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Exposure to peer deviance during childhood and risk for drug abuse: a Swedish national co-relative control study

Published online by Cambridge University Press:  17 September 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
H. Ohlsson
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden
B. Mezuk
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Family Medicine and Population Health, Division of Epidemiology, Virginia Commonwealth University, Richmond, VA, 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
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
*
*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.

Peer deviance (PD) is associated with risk for drug abuse (DA). Is this association causal?

Method.

DA was recorded in official records. PD was defined as the percentage of peers residing in small communities with future DA registrations. We examined offspring in families whose community PD changed when the offspring was 0–15 years of age and then examined families where cousins or siblings differed in their years of exposure to low or high PD communities.

Results.

The duration of exposure to PD was strongly associated with future DA. Co-relative analyses for families whose exposure to PD declined suggested that the PD–DA association was largely non-causal. Within full-sibling pairs in such families, the length of exposure to low PD environments was unrelated to risk for DA. By contrast, co-relative analyses in families where exposure to PD increased over time indicated that the PD–DA association was largely causal. In such families, siblings who differed in the duration of their exposure to high PD differed in their risk for subsequent DA. These results were replicated in families whose PD changed because they moved or because of changes in the community in which they resided.

Conclusions.

Within families whose social environment is improving over time, the association between PD exposure and offspring DA outcomes is not causal but is due to familial confounding. Within families whose social environment is deteriorating, the PD–DA association seems to be largely causal. Our measure of PD may also reflect broader aspects of the community environment beyond peers.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2014 

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