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(Fodmaps) and Nonallergic Food Intolerance

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(Fodmaps) and Nonallergic Food Intolerance 436241TAG Therapeutic Advances in Gastroenterology Review Ther Adv Gastroenterol Fermentable oligosaccharides, (2012) 5(4) 261 –268 DOI: 10.1177/ disaccharides, monosaccharides and 1756283X11436241 © The Author(s), 2012. polyols (FODMAPs) and nonallergic food Reprints and permissions: http://www.sagepub.co.uk/ intolerance: FODMAPs or food chemicals? journalsPermissions.nav Jacqueline S. Barrett and Peter R. Gibson Abstract: Food intolerance in irritable bowel syndrome (IBS) is increasingly being recognized, with patients convinced that diet plays a role in symptom induction. Evidence is building to implicate fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) in the onset of abdominal pain, bloating, wind and altered bowel habit through their fermentation and osmotic effects. Hypersensitivity to normal levels of luminal distension is known to occur in patients with IBS, with consideration of food chemical intolerance likely to answer many questions about this physiological process. This paper summarizes the evidence and application of the most common approaches to managing food intolerance in IBS: the low-FODMAP diet, the elimination diet for food chemical sensitivity and others including possible noncoeliac gluten intolerance. Keywords: FODMAPs, food chemicals, food intolerance, fructose, gluten, irritable bowel syndrome, salicylates Introduction role of food intolerance as a major contributor to Correspondence to: Jacqueline S. Barrett, The role of dietary components in inducing IBS symptoms. Foods are not the cause of the PhD, BSc(Biomed)(Hons), gastrointestinal symptoms of abdominal pain, condition. Rather, in the presence of IBS, patients M Nutr Diet Eastern Health Clinical bloating, flatus and altered bowel habit in irrita- can begin to experience symptoms of bloating, School, Monash University, ble bowel syndrome (IBS) is difficult to explore. abdominal pain and motility changes to specific Level 2, 5 Arnold Street, Box Hill, Victoria 3128, Food intolerances have been considered but food components. This is due to the IBS condi- Australia issues surrounding diagnostic tools and well tion, which causes altered microflora, potential jacqueline.barrett@ monash.edu.au designed dietary trials result in questionable small intestinal bacterial overgrowth (SIBO), and Peter R. Gibson, MD, outcomes. Historically, patients have identified visceral hypersensitivity. Food intolerance reac- FRACP caffeine, alcohol, fibre and fats as symptom trig- tions can be delayed and the severity of symptoms Eastern Health Clinical School, Monash University, gers, although strong evidence is conflicting in can be dose dependent [Shepherd et al. 2008]. Box Hill, Victoria, Australia some and lacking in most [Francis and Whorwell, It is much more difficult to pinpoint trigger foods 1994; Olesen and Gudmand-Hoyer, 2000; Rao in the case of food intolerance. Many published et al. 1998; Simren et al. 2001, 2007]. Asking studies report specific food intolerances accord- patients to identify which foods contribute to ing to patient questionnaires [Ballegaard et al. symptoms is fraught with inaccuracies given meals 1997; Niec et al. 1998]. This is unreliable meth- are complex mixtures of dietary components, and odology given the mix of foods included in meals the timing of symptom onset following a trigger and snacks and the likelihood of pinpointing the food can vary. wrong culprit. There is consistently a lack of evidence for food In recent decades, the role of dietary components allergy in IBS, with no change in reliable immu- in inducing IBS symptoms has been explored. nological markers following rechallenge of sus- There is evidence that certain food components pect trigger foods [Jones et al. 1982]. Evidence can contribute to symptoms through the effects of encourages researchers to further investigate the malabsorption of carbohydrates [Barrett et al. http://tag.sagepub.com 261 Therapeutic Advances in Gastroenterology 5 (4) 2010; Shepherd et al. 2008], and stimulation of the UK has shown it superior to a dietary approach hypersensitivity through food chemical ingestion previously considered as best practice [Staudacher [Niec et al. 1998]. Noncoeliac gluten intolerance et al. 2011]. also exists [Biesiekierski et al. 2010] and may be important in a subgroup of patients with IBS. This The mechanism by which FODMAPs were exert- paper summarizes the evidence and application of ing their effects was then studied via two separate the most common approaches to managing food trials. Using an ileostomