ABSTRACT
BACKGROUND: To investigate the extent to which three putative 'environmental' risk factors, maternal punitive discipline (MPD), paternal punitive discipline (PPD) and negative life events (NLEs), share genetic influences with, and moderate the heritability of, externalizing behavior. METHOD: The sample consisted of 2647 participants, aged 12-19 years, from the G1219 and G1219Twins longitudinal studies. Externalizing behavior was measured using the Youth Self-Report, MPD, PPD and exposure to NLEs were assessed using the Negative Sanctions Scale and the Life Event Scale for Adolescents respectively. RESULT: Genetic influences overlapped for externalizing behavior and each 'environmental' risk, indicating gene-environment correlation. When controlling for the gene-environment correlation, genetic variance decreased, and both shared and non-shared environmental influences increased, as a function of MPD. Genetic variance increased as a function of PPD, and for NLEs the only interaction effect was on the level of non-shared environment influence unique to externalizing behavior. CONCLUSION: The magnitude of the influence of genetic risk on externalizing behavior is contextually dependent, even after controlling for gene-environment correlation.
Subject(s)
Child Behavior Disorders/genetics , Child Behavior Disorders/psychology , Life Change Events , Parent-Child Relations , Punishment/psychology , Social Environment , Adolescent , Adult , Child , Child Behavior Disorders/diagnosis , Diseases in Twins/genetics , Female , Genetic Predisposition to Disease/genetics , Genetics, Behavioral , Humans , Longitudinal Studies , Male , Models, Genetic , Models, Psychological , Psychiatric Status Rating Scales , Risk FactorsABSTRACT
BACKGROUND: There is substantial evidence that maternal smoking during pregnancy is associated with both antisocial behaviour and symptoms of attention-deficit hyperactivity disorder (ADHD) in offspring. However, it is not clear whether maternal smoking during pregnancy is independently associated with antisocial behaviour or whether the association arises because antisocial behaviour and ADHD covary. AIMS: To examine the relationship between maternal smoking during pregnancy, antisocial behaviour and ADHD in offspring. METHOD: Questionnaires concerning behaviour and environmental factors were sent to twins from the CaStANET study and data analysed using a number of bivariate structural equation models. RESULTS: Maternal prenatal smoking contributed small but significant amounts to the variance of ADHD and of antisocial behaviour. The best fitting bivariate model was one in which maternal prenatal smoking had a specific influence on each phenotype, independent of the effect on the other phenotype. CONCLUSIONS: Both antisocial behaviour and ADHD symptoms in offspring are independently influenced by maternal prenatal smoking during pregnancy.
