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Healthcare professional Resource for Gluten Related Disorders.

Dr. Schär Institute

FODMAPs: is the evidence stacking up?

Dr. Schär Institute low-FODMAP-diet Gluten intolerance Gluten-free diet
A diet low in short-chain fermentable carbohydrates (FODMAPs) is fast becoming an accepted dietary treatment for irritable bowel syndrome (IBS) and other functional bowel disorders due to its powerful effect on reducing gastrointestinal symptoms. [1]
The concept that certain individual carbohydrates, e.g. lactose, fructose and sorbitol induce IBS-like symptoms in susceptible individuals is not new, however grouping shortchain fermentable carbohydrates together and reducing their overall dietary intake is novel. [2] The low FODMAP diet originated in Australia and was successfully introduced to the UK five years ago.

What are FODMAPs and where do they occur?

The term FODMAP is an acronym for fermentable oligisaccharides, disaccharides, monosacharides and polyols. Oligosaccharides include fructans and galacto-oligosaccharides which are chains of varying length of either fructose or galactose units, respectively, with a glucose terminal end. Fructans include inulin (DP 2-60), oligofructose (DP 2-8) and fructo-oligosaccharides (DP <10) [3] and dietary sources include wheat, onion and garlic. Galacto-oligosaccharides include raffinose and stachyose and typical dietary sources are beans and legumes. Oligosaccharide absorption in the gastrointestinal tract is very limited (less than 5%) due to humans lacking the enzymes that are able to break down the glycosidic bonds. [4,5]

Lactose is a disaccharide that is hydrolysed in the jejunum by a ß-galactosidase enzyme called lactase. Lactase expression is at its peak just after birth, however it starts to decline after the first few months of life in up to 70% of humans. In some susceptible individuals, a dose of greater than 4 g of lactose can be malabsorbed and lead to IBS-like symptoms. [6]

Lactose naturally occurs in mammalian milk and is often added to manufactured foods to improve taste and texture and to pharmaceutical agents as a bulking agent.

The monosaccharide fructose is absorbed across the intestinal membrane by facultative transport pathways, two of which are reasonably well understood. The first transporter is GLUT5, which is specific to fructose but there is a limit to the absorption capacity. The second is a hexose transporter called GLUT2 which co-transports glucose and fructose. [7] An equal amount of fructose and glucose is optimal for fructose absorption, however, fructose malabsorption is not uncommon and is observed in 30-60% of people. [8] Fructose is found naturally in fruit and honey and fructose ingredients are increasingly used in the food industry to enhance taste and texture in food products.

Polyols are sugar alcohols (e.g. sorbitol, mannitol, xylitol) and are passively absorbed along the small intestine at a variable rate depending on their molecular size, the intestinal pore size, organic disease and small intestinal transit time. [1] Malabsorption of a 10g dose of sorbitol has been reported in 60-70% of people. [9]

Lactose, fructose and polyols have the potential to become FODMAPs when they are malabsorbed.

Mechanisms of symptom generation

There are two well described mechanisms that FODMAPs exert in the gastrointestinal tract that can lead to IBS-like symptoms in susceptible individuals.

Osmotic activity
Malabsorption of short-chain carbohydrates renders them as osmotically active in the gastrointestinal lumen. In patients with an ileostomy, a high FODMAP diet produced approximately 20% more total ileal effluent, water and dry weight when compared to a low FODMAP diet. [10] Furthermore, in healthy subjects, mannitol or fructose lead to a ten-fold increased small intestinal water content on magnetic resonance imaging (MRI) when compared with glucose or a combination of equal quantities of glucose and fructose. [11,12] An increase in small intestinal water content may lead to luminal distension, abdominal pain, borborygmi and eventual diarrhea in susceptible individuals.

Colonic fermentation
When FODMAPs reach the colon they are readily fermented by the colonic microbiota producing gas e.g. hydrogen. In patients with visceral hypersensitivity, increased gas production can lead to symptoms of abdominal distension and abdominal pain. Hydrogen breath tests are useful to measure colonic gas production following specific carbohydrate doses. Several studies have indeed reported increased hydrogen production in healthy volunteers and patients with IBS following consumption of individual or combinations of FODMAPs. [12,13] Furthermore, patients with IBS reported increased gastrointestinal symptoms on a high FODMAP diet. [13]
Dr. Schär Institute low-FODMAP-diet Gluten intolerance Fructose transport

