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Genetic and environmental risk factors in males for self-report externalizing traits in mid-adolescence and criminal behavior through young adulthood

Published online by Cambridge University Press:  01 February 2013

K. S. Kendler*
Affiliation:
Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA Department of Human and Molecular Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA
C. J. Patrick
Affiliation:
Department of Psychology, Florida State University, Tallahassee, FL, USA
H. Larsson
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden Karolinska Institute Center for Neurodevelopmental Disorders, Stockholm, Sweden
C. O. Gardner
Affiliation:
Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA
P. Lichtenstein
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden
*
*Address for correspondence: K. S. Kendler, M.D., Virginia Institute for Psychiatric and Behavioral Genetics of VCU, Box 980126, Richmond, VA 23298-0126, USA. (Email: [email protected])

Abstract

Background

Externalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors.

Method

We examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx.

Results

The best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2 = 0.48) and familial–environmental factors (c2 = 0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors.

Conclusions

In adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB. Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2013 

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