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. 2014 Mar;10(3):164-74.

Irritable bowel syndrome: the role of food in pathogenesis and management

Paula A Hayes  1 , Marianne H Fraher  1 , Eamonn M M Quigley  1
Affiliations

Irritable bowel syndrome: the role of food in pathogenesis and management

Paula A Hayes et al. Gastroenterol Hepatol (N Y). 2014 Mar.

Abstract

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder that affects approximately 10% to 20% of the general adult population in Europe and the Americas and is characterized by abdominal pain and altered bowel habits in the absence of reliable biomarkers. The pathophysiology of IBS is poorly understood and is currently thought to represent a complex interplay among the gut microbiota, low-grade inflammation, impaired mucosal barrier function, visceral hypersensitivity, gut motility, and alterations in the gut-brain axis. In any individual patient, 1 or more of these factors may interact to generate symptoms. Although up to 50% of patients report postprandial exacerbation of symptoms, few studies have critically assessed the role of diet in IBS. Furthermore, although many patients with IBS adopt any one of a host of dietary changes in an attempt to alleviate their symptoms, there has been, up until recently little scientific basis for any dietary recommendation in IBS. This review discusses the contribution of diet to the pathophysiology and symptoms of IBS.

Keywords: FODMAPs; Irritable bowel syndrome; diet; food allergy; food intolerance; gluten; gut hormones.

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Figures

Figure
Figure
Potential interactions between diet and the host in irritable bowel syndrome. Input from the central nervous system, mediated by the autonomic nerves (and/or hormonally), may influence gut function and lead to an exaggerated response to food ingestion. Stress may exaggerate these effects, which may be further exacerbated by gut hypersensitivity. Food allergens may generate immune/inflammatory responses. Several food components or their metabolites may directly or indirectly impact symptoms. Interactions between the commensal microbiota and food may lead to the generation of short-chain fatty acids, bile acids, and gases that cause symptoms. Changes in the microbiota, whether gross with the introduction of pathogens or more subtle, will lead to inflammatory responses or immune activation in the gut wall and trigger sensory, motor, and secretory responses. FODMAPs, fermentable oligo-, di-, and monosaccharides and polyols.
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