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Sex differences and developmental stability in genetic and environmental influences on psychoactive substance consumption from early adolescence to young adulthood

Published online by Cambridge University Press:  20 January 2011

J. H. Baker
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA, USA Department of Psychology, Virginia Commonwealth University, Richmond, VA, USA
H. H. Maes
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA, USA Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA
H. Larsson
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
P. Lichtenstein
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
K. S. Kendler*
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA, USA Department of Human Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Virginia Commonwealth University, Richmond, VAUSA
*
*Address for correspondence: K. S. Kendler, M.D., Virginia Commonwealth University, Department of Psychiatry, Box 980126, Richmond, VA 23298, USA. (Email: kendler@vcu.edu)

Abstract

Background

Genetic and environmental factors are important in the etiology of substance use. However, little is known about the stability of these factors across development. We aimed to answer three crucial questions about this etiology that have never been addressed in a single study: (1) Is there a general vulnerability to substance consumption from early adolescence to young adulthood? (2) If so, do the genetic and environmental influences on this vulnerability change across development? (3) Do these developmental processes differ in males and females?

Method

Subjects included 1480 twin pairs from the Swedish Twin Study of Child and Adolescent Development who have been followed since 1994. Prospective, self-reported regular smoking, alcohol intoxication and illicit drug use were assessed at ages 13–14, 16–17 and 19–20 years. Structural modeling was performed with the program Mx.

Results

An underlying common factor accounted for the association between smoking, alcohol and illicit drug consumption for the three age groups. Common genetic and shared environmental effects showed substantial continuity. In general, as participants aged, the influence of the shared environment decreased, and genetic effects became more substance specific in their effect.

Conclusions

The current report answers three important questions in the etiology of substance use. The genetic and environmental risk for substance consumption is partly mediated through a common factor and is partly substance specific. Developmentally, evidence was strongest for stability of common genetic effects, with less evidence for genetic innovation. These processes seem to be the same in males and females.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2011

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