Essentiality was proposed in the field of lipid by Burr and Burr in 1929. When rats were raised on the fat-free diet, their growth retarded and their skin and tails showed the characteristic deficient symptoms, which were relieved by the addition of Ω6(n-6) polyunsaturated fatty acids as linoleic(LA) and arachidonic(AA) acids to the basal diet. LA is dehydrogenated to γ-linolenic acid(GLNA) by δ6 desaturase, then GLNA is 2 carbon chain elongated by elongase to dihomo-γ-linolenic acid(DGLNA), which is desaturated by δ5 desaturase to AA. These acids are called LA family or Ω6(n-6) polyunsaturated fatty acids(PUFA). α-Linolenic acid(ALNA) is converted through the series of desaturation and elongation steps to docosahexaenic acid(DHA) via eicosapentaenoic acid(EPA). These acids belong to ALNA family or Ω3(n-3)PUFA. Human who consume large amounts of EPA and DHA, which are present in fatty fish and fish oils, have increased levels of these two fatty acids in their plasma and tissue lipids at the expense of LA and AA. Alternately, vegetarians, whose intake of LA in high, have more elevated levels of LA and AA and lower levels of EPA and DHA in plasma lipids and in cell membranes than omnivores. AA and EPA are metabolized to substances called eicosanoids. Those derived form AA are known as prostanocids(prostaglandins and prostacyclins) of the 2-types and leukotrienes of the 4-series, whereas those derived from EPA are known as prostanoids of the 3-types and leukotrienes of the 5-series. DGLNA is a precursor of the 1-types of prostaglandins. The metabolites of AA and EPA have competitive functions. Ingestion of EPA from fish or fish oil replaces AA from membrane phospholipids in practically all cells. So this leads to a more physiological state characterized by the production of proatanoids and leukotrienes that have antithrombic, antichemotactic, antivasoconstrictive and antiinflammatory properties. It is evident that Ω3 fatty acids can affect a number of chronic diseases through eicosanoids alone.