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FODMAP

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FODMAPs are short chain carbohydrates that are poorly absorbed in the small intestine. They include short chain oligo-saccharide polymers of fructose (fructans) and galactooligosaccharides (GOS, stachyose, raffinose), disaccharides (lactose), monosaccharides (fructose), and sugar alcohols (polyols), such as sorbitol, mannitol, xylitol and maltitol.[1][2][3]

The term FODMAP is an acronym, derived from "Fermentable, Oligo-, Di-, Mono-saccharides And Polyols".[1] Although FODMAPs are naturally present in food and the human diet, FODMAP restriction has been found to improve symptom control in people with irritable bowel syndrome (IBS) and other functional gastrointestinal disorders (FGID).[4][5][6][7][8][9] Prior to the formation of the FODMAP concept, diet was seldom used as first line therapy for management of IBS and other FGID.

History

Over many years, there have been multiple observations that ingestion of certain short-chain carbohydrates, including lactose, fructose and sorbitol, fructans and galactooligosaccharides, induced IBS-like symptoms.[10][11][12][13][14][15][16][17][18][19] These studies also showed that dietary restriction of short-chain carbohydrates was associated with symptom improvement in some people with IBS.[8][9][10][11][12][13][14][15][16][17][18][19]

These short-chain carbohydrates (lactose, fructose and sorbitol, fructans and GOS) behave similarly in the intestine. Firstly, being small molecules and either poorly absorbed or not absorbed at all, they drag water into the intestine via osmosis.[15][20] Secondly, these molecules are readily fermented by colonic bacteria, so upon malabsorption in the small intestine they enter the large intestine where they generate gases (hydrogen, carbon dioxide and methane).[5] The dual actions of these carbohydrates cause an expansion in volume of intestinal contents, which stretches the intestinal wall and stimulates nerves in the gut. It is this 'stretching' that triggers the sensations of pain and discomfort that are commonly experienced by IBS sufferers.[3][5][7]

The FODMAP concept was first published in 2005 as part of a hypothesis paper.[1] In this paper, it was proposed that a collective reduction in the dietary intake of all indigestible or slowly absorbed, short-chain carbohydrates would minimise stretching of the intestinal wall. This was proposed to reduce stimulation of the gut's nervous system and provide the best chance of reducing symptom generation in people with IBS (see below). At the time, there was no collective term for indigestible or slowly absorbed, short-chain carbohydrates, so the term 'FODMAP' was created to improve understanding and facilitate communication of the concept.[1]

The low FODMAP diet was originally developed by a research team at Monash University in Melbourne, Australia.[21] The Monash team undertook the first research to investigate whether a low FODMAP diet improved symptom control in patients with IBS and established the mechanism by which the diet exerted its effect.[3][5][22] Monash University also established a rigorous food analysis program to measure the FODMAP content of a wide selection of Australian and international foods.[23][24][25] The FODMAP composition data generated by Monash University updated previous data that was based on limited literature, with guesses (sometimes wrong) made where there was little information.[26]

As a result of this program of research and FODMAP food analysis, a comprehensive and accurate database now exists describing the FODMAP content of food;[23][24][25] scientists now understand the mechanism by which the diet works[20][22] and there is sound evidence indicating that a low FODMAP diet improves symptom control in approximately three out of every four people with IBS and other FGIDs (such as simple bloating).[3][5][7][8][9][27][28][29][30]

FGID

The basis of many functional gastrointestinal disorders (FGIDs) is distension of the intestinal lumen. Such luminal distension may induce pain, a sensation of bloating, abdominal distension and motility disorders. Therapeutic approaches seek to reduce factors that lead to distension, particularly of the distal small and proximal large intestine. Food substances that can induce distension are those that are poorly absorbed in the proximal small intestine, osmotically active, and fermented by intestinal bacteria with hydrogen (as opposed to methane) production. The small molecule FODMAPs exhibit these characteristics.[4]

Absorption

Poor absorption of most FODMAP carbohydrates is common to everyone. Any FODMAPs that are not absorbed in the small intestine pass into the large intestine, where bacteria ferment them. The resultant production of gas potentially results in bloating and flatulence. Most individuals do not suffer significant symptoms but some may suffer the symptoms of IBS. Restriction of FODMAP intake in the latter group has been found to result in improvement of symptoms.

