Abstract
Irritable bowel syndrome (IBS) is a debilitating, complex, chronic disorder with a multifactorial etiopathogenesis, pathophysiology and clinical phenotype. IBS is the most common disorder of gut-brain interaction (DGBI), with a prevalence ranging from 7% to 23% globally. The burden of IBS on patients is considerable in terms of reduced quality of life. Furthermore, the costs to healthcare systems and society are substantial as IBS accounts for billions of dollars in direct and indirect medical costs. Common symptoms of IBS are bloating, reoccurring episodes of abdominal pain, excessive flatus, constipation, diarrhea or alternating bowel habits. Many IBS patients have associated ingestion of specific foods with GI symptoms onset or exacerbation and have therefore, attempted dietary therapy for the treatment and control of their GI symptoms. The low fermentable oligo-, di-, mono-saccharides, and polyols (FODMAP) diet is currently the most evidence-based and internationally accepted viable first-line dietary therapy for IBS. FODMAPs are short-chain carbohydrates that are poorly or incompletely absorbed in the small intestine and subsequently fermented by the colonic microbiota, leading to the production of gases, such as hydrogen, carbon dioxide, and methane. There is a recognized need to elucidate how FODMAPs induce GI symptoms and to understand how the 3-phase (restriction, re-introduction and personalization) FODMAP diet works. Hence, the objective of this review article is to elucidate the pathophysiological central and peripheral gutrelated mechanisms through which FODMAPs cause GI- symptoms, to expound the implementation of the FODMAP diet and to highlight and confute concerns around the safety and risks of the FODMAP diet long-term.
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