Polyunsaturated Fatty Acids and Risk of Ischemic Stroke

Ischemic stroke is a major cause of death and morbidity worldwide. It has been suggested that polyunsaturated fatty acids (PUFAs) may be associated with a lower risk ischemic stroke, but this has been far less studied than their role for coronary heart disease. In this paper, we summarize the main findings from previous follow-up studies investigating associations between intake or biomarkers of the major PUFAs including alpha-linolenic acid (ALA), marine n-3 PUFAs and linoleic acid (LA) and the development of ischemic stroke. Several follow-up studies have suggested that marine n-3 PUFAs may be associated with a lower risk of ischemic stroke although results have not been consistent and limited knowledge exist on the individual marine n-3 PUFAs and ischemic stroke and its subtypes. The role of ALA is less clear, but most studies have not supported that ALA is appreciably associated with ischemic stroke risk. Some studies have supported that LA might be associated with a lower risk of total ischemic stroke, while limited evidence exist on PUFAs and ischemic stroke subtypes. The associations may depend on the macronutrients that PUFAs replace and this substitution aspect together with focus on dietary patterns represent interesting areas for future research

The Effect of Low-Dose Marine <em>n</em>-3 Fatty Acids on Plasma Levels of sCD36 in Overweight Subjects:A Randomized, Double-Blind, Placebo-Controlled Trial

CD36 is a scavenger receptor involved in lipid uptake and inflammation. Recently, non-cell-bound CD36 (sCD36) was identified in plasma and suggested to be a marker of lipid accumulation in the vessel wall. Marine n-3 polyunsaturated fatty acids (PUFA) may have cardioprotective effects. This study evaluated the effect of marine n-3 PUFA on sCD36 levels in overweight subjects. Fifty overweight subjects were randomized to 1.1 g of n-3 PUFA or 2 g of olive oil daily for six weeks. Neutrophils were isolated at baseline and after six weeks of treatment while an adipose tissue biopsy was obtained at baseline. The content of n-3 PUFA in adipose tissue and neutrophils was analyzed by gas chromatography, while plasma levels of sCD36 were determined using an enzyme-linked immunosorbent assay (ELISA). After six weeks of supplement plasma sCD36 did not differ between supplements (P = 0.18). There was no significant correlation between plasma sCD36 levels and n-3 PUFA in neutrophils at baseline (r = −0.02, P = 0.88), after six weeks supplement (r = −0.03, P = 0.85) or in adipose tissue (r = 0.14, P = 0.34). This study therefore does not provide evidence for a cardioprotective effect of n-3 PUFA acting through a CD36-dependent mechanism