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Irritable Bowel Disease

Diet is thought to be one of the most important factors in the cause of diseases of the large bowel, including colorectal cancer and inflammatory bowel disease (IBD). Whilst the role of individual fatty acids in human colorectal cancer risk is not clear, the amount and type of fat appears to be important. Epidemiological studies indicate that diets high in saturated fats increase the risk of cancer, whereas diets high in polyunsaturated fats rich in omega-3 fatty acids derived from oily fish or fish oil are thought to decrease the risk of cancer. [i] Patients with colon tumours have an abnormal cell turnover rate and are at increased risk of developing further colorectal malignancies; high doses of fish oil have been shown to reduce the rate of cell growth in such individuals.[ii] Indeed current research is investigating the potential efficacy of EPA supplementation in reducing the risk of colorectal cancer.[iii]

Inflammatory bowel disease includes both Crohn’s disease and ulcerative colitis. Both conditions are the result of an exaggerated or insufficiently suppressed immune response, leading to damage of the mucous membrane, allowing toxins and bacteria to seep through the intestinal wall and into the blood stream, further accelerating the inflammatory process. [iv] Diverticulosis coli is another common condition involving development of mucosal folds and inflammation of the colon. [v]

Substances produced from the omega-6 fatty acid arachidonic acid are considered primarily responsible for inflammatory processes and the intestinal inflammation seen in inflammatory bowel disease. Prostaglandin formation from omega-3 and omega-6 fatty acids uses different pathways that share common enzymes. The ratio of omega-3 to omega-6 will therefore affect which pathway is the most active. Unfortunately the ratio of inflammatory omega-6 fatty acids in the diet is much higher than that of anti-inflammatory omega-3 fatty acids. If there is a higher intake of EPA, however, this causes competition with arachidonic acid (AA) for the utilisation of specific enzymes, and inhibits the production of inflammatory prostaglandins. [vi] The ability of EPA to reduce the inflammatory response suggests great potential for alleviating symptoms of inflammatory bowel disease.

[i] Lipkin, L., Reddy, B., Newmark, H. & Lamprecht, S.A., Dietary factors in human colorectal cancer, Annual Review of Nutrition, (1999) Vol. 19: 545-586. See also Reddy, A. & Lawrence, R.A. et al. (2002) Inhibition of intracellular peroxides and apoptosis of lymphocytes in lupus-prone B/W mice by dietary n-6 and n-3 lipids with calorie restriction. J Clin Immunol 22(4): 206-19.

[ii] Anti, M., Armelao, F., Marra, G., Percesepe, A., Bartoli, G.M., Palozza, P., Parrella, P., Canetta, C., Gentiloni, N., De Vitis, I., et al. Effects of different doses of fish oil on rectal cell proliferation in patients with sporadic colonic adenomas. (1994) Gastroenterology. 107(6):1709-18.

[iii] Courtney, E.D., Matthews, S., Finlayson, C., Di Pierro, D., Belluzzi, A., Roda, E., Kang, J.Y., Leicester, R.J. Eicosapentaenoic acid (EPA) reduces crypt cell proliferation and increases apoptosis in normal colonic mucosa in subjects with a history of colorectal adenomas. Int J Colorectal Dis. 2007 Jul;22(7):765-76.

[iv] Schmidt, C. & Stallmach, A. Etiology and pathogenesis of inflammatory bowel disease, (2005), Minerva Gastroenterol Dieteol , 51(2)l127-45.

[v] West, A.B. Losada, M. The pathology of diverticulosis coli, J Clin Gastroenterol, (2004) 38(5):S11-6.

[vi] Obajimi, O., Black, K.D., MacDonald, D.J., Boyle, M., Glen, I. & Ross, B.M. Differential effects of eicosapentaenoic and docosahexaenoic acids upon oxidant-stimulated release and uptake of arachidonic acid in human lymphoma U937 cells, Pharmacological Research, (2005) Vol 52:2 pp.183-191.

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