Abstract

Inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn’s disease, is a chronic relapsing intestinal inflammatory disorder of the gastrointestinal tract. IBD is occurring with increasing frequency among Western populations and is emerging in countries that have traditionally had a low prevalence of the component diseases. IBD is a multifactorial, heterogeneous disease that occurs in genetically susceptible individuals in response to environmental and immunological factors associated with a dysregulated intestinal mucosal immunological response. The increase in incidence of IBD parallels the increase in dietary intake of omega-6 (n-6) polyunsaturated fatty acids and the change in balance of intake of n-6 to n-3 fatty acids. Experimental data suggest that high intake of n-6 fatty acids may contribute to the development and severity of IBD through increased synthesis and membrane incorporation of arachidonic acid (ARA) with the accompanying production of pro-inflammatory mediators, and increased oxidative stress in n-6 fatty acid rich membranes. Conversely, the n-3 polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid (DHA) partly replace ARA in cell membranes and are metabolized to weaker pro-inflammatory eicosanoids and to strong pro-resolving mediators with roles in inflammation cessation. Consequently, high dietary n-6 fatty acid intake and high n-6–n-3 fatty acid ratios may be an important environmental modifier that contributes to the development of IBD in genetically susceptible individuals, while increased intake of n-3 fatty acids may lower risk of IBD and could be therapeutic.

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