Inflammatory bowel disease is an idiopathic disease caused by dysregulated immune response to host intestinal microflora. The two major types of inflammatory bowel disease are ulcerative colitis, which is limited to the colon, and Crohn’s disease, which can affect any segment of the gastrointestinal tract from the mouth to the anus. There is also genetic predisposition for inflammatory bowel disease, and patients with this condition are more prone to the development of cancer.
Researchers are exploring microbiome of the gut in Inflammatory bowel disease. The cause of inflammatory bowel is dysbiosis (disruption of normal flora) due to viral, bacterial, fungal or topographical changes in the digestive system. One newly published study shows “the long-term dynamic behavior of the gut microbiome in inflammatory bowel disease and differentiate this from normal variation”.
Those with inflammatory bowel disease were found to have microbiomes which fluctuate more than those of healthy individuals. Interestingly, the microbiomes of some inflammatory bowel disease patients were found to become normal, but then will deviate again. Inflammation was correlated with fluctuations in the gut microbiome (Halfvarson, et al., 2017). Research showed that functional activity of the microbiome plays an important role in both healthy and disease states. Current strategies employed to therapeutically alter the microbiome include dietary modification, prebiotics, probiotics, antibiotics, and even fecal transplantation to restore a state of health. (Schulberg & De Cruz, 2016)
Another study from 2016 in which researchers found that the mucus layer which lines the intestines is key in establishing this symbiotic relationship between host and microbe. This lining protects the intestines from chemical (enzymatic and environmental) and microbial damage and also helps determine bacterial colonies and their food supply. Mucins are the major component of this mucus layer; Muc2 is the most prominent mucin, secreted by goblet cells, in the colon. Mice which lack the Muc2 gene, spontaneously, and experimentally, develop colitis. Decreased Muc2 expression has also been implicated in the inflammatory bowel disease and colon cancers (Huang et al., 2015).
If you do not have healthy gut microbiome, you do not digest food, lack vitamin transport, and at risk of developing bowel disease, chronic inflammation, and even cancers, you can help yourself by eating whole foods. Most vegetables and fruits carry the helpful bacteria required to digest the foods, we just need to eat them as close to their whole state as possible. Taking a broad-spectrum probiotic helps to keep your gut flora replenished. Fermented foods like yogurt, lassi, kim chi, sauerkraut, and pickled vegetables can help establish normal flora. Make sure also to ingest pre-biotics to give your microbiome its own food supply. Using ghee or coconut oil, sesame oil, olive oil and others healthy oils provides pre-biotic to the microbiota for propagating healthy gut flora. (Besten, et al., 2013).
Halfvarson, J., Brislawn, C. J., Lamendella, R., Vázquez-Baeza, Y., Walters, W. A., Bramer, L. M., Jansson, J. K. (2017). Dynamics of the human gut microbiome in inflammatory bowel disease. Nature Microbiology, 2, 17004. doi:10.1038/nmicrobiol.2017.4
Schulberg, J., & De Cruz, P. (2016). Characterisation and therapeutic manipulation of the gut microbiome in inflammatory bowel disease. Internal Medicine Journal, 46(3), 266–273. https://doi.org/10.1111/imj.13003
Tytgat KMAJ, Buller HA, Opdam FJM, et al. Biosynthesis of human colonic mucin: Muc2 is the prominent secretory mucin. Gastroenterology. 1994; 107:1352–1363. [PubMed: 7926500]
Velcich A, Yang W, Heyer J, et al. Colorectal cancer in mice genetically deficient in the mucin Muc2. Science. 2002; 295:1726–1729. [PubMed: 11872843]
Besten, G. D., Eunen, K. V., Groen, A. K., Venema, K., Reijngoud, D., & Bakker, B. M. (2013). The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. The Journal of Lipid Research, 54(9), 2325-2340. doi:10.1194/jlr.r036012
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