From the limited study **data** in this review, EPA and DHA appear to have differential roles in platelet function with EPA reducing mean platelet volume and count, and DHA reducing collagen-induced platelet aggregation [61,65]. Furthermore, von Schacky and Weber demonstrated in a small uncontrolled study that DHA had a greater antithrombotic effect (via reduced platelet responsiveness) compared to EPA in healthy volunteers after just six days of 6 g/day EPA or DHA [45]. Both EPA and DHA are able to displace a proportion of AA in platelet membrane phospholipids, thus decreasing the amount of AA-derived pro-aggregatory mediators such as TXA 2 that are formed from the metabolism of AA by COX-2 [2]. EPA is also a substrate for COX-2, resulting in synthesis of weaker pro-aggregatory mediators such as TXA 3 . Both EPA and AA also form equipotent prostacyclins PGI 3 and PGI 2 , respectively, which inhibit platelet aggregation. Thus, the overall effect of EPA and DHA is to create a less thrombogenic environment [2]. This competitive displacement of AA is supported by the strong association of DHA's positive effect on platelet aggregation with decreases in platelet-derived TXB 2 , an inactive metabolite of AA-derived TXA 2 [65]. This may also be due to DHA's competitive inhibition of COX-2 or to the inhibition of TXA 2 synthetase or TXA 2 receptor function [23].