Nutritional Modulation of Inflammation by Polyunsaturated Fatty Acids/Eicosanoids

Abstract

The first indication that dietary fat may be essential for healthy growing animals was presented in 1918 by Aron, who proposed that butter has a nutrient value that cannot be provided by other dietary components (1). This report suggested that there was a special nutritive value inherent in fat apart from its caloric contribution and that this possibly was related to the presence of certain lipids. In 1929, Burr and Burr (2) presented the first in a series of articles outlining a “new deficiency disease produced by the rigid exclusion of fat from the diet.” In the series of conclusions put forth, they developed the hypothesis that warm-blooded animals, in general, cannot synthesize appreciable quantities of certain fatty acids. In 1930, both investigators significantly added to their earlier work by presenting evidence that the dietary inclusion of linoleic acid alone could reverse all deficiency symptoms resulting from a fat-free diet and thus linoleic acid (LA or 18:2n-6)’ was heralded as an essential fatty acid (EFA) (3). The recognition that some unsaturated fatty acids could not be synthesized from endogenous precursors by mammals and were essential dietary elements led to the designation of essential and nonessential fatty acids. It was originally thought that there are only two essential fatty acids, linoleic acid (9,12-octadecadienoic acid, LA, 18:2n-6) and α-linolenic acid (9,12,15-octadecatrienoic acid [ALA], 18:3n-3), but continued nutritional studies revealed positive essential growth responses not only for linoleic acid and a-linolenic acid, but also for arachidonic acid as well as the long-chain highly unsaturated fatty acids in fish oil (eicosapentaenoic acid, 20:5n-3) and docosahexaenoic acid, 22:n-3) (4–6). More recent reports on the biological significance of the longer-chain n-3 PUFAs do qualify these long-chain fatty acids as essential PUFAs.