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Towards a molecular epidemiology of alcohol dependence: analysing the interplay of genetic and environmental risk factors

P. A. F. MADDEN, PhD., K.K. BUCHOLZ, PhD. and L.J. BIERUT, MD

Missouri Alcoholism Research Center at Washington University, and Departments of Psychiatry, Psychology and Genetics, Washington University School of Medicine, St Louis, Missouri, USA

J.B. WHITFIELD, PhD.

Department of Clinical Biochemistry, Royal Prince Alfred Hospital, Sydney, Australia

S.H. DINWIDDIE, MD

Department of Psychiatry, North Chicago Medical School, Chicago, Illinois, USA

W. S. SLUTSKE, PhD.

Missouri Alcoholism Research Center at the University of Missouri, and Department of Psychology, University of Missouri, Columbia, Missouri, USA

D. B. STATHAM, MA and NICHOLAS G. MARTIN, PhD

Department of Epidemiology and Population Health, Queensland Institute of Medical Research, Brisbane, Australia

Correspondence: Dr Andrew C. Heath, 40 North Kingshighway, Suite I, St Louis, MO 63108, USA. Tel: + 1314 286 2204; fax: + 1314 286 2213; email: andrew{at}matlock.wustl.edu

Declaration of interest This research was supported by grants from the US National Institutes of Health, the US Alcohol Beverage Medical Research Foundation and the Australian National Health and Medical Research Council.

ABSTRACT

Background Progress in identifying genetic factors protective against alcohol dependence (AlcD) requires a paradigm shift in psychiatric epidemiology.

Aims To integrate analysis of research into the genetics of alcoholism.

Method Data from prospective questionnaire and interview surveys of the Australian twin panel, and from a subsample who underwent alcohol challenge, were analysed.

Results In men, effects of alcohol dehydrogenase ADH2^*1/^*2 genotype or high alcohol sensitivity (risk-decreasing), and of history of childhood conduct disorder, or having monozygotic co-twin or twin sister with AlcD (risk-increasing) were significant and comparable in magnitude. Religious affiliation (Anglican versus other) was associated with the ADH2 genotype, but did not explain the associations with AlcD symptoms. No protective effect of the ADH2^*1/^*2 genotype was observed in women.

Conclusions The early onset and strong familial aggregation of AlcD, and opportunity for within-family tests of genetic association to avoid confounding effects, make epidemiological family studies of adolescents and young adults and their families a priority.

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