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Environmental transmission of violent criminal behavior in siblings: a Swedish national study

Published online by Cambridge University Press:  28 April 2014

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
N. A. Morris
Affiliation:
Department of Criminal Justice, Virginia Commonwealth University, Richmond VA USA
S. L. Lönn
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden
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
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, Virginia Commonwealth University, Box 980126, Richmond, VA 23298-0126, USA. (Email: kendler@vcu.edu)

Abstract

Background.

Violent criminal behaviour (VCB) runs strongly in families partly because of shared environmental factors. Can we clarify the environmental processes that contribute to similarity of risk for VCB in siblings?

Method.

We assessed VCB from the Swedish National Crime Register for the years 1973–2011 in siblings born 1950–1991. We examined by conditional logistic and Cox proportional hazard regression, respectively, whether resemblance for VCB in sibling pairs was influenced by their age difference and whether VCB was more strongly ‘transmitted’ from older→younger versus younger→older siblings.

Results.

In our best-fit logistic model, for each year of age difference in full sibling pairs, the risk for VCB in the sibling of a case versus control proband declined by 2.6% [95% confidence interval (CI) 2.2–3.0]. In our best-fit Cox model, the hazard rate for VCB in a sibling when the affected proband was older versus younger was 1.4, 2.1 and 2.9 respectively for a 1-, 5- and 10-year difference in siblings.

Conclusions.

Controlling for genetic effects by examining only full siblings, sibling resemblance for risk for VCB was significantly greater in pairs closer versus more distant in age. Older siblings more strongly transmitted risk for VCB to their younger siblings than vice versa. These results strongly support the importance of familial–environmental influences on VCB and provide some insight into the possible mechanisms at work.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2014 

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