Why celiac disease develops in 1% of people in the world who eat gluten-containing grains but not in the other 35-45% who are genetically at risk is not known. Having abnormal levels of gut bacteria levels is a risk. A 2005 study from Sweden revealed that altered short chain fatty acids (SCFA) levels produced by gut bacteria are a new piece to the puzzle. This also provides further support for the use of probiotics in the treatment and prevention of celiac disease.
The healthy human gastrointestinal tract contains millions of live microbes that aid in digestion and produce various nutrients including SCFAs. These short fragments of fats when unbranched are health food for the intestine. Altered levels of SCFAs are measurable and result from an inbalance of gut microflora. Tjellström et al measured short chain fatty acids levels as an indicator of gut bacteria levels in children with celiac disease and healthy children and found significant differences.
The found both untreated CD and treated CD children had presence of unhealthy longer branched SCFAs. These branched SCFAs cause more intestinal lining cell turnover. This can result in villous atrophy, impaired absorption and an overload of undigested proteins to the distal small bowel and colon resulting in diarrhea. They conclude “our finding may well reflect a deviant gut flora in CD, which may be a new piece in the intriguing puzzle…”
Normal gut bacteria promote healthy gut lining cells thereby preventing a leaky gut by preserving protective intestinal barrier function. Finding altered SCFA levels as a marker of altered gut flora suggests that restoring the normal balance with probiotics could help protect against the development of CD. This concept is supported by other research showing beneficial effects of probiotics in the treatment of colitis, Crohn’s disease, IBS, antibiotic associated diarrhea and HIV/AIDS diarrhea. Maybe we should all be on probiotics.
References:
Gut microflora associated characteristics in children with celiac disease. Tjellström, B, et al. American Journal of Gastroenterology 2005; 100: 2784-2788
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