World Digestive Health Day WDHD – May 29, 2016 THE GUT RESPONSE TO FOOD; A PHYSIOLOGICAL PERSPECTIVE ON FOOD-INDUCED GASTROINTESTINAL SYMPTOMS, continued delayed gastric emptying and small bowel transit in an attempt to halt caloric losses: the so-called ileal brake.22 ROLE OF NEUROMODULATORS AND NEUROTRANSMITTERS Serotonin is a neurotransmitter and paracrine signaling molecule and is secreted primarily from enterochromaffin (EC) cells, which accounts for approximately 80% of total body serotonin secretion. Increased enterochromaffin (EC) cells, elevated postprandial serotonin levels and decreased serotonin reuptake due to decreased affinity for the reuptake transporter protein have been reported in different IBS subtypes; the former being observed in post-infectious IBS and the latter two in IBS-D.23- 25Serotonin stimulates receptors responsible for peristalsis and secretion in the GI tract, and acts to promote communication along the got and on the gut-brain axis. The post-prandial diarrhea and urgency commonly reported by sufferers with IBS-D may be due to an exaggerated serotonin response leading to increased peristalsis and secretions.23 FOOD-MICROBIOTA INTERACTIONS The gut microbiota plays a pivotal role in gut homeostasis in health and in the pathogenesis of a number of intestinal and extra-intestinal diseases. It includes a diverse population of approximately 1014 bacterial cells; 10 times more than that total number of human cells. The functions of the gut microbiota include the protection of the host from enteric pathogens, the development of the host immune system, participation in host metabolism and contributing to nutrition. Our diet has a major impact on the composition of the microbiota and differences in dietary patterns are a major determinant of interindividual variations in microbiota diversity. For an excellent overview of many aspects of the gut microbiota, please refer to the 2014 World Digestive Health Day publication “WGO Handbook on Gut Microbes”, which can be downloaded for free at: http://www.worldgastroenterology.org/UserFiles/file/ WDHD-2014-handbook-FINAL.pdf. Interactions between components of the diet and/or the products of digestion could play a role in the genesis of food related symptoms and changes in diet or microbiota could exacerbate or alleviate such symptoms. As a by-product of bacterial fermentation is liberation of gases (e.g. nitrogen, hydrogen, carbon dioxide and methane) an increase in the numbers of gas-producing organisms (e.g. E. coli, Veillonella species) may cause flatulence and bloating.26 Flatulence could occur as a consequence of a reduction in methanogenic bacteria, (Methanobrevibacter smithii and certain Clostridium and Bacteroides species) which convert hydrogen produced by other intestinal bacteria to methane and greatly reduce gas production.27,28 In contrast, excess methane production has been linked to constipation.27 The arrival of undigested carbohydrates into the colon will provide more substrate for fermentation, as well as acting as a prebiotic. Local changes in gas production, in conjunction with enhanced sensitivity to gas distension may contribute to bloating, a remarkably prevalent post-prandial symptom in a number of functional gastrointestinal disorders. Bacterial metabolism of carbohydrates also produce short chain fatty acids which stimulate colonic and ileo-colonic motility and secretion29,30 and could cause diarrhea; stool volume and consistency will also be influenced by the extent of bacterial deconjugation of bile acids. CONCLUSION Many are the physiological interactions between the act eating and gut function; interactions that can be accentuated in a variety of diseases and disorders and that could account for postprandial symptomatology without having to invoke food intolerance or allergy. REFERENCES 1. Grenham S, Clarke G, Cryan JF, Dinan TG. Brain-gut-microbe communication in health and disease. Front Physiol. 2011;2:94. 2. Cryan JF, O’Mahony SM. The microbiome-gut-brain axis: from bowel to behavior. Neurogastroenterol Motil. 2011;23:187-192. 3. Fichna J, Storr MA. Brain-Gut Interactions in IBS. Front Pharmacol. 2012;3:127. 4. Snape WJ Jr, Carlson GM, Matarazzo SA, Cohen S. Evidence that abnormal myoelectrical activity produces colonic motor dysfunction in the irritable bowel syndrome. Gastroenterology. 1977;72:383-7. 5. Simren M, Abrahamsson H, Bjornsson ES. An exaggerated sensory component of the gastrocolonic response in patients with irritable bowel syndrome. Gut 2001;48:20–27. 6. McKee DP, Quigley EMM. Intestinal motility and the irritable bowel syndrome - Is IBS a motility disorder? Part 1. Definition of IBS and colonic motility. Dig Dis Sci 1993;38:1761- 1772. 58 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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