Diet in the pathophysiology and management of irritable bowel syndrome

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Diet plays an important role in the pathophysiology of irritable bowel syndrome (IBS) and is an effective tool in managing this disorder. This includes a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs).

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These indigestible and poorly absorbed short-chain carbohydrates trigger IBS symptoms and are thought to exert their effects by increasing osmotic pressure in the lumen of the intestine and by providing a substrate for bacterial fermentation with consequent gas production. 1 The gas causes abdominal distention, and the change in pressure in the lumen of the large intestine affects the release of serotonin, causing abdominal pain and discomfort.


Recent studies have shown that the mechanisms by which FODMAPs exert their effects are more complicated than originally thought. 1

All segments of the gastrointestinal tract contain endocrine cells scattered between the mucosal epithelial cells facing the intestinal lumen. 1,2 There are at least 10 types of endocrine cell, and they regulate gastrointestinal motility, secretion, absorption, visceral sensitivity, local immune defense, cell proliferation, and appetite. 2–4 Abnormal densities of gastrointestinal endocrine cells have been reported in patients with IBS, which may explain the dysmotility, visceral hypersensitivity, and abnormal intestinal secretion seen in these patients. 5

But other factors such as diet, intestinal microbiota, genetics, and low-grade inflammation also play pivotal roles in the pathophysiology of IBS by exerting effects on gastrointestinal endocrine cells. The abnormalities in the gastrointestinal endocrine cells in IBS are thought to be brought about by aberrant differentiation of stem cells into endocrine cells ( Figure 1 ).6

A diet low in FODMAPs appears to induce changes in the intestinal microbiota and gastrointestinal endocrine cells and to reduce IBS symptoms. 6

Figure 1. Symptoms of irritable bowel syndrome are believed to be triggered by the consumption of a diet rich in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) via mechanisms involving the intestinal endocrine cells. FODMAPs act as prebiotics, providing a substrate selecting unfavorable bacteria, resulting in the fermentation of FODMAPs. The by-products of the interaction between FODMAPs and intestinal microbiota act on intestinal stem cells, resulting in abnormal clonogenic activity and differentiation progeny. Abnormal stem cell activity leads to an altered density of endocrine cells, causing gastrointestinal dysmotility, visceral hypersensitivity, and abnormal intestinal secretion.


Another dietary factor in IBS is gluten. Symptoms of IBS and celiac disease overlap: most studies have found that fewer than 5% of patients with celiac disease are misdiagnosed as having IBS based on the symptom criteria for IBS, but some studies report a rate as high as 32%. 7 In addition, 38% of patients with celiac disease who consume a gluten-free diet fulfill the symptom-based Rome criteria for IBS. 7

The contribution of gluten to IBS does not end with the coexistence of IBS and celiac disease, but also includes the newly debated diagnosis of nonceliac gluten sensitivity, characterized by gastrointestinal symptoms (abdominal pain, diarrhea, constipation, nausea, and vomiting) and other symptoms (headache, musculoskeletal pain, “brain fog,” fatigue, and depression) that are similar to those of IBS. Symptoms are triggered by the ingestion of wheat products, are improved after wheat products are removed from the diet, and relapse after a wheat challenge. 7

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