Good fats of course, those being ω-3 fatty acids (a type of polyunsaturated fatty acid [PUFA], another being the ω-6 fatty acids; these are also referred to as n-3 and n-6 fatty acids). Members of these families are derived from the essential fatty acids linoleate (LA) and α-linolenate (LNA). Strictly speaking, these two are the only essential fatty acids (required through diet), although that term is often extended to the entire family of PUFAs (Cunnane, 2003). The ω-3 and ω-6 fatty acids are critical for a host of bodily functions, which you can read about in reviews by Das (2006) and Wijendran and Hayes (2004). Very roughly speaking ω-6 fatty acids are pro-inflammatory whereas ω-3 fatty acids are anti-inflammatory. More specifically, the ω-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are antithrombotic and antiarryhthmic, and dietary intake of these fatty acids is associated with reduced risk of death from cardiovascular disease.
Although current evidence indicates that the relative dietary ratios of ω-3 and ω-6 fatty acids is a indicator for overall health (
Wijendran and Hayes 2004; Simopoulos, 2002), the mechanisms by which EPA and DHA reduce the risk of cardiac mortality remain unclear. The assumption is that direct incorporation of these fatty acids into the myocardium of the heart underlies their health benefits. That dietary intake directly modulates myocardial phospholipid profile was recently documented by
Metcalf et al. (2007). The authors examined the atrial tissue of people undergoing elective cardiac surgery following varying durations of dietary supplementation with fish oil (6 g EPA+DHA/day, for 7-60 days). They found that fish oil supplementation increased the amount of EPA and DHA in the cell membranes of both atrial tissue as well as red blood cells.
It has been proposed that the cardioprotective effects of EPA and DHA result from replacement of arachidonic acid (AA) in cardiac membranes. AA is a precursor of a wide array of eicosanoids (
Funk, 2001). These compounds promote inflammatory responses, platelet aggregation, and vasoconstriction. Although these are essential metabolic functions, excess AA-derived eicosanoids can promote atherosclerotic disease and thrombosis.
Metcalf et al. also showed that dietary fish oil supplementation reduced atrial AA concentrations, consistent with the idea that part of the benefit of EPA and DHA may be due to the reduction in AA-derived pro-inflammatory factors.
These phosphospholipid adaptations in atrial tissue may thus underlie the cardioprotective effects of dietary fish oil. In support of this, the timescale and magnitude of these changes is broadly consistent with the observation that the protective effects of ω-3 fatty acid supplementation begin early, but reach significance only after about three months.
Also of note is the fact that supplementing with flaxseed oil (
high in ALA) did not result in any changes in ω-3 fatty acid concentrations. This is likely due to the fact that dietary ALA is converted to EPA and DHA at extremely low rates (
Plourde & Cunnane 2007), which is consistent with suggestions that ALA supplementation is not cardioprotective (
Matthan et al. 2005;
Wang et al. 2006).
