Polyunsaturated Fatty Acids and Cardiovascular Disease: Implications for Nutrigenetics

Abstract

Cardiovascular disease (CVD) arises as a result of genetic predisposition in the context of a disease-promoting environment. While several risk factors have been identified for CVD, such as elevated serum lipid levels and hypertension, most of the genes identified thus far do not appear to involve such ‘conventional’ risk factors. Moreover, the interactions between genes and environment, such as a diet high in certain fats, adds another level of complexity to CVD and renders identification of the underlying genetic factors even more difficult. Polyunsaturated fatty acids (PUFAs), such as the ω–6 and ω–3 fatty acids, which have multiple roles in membrane structure, lipid metabolism, blood clotting, blood pressure, and, in particular, inflammation, have been linked to the reduction in CVD. Linoleic (ω–6) and α-linolenic acid (ω–3) are essential fatty acids that can be converted into long-chain PUFAs, such as arachidonic acid (AA) and eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA), respectively. These long-chain PUFAs are metabolized by enzymatically catalyzed systems via cyclooxygenases and lipoxygenases. The 5-lipoxygenase (5-LO)/leukotriene (LT) biosynthesis pathway has been biochemically and genetically associated with CVD traits in mice and humans, particularly in the context of dietary AA and EPA/DHA. In this review, we summarize the biochemical metabolism of ω–3 and ω–6 PUFAs, evaluate the evidence for genetic and nutrigenetic contributions of 5-LO pathway genes to CVD, and discuss the potential of future studies that could identify other gene-dietary interactions between PUFAs and CVD traits.

Fatty acid profile of fillet, liver and mesenteric fat in tilapia (<i>Oreochromis niloticus</i>) fed vegetable oil supplementation in the finishing period of fattening

“…In accordance with this assumption, an increase was experienced for arachidonic acid (AA) in vegetable oil groups, which was the most expressed by the SO diet. This can be regarded as a less favourable tendency, as AA is the precursor of the most effective inflammation mediators, thromboxanes, prostaglandins and leukotrienes (Allayee et al 2009). The ratio of arachidonic acid to long-chain n-3 PUFAs (EPA and DHA) in human diets is also an important factor.…”

Endogenously Decreasing Tissue n-6/n-3 Fatty Acid Ratio Reduces Atherosclerotic Lesions in Apolipoprotein E –Deficient Mice by Inhibiting Systemic and Vascular Inflammation

“…[1][2][3][4][5] The beneficial effects of n-3 PUFAs in atherosclerotic cardiovascular disease are associated with the reduction of endothelial adhesion molecules, 3 the stabilization of atherosclerotic lesions, 4 the modulation of oxidative stress in macrophages, 6 and improvement in the function of endothelium 5,7 and macrophages. 8 However, several studies on animals and humans have shown somewhat contradictory results, 9 -11 possibly because they did not account for the tissue background level of n-6 PUFAs, a potential confounding factor.…”

Nutrigenomics: interaction between certain genetic polymorphisms and a diet

“…Najverjetneje arahidonska kislina in njen prekurzor stopnjujeta aterogenski u~inek pri variantnih genotipih z vi{anjem produkcije eikozanoidov. Nasproten u~inek pa bi lahko imel pove~an vnos DHA in EPA, saj bi se tvorba vnetnih levkotrienov posledi~no zni`ala (17,54,56).…”