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Quotation

I hmmed because you first say it's not bacteria and then finish by saying that it's fatty acid producing bacteria. Little bit of a contradiction. By the way, it's pretty well established that chronically elevated cortisol is a cause of colitis. If you doubt that you might wanna read Sapolsky's Why Zebras Don't Get Ulcers. Cortisol can be useful for short term management of colitis and ulcers, but the underlying problem is surely not a chronic cortisol deficiency. Histamine seems to play an important role in the development of chronic inflammation in the gut, but before you dismiss the role of bacteria you should note that histamine is one of the most important mediators of endotoxic inflammation resulting from bacteria. I am not sure what you mean by low potassium, but since low systemic potassium is virtually non-existent I can't see how this would be an important factor. I also don't know where you would get the idea that colitis is characterized by low methylation, when the connection between increased methylation, inflammation, colitis, and cancer is so well established. For example, RARB, a gene previously identified as a tumor suppressor in colorectal adenocarcinoma is turned of by the increased methylation in colitis. Colitis is a hypermethylated state! I seriously recommend you read this good review on methylation and colitis. You can get the full text via sci-hub." In conclusion, we have shown a step-wise increase in methylation status of the genome between a healthy colon, a quiescent and an inflamed UC colon. Data have been collated in relation to inflammatory genes, individual SNPs, methylation status, phenotype and presentation. Although the aetiological role of methylation remains contested, there is evidence for specific methylation alterations in genes involved in the inflammatory process, such as ESR1, CD1 and BRINP3, both upstream and downstream of inflammation in UC, and of the relationship between methylation status andclinical phenotypes. This gives credence to the theor yof UC as a model of mucosal inflammatory process driven by epigenetic markers." (Davidson, Nwokolo, Arasaradnam 2016)Epigenomics. 2016 May;8(5):667-84. doi: 10.2217/epi-2016-0006. Epub 2016 Apr 20. A systematic review of the role of DNA methylation on inflammatory genes in ulcerative colitis. Gould NJ1, Davidson KL1, Nwokolo CU2, Arasaradnam RP2,3.BACKGROUND: Ulcerative colitis (UC) is an idiopathic disease of the large intestine with evidence pointing to the role of epigenetic changes.METHODS Searches were performed in three databases (EMBASE, MEDLINE and Web of Science), following PRISMA protocol. DNA methylation was the only epigenetic mechanism affecting genes linked to inflammatory response in UC.RESULTS: A total of 25 differentially methylated inflammatory genes were identified. Hypermethylation of miR-1247 significantly correlates (p = 0.0006) with refractory UC while PAR2 hypermethylation correlates (p = 0.007) with corticosteroid dependence.CONCLUSION: Evidence points to a step-wise increase in methylation status of the genome between a healthy colon, quiescent UC and when inflamed. Inflammatory genes (which are aberrantly methylated), have also been implicated in cancer development in UC.