Cardiovascular disease is one of the major public concerns other than diabetes, obesity and cancer. Cardiovascular have both modifiable (ie, behavior, diet and lifestyle) and nonmodifiable (ie, genetic, age and sex) risk factors. In this article, Ordovas JM is concern about how genes and the environment act together to cause cardiovascular disease and how the environment (eg, diet) might be modified in a more personalised fashion to help prevent or delay the onset of disease.
Lipoproteins are macromolecular complexes of lipids and specific proteins (apolipoprotein or apoprotein) that originate mainly from the liver and intestine and are involved in the transport and redistribution of lipids in the body. Lipoprotein metabolism is linked to the development of atherosclerosis. Thus, genetic variants involved in lipid metabolism that may affect dietary response and potentially cardiovascular disease is being studied.
Genetic variation at the APOE locus with the alleles E4, E3 or E2 affects the level of plasma cholesterol, LDL-cholesterol and intestinal cholesterol absorption. Individuals with different APOE phenotypes respond differently to dietary saturated fat and cholesterol. APOE4 carriers tend to absorb more cholesterol, have higher plasma cholesterol and LDL-cholesterol than non-APOE4 carriers.
Therefore, genetic variation at those loci is expected to explain some of the dramatic interindividual variations in lipoprotein response to dietary change. However, lipoprotein response to dietary factors is extremely complex. Thus, further studies are needed to test for the gene-diet interactions.
Reference:
http://www.ajcn.org/ (cited on May 10, 2009)
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