Evidence-based Dietary Management of Functional Gastrointestinal Symptoms: The FODMAP Approach

Peter R Gibson; Susan J Shepherd


J Gastroenterol Hepatol. 2010;25(2):252-258. 

In This Article


The acronym, 'FODMAP'—Fermentable Oligo-, Di- and Mono-saccharides and Polyols—was coined to describe a previously-unrelated group of short-chain carbohydrates and sugar alcohols (polyols).[4] They comprise fructose, lactose, fructo- and galacto-oligosaccharides (fructans, and galactans), and polyols (such as sorbitol, mannitol, xylitol and maltitol) all of which putatively have three common functional properties:

  • Poorly absorbed in the small intestine: Poor absorption occurs by virtue of slow, low-capacity transport mechanisms across the epithelium (fructose), reduced activity of brush border hydrolases (lactose), lack of hydrolases (fructans, galactans), or molecules being too large for simple diffusion (polyols).

  • Small and therefore osmotically-active molecules: This effect has been demonstrated with, for example, a synthetic FODMAP, lactulose, which exerts a laxative effect when given in sufficient dose by increasing the liquidity of luminal contents and subsequently affecting gut motility.[5]

  • Rapidly fermented by bacteria: The rapidity of fermentation by bacteria is dictated by the chain length of the carbohydrate; oligosaccharides and sugars are very rapidly fermented compared with polysaccharides such as soluble dietary fibre.[6]

These functional properties have recently been confirmed in studies in which diets high and low in FODMAPs (rather than pure individual FODMAPs) have been fed to volunteers. In a study of 10 ileostomates, changes in dry-weight ileostomy effluent could be explained entirely on the basis of dietary FODMAPs and the effluent volume increased by a mean of 22% on the high FODMAP diet.[7] Fermentation of FODMAPs in the small intestine was suggested by the recovery of only 34% of FODMAPs consumed in the ileostomy effluent, although some fermentation in the ileostomy bag ex vivo also would have contributed. When the diets were fed to healthy volunteers, breath hydrogen production, a marker of gas production in the intestine, was markedly elevated throughout the day.[8] Furthermore, in methane-producers, high FODMAP intake favored production of hydrogen over methane, which occupies a smaller volume per hydrogen molecule generated. Thus, all the putative functional properties have been confirmed to occur in vivo in association with dietary intake of FODMAPs.

There is considerable evidence that individual FODMAPs induce abdominal symptoms. Acute provocation tests with lactose,[9] fructose[9–11] fructo-oligosaccharides (FOS)[12,13] or sorbitol[9,14–17] cause abdominal symptoms such as bloating, pain, nausea and disturbed bowel habit (diarrhea and/or constipation) in many people, especially those with IBS.[15] The role of lactose and polyols in the induction of gut symptoms has been well-described in clinical practice; the dietary regimen for the management of lactose malabsorption has been comprehensively addressed[18] and mandatory declaration of 'excess consumption may have a laxative effect' is in place for food products containing polyols. Increased flatulence and change of bowel habits after consuming 'windy vegetables', such as lentils and baked beans, are common knowledge although identification of galactans, in addition to resistant starch, as the culprit molecules may not be. Additive effects fructose and sorbitol[10,19,20] and lactose and fructans[21] on abdominal symptoms are also well-described.


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