World Digestive Health Day WDHD – May 29, 2016 DAVID S. SANDERS, MD Academic Unit of Gastroenterology Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Foundation Trust Sheffield, South Yorkshire, UK WHAT IS THE ROLE OF FOOD IN IBS? PETER GIBSON, MD Alfred Hospital Dept. of Gastroenterology Melbourne, VIC, Australia Irritable bowel syndrome (IBS) is common, with a pooled global prevalence of 11.2%.1 The etiology of IBS is not entirely clear, but 40% to 84% of IBS patients believe that food-items are important triggers of their gastrointestinal symptoms. Carbohydrates are reported as a source of symptoms in 70% and gluten-based products cited as an offending culprit by roughly one-in-four.2 Furthermore, IBS patients who report adverse food reactions tend to have more severe symptoms, associated subjective health complaints of musculoskeletal pains and chronic fatigue, and reduced quality of life.2,3,4 Most recent work has focused on wheat, gluten, and FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols). Carbohydrate malabsorption (e.g. lactose malabsorption), by virtue of its resultant distension of the intestine with increased water content and gas from bacterial fermentation, has long been documented to cause IBS-like symptoms and restriction of perceived culprits has been an adjunct to standard therapy. Restricting all slowly-absorbed and indigestible short-chain carbohydrates (a low FODMAP diet) has randomized controlled evidence from multiple centers across many countries of efficacy in patients with IBS. It benefits up to three of four patients with IBS and is proposed as a primary therapy for IBS. Most patients who benefit can de-restrict the diet and maintain the benefits. More controversial has been the role of gluten in IBS; and the entity of non-celiac gluten sensitivity (NCGS) is now accepted by consensus. Unfortunately, the study of its epidemiology, pathophysiology, and characteristics has been hindered by the lack of objective diagnostic criteria and reliance upon self-report of improvement with a gluten-free diet and exacerbation by subsequent ingestion of wheat. Furthermore, what component(s) of wheat that is/are driving symptoms in any individual is difficult to define. The population prevalence of NCGS when self-reported ranges from 0.6% to 13%.5 The pathophysiology of NCGS may involve an innate immune responses being driven by gluten or non-gluten wheat-associated proteins, such as alpha-amylase trypsin inhibitors, or the FODMAPs, which co-exist with gluten in cereals.5 Some may have celiac disease that has yet to fulfill all diagnostic criteria. Definitive demonstration of gluten/wheat-protein sensitivity is by randomized, placebo-controlled, double blind cross-over studies using FODMAP-depleted gluten. Three prospective studies have been reported in patients with self-reported NCGS, with the consistent finding of less than 5% of such patients having specific responses to gluten. A major hurdle has been strong nocebo effects in these studies. Results of double-blind placebo-controlled challenges in 920 adults with self-reported wheat sensitivity but not celiac disease or wheat allergy found minimal nocebo response in general and were able to detect 30% with positive wheat reactions, although the majority of these also reacted to other foods, particularly milk protein.6 Nearly all of the patients had evidence of immune activation in the intestine and/or colon, particularly increased density of intraepithelial lymphocytes and eosinophilic infiltration. This contrasted with patients in the randomized controlled trials (RCTs) where such patients were mostly excluded. Interestingly, when patients with apparent NCGS were re-challenged with gluten or placebo in parallel-group studies, significant differences were observed with greater symptom severity in the gluten-treated group. Hence, gluten-containing cereal sensitivity is likely to represent one or more entity in individual patients – previously undiagnosed celiac disease, FODMAP sensitivity, gluten or other wheat protein sensitivity, multiple food protein sensitivity, or none. Defining the specificities in an individual is largely done by judicious clinical evaluation including assessment of duodenal histology, and ‘n-of-one’ dietary re-challenge studies with the ultimate aim of gaining the greatest symptomatic benefit with the least dietary restriction and of achieving sustained benefits. 18 WGO Handbook on DIET AND THE GUT World Digestive Health Day WDHD May 29, 2016
WGO Handbook on Diet and the Gut_2016_Final
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