Dietary lipids and intestinal inflammatory disease

Inflammatory bowel diseases (IBD) are chronic recurrent intestinal inflammatory disorders that are occurring with an increasing prevalence among Westernized nations and younger age groups. IBD is multifactorial, involving genetic, environmental, and immunologic factors that combine to promote an exaggerated immune response associated with failure of appropriate regulatory feedback mechanisms that terminate the response to stimuli. The increase in IBD has followed a similar pattern to the increase in dietary n-6 fatty acids and n-6/n-3 fatty acid ratio. Plausible mechanisms to suggest that high intakes of linoleic acid may contribute to IBD include inhibition of eicosapentaenoic acid and docosahexaenoic acid synthesis, increased synthesis and membrane incorporation of arachidonic acid with production of proinflammatory mediators, and increased oxidative stress in LA-rich membranes. High n-6 fatty acids in the neonatal milk diet result in increased colonic n-6 fatty acids and an exaggerated response to chemically induced colitis, whereas a milk diet low in n-6 and high in n-3 fatty acids increases colonic n-3 fatty acids and lowers colonic damage. High dietary n-6 fatty acids and n-6/n-3 fatty acid ratios may be important environmental modifiers that contribute to IBD.

Abbreviations: ALA, α Linolenic acid, ARA, Arachidonic acid, CD, Crohn’s disease, COX, Cyclo-oxygenase, DHA, Docosahexaenoic acid, EPA, Eicosapentaenoic acid, IBD, Inflammatory bowel disease, IL, Interleukin, LA, Linoleic acid, PC, Phosphatidylcholine, PE, Phosphatidylethanolamine, PUFA, Polyunsaturated fatty acids, UC, Ulcerative colitis