Clinical evidence

Despite all this high quality data, does the low FODMAP diet improve symptoms of IBS in clinical practice? The evidence base for uncontrolled and more recently controlled studies on the efficacy of the low FODMAP diet is increasing. A retrospective assessment of patients with fructose malabsorption who had adhered to a low FODMAP diet showed that 85% had improvement for all IBS symptoms. [14] This study was followed by a FODMAP challenge cross-over feeding study by the same group. Patients who had previously had success with the low FODMAP diet were challenged with increasing doses of fructose and/or fructans and glucose as a control while following a low FODMAP diet where the majority of food was provided for the duration of the study. Symptoms were assessed during each challenge and showed that fructose and/or fructans significantly induced overall and individual (bloating, abdominal pain and flatulence) IBS symptoms. In addition this study demonstrated a dose response to fructose and/or fructans with increasing symptoms at higher doses. [15]

A non-randomised controlled trial compared IBS symptoms at follow-up in patients who had been treated with a low FODMAP diet or as the control, standard dietary advice based on the NICE guidelines (National Institute for Health and Care Excellence). [16] This study demonstrated that 76% of patients who had been given low FODMAP advice had an improvement in overall symptoms compared to 54% in the standard dietary advice group. [17]

However, major limitations of this study were that it was not randomised and only recorded symptoms at follow-up.

Three randomised controlled trials (RCTs) assessing a low FODMAP diet in IBS have been completed. The first was a cross-over feeding study comparing 4 days of a low and a high FODMAP diet. This study showed that symptoms were much lower on the low FODMAP diet. [13] The next RCT, another feeding study, had a cross-over design and showed that overall symptoms, abdominal pain, bloating and flatulence were all significantly lower after 3 weeks of a low FODMAP diet when compared to a high FODMAP diet. [18] The problem with feeding studies is that they do not reflect normal every day challenges faced when choosing food on a restrictive diet. The last RCT to date compared 4 weeks of a low FODMAP diet with a habitual diet. Both groups received dietary advice from a specialist dietitian and showed that symptoms were adequately controlled in 68% of patients following the low FODMAP diet compared to only 23% in the control group. [19]


A low FODMAP diet restricts a wide variety of foods from some starchy cereal grains, fruit and vegetables, milk and milk products and processed foods containing any high FODMAP ingredients. Alternative foods are a key component of patient education and even under strict advice from a dietitian, it has been shown that nutrient intakes, calcium in particular, can be compromised on a low FODMAP diet. [19] Diet has a dramatic effect on the composition of the gastrointestinal microbiota and patients with IBS have been reported to have dysbiosis. The prebiotic effects of some carbohydrates (e.g. fructo-oligosaccharides and galacto-oligosaccharides) is well established, so reducing their intake as part of a low FODMAP diet is of potential concern. Indeed, a significant decrease in the concentration of luminal bifidobacteria after 4 weeks of a low FODMAP diet has been observed. [19] However, whether this reduction is problematic in the short or long term is currently unknown but warrants further investigation.

