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The term FODMAP is an acronym, derived from "Fermentable Oligo-, Di-, Mono-saccharides And Polyols".[1]

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] FODMAPs are naturally present in food and the human diet.

FODMAPs can cause digestive discomfort in some people, but they do not cause intestinal inflammation. In fact, FODMAPs help avert digestive discomfort because they produce beneficial alterations in the gut flora.[3][4][5]

FODMAPs are not the cause of these disorders,[6] but FODMAPs restriction (a low-FODMAP diet) might help to improve short-term digestive symptoms in adults with irritable bowel syndrome (IBS) and other functional gastrointestinal disorders (FGID).[6][7][8][9][10] Avoiding FODMAPs long-term can have a detrimental impact on the gut microbiota and metabolome.[2][8][10][11]

Also, a low FODMAP diet used without a previous complete medical evaluation can cause serious health risks. It can ameliorate and mask the digestive symptoms of serious diseases, such as celiac disease, inflammatory bowel disease and colon cancer, avoiding their correct diagnosis and therapy.[12][13]

Contents

AbsorptionEdit

FODMAPs are poorly absorbed in the small intestine and subsequently fermented by the bacteria in the distal small and proximal large intestine. This is a normal phenomenon, common to everyone. The resultant production of gas potentially results in bloating and flatulence.[6]

Nevertheless, although FODMAP can cause certain digestive discomfort in some people, not only do they not cause intestinal inflammation, but they avoid it, because they produce beneficial alterations in the intestinal flora that contribute to maintain the good health of the colon.[3][4][5]

FODMAPs are not the cause of irritable bowel syndrome nor other functional gastrointestinal disorders, but rather a person develops symptoms when the underlying bowel response is exaggerated or abnormal.[6]

Fructose malabsorption and lactose intolerance may produce IBS symptoms through the same mechanism but, unlike with other FODMAPs, poor absorption of fructose is found in only a minority and, in certain populations, notably those of European descent, lactose intolerance is found in only a minority.[14] 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.[6]

Sources in the dietEdit

The significance of sources of FODMAPs varies through differences in dietary groups such as geography, ethnicity and other factors.[6] Commonly used FODMAPs comprise the following:[15]

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

Fructans, galactans and polyolsEdit

Sources of fructansEdit

Sources of fructans include wheat, rye, barley, onion, garlic, Jerusalem and globe artichoke, beetroot, dandelion leaves, the white part of leeks, the white part of spring onion, brussels sprouts, savoy cabbage and prebiotics such as fructooligosaccharides (FOS), oligofructose and inulin.[6][16][17] Asparagus, fennel, red cabbage and radicchio contain moderate amounts but may be eaten if the advised portion size is observed.[17]

Sources of galactansEdit

Pulses and beans are the main dietary sources (though green beans, canned lentils, sprouted mung beans, tofu (not silken) and tempeh contain comparatively low amounts).[17][16] Supplements of the enzyme supplement alpha-galactosidase may reduce symptoms[18] (if brands containing other FODMAPs, such as polyol artificial sweeteners, are avoided).

Sources of polyolsEdit

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.[6][16] Cabbage, chicory and fennel contain moderate amounts but may be eaten if the advised portion size is observed.[17]

Fructose and lactoseEdit

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 fructoseEdit

Sources of lactoseEdit

Low-FODMAP dietEdit

A low-FODMAP diet consists in the global restriction of all fermentable carbohydrates (FODMAPs).[6]

Suggested foodsEdit

Below are low-FODMAP foods categorized by group according to the Monash University "Low-FODMAP Diet".[17][19]

  • Vegetables: alfalfa, bean sprouts, green beans, bok choy, capsicum (bell pepper), carrot, chives, fresh herbs, choy sum, cucumber, lettuce, tomato, zucchini, the green parts of leeks and spring onions
  • Fruits: orange, grapes, melon
  • Protein: meats, fish, chicken, tofu (not silken), tempeh
  • Dairy: lactose-free milk, lactose-free yoghurts, hard cheese
  • Breads and cereals: rice, crisped rice, maize/corn, potatoes, quinoa and gluten-free breads made with their flours. Oats and spelt are relatively low in FODMAPs.
  • Biscuits (cookies) and snacks: made with flour of cereals listed above, without high FODMAP ingredients added (such as onion, pear or honey).
  • Nuts and seeds: almonds (no more than 10 nuts per serving), pumpkin seeds; not cashews or pistachios
  • Beverage options: water, coffee, tea

Other sources confirm the suitability of these and suggest some additional foods.[20]

Effectiveness and risksEdit

A low-FODMAP diet might help to improve short-term digestive symptoms in adults with irritable bowel syndrome,[7][8][9][10] but its long-term follow-up can have negative effects because it causes a detrimental impact on the gut microbiota and metabolome.[2][8][10][11] It should only be used for short periods of time and under the advice of a specialist.[21] More studies are needed to evaluate its effectiveness in children with irritable bowel syndrome.[7] There is only a little evidence of its effectiveness in treating functional symptoms in inflammatory bowel disease from small studies which are susceptible to bias.[22][23] More studies are needed to assess the true impact of this diet on health.[8][10]

In addition, the use of a low-FODMAP diet without medical advice can lead to serious health risks, including nutritional deficiencies, cancer risk or even mortality. A low-FODMAP diet can ameliorate and mask the digestive symptoms of serious diseases that usually present digestive symptoms similar to those of irritable bowel syndrome, such as celiac disease, inflammatory bowel disease and colon cancer. It is crucial to conduct a complete medical evaluation before starting a low-FODMAP diet to ensure a correct diagnosis and that the appropriate therapy can be undertaken.[12] This is especially relevant in the case of celiac disease. Since the consumption of gluten is suppressed or reduced with a low-FODMAP diet, the improvement of the digestive symptoms with this diet may not be related to the withdrawal of the FODMAPs, but of gluten, indicating the presence of an unrecognized celiac disease, avoiding its diagnosis and correct treatment, with the consequent risk of several serious health complications, including various types of cancer.[12][13]

A low-FODMAP diet is highly restrictive in various groups of nutrients, can be impractical to follow in the long-term and may add an unnecessary financial burden.[23]

HistoryEdit

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.[6]

Over many years, there have been multiple observations that ingestion of certain short-chain carbohydrates, including lactose, fructose and sorbitol, fructans and galactooligosaccharides, can induce gastrointestinal discomfort similar to that of people with irritable bowel syndrome. These studies also showed that dietary restriction of short-chain carbohydrates was associated with symptoms improvement.[24]

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.[25] 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).[6] 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.[2]

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.[17] 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.[2][26] Monash University also established a rigorous food analysis program to measure the FODMAP content of a wide selection of Australian and international foods.[27][28][29] 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.[30]

See alsoEdit

ReferencesEdit

  1. ^ a b c d Gibson PR, Shepherd SJ (June 2005). "Personal view: food for thought--western lifestyle and susceptibility to Crohn's disease. The FODMAP hypothesis". Alimentary Pharmacology & Therapeutics. 21 (12): 1399–409. doi:10.1111/j.1365-2036.2005.02506.x. PMID 15948806.
  2. ^ a b c d e Tuck CJ, Muir JG, Barrett JS, Gibson PR (September 2014). "Fermentable oligosaccharides, disaccharides, monosaccharides and polyols: role in irritable bowel syndrome". Expert Review of Gastroenterology & Hepatology. 8 (7): 819–34. doi:10.1586/17474124.2014.917956. PMID 24830318.
  3. ^ a b Makharia A, Catassi C, Makharia GK (December 2015). "The Overlap between Irritable Bowel Syndrome and Non-Celiac Gluten Sensitivity: A Clinical Dilemma". Nutrients (Review). 7 (12): 10417–26. doi:10.3390/nu7125541. PMC 4690093. PMID 26690475.
  4. ^ a b Greer JB, O'Keefe SJ (2011). "Microbial induction of immunity, inflammation, and cancer". Frontiers in Physiology (Review). 1: 168. doi:10.3389/fphys.2010.00168. PMC 3059938. PMID 21423403.
  5. ^ a b Andoh A, Tsujikawa T, Fujiyama Y (2003). "Role of dietary fiber and short-chain fatty acids in the colon". Current Pharmaceutical Design (Review). 9 (4): 347–58. PMID 12570825.
  6. ^ a b c d e f g h i j k Gibson PR, Shepherd SJ (February 2010). "Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach". Journal of Gastroenterology and Hepatology. 25 (2): 252–8. doi:10.1111/j.1440-1746.2009.06149.x. PMID 20136989.
  7. ^ a b c Turco R, Salvatore S, Miele E, Romano C, Marseglia GL, Staiano A (May 2018). "Does a low FODMAPs diet reduce symptoms of functional abdominal pain disorders? A systematic review in adult and paediatric population, on behalf of Italian Society of Pediatrics". Italian Journal of Pediatrics (Systematic Review). 44 (1): 53. doi:10.1186/s13052-018-0495-8. PMC 5952847. PMID 29764491.
  8. ^ a b c d e Staudacher HM, Irving PM, Lomer MC, Whelan K (April 2014). "Mechanisms and efficacy of dietary FODMAP restriction in IBS". Nature Reviews. Gastroenterology & Hepatology (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, further work is urgently needed both to confirm clinical efficacy of fermentable carbohydrate restriction in a variety of clinical subgroups and to fully characterize the effect on the gut microbiota and the colonic environ¬ment. Whether the effect on luminal bifidobacteria is clinically relevant, preventable, or long lasting, needs to be investigated. The influence on nutrient intake, dietary diversity, which might also affect the gut microbiota, and quality of life also requires further exploration as does the possible economic effects due to reduced physician contact and need for medication. Although further work is required to confirm its place in IBS and functional bowel disorder clinical pathways, fermentable carbohydrate restriction is an important consideration for future national and international IBS guidelines.
  9. ^ a b Marsh A, Eslick EM, Eslick GD (April 2016). "Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis". European Journal of Nutrition. 55 (3): 897–906. doi:10.1007/s00394-015-0922-1. PMID 25982757.
  10. ^ a b c d e Rao SS, Yu S, Fedewa A (June 2015). "Systematic review: dietary fibre and FODMAP-restricted diet in the management of constipation and irritable bowel syndrome". Alimentary Pharmacology & Therapeutics. 41 (12): 1256–70. doi:10.1111/apt.13167. PMID 25903636.
  11. ^ a b Heiman ML, Greenway FL (May 2016). "A healthy gastrointestinal microbiome is dependent on dietary diversity". Molecular Metabolism (Review). 5 (5): 317–320. doi:10.1016/j.molmet.2016.02.005. PMC 4837298. PMID 27110483.
  12. ^ a b c Barrett JS (March 2017). "How to institute the low-FODMAP diet". Journal of Gastroenterology and Hepatology (Review). 32 Suppl 1: 8–10. doi:10.1111/jgh.13686. PMID 28244669. Common symptoms of IBS are bloating, abdominal pain, excessive flatus, constipation, diarrhea, or alternating bowel habit. These symptoms, however, are also common in the presentation of coeliac disease, inflammatory bowel disease, defecatory disorders, and colon cancer. Confirming the diagnosis is crucial so that appropriate therapy can be undertaken. Unfortunately, even in these alternate diagnoses, a change in diet restricting FODMAPs may improve symptoms and mask the fact that the correct diagnosis has not been made. This is the case with coeliac disease where a low-FODMAP diet can concurrently reduce dietary gluten, improving symptoms, and also affecting coeliac diagnostic indices. Misdiagnosis of intestinal diseases can lead to secondary problems such as nutritional deficiencies, cancer risk, or even mortality in the case of colon cancer.
  13. ^ a b "Celiac disease". World Gastroenterology Organisation Global Guidelines. July 2016. Archived from the original on 17 March 2017. Retrieved 4 June 2018.
  14. ^ Storhaug CL, Fosse SK, Fadnes LT (October 2017). "Country, regional, and global estimates for lactose malabsorption in adults: a systematic review and meta-analysis". The Lancet. Gastroenterology & Hepatology. 2 (10): 738–746. doi:10.1016/S2468-1253(17)30154-1. PMID 28690131.
  15. ^ Bayless TM, Hanauer SB (2014). Advanced Therapy of Inflammatory Bowel Disease: Ulcerative Colitis. 1, 3e. PMPH-USA. pp. 250–. ISBN 978-1-60795-216-9.
  16. ^ a b c Gibson PR, Varney J, Malakar S, Muir JG (May 2015). "Food components and irritable bowel syndrome". Gastroenterology. 148 (6): 1158–74.e4. doi:10.1053/j.gastro.2015.02.005. PMID 25680668.
  17. ^ a b c d e f "The Monash University Low FODMAP diet". Melbourne, Australia: Monash University. 2012-12-18. Retrieved 2014-05-26.
  18. ^ "New research: Enzyme therapy can help reduce symptoms in IBS patients sensitive to galacto-oligosaccharides (GOS) present in legumes, soy milk and nuts". www.monashfodmap.com.
  19. ^ "The Monash University Low FODMAP diet. Frequently asked questions". Melbourne, Australia: Monash University. Retrieved 3 June 2018.
  20. ^ "Low FODMAP foods" (PDF). IBS Group. Archived from the original (PDF) on 14 December 2015. Retrieved 16 May 2016.
  21. ^ Staudacher HM, Whelan K (August 2017). "The low FODMAP diet: recent advances in understanding its mechanisms and efficacy in IBS". Gut (Review). 66 (8): 1517–1527. doi:10.1136/gutjnl-2017-313750. PMID 28592442.
  22. ^ Gearry RB, Irving PM, Barrett JS, Nathan DM, Shepherd SJ, Gibson PR (February 2009). "Reduction of dietary poorly absorbed short-chain carbohydrates (FODMAPs) improves abdominal symptoms in patients with inflammatory bowel disease-a pilot study". Journal of Crohn's & Colitis. 3 (1): 8–14. doi:10.1016/j.crohns.2008.09.004. PMID 21172242.
  23. ^ a b Hou JK, Lee D, Lewis J (October 2014). "Diet and inflammatory bowel disease: review of patient-targeted recommendations". Clinical Gastroenterology and Hepatology (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 diet. Furthermore, the practicality of maintaining these interventions over long periods of time is doubtful. 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.
  24. ^ Gibson PR (March 2017). "History of the low FODMAP diet". Journal of Gastroenterology and Hepatology (Review). 32 Suppl 1: 5–7. doi:10.1111/jgh.13685. PMID 28244673.
  25. ^ Murray K, Wilkinson-Smith V, Hoad C, Costigan C, Cox E, Lam C, Marciani L, Gowland P, Spiller RC (January 2014). "Differential effects of FODMAPs (fermentable oligo-, di-, mono-saccharides and polyols) on small and large intestinal contents in healthy subjects shown by MRI". The American Journal of Gastroenterology. 109 (1): 110–9. doi:10.1038/ajg.2013.386. PMC 3887576. PMID 24247211.
  26. ^ Barrett JS, Gearry RB, Muir JG, Irving PM, Rose R, Rosella O, Haines ML, Shepherd SJ, Gibson PR (April 2010). "Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon". Alimentary Pharmacology & Therapeutics. 31 (8): 874–82. doi:10.1111/j.1365-2036.2010.04237.x. PMID 20102355.
  27. ^ Muir JG, Rose R, Rosella O, Liels K, Barrett JS, Shepherd SJ, Gibson PR (January 2009). "Measurement of short-chain carbohydrates in common Australian vegetables and fruits by high-performance liquid chromatography (HPLC)". Journal of Agricultural and Food Chemistry. 57 (2): 554–65. doi:10.1021/jf802700e. PMID 19123815.
  28. ^ Muir JG, Shepherd SJ, Rosella O, Rose R, Barrett JS, Gibson PR (August 2007). "Fructan and free fructose content of common Australian vegetables and fruit". Journal of Agricultural and Food Chemistry. 55 (16): 6619–27. doi:10.1021/jf070623x. PMID 17625872.
  29. ^ Biesiekierski JR, Rosella O, Rose R, Liels K, Barrett JS, Shepherd SJ, Gibson PR, Muir JG (April 2011). "Quantification of fructans, galacto-oligosacharides and other short-chain carbohydrates in processed grains and cereals". Journal of Human Nutrition and Dietetics. 24 (2): 154–76. doi:10.1111/j.1365-277X.2010.01139.x. PMID 21332832.
  30. ^ Southgate DA, Paul AA, Dean AC, Christie AA (October 1978). "Free sugars in foods". Journal of Human Nutrition. 32 (5): 335–47. doi:10.3109/09637487809143898. PMID 363937.

Further readingEdit

External linksEdit