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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1190.)
© 2003 American Heart Association, Inc.

Special Article

Genes, Environment, and Cardiovascular Disease

Charles F. Sing; Jari H. Stengård; Sharon L.R. Kardia

From the Departments of Human Genetics (C.F.S., J.H.S.) and Epidemiology (S.L.R.K.), University of Michigan, Ann Arbor, and the National Public Health Institute (J.H.S), Helsinki, Finland.

Correspondence to Dr Charles F. Sing, Department of Human Genetics, University of Michigan, 1241 E Catherine St, 5928 Buhl Bldg, Ann Arbor, MI 48109-0618. E-mail csing{at}umich.edu

Abstract

In this essay, we call to attention what every medical researcher knows about the etiology of cardiovascular disease but most deny, or choose to ignore, when designing, carrying out, and reporting genetic studies. Medical research is entering an era of synthesis that will take advantage of the successes of reductionism over the past decade in defining and describing human genome variations. Meaningful insights into the role of such variation requires a biological model of genome-phenotype relationships that incorporates interactions between subsets of possible genetic and environmental agents as causations in particular contexts indexed by time and space. We make recommendations for what needs to be done to cope with these complexities.

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