Clinical practice

The evidence clearly supports using a low FODMAP diet in clinical practice, however, research only supports its use as a dietitian led intervention. Dietitians need to have the expertise in the low FODMAP approach to be able to effectively educate patients and use appropriate outcomes to measure symptom response. [20] Furthermore, strict FODMAP restriction is advised only over a short period of up to 8 weeks, following which, FODMAP reintroduction to individual tolerance in relation to gastrointestinal symptoms is recommended to increase dietary variety, ensure nutritional adequacy and have as minimal impact on the gastrointestinal microbiota.
  • Senior Consultant Dietitian, Guy’s and St Thomas’ NHS Foundation Trust und Honorary Senior Lecturer, King’s College London
Miranda Lomer is a Consultant Dietitian with over 20 years of experience in gastroenterology. She has published widely in the dietary management of functional gastrointestinal disorders and inflammatory bowel diseases. She has led the successful development and implementation of a patient pathway and a dietetic training programme for FODMAP education in the UK.
  1. Staudacher H. M., Irving P. M., Lomer M. C., Whelan K. Mechanisms and efficacy of dietary FODMAP restriction in IBS. Nature Gastro Hep. 2014 [Epub ahead of print]
  2. Shepherd S. J., Lomer M. C., Gibson P. R. Short-chain carbohydrates and functional gastrointestinal disorders. Am J Gastroenterol 2013;108(5):707–717
  3. Roberfroid M. B. Inulin-type fructans: functional food ingredients. J. Nutr. 2007:137 (Suppl. 11), 2493S–2502S
  4. Bach Knudsen K. E., Hessov I. Recovery of inulin from Jerusalem artichoke (Helianthus tuberosus L.) in the small intestine of man. Br. J. Nutr. 1995:74, 101–113
  5. Macfarlane G. T., Steed H., Macfarlane S. Bacterial metabolism and health-related effects of galacto-oligosaccharides and other prebiotics. J. Appl. Microbiol. 2008:104, 305–344
  6. Lomer M. C. E., Parkes G. C., Sanderson J. D. Lactose intolerance in clinical practice: myths and realities Aliment Pharmacol Ther 2008: 27; 93–103
  7. Jones H. F., Butler R. N., Brooks D. A. Intestinal fructose transport and malabsorption in humans. Am. J. Physiol. Gastrointest. Liver Physiol. 2011:300, G202–G206
  8. Rumessen J. J., Gudmandhoyer E. Absorption capacity of fructose in healthy-adults – comparison with sucrose and its constituent monosaccharides. Gut 1986:27, 1161–1168
  9. Yao C. K., Tan H. L., van Langenberg D. R., Barrett J. S., Rose R., Liels K., Gibson P. R., Muir J. G. Dietary sorbitol and mannitol: food content and distinct absorption patterns between healthy individuals and patients with irritable bowel syndrome. J. Hum. Nutr. Diet 2013 [Epub ahead of print]
  10. Barrett J. S., Gearry R. B., Muir J. G., Irving P. M., Rose R., Rosella O., Haines M. L., Shepherd S. J., Gibson P. R. Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon. Aliment. Pharmacol. Ther. 2010:31, 874–882
  11. Marciani L., Cox E. F., Hoad C. L., Pritchard S., Totman J. J., Foley S., Mistry A., Evans S., Gowland P. A., Spiller R. C. Postprandial changes in small bowel water content in healthy subjects and patients with irritable bowel syndrome. Gastroenterology 2010:138, 469–477.e1
  12. Murray K., Wilkinson-Smith V., Hoad C., Costigan C., Cox E., Lam C., Marciani L., Gowland P., Spiller R. C. Differential effects of FODMAPs (fermentable oligo, di, mono-saccharides and polyols) on small and large intestinal contents in healthy subjects shown by MRI. Am. J. Gastroenterol. 2013 [Epub ahead of print]
  13. Ong D. K., Mitchell S. B., Barrett J. S., Shepherd S. J., Irving P. M., Biesiekierski J. R., Smith S., Gibson P. R., Muir J. G. Manipulation of dietary short chain carbo-hydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. J. Gastroenterol. Hepatol. 2010:25, 1366–1373
  14. Shepherd S. J., Gibson P. R. Fructose malabsorption and symptoms of irritable bowel syndrome: guidelines for effective dietary management. J. Am. Diet Assoc. 2006:106, 1631–1639
  15. Shepherd S. J., Parker F. C., Muir J. G., Gibson P. R. Dietary triggers of abdominal symptoms in patients with irritable bowel syndrome: randomized placebo-controlled evidence. Clin. Gastroenterol. Hepatol. 2008:6, 765–771
  16. National Institute for Health and Care Excellence Guideline Development Group. Irritable bowel syndrome in adults: Diagnosis and management of irritable bowel syndrome in primary care London: NICE, 2008. [accessed 11/03/2014]
  17. Staudacher H. M., Whelan K., Irving P., Lomer M. C. Comparison of symptom response following advice for a diet low in fermentable carbohydrates (FODMAPs) versus standard dietary advice in patients with irritable bowel syndrome. J Hum Nutr Diet 2011:24(5);487–495
  18. Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG. A diet low in FODMAPs reduces symptoms of irritable bowel syndrome. Gastroenterology Sept 2013 [Epub ahead of print]
  19. Staudacher H. M., Lomer M. C., Anderson J. L., Barrett J. S., Muir J. G., Irving P. M., Whelan K. Fermentable carbohydrate restriction impacts on luminal bifidobacteria and gastrointestinal symptoms in a randomized controlled trial of patients with irritable bowel syndrome. J Nutr 2012:142(8);1510–1518
  20. McKenzie Y., Alder A., Anderson W., Brian A., Goddard L., Jankovich E., Mutch P., Reeves L., Singer A., Lomer M. C. E. British Dietetic Association evidence-based practice guidelines for the dietetic management of irritable bowel syndrome (IBS) in adults. J Hum Nutr Diet. 2012:25(3);260–274