Microcirculation, Vitamin E and Omega 3 Fatty Acids: An Overview

Abstract

Epidemiological and clinical studies suggest that ingestion of diets rich in fish and fish oils (FO) may be related to reduced incidence of cardiovascular disease (CVD). Our studies^1,2, and many other studies, in humans and using animal models for atherosclerosis, have shown that FOs significantly reduce serum lipoproteins (in particular very low density lipoproteins-VLDL), and decreases platelet reactivity^{3,4,5,6,7,8,9,}. It has been recently demonstrated that the hypotriglyceridemic effect may be due to decreased hepatic mRNA encoding for fatty acid synthase¹⁰,. However, not all reported effects of n-3 fatty acids appear to be beneficial^11,12,13,14,. Fatty acids of the three series are susceptible to rapid oxidation and the resulting free radicals can elicit cellular damage^15,. In this regard, a poor antioxidant status has been found to be associated with an increased risk for CVD^16,17,18,. Some studies have reported that FO consumption increases the dietary vit. E requirement^16,19,20,21, while a study recently conducted by Berlin et al.^22, found that dietary FO vs a blend of stripped lard, beef tallow and corn oil supplementation increased red blood cell (RBC) membrane vit. E concentration; surprisingly, plasma and tissue lipid oxidation products were not measured. In line with these observations, Chen et al^23, reported that FO supplementation may in fact attenuate free radical generation (measured as MDA) in rabbits following coronary occlusion, presumably by serving as the substrate for peroxidation at the expense of other membrane constituents. They also found that in the FO fed group the level of myocardial Superoxide dismutase and the 6-keto-PGF₁ α/TXB₂ ratio increased versus a coconut oil control (FO vs chow fed did not differ significantly). An alternative explanation might be related to the decreased TXB₂ which results in equimolar reductions in HHT and MDA. Most likely, as suggested by others^21,, the oxidative stress induced by high levels of dietary FO can be countered by vit. E supplementation in animals where other antioxidant mechanisms are not compromised, although the amounts required are unclear.