Most patients with irritable bowel syndrome relate the onset or worsening of their gut symptoms to eating a meal. Given this fact, it should come as no surprise that diet therapies are growing increasingly popular as a treatment for IBS. Currently, the low FODMAP diet is the most evidence-based diet intervention for IBS patients. Randomized controlled trials (RCT) report that 50% to 80% of patients with IBS experience significant clinical improvement with the low FODMAP diet.
FODMAPs are short chain carbohydrates that are difficult or impossible for the human small intestine to digest or absorb. Because they are not absorbed, they are available for fermentation by the microbiota in the distal small bowel and colon producing short chain fatty acids and gases that can trigger symptoms in IBS patients who have underlying abnormalities in motility and visceral sensation.
In patients with intestinal brush border lactase deficiency, lactose cannot be digested and thus cannot be absorbed. Thus, in patients with lactase deficiency, lactose becomes a FODMAP. On the other hand, in patients with normal levels of intestinal lactase, lactose can be digested and the resultant monosaccharides, glucose and galactose are normally absorbed. The other main intestinal disaccharidase in the intestinal brush border epithelium is sucrase isomaltase (SI). SI is responsible for the digestion of sucrose to glucose and fructose and starch to glucose monomers. A number of SI gene variants associated with decreased SI function have been found to be more prevalent in patients with IBS. In patients with SI deficiency, sucrose and starch become FODMAPs. This is potentially important as current teaching of the LFD does not account for patients with SI deficiency.
The study from the University of Michigan by Eswaran et al, found that the presence of mutations in the SI gene were associated with a lower likelihood of clinical response to the low FODMAP diet in patients with IBS-D. This provocative, post-hoc analysis requires validation in a larger, prospective trial. If confirmed, it may be useful to test for SI deficiency either before initiating the low FODMAP diet or in patients who fail to respond to the low FODMAP diet.
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Garcia-Etxebarria K, et al. Clin Gastroenterol Hepatol. 2018;16:1673-1676.
Zheng T, et al. Gut. 2019; in press.
William D. Chey, MD
Professor of medicine
Director of the GI Physiology Laboratory
University of Michigan Health System
Disclosures: Chey reports financial ties to Allergan, Conti, IM Health, Ironwood, MyGiHealth, Nestle, QOL Medical, Ritter, Salix, Shire, True Self Foods, Volcant and Zespori.