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Examination of the Causes of Covariation Between Conduct Disorder Symptoms and Vulnerability to Drug Dependence

Published online by Cambridge University Press:  21 February 2012

Tanya M. M. Button*
Affiliation:
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, United States of America. tanya.button@colorado.edu
John K. Hewitt
Affiliation:
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, United States of America; Department of Psychology, University of Colorado, Boulder, Colorado, United States of America.
Soo Hyun Rhee
Affiliation:
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, United States of America; Department of Psychology, University of Colorado, Boulder, Colorado, United States of America.
Susan E. Young
Affiliation:
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, United States of America.
Robin P. Corley
Affiliation:
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, United States of America.
Michael C. Stallings
Affiliation:
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado, United States of America; Department of Psychology, University of Colorado, Boulder, Colorado, United States of America.
*
*Address for correspondence: Tanya Button, Institute for Behavioral Genetics, 447 University of Colorado, Boulder, CO 80309-0447, USA.

Abstract

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Conduct disorder (CD) symptoms and substance dependence commonly co-occur. Both phenotypes are highly heritable and a common genetic influence on the covariation has been suggested. The aim of this study was to determine the extent to which genes and environment contribute to the covariance between CD and drug dependence using twins from the Colorado Longitudinal Twin Sample and the Colorado Twin Registry. A total of 880 twin pairs (237 monozygotic [MZ] female, 195 MZ male, 116 dizygotic [DZ] female, 118 DZ male and 214 DZ opposite-sex) aged 13 to 18 (mean = 15.65) were included in the analysis. CD was assessed by lifetime Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) symptom count and a polysubstance dependence vulnerability index was developed from responses to the Composite International Diagnostic Interview — Substance Abuse Module. A bivariate Cholesky Decomposition model was used to partition the cause of variation and covariation of the two phenotypes. No sex-limitation was observed in our data, and male and female parameter estimates were constrained to be equal. Both CD symptoms and dependence vulnerability were significantly heritable, and genes, shared environment and nonshared environment all contributed to the covariation between them. Genes contributed 35% of the phenotypic covariance, shared environment contributed 46%, and nonshared environmental influences contributed the remaining 19% to the phenotypic covariance. Therefore, there appears to be pleiotropic genetic influence on CD symptoms and dependence vulnerability.

Type
Articles
Copyright
Copyright © Cambridge University Press 2006