a1 Virginia Institute for Psychiatric and Behavioral Genetics, Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA
a2 Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, London, UK
a3 Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA
Background Longitudinal, genetically informed, prospective data collected on a large population of male twins (n=1037) were used to examine developmental differences in the etiology of antisocial behavior.
Method Analyses were carried out on both mother- and child-reported symptoms of conduct disorder (CD) in 10- to 17-year-old twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) and self-reported antisocial behavior by the twins as young adults from the Young Adult Follow-Up (YAFU) study.
Results The following trends were identified: (1) a single genetic factor influencing antisocial behavior beginning at age 10 through young adulthood (‘life-course persistent’); (2) a shared-environmental effect beginning in adolescence (‘adolescent-onset’); (3) a transient genetic effect at puberty; and (4) a genetic influence specific to adult antisocial behavior.
Conclusions Overall, these etiological findings are consistent with predictions from Moffitt's developmental theory of antisocial behavior. The genetic effect at puberty at ages 12–15 is also consistent with a genetically mediated influence on the timing of puberty affecting the expression of genetic differences in antisocial outcomes.
(Online publication March 22 2007)
c1 *Address for correspondence: Judy L. Silberg, Virginia Institute for Psychiatric and Behavioral Genetics, Department of Human Genetics, Virginia Commonwealth University, P.O. Box 980003, Richmond, VA 23298-0003, USA. (Email: firstname.lastname@example.org)