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Alcohol, sucrose and genetics influence cardiovascular risk

Cardiovascular disease (CVD) risk is determined in part by individual variations in diet and polymorphisms of the apolipoprotein-E (APOE) gene that regulate lipid metabolism. Three polymorphisms of APOE-E—E2, E3 and E4—influence the cholesterol response to changes in dietary fat. Two studies in the current issue of the American Journal of Clinical Nutrition examine how the APOE genotype interacts with alcohol in a population without CVD, and with sucrose in a population with CVD.

Both studies proceed from prior observations that carriers of the APOE E2 allele have lower serum LDL-cholesterol levels and higher triacylglycerol levels, whereas carriers of the APOE E4 allele have the highest LDL-cholesterol levels and the highest overall CVD risk. Corella et al. focused on the interaction of alcohol and APOE genotype in a cohort of the Framingham Offspring Study consisting of 1014 men and 1133 women averaging age 54, all free of CVD. Among carriers of the E2 allele, alcohol consumers had significantly lower LDL levels than nondrinkers. Conversely, among carriers of the E4 allele, LDL concentrations were higher in drinkers than in nondrinkers. The interaction between alcohol and APOE appeared to be limited to men. Whether they were drinkers or non-drinkers, women with the E2 allele had equally low LDL levels, whereas women with the E4 allele had the same modest elevation of LDL cholesterol levels regardless of their alcohol consumption. Conversely, male drinkers with the E4 allele had significantly higher (14.8%) LDL levels than male drinkers with the E2 allele.

A different study from Finland by Erkkilä et al. examined interactions between sucrose consumption, APOE E genotype and serum lipid metabolism. Participants included 284 males and 130 females who averaged 61 years of age and who had experienced one previous hospitalization for treatment of a CVD-related condition such as acute myocardial infarction or coronary artery bypass surgery. Serum total cholesterol and LDL cholesterol concentrations were lowest among carriers of the E2 allele. However, high sucrose intake was associated with triacylglycerol concentrations that were more than one third higher in carriers of the E2 allele than in carriers of the E3 and E4 alleles. On the other hand, saturated fat consumption had only a weak association with serum cholesterol levels in all three genotypes. Since subjects with the E2 allele made up only 5% of the study, the usefulness of this information in designing preventive treatment regimes for CVD patients may be limited.

An editorial by Lars Berglund provides an overview of APOE E investigations to date and suggests possible mechanisms whereby E2 and E4 alleles cause different lipid metabolism responses to nutrients. He suggests that, in such complex research, it is important to keep in mind that multiple comparisons of genotypes and different nutrients, as well as a low frequency of some genotypes, call for additional verifications of individual findings by further studies.

Corella, Dolores, et al. Alcohol drinking determines the effect of the APOE locus on LDL-cholesterol concentrations in men: the Framingham Offspring Study. Am J Clin Nutr 2001;73:736-45.

Erkkilä, Arja T., et al. APOE polymorphism and the hypertriacylglyceridemic effect of dietary sucrose. Am J Clin Nutr 2001;73:746-52.

Berglund, Lars. The APOE gene and diets—food (and drink) for thought. Am J Clin Nutr 2001;73:669-70.

This media release is provided by The American Society for Clinical Nutrition, to provide current information on nutrition-related research. This information should not be construed as medical advice.

If you have a medical concern, consult your doctor. To see the complete text of these articles, please go to: http://faseb.org/ajcn/April/11914-Ordovas.pdf, http://faseb.org/ajcn/April/12529-Berglund.pdf http://faseb.org/ajcn/April/11942-Erkkila.pdf

For more information please contact: Corella et al. at: ordovas@hnrc.tufts.edu Erkkilä et al. at: arja.erkkila@uku.fi Berglund et al.at: lfb9@columbia.edu

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