences on aggression and rule-breaking in order to examine change and stability across the span of childhood to mid-adolescence. METHODS Behavioral assessments were conducted at two time points: age 9-10 years and 14-15 years. Using behavioral genetics biometric modeling, the longitudinal structure of influences was investigated. RESULTS Aggression and rule-breaking were found to be influenced by a latent common factor of antisocial behavior (ASB) within each wave of data collection. The childhood-age common factor of ASB was influenced by 41% genetics, 40% shared environment and 19% nonshared environment. In adolescence, 41% of influences on the common factor were novel and entirely genetic, while the remainder of influences were stable across time. Additionally, both aggression and rule-breaking within each wave were found to have unique influences not common across subscales or across waves, highlighting specificity of influences on different problem behaviors at both ages. CONCLUSIONS This research sheds light on the commonality of influences on etiology of different forms of antisocial behavior, and suggests future directions for research into intervention for antisocial behavior problems in youth, such as investigation of adolescence-specific environmental influences on the development of antisocial behavior problems.

The Biology of Childhood Crime and Antisocial Behavior

Research into the biological underpinnings of antisocial behavior has not only been increasingly integrated into criminological research, but has also expanded its scope to focus on antisocial behavior that develops during childhood. Many of the biological risk factors that are associated with antisocial behavior during adulthood have also been found to characterize young antisocials. Structural and functional brain imaging studies have implicated several brain regions in the development of antisocial behavior in children, including the amygdala, the ventromedial prefrontal cortex, and the temporal region. Neuropsychological studies indicate that antisocial children display multiple behavioral indices of brain dysfunction, including executive dysfunction and IQ deficits. Psychophysiological studies have revealed that antisocial children are characterized by underarousal and diminished responses to stimuli and stressors. Early health factors, including minor physical anomalies and prenatal nicotine exposure, both independently and in interaction with social risk factors are associated with antisocial behavior in children. Future research should focus on incorporating a life-course criminological perspective into the study of the biology of childhood crime and antisocial behavior. Longitudinal studies that measure both biological and social risk factors over time will be critical to advancing our understanding of the development of antisocial behavior both during childhood and throughout the life-course.

Childhood EEG frontal alpha power as a predictor of adolescent antisocial behavior: a twin heritability study.

High EEG frontal alpha power (FAP) is thought to represent a state of low arousal in the brain, which has been related in past research to antisocial behavior (ASB). We investigated a longitudinal sample of 900 twins in two assessments in late childhood and mid-adolescence to verify whether relationships exist between FAP and both aggressive and nonaggressive ASB. ASB was measured by the Child Behavioral Checklist, and FAP was calculated using connectivity analysis methods that used principal components analysis to derive power of the most dominant frontal activation. Significant positive predictive relationships emerged in males between childhood FAP and adolescent aggressive ASB using multilevel mixed modeling. No concurrent relationships were found. Using bivariate biometric twin modeling analysis, the relationship between childhood FAP and adolescent aggressive ASB in males was found to be entirely due to genetic factors, which were correlated r=0.22.

Genetics of Personality

This article is a revision of the previous edition article by N.L. Pedersen, volume 9, pp. 6116–6118,