Fructose malabsorption and lactose intolerance may produce IBS symptoms through the same mechanism but, unlike with other FODMAPs, poor absorption is found only in a minority of people. Many who benefit from a low FODMAP diet need not restrict fructose or lactose. It is possible to identify these two conditions with hydrogen and methane breath testing and thus eliminate the necessity for dietary compliance if possible.[4]

Sources in the diet

The significance of sources of FODMAPs varies through differences in dietary groups such as geography, ethnicity and other factors.[4] Commonly used FODMAPs comprise the following:[31]

  • oligosaccharides, including fructans and galacto-oligosaccharides;
  • disaccharides, including lactose;
  • monosaccharides, including fructose;
  • polyols, including sorbitol, xylitol, and mannitol.

Fructans, galactans and polyols

Sources of fructans

Sources of fructans include wheat (although some wheat strains such as spelt contain lower amounts),[32] rye, barley, onion, garlic, Jerusalem and globe artichoke, asparagus, beetroot, chicory, dandelion leaves, leek, radicchio, the white part of spring onion, broccoli, brussels sprouts, cabbage, fennel and prebiotics such as fructooligosaccharides (FOS), oligofructose and inulin.[4][33]

Sources of galactans

Pulses and beans are the main dietary sources (though green beans, tofu and tempeh contain comparatively low amounts).[21][33]

Sources of polyols

Polyols are found naturally in some fruit (particularly stone fruits), including apples, apricots, avocados, blackberries, cherries, lychees, nectarines, peaches, pears, plums, prunes, watermelon and some vegetables, including cauliflower, mushrooms and mange-tout peas. They are also used as bulk sweeteners and include isomalt, maltitol, mannitol, sorbitol and xylitol.[4][33]

Fructose and lactose

People following a low-FODMAP diet may be able to tolerate moderate amounts of fructose and lactose, particularly if they have lactase persistence.

Sources of fructose

Main article: Fructose malabsorption § Foods with high fructose content

Sources of lactose

Main article: Lactose intolerance § Avoiding lactose-containing products

Low-FODMAP diet suggested foods

Below are low-FODMAP foods categorized by group according to the Monash University "Low FODMAP Diet".[21]

  • Vegetables: Alfalfa, bean sprouts, green beans, bok choy, capsicum (bell pepper), carrot, chives, fresh herbs, choy sum, cucumber, lettuce, tomato, zucchini (courgette)
  • Fruits: Banana, orange, mandarin, grapes, melon
  • Protein: Meats, fish, chicken, tofu, tempeh
  • Dairy: Lactose-free milk, lactose-free yoghurts, hard cheese
  • Breads and cereals: Gluten-free bread and sourdough spelt bread, rice bubbles, oats, gluten-free pasta, rice, quinoa
  • Biscuits (cookies) and snacks: Gluten-free biscuits, rice cakes, corn thins
  • Nuts and seeds: Almonds (<10 nuts), pumpkin seeds
  • Beverage options: water, coffee or tea

Other sources confirm the suitability of these and suggest some additional foods.[34]

Effectiveness and nutritional adequacy

Evidence from randomized trials indicates that a low FODMAP diet can help to treat irritable bowel syndrome in adults and in children.[6][35][36] A comprehensive systematic review and meta-analysis supports the efficacy of this diet in the treatment of functional gastrointestinal symptoms of IBS[37] although the evidence is less good for constipation.[38]

There is only a little evidence of effectiveness in treating functional symptoms in inflammatory bowel disease from small studies which are susceptible to bias.[39][40][41]

In common with other defined diets, the low FODMAP diet can be impractical to follow[41] and risks imposing an undue financial burden and worsening malnutrition.[42]

See also

References

  1. ^ a b c d Gibson, PR; Shepherd, SJ (2005). "Personal view: food for thought--western lifestyle and susceptibility to Crohn's disease. The FODMAP hypothesis". Aliment Pharmacol Ther. 21 (12): 1399–1409. doi:10.1111/j.1365-2036.2005.02506.x. PMID 15948806.
  2. ^ Dunlop, S; Hebden, J; Naesdal, J; et, al. (2006). "Abnormal intestinal permeability in subgroups of diarrhea-predominant irritable bowel syndromes". Am J Gastroenterol. 101 (6): 1288–94. doi:10.1111/j.1572-0241.2006.00672.x. PMID 16771951.
  3. ^ a b c d Tuck, CJ; Muir, JG; Barrett, JS; Gibson, PR (2014). "Fermentable oligosaccharides, disaccharides, monosaccharides and polyols: role in irritable bowel syndrome". Expert Rev Gastroenterol Hepatol. 8 (7): 819–834. doi:10.1586/17474124.2014.917956. PMID 24830318.
  4. ^ a b c d e f Peter R Gibson; Susan J Shepherd (2010). "Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach". Journal of Gastroenterology and Hepatology. 25 (2): 252–258. doi:10.1111/j.1440-1746.2009.06149.x. PMID 20136989. {{cite journal}}: Unknown parameter |last-author-amp= ignored (|name-list-style= suggested) (help)
  5. ^ a b c d e Ong, DK; Mitchell, SB; Barrett, JS; Shepherd, SJ; Irving, PM; Biesiekierski, JR; Smith, S; Gibson, PR; Muir, JG (2010). "Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. Journal of gastroenterology and hepatology". J Gastroenterol Hepatol. 25 (8): 1366–1373. doi:10.1111/j.1440-1746.2010.06370.x. PMID 20659225.
  6. ^ a b Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG (2014). "A diet low in FODMAPs reduces symptoms of irritable bowel syndrome". Gastroenterology. 146 (1): 67–75.e5. doi:10.1053/j.gastro.2013.09.046. PMID 24076059.
  7. ^ a b c Staudacher, HM; Whelan, K; Irving, PM; Lomer, MC (2011). "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. 24 (5): 487–495. doi:10.1111/j.1365-277X.2011.01162.x. PMID 21615553.
  8. ^ a b c Maagaard, L; Ankersen, DV; Végh, Z; Burisch, J; Jensen, L; Pedersen, N (2016). "Follow-up of patients with functional bowel symptoms treated with a low FODMAP diet". World Journal of Gastroenterology. 22 (15): 4009–19. doi:10.3748/wjg.v22.i15.4009.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  9. ^ a b c McIntosh, K; Reed, DE; Schneider, T; Dang, F; Keshteli, AH; De Palma, G (2016). "FODMAPs alter symptoms and the metabolome of patients with IBS: a randomised controlled trial". Gut. doi:10.1136/gutjnl-2015-311339. PMID 26976734.
  10. ^ a b Cann, PA; Read, NW; Brown, C; Hobson, N; Holdsworth, CD (1983). "Irritable bowel syndrome: relationship of disorders in the transit of a single solid meal to symptom patterns". Gut microbes. 24 (5): 405–11. doi:10.1136/gut.24.5.405. PMC 1419989. PMID 6840614.
  11. ^ a b Evans, PR; Piesse, C; Bak, YT; Kellow, JE (1998). "Fructose-sorbitol malabsorption and symptom provocation in irritable bowel syndrome: relationship to enteric hypersensitivity and dysmotility". Scand J Gastroent. 33: 1158–63. doi:10.1080/00365529850172502. PMID 9867093.
  12. ^ a b Dear, K; Elia, M; Hunter, J (2005). "Do Interventions Which Reduce Colonic Bacterial Fermentation Improve Symptoms of Irritable Bowel Syndrome?". Digestive diseases and sciences. 50 (4): 758–66. doi:10.1007/s10620-005-2570-4. PMID 15844715.
  13. ^ a b King, TS; Elia, M; Hunter, JO (1998). "Abnormal colonic fermentation in irritable bowel syndrome". The Lancet. 352: 1187–9. doi:10.1016/s0140-6736(98)02146-1. PMID 9777836.
  14. ^ a b Cummings, JH; Macfarlane, GT (2002). "Gastrointestinal effects of prebiotics". The British journal of nutrition. 87 Suppl 2: 145–51. doi:10.1079/BJNBJN/2002530. PMID 12088511.
  15. ^ a b c Marciani, L; Cox, EF; EF, CL; Pritchard, S; Totman, JJ; Foley, S (2010). "Postprandial changes in small bowel water content in healthy subjects and patients with irritable bowel syndrome". Gastroenterology. 138 (2): 469–77. doi:10.1053/j.gastro.2009.10.055. PMID 19909743.
  16. ^ a b Briet, F; Achour, L; Flourie, B; Beaugerie, L; Pellier, P; Franchisseur, C (1995). "Symptomatic response to varying levels of fructo-oligosaccharides consumed occasionally or regularly". European journal of clinical nutrition. 49 (7): 501–7. PMID 7588500.
  17. ^ a b Stone-Dorshow, T; Levitt, MD (1987). "Gaseous response to ingestion of a poorly absorbed fructo-oligosaccharide sweetener". The American Journal of Clinical Nutrition. 46 (1): 61–5. PMID 3604970.
  18. ^ a b Wagner, JR; Becker, R; Gumbmann, MR; Olson, AC (1976). "Hydrogen production in the rat following ingestion of raffinose, stachyose and oligosaccharide-free bean residue". The Journal of Nutrition. 106 (4): 466–70. PMID 1255266.
  19. ^ a b Clausen, MR; Jorgensen, J; Mortensen, PB (1998). "Comparison of diarrhea induced by ingestion of fructooligosaccharide idolax and disaccharide lactulose (role of osmolarity versus fermentation of malabsorbed carbohydrate)". Digestive diseases and sciences. 43: 2696–707. PMID 9881502.
  20. ^ a b Murray, K; Wilkinson-Smith, V; Hoad, C; Costigan, C; Cox, E; Lam, C; Marciani, L; Gowland, P; Spiller, RC (2014). "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. 109 (1): 110–119. doi:10.1038/ajg.2013.386. PMC 3887576. PMID 24247211.
  21. ^ a b c "The Monash University Low FODMAP diet". Monash University, Melbourne, Australia. 2012-12-18. Retrieved 2014-05-26.
  22. ^ a b Barrett, JS; Gearry, RB; Muir, JG; Irving, PM; Rose, R; Rosella, O; Haines, ML; Shepherd, SJ; Gibson, PR (2010). "Dietary poorly absorbed, short‐chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon". Aliment Pharmacol Ther. 31 (8): 874–882. doi:10.1111/j.1365-2036.2010.04237.x. PMID 20102355.
  23. ^ a b Muir, JG; Rose, R; Rosella, O; Liels, K; Barrett, JS; Shepherd, SJ; Gibson, PR (2009). "Measurement of short-chain carbohydrates in common Australian vegetables and fruits by high-performance liquid chromatography (HPLC)". J Agric Food Chem. 57 (2): 554–565. doi:10.1021/jf802700e. PMID 19123815.
  24. ^ a b Muir, JG; Shepherd, SJ; Rosella, O; Rose, R; Barrett, JS; Gibson, PR (2007). "Fructan and free fructose content of common Australian vegetables and fruit". J Agric Food Chem. 55 (16): 6619–6627. doi:10.1021/jf070623x. PMID 17625872.
  25. ^ a b Biesiekierski, JR; Rosella, O; Rose, R; Liels, K; Barrett, JS; Shepherd, SJ; Gibson, PR; Muir, JG (2011). "Quantification of fructans, galacto-oligosacharides and other short-chain carbohydrates in processed grains and cereals". J Hum Nutr Diet. 24 (2): 154–176. doi:10.1111/j.1365-277X.2010.01139.x. PMID 21332832.
  26. ^ Southgate, DA; Paul, AA; Dean, AC; Christie, AA (1978). "Free sugars in foods". J Hum Nutr. 32 (5): 335–347. doi:10.3109/09637487809143898. PMID 363937.
  27. ^ de Roest, RH; Dobbs, BR; Chapman, BA; Batman, B; O'Brien, LA; Leeper, JA; Hebblethwaite, CR; Gearry, RB (2013). "The low FODMAP diet improves gastrointestinal symptoms in patients with irritable bowel syndrome: a prospective study". Int J Clin Pract. 67 (9): 895–903. doi:10.1111/ijcp.12128. PMID 23701141.
  28. ^ Staudacher, HM; Lomer, MC; Anderson, JL; Barrett, JS; Muir, JG; Irving, PM; Whelan, K (2012). "Fermentable carbohydrate restriction reduces luminal bifidobacteria and gastrointestinal symptoms in patients with irritable bowel syndrome". J Nutr. 142 (8): 1510–1518. doi:10.3945/jn.112.159285. PMID 22739368.
  29. ^ Biesiekierski, JR; Peters, SL; Newnham, ED; Rosella, O; Muir, JG; Gibson, PR (2013). "No effects of gluten in patients with self-reported non-celiac gluten sensitivity following dietary reduction of low-fermentable, poorly-absorbed, short-chain carbohydrates". Gastroenterology. 145 (2): 320–328. doi:10.1053/j.gastro.2013.04.051. PMID 23648697.
  30. ^ Chumpitazi, BP; Hollister, EB; Oezguen, N; Tsai, CM; McMeans, AR; Luna, RA; Savidge, TC; Versalovic, J; Shulman, RJ (2014). "Gut microbiota influences low fermentable substrate diet efficacy in children with irritable bowel syndrome". Gut Microbes. 5 (2): 165–175. doi:10.4161/gmic.27923. PMC 4063841. PMID 24637601.
  31. ^ Bayless; Theodore M. Bayless; Stephen B. Hanauer; Professor Theodore M Bayless (14 May 2014). Advanced Therapy of Inflammatory Bowel Disease: Ulcerative Colitis (Volume 1), 3e. PMPH-USA. pp. 250–. ISBN 978-1-60795-216-9.
  32. ^ "Frequently asked questions in the area of diet and IBS". Med.monash.edu. 2013-08-30. Retrieved 2014-05-26.
  33. ^ a b c Gibson PR, Varney J, Malakar S, Muir JG (2015). "Food components and irritable bowel syndrome". Gastroenterology. 148 (6): 1158–74.e4. doi:10.1053/j.gastro.2015.02.005. PMID 25680668.
  34. ^ "Low FODMAP foods" (PDF). IBS Group. Retrieved 16 May 2016.
  35. ^ Staudacher HM, Irving PM, Lomer MC, Whelan K (April 2014). "Mechanisms and efficacy of dietary FODMAP restriction in IBS". Nat Rev Gastroenterol Hepatol (Review). 11 (4): 256–66. doi:10.1038/nrgastro.2013.259. PMID 24445613. An emerging body of research now demonstrates the efficacy of fermentable carbohydrate restriction in IBS; however, limitations still exist with this approach owing to a limited number of randomized trials, in part due to the fundamental difficulty of placebo control in dietary trials. Evidence also indicates that the diet can influence the gut microbiota and nutrient intake. Fermentable carbohydrate restriction in people with IBS is promising, but the effects on gastrointestinal health require further investigation.
  36. ^ Chumpitazi BP, Cope JL, Hollister EB, Tsai CM, McMeans AR, Luna RA, Versalovic J, Shulman RJ (2015). "Randomised clinical trial: gut microbiome biomarkers are associated with clinical response to a low FODMAP diet in children with the irritable bowel syndrome". Aliment. Pharmacol. Ther. 42 (4): 418–27. doi:10.1111/apt.13286. PMID 26104013.
  37. ^ Marsh A, Eslick EM, Eslick GD (2015). "Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis". Eur J Nutr. doi:10.1007/s00394-015-0922-1. PMID 25982757.
  38. ^ Rao SS, Yu S, Fedewa A (2015). "Systematic review: dietary fibre and FODMAP-restricted diet in the management of constipation and irritable bowel syndrome". Aliment. Pharmacol. Ther. 41 (12): 1256–70. doi:10.1111/apt.13167. PMID 25903636.
  39. ^ Gearry RB, Irving PM, Barrett JS, Nathan DM, Shepherd SJ, Gibson PR (2009). "Reduction of dietary poorly absorbed short-chain carbohydrates (FODMAPs) improves abdominal symptoms in patients with inflammatory bowel disease-a pilot study". J Crohns Colitis. 3 (1): 8–14. doi:10.1016/j.crohns.2008.09.004. PMID 21172242.
  40. ^ Charlebois A, Rosenfeld G, Bressler B (2015). "The Impact of Dietary Interventions on the Symptoms of Inflammatory Bowel Disease: A Systematic Review". Crit Rev Food Sci Nutr. doi:10.1080/10408398.2012.760515. PMID 25569442.
  41. ^ a b Hou JK, Lee D, Lewis J (October 2014). "Diet and inflammatory bowel disease: review of patient-targeted recommendations". Clin. Gastroenterol. Hepatol. (Review). 12 (10): 1592–600. doi:10.1016/j.cgh.2013.09.063. PMC 4021001. PMID 24107394. Even less evidence exists for the efficacy of the SCD, FODMAP, or Paleo diets. Furthermore, the practicality of maintaining these interventions over long periods of time is doubtful.
  42. ^ Hou et al. (p. 1598) write: "At a practical level, adherence to defined diets may result in an unnecessary financial burden or reduction in overall caloric intake in patients who are already at risk for protein-calorie malnutrition".

Further reading

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