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Etiological heterogeneity in the development of antisocial behavior: the Virginia Twin Study of Adolescent Behavioral Development and the Young Adult Follow-Up

Published online by Cambridge University Press:  22 March 2007

JUDY L. SILBERG ,
MICHAEL RUTTER ,
KELLY TRACY ,
HERMINE H. MAES  and
LINDON EAVES
JUDY L. SILBERG*
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA
MICHAEL RUTTER
Affiliation:
Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, London, UK
KELLY TRACY
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA
HERMINE H. MAES
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA
LINDON EAVES
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA
*
*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: jsilberg@hsc.vcu.edu)
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Abstract

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.

Type
Original Article
Information
Psychological Medicine , Volume 37 , Issue 8 , August 2007 , pp. 1193 - 1202
Copyright
Copyright © Cambridge University Press 2007

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