FAs as modulators of genetic effects in lipid metabolism," write the authors. They go on to explain that "a more complete understanding of these factors and a thoughtful use of this information should help in the identification of vulnerable populations who will benefit from more personalized dietary recommendations."
A second study published by Ordovas, Lai, and colleagues in the Journal of Lipid Research also studied variants of the APOA5 gene in participants in the Framingham Heart Study to determine if the gene is related to atherosclerosis. The authors, including corresponding author Christopher O'Donnell of the National Heart, Lung, and Blood Institute's Framingham Heart Study, and first author Roberto Elosua, a former Fulbright-Generalitat de Catalu?a fellow who works with Ordovas, found that while most variants of the APOA5 gene were not associated with carotid intimal medial thickness (IMT), a surrogate measure of atherosclerosis burden, particular gene variants were "significantly associated with carotid IMT in obese participants."
Carriers of the particular gene variants who were obese expressed the effects of the gene variant differently than carriers who were not obese, showing a greater build-up of plaque in the heart. This was true for participants who were obese regardless of fat and cholesterol levels in the blood, age, gender, smoking or diabetes status, weight-for-height and blood pressure, all factors which are thought to influence risk of heart disease. Lai notes that "although obesity is a known contributing factor to heart disease, the association was strengthened in carriers of the rare APOA5 variant who were obese."
"It may be more important for some people to make preventive dietary and lifestyle changes than others, depending on their genetic makeup," says Ordovas. "The 'bad' genotype, in this study, doesn't seem to be that bad unless it's triggered by obesity," he concludes. "The observations, while strong,
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