Dietary polyunsaturated fats and inflammation

Dietary polyunsaturated fats are classified as n-3 or n-6 according to their double bond chemistry and these chemical differences confer differential biological effects on fatty acids from these two classes. In the modern Australian diet, the intake of n-6 fats exceeds that of n-3 fats by approximately 25-fold. This relative abundance of n-6 fat intake is reflected in the cell membranes where the ratio of n-6:n-3 PUFA is approximately 7:1. While this relative excess of n-6 to n-3 fat has been driven by agricultural and industrial changes as well as dietary changes aimed at lowering blood cholesterol levels, there is considerable evidence that increasing the amount of dietary n-3 fat can suppress inflammatory mediator production and can suppress inflammation. Animal studies using models of inflammatory disease have demonstrated that ingestion of fish oil, rich in n-3 fats, can suppress inflammation. In human studies, at least 11 double-blind, placebo-controlled clinical trials with rheumatoid arthritis patients have demonstrated that dietary supplements of fish oil can provide symptomatic benefits. The mechanisms for these clinical responses lie in the effects which n-3 fats have on the production of inflammatory mediators. Dietary fish oil which contains 20- and 22-carbon n-3 fatty acids and flaxseed oil which contains their 18-carbon n-3 progenitor fatty acid, can inhibit the production of the eicosanoid inflammatory mediators, prostaglandin E(2) (PGE(2)) and leukotriene B-4 (LTB(4)) and the cytokine inflammatory mediators, interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF alpha). Because n-6 fats can decrease the levels of n-3 fats in cell membranes, it is most likely that the optimum anti-inflammatory effects of n-3 fats will be within the context of diets also containing lower levels of n-6 fats than those in the current Australian diet.