Behavioural performance in the Go/NoGo task was compared with caregiver and teacher reports of inattention and hyperactivity–impulsivity in 1,151 children (N = 557 boys; N = 594 girls) age 9–10 years old. Errors of commission (NoGo errors) were significantly correlated with symptom counts of hyperactivity–impulsivity, while errors of omission (Go errors) were significantly correlated with symptom counts for inattention in both caregiver and teacher reports. Cross-correlations were also evident, however, such that errors of commission were related to inattention symptoms, and errors of omission were related to hyperactivity–impulsivity. Moreover, hyperactivity–impulsivity and inattention symptoms were highly intercorrelated in both caregiver (r = .52) and teacher reports (r = .70), while errors of commission and omission were virtually uncorrelated in the Go/NoGo task (r = .06). The results highlight the difficulty in disentangling hyperactivity–impulsivity and inattention in questionnaires, and suggest that these constructs may be more clearly distinguished in laboratory measures such as the Go/NoGo task.

A meta-analysis of twin, family and adoption studies was conducted to estimate the magnitude of genetic and environmental influences on impulsivity. The best fitting model for 41 key studies (58 independent samples from 14 month old infants to adults; N = 27,147) included equal proportions of variance due to genetic (0.50) and non-shared environmental (0.50) influences, with genetic effects being both additive (0.38) and non-additive (0.12). Shared environmental effects were unimportant in explaining individual differences in impulsivity. Age, sex, and study design (twin vs. adoption) were all significant moderators of the magnitude of genetic and environmental influences on impulsivity. The relative contribution of genetic effects (broad sense heritability) and unique environmental effects were also found to be important throughout development from childhood to adulthood. Total genetic effects were found to be important for all ages, but appeared to be strongest in children. Analyses also demonstrated that genetic effects appeared to be stronger in males than in females. Method of assessment (laboratory tasks vs. questionnaires), however, was not a significant moderator of the genetic and environmental influences on impulsivity. These results provide a structured synthesis of existing behavior genetic studies on impulsivity by providing a clearer understanding of the relative genetic and environmental contributions in impulsive traits through various stages of development.

Genetic and environmental influences on childhood antisocial and aggressive behavior (ASB) during childhood were examined in 9-to 10-year-old twins, using a multi-informant approach. The sample (605 families of twins or triplets) was socioeconomically and ethnically diverse, representative of the culturally diverse urban population in Southern California. Measures of ASB included symptom counts for conduct disorder, ratings of aggression, delinquency, and psychopathic traits obtained through child self-reports, teacher, and caregiver ratings. Multivariate analysis revealed a common ASB factor across informants that was strongly heritable (heritability was .96), highlighting the importance of a broad, general measure obtained from multiple sources as a plausible construct for future investigations of specific genetic mechanisms in ASB. The best fitting multivariate model required informant-specific genetic, environmental, and rater effects for variation in observed ASB measures. The results suggest that parent, children, and teachers have only a partly "shared view" and that the additional factors that influence the "rater-specific" view of the child's antisocial behavior vary for different informants. This is the first study to demonstrate strong heritable effects on ASB in ethnically and economically diverse samples. Keywords antisocial behavior; aggression; genes; environment Why do some children grow up to be prosocial, law-abiding individuals, whereas others engage in patterns of disruptive, defiant, and delinquent behavior, even falling into the criminal justice system well before reaching adulthood? A plethora of studies have investigated the etiology of such individual differences, with abundant evidence demonstrating the importance of both social circumstances and biological risk factors in antisocial behavior across the life span (Baker, 1999;Raine, 1993Raine, ,2002Raine, Brennan, Farrington, & Mednick, 1997;Stoff, Breiling, & Maser, 1997). Among these risk factors, genetic and environmental influences have been of considerable interest and are likely to play a key role in our understanding of aggression and other antisocial behaviors and, thus, our ability to avert them.

Background The current study investigates whether the underlying factor structure of psychopathic personality traits found in adults is similar to that in children and what the extent of the genetic and environmental influences are on these psychopathic traits. Method Psychopathic personality traits were assessed in a community sample of 1219 twins and triplets (age 9–10 years) through caregiver reports of each child’s behavior using the Child Psychopathy Scale (CPS). Results Confirmatory factor analyses revealed an optimal two-factor solution (callous/disinhibited and manipulative/deceitful) to the CPS subscales. Bivariate genetic modeling of the two computed factor scores revealed significant genetic as well as unique environmental influences on psychopathic personality traits in both boys and girls, with heritability estimates of 0.64 and 0.46, respectively, in boys and 0.49 and 0.58, respectively, in girls. No shared environmental influences on psychopathic personality traits were found. Conclusions The relationship between the two factors was mediated by both genetic and unique environmental factors common to both traits.

The current versions of the DSM (DSM-IV-TR) and ICD