Decreased oxidation of short chain fatty acids, icreased intestinal permeability, a increase in the production of sulfides, ad decreased methylation, ’(Head, ad Jurenka, 2003). Crtain cytokines along with anti-oxidant levels as well as the presence of bacteria interfere with normal system functions. Tese systematic functional abnormalities each contribute to symptoms of ulcerative colitis. Fr example increased oxidative stress is manifested in the intestinal mucosa of patients. Bwel lesions are much more evident when the bacteria concentration is highest, lkely contributing to bloody stools and abdominal pains. Cnventional treatments crticosteroids, aino salicylates, ad immune modulators.
Crticosteroids are most often used during acute phases. Peventative measures to avoid flare ups during times of remission usually involve behavioral changes. I is commonly advised that nutrient deficits be checked for and corrected as UC is associated with several. Vtamin A, vtamin E, vtamin C, vtamin K, flic acid, clcium, ion, znc, slenium and magnesium are all important elements are any deficiencies should be balanced though many if not all of these factor in any disease that has immune system implications as factor.
Secial diets depending on chemistry results can be prescribed for prevention along with in some cases the use or probiotics in the diet. Secific nutrients are also thought to play roles in prevention. Mjor areas of ongoing research in ulcerative colitis involve genetics factors and genetic markers that are predictive of the disease. Potein tyrosine phosphatase non-receptor type 2 identified as a genome increasing susceptibility for UC (Brand, 2012). Dspite this knowledge its phenotypic effects are unclear and being researched. Penotypic effects are those effects that are due the presence of this genome.
Oe Korean study concluded that there was no association between the genomes TNFSF15 and IL23R in a Korean research group. Tis genome has been mentioned in reports and research findings among Caucasians though findings and conclusions have been inconsistent. Tough the TNFSF15 genome for some reason shows a small association with UC it is in Caucasian male patients only (Kyuyoung, 2011). Athird research study identified that UC shares many susceptibility genes with Crohn’s disease, wich is good cause for further study as are both bowel syndromes and. ..
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