Affiliation:
1. From the Hyperlipidemia and Atherosclerosis Research Group (S.L.-C., A.B., M.X.), Clinical Research Institute of Montreal, Montreal, Quebec, Canada; Département de médecine familiale (M.X.), Faculté de médecine, Université de Sherbrooke and Centre de recherche clinique (M.X., T.N.), Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Québec, Canada; Department of Human Genetics (C.F.S.), University of Michigan, Ann Arbor, Mich.
Abstract
Hyperlipidemia, smoking, and obesity are well-known risk factors for cardiovascular disease. Conversely, moderate alcohol intake is associated with lower atherosclerosis risk. However, the influence of taking alcohol on the interrelationships of these factors in a particular context has not been thoroughly investigated. In this study, we asked whether the association between plasma measures of lipid metabolism and alcohol intake is dependent on context defined by gender, age, body mass index (BMI), smoking, and
apolipoprotein E
(
APOE)
genotype. Data were obtained in a sample of 869 women and 824 men who participated in the Quebec Heart Health Survey. There was no evidence that variation among
APOE
genotypes influenced the association between LDL cholesterol (LDL-C) or HDL cholesterol (HDL)-C and alcohol, after adjustment for age and BMI. Further, the positive (LDL-C and BMI) and the negative (HDL-C and BMI) associations that were observed in men and women with the
ε
3/2
and
ε
3/3
genotypes were not modified by alcohol intake. However, in women with the
ε
4/3
genotype only, we found a significant influence of an alcohol by BMI interaction on the prediction of total cholesterol, LDL-C, HDL-C, apoA-I, and apoB, and this interaction was influenced by the status of smoking. Whereas the influence of an alcohol by BMI interaction on total cholesterol and LDL-C was significant in smokers, its influence on HDL-C was significant only in non-smokers. This study emphasizes the context dependency of the influence of alcohol on lipid metabolism and demonstrates how biological, environmental, and genetic factors interact to determine cardiovascular disease risk.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine
Cited by
45 articles.
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