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A Swedish national adoption study of criminality

Published online by Cambridge University Press:  04 November 2013

K. S. Kendler*
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA, USA
S. Larsson Lönn
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden
N. A. Morris
Affiliation:
Department of Criminal Justice, Virginia Commonwealth University, Richmond, VA, USA
J. Sundquist
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, CA, USA
N. Långström
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden
K. Sundquist
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, CA, USA
*
*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: kendler@vcu.edu)

Abstract

Background

To clarify the role of genetic and environmental factors in criminal behavior (CB), we examined all CB and violent and non-violent subtypes (VCB and NVCB, respectively) in a Swedish national sample of adoptees and their relatives.

Method

CB was defined by a conviction in the Swedish Crime Register with standard definitions for VCB and NVCB subtypes. We examined adoptees born 1950–1991 (n = 18 070) and their biological (n = 79 206) and adoptive (n = 47 311) relatives.

Results

The risk for all CB was significantly elevated in the adopted-away offspring of biological parents of which at least one had CB [odds ratio (OR) 1.5, 95% confidence interval (CI) 1.4–1.6] and in the biological full and half-siblings of CB adoptees (OR 1.4, 95% CI 1.2–1.6 and OR 1.3, 95% CI 1.2–1.3, respectively). A genetic risk index (including biological parental/sibling history of CB and alcohol abuse) and an environmental risk index (including adoptive parental and sibling CB and a history of adoptive parental divorce, death, and medical illness) both strongly predicted probability of CB. These genetic and environmental risk indices acted additively on adoptee risk for CB. Moderate specificity was seen in the transmission of genetic risk for VCB and NVCB between biological parents and siblings and adoptees.

Conclusions

CB is etiologically complex and influenced by a range of genetic risk factors including a specific liability to CB and a vulnerability to broader externalizing behaviors, and by features of the adoptive environment including parental CB, divorce and death. Genetic risk factors for VCB and NVCB may be at least partially distinct.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2013 

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