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Published Online: 1 February 2014

Genetic and Family and Community Environmental Effects on Drug Abuse in Adolescence: A Swedish National Twin and Sibling Study

Abstract

Objective

Using Swedish nationwide registry data, the authors investigated genetic and environmental risk factors in the etiology of drug abuse by twin sibling modeling. The authors followed up with epidemiological analyses to identify shared environmental influences on drug abuse.

Method

Drug abuse was defined using public medical, legal, or pharmacy records. Twin and sibling pairs were obtained from the national twin and genealogical registers. Information about sibling pair residence within the same household, small residential area, or municipality was obtained from Statistics Sweden. The authors predicted concordance for drug abuse by years of co-residence until the older sibling turned 21 and risk for future drug abuse in adolescents living with parental figures as a function of family-level socioeconomic status and neighborhood social deprivation.

Results

The best twin sibling fit model predicted substantial heritability for drug abuse in males (55%) and females (73%), with environmental factors shared by siblings operating only in males and accounting for 23% of the variance in liability. For each year of living in the same household, the probability of sibling concordance for drug abuse increased 2%−5%. When not residing in the same household, concordance was predicted from residence in the same small residential area or municipality. Risk for drug abuse was predicted both by family socioeconomic status and neighborhood social deprivation. Controlling for family socioeconomic status, each year of living in a high social deprivation neighborhood increased the risk for drug abuse by 2%.

Conclusions

Using objective registry data, the authors found that drug abuse is highly heritable. A substantial proportion of the shared environmental effect on drug abuse comes from community-wide rather than household-level influences. Genetic effects demonstrated in twin studies have led to molecular analyses to elucidate biological pathways. In a parallel manner, environmental effects can be followed up by epidemiological studies to clarify social mechanisms.

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Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 209 - 217
PubMed: 24077613

History

Received: 11 October 2012
Revision received: 12 March 2013
Revision received: 13 June 2013
Accepted: 17 June 2013
Published online: 1 February 2014
Published in print: February 2014

Authors

Details

Kenneth S. Kendler, M.D.
From the Departments of Psychiatry and Human and Molecular Genetics, the Virginia Institute for Psychiatric and Behavioral Genetics, and the Massey Cancer Center, Virginia Commonwealth University, Richmond, Va.; the Center for Primary Health Care Research, Lund University, Malmö, Sweden; and Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, Calif.
Hermine H. Maes, Ph.D.
From the Departments of Psychiatry and Human and Molecular Genetics, the Virginia Institute for Psychiatric and Behavioral Genetics, and the Massey Cancer Center, Virginia Commonwealth University, Richmond, Va.; the Center for Primary Health Care Research, Lund University, Malmö, Sweden; and Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, Calif.
Kristina Sundquist, M.D., Ph.D.
From the Departments of Psychiatry and Human and Molecular Genetics, the Virginia Institute for Psychiatric and Behavioral Genetics, and the Massey Cancer Center, Virginia Commonwealth University, Richmond, Va.; the Center for Primary Health Care Research, Lund University, Malmö, Sweden; and Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, Calif.
Henrik Ohlsson, Ph.D.
From the Departments of Psychiatry and Human and Molecular Genetics, the Virginia Institute for Psychiatric and Behavioral Genetics, and the Massey Cancer Center, Virginia Commonwealth University, Richmond, Va.; the Center for Primary Health Care Research, Lund University, Malmö, Sweden; and Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, Calif.
Jan Sundquist, M.D., Ph.D.
From the Departments of Psychiatry and Human and Molecular Genetics, the Virginia Institute for Psychiatric and Behavioral Genetics, and the Massey Cancer Center, Virginia Commonwealth University, Richmond, Va.; the Center for Primary Health Care Research, Lund University, Malmö, Sweden; and Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, Calif.

Notes

Address correspondence to Dr. Kendler ([email protected]).

Funding Information

The authors report no financial relationships with commercial interests.
Supplementary Material
Supported by the National Institute of Drug Abuse (grant RO1 DA030005); the Swedish Research Council (2011-3340 and 2012-2378); the ALF project grant, Lund, Sweden; the Swedish Council for Information on Alcohol and Other Drugs; and the Swedish Council for Working Life and Social Research (2007-1754).

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