Abstract

Rheumatoid arthritis (RA) is an autoimmune disease, characterized by very painful joint as well as erosive and progressive chronic inflammation and thickening of the synovial lining in addition to cartilage damage. Chronic inflammationsyndrome is considered as the major cause and pathogenesis of RA. RA has a prevalence of about 2 percent worldwide and ismore common in women with symptoms typically appearing during middle age. Nutritional factors have been shown to have favourable influences on pathophysiological processes in RA, including oxidative damage, cartilage matrix degradation and repair, and chondrocyte function and responses in adjacent bone. Oxidative stress and low antioxidant status have been amajor factor in RA patients, most of which are nutritionally deficient. It has been shown in several studies that adequate intakes of antioxidants and n-3 PUFAs alleviate inflammation by decreasing the release and activity proinflammatory compounds includingIL-1, TNF-α and nuclear factor kappa B (NFkB). Western diets contain large amounts of linoleic acid (C18:2 n-6), which is considered a proinflammatory fatty acid and contributes to the high ratio of n-6 to n-3 fatty acids verified in such diets. This high ratio may lessen the more positive results expected with fish oil n-3 fatty acids in patients with RA. However, a diet rich inmonounsaturated fatty acids and oils rich in α-linolenic acid (C18:3 n-3) can overcome this. Olive oil contains large amounts of oleic acid. Oleic acid is an n-9 monounsaturated fatty acid (C18:1 n-9) that is converted to eicosatrienoic acid (ETA; C20:3 n-9).ETA is converted to LTA3, which is a potent inhibitor of leukotrienes B4 synthesis. Therefore, ETA may exert its anti-inflammatoryaction through a mechanism analogous to that of fish oil, which contains eicosapentaenoic acid. Numerous studies have alsodemonstrated that certain nutraceuticals, including glucosamine and chondroitin sulphate, methylsulfonylmethane (MSM),bromelain, hyaluronic acid and type II collagen may influence RA pathophysiology.