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The causal nature of the association between neighborhood deprivation and drug abuse: a prospective national Swedish co-relative control study

Published online by Cambridge University Press:  27 March 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
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, Virginia Commonwealth University, Box 980126, Richmond, VA 23298-0126, USA. (Email: kendler@vcu.edu)

Abstract

Background

Risk for drug abuse (DA) is strongly associated with neighborhood social deprivation (SD). However, the causal nature of this relationship is unclear.

Method

Three Swedish population-based cohorts were followed up over 5 years for incident registration of DA in medical, legal or pharmacy records. In each cohort, we examined the SD–DA association, controlling carefully for individual socio-economic status (SES) with multiple measures, in the entire sample and among pairs of first cousins, paternal and maternal half-siblings, full siblings and monozygotic (MZ) twins discordant for SD exposure. The number of informative relative pairs ranged from 6366 to 166 208.

Results

In all cohorts, SD was prospectively related to risk for incident DA. In relative pairs discordant for SD exposure, the SD–DA association was similar to that seen in the entire population in cousins, half-siblings, full siblings and MZ twins. Eliminating subjects who were residentially unstable or had DA in the first two follow-up years did not alter this pattern. When divided by age, in the youngest groups, the SD–DA association was weaker in siblings than in the entire population.

Conclusions

Across three cohorts, controlling for individual SES and confounding familial factors, SD prospectively predicted risk for incident DA registration. These results support the hypothesis that the SD–DA association is in part causal and unlikely to result entirely from personal attributes, which both increase risk for DA and cause selection into high SD environments. At least part of the SD–DA association arises because exposure to SD causes an increased risk of DA.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2014 

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