EPA (Eicosapentaenoic acid)

Mechanism

As a long-chain n-3 fatty acid, EPA is incorporated into cell-membrane phospholipids, where it displaces arachidonic acid (C20:4 n-6). Upon activation, the altered substrate pool gives rise to less strongly pro-inflammatory 3-series prostaglandins/thromboxanes and 5-series leukotrienes, along with EPA-derived resolvins. Much of the robust mechanistic evidence comes from human and monogastric models and is extrapolated to the horse; individual controlled equine studies suggest a modulation of inflammatory markers. Marine EPA/DHA intake has been associated with the field of joint and skin health, although study designs and dosages are heterogeneous. Horses take up n-3 in their basal forage primarily as ALA from pasture grass and flaxseed; preformed EPA must be supplied via marine sources (fish oil, algal oil), since endogenous conversion from ALA is low.

Cautions

• · Marine oils oxidise easily (rancidity) - feed cool, dark and fresh.
• · Higher PUFA intake raises the vitamin E requirement; factor in antioxidant coverage.
• · Very high doses may affect platelet function/clotting (relevant perioperatively, equine data limited).
• · Fish oil can reduce palatability; algal oil as an alternative.

Sources