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Omega-6 fatty acids and inflammation.

Ever since I can remember, there has been an idea promulgated among many nutritionists that omega-6 fatty acids are "bad for you" because they have a pro-inflammatory effect. In contrast, omega-3 fatty acids are said to be "good for you" because they have an anti-inflammatory effect. The basis of the concern about omega-6 fatty acids is that linoleic acid (the major omega-3 fatty acid in the diet) is converted in part to arachidonic acid, which is a precursor for pro-inflammatory eicosanoids such as prostaglandin E2, leukotriene B4, and thromboxane A2. In addition, high linoleic acid intake might result in decreased conversion of alpha-linolenic acid (an omega-3 fatty acid) to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), due to competition for the enzyme, delta-6 desaturase. Decreased synthesis of EPA and DHA would presumably result in decreased production of anti-inflammatory eicosanoids that are derived from these fatty acids. During the past century, per capita consumption of omega-6 fatty acids has increased while consumption of omega-3 fatty acids has decreased, resulting in a marked change in the ratio between these two classes of fatty acids in the diet. It has been argued that the reduction in the ratio of omega-6 to omega-3 in the diet is responsible in part for the increased incidence of various diseases that have an inflammatory component, including cardiovascular disease and asthma.

The idea that omega-6 fatty acids are pro-inflammatory has always been difficult to understand, considering the available data. First, the bulk of the research indicates that omega-6 fatty acids, including linoleic acid, reduce the risk of developing cardiovascular disease. Moreover, two diseases with a major inflammatory component--rheumatoid arthritis and atopic dermatitis--have been shown to be ameliorated by supplementation with omega-6 fatty acids.

In one study, 37 patients with active rheumatoid arthritis were randomly assigned to receive, in double-blind fashion, borage oil (providing 1.4 g per day of the omega-6 fatty acid gamma-linolenic acid) or placebo for 24 weeks. Compared with baseline, borage oil reduced the number of tender joints by 36%, improved the tender-joint score by 45%, improved the swollen-joint score by 41%, and reduced the swollen-joint count by 28%. Each of these parameters worsened in the placebo group, and the difference in the change between groups was statistically significant for each comparison (p = 0.02 to 0.003). Compared with placebo, borage oil also significantly reduced pain (p = 0.01).

In another study, 48 adults (mean age, 24 years) with chronic, severe atopic dermatitis were randomly assigned to receive, in double-blind fashion, sunflower oil (4.76 g per day, providing about 3 g per day of linoleic acid), fish oil (providing daily 2.0 g of EPA and 1.3 g of DHA), or placebo (olive oil) for 12 weeks. Disease severity was assessed by the Rajka score, which takes into account disease extension, course of eczema, and itch intensity. The mean Rajka score improved in the sunflower oil group by 73% after 6 weeks and by 81% after 12 weeks. The improvement was significant compared with the changes in the fish oil and placebo groups (p < 0.0001 for each) and compared with baseline (p < 0.01).

The view that omega-6 fatty acids are primarily pro-inflammatory fails to consider the complex nature of omega-6 fatty acid metabolism. For example, dihomo-gamma-linolenic acid is a metabolite of linoleic acid that is converted both to arachidonic acid (which promotes inflammation in some circumstances) and to prostaglandin El (which has anti-inflammatory activity). There is no clear evidence that the pro-inflammatory metabolic pathways dominate the anti-inflammatory pathways under normal circumstance.

Scientists recently conducted a meta-analysis of 15 randomized controlled trials that examined the effect of dietary linoleic acid intake on markers of chronic inflammation in healthy noninfant populations. None of the trials reported significant findings for a wide array of inflammatory markers, including C-reactive protein, fibrinogen, plasminogen activator inhibitor type 1, cytokines, or tumor necrosis factor-alpha. The only reported significant effects of higher linoleic acid intakes were greater excretion of prostaglandin E2 and lower excretion of 2,3-dinor-thromboxane B2 in one study and higher excretion of tetranorprostanedioic acid in another study. However, the authors of those studies stated that these effects were not indicative of increased inflammation. Based on this evidence, it seems that the commonly held belief that omega-6 fatty acids are pro-inflammatory is incorrect.

These findings do not rule out the possibility that the increased ratio of omega-6 to omega-3 fatty acids in the modern diet does have deleterious effects. For example, studies in rats suggest that a 4 to 1 ratio of omega-6 to omega-3 is optimal for improving learning performance. That ratio is much lower than the current 10 to 1 ratio in the typical American diet. However, if a relative excess of omega-6 fatty acids does lead to adverse consequences, the mechanism is likely unrelated to increased inflammation.

Alan R. Gaby, MD
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Author:Gaby, Alan R.
Publication:Townsend Letter
Article Type:Editorial
Geographic Code:1USA
Date:Nov 1, 2012
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