Genes, environment, and cardiovascular disease.
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.
Sing
Charles F
CF
Department of Human Genetics, University of Michigan, 1241 E Catherine St, 5928 Buhl Bldg, Ann Arbor, MI 48109-0618, USA. csing@umich.edu
Stengård
Jari H
JH
Kardia
Sharon L R
SL
D002318:Cardiovascular Diseases / Q000209:etiology* / Q000235:genetics; D015984:Causality; D004777:Environment; D020022:Genetic Predisposition to Disease; D005828:Genetics, Population; D015894:Genome, Human; D005838:Genotype; D006801:Humans; D008957:Models, Genetic