Omega-3 long-chain PUFA and triglycride lowering: Minimum effective intakes

Early studies on the cardioprotective effects of high doses (up to 20 g of eicosapentaenoic and docosahexaenoic acids, EPA and DHA, per day) of omega-3 fatty acids (FAs) suggested that these FAs primarily lowered triglyceride levels. These supraphysiological intake studies soon gave way to trials using lower and lower intakes of omega-3 FAs such that it is now clear that up to 45% lowering of serum triglyceride levels can be achieved with 3-4 g of EPA+DHA. This is an intake that can hardly be achieved by dietary means; direct supplementation is required. This is a public health challenge since implementing wide-scale supplementation programmes would be difficult. Relatively few investigators have examined the effects of low (<2 g) EPA+DHA on serum lipid profiles, presumably because until recently there was little expectation that any benefit would be detectable. With the publication of the DART study and more recently the GISSI-Prevenzione Study, it is becoming clear that small intakes of omega-3 FAs can significantly impact CHD risk. A review of the studies on the effects of small doses (<2 g . day^-1) of omega-3 FAs on serum triglyceride levels suggests that serum triglyceride levels decreased in every study (compared with control or placebo treatment). The decreases were often not statistically significant, but this is to be expected with small doses given for short time-periods. Four of the five studies that examined postprandial lipids (PPL) reported significant reductions in this parameter even when fasting levels were not altered. This suggests that chronic intake of small amounts of omega-3 FAs may reduce overall (day-long) triglyceride-rich lipoprotein levels which could have long-term implications for the reduction of CHD risk. Whilst the cardioprotective effects of omega-3 FAs are becoming well documented, the question of whether such beneficial effects of omega-3 FAs are at least partially mediated by changes in serum levels of triglyceride-rich lipoproteins or their remnants remains open. Further studies to examine the effects of this low level of intake are clearly needed to determine the relative contribution of hypolipidaemic mechanisms versus those involving diminished platelet function, altered adhesion molecule expression, improvements in endothelial function and antiarrhythmic or hypotensive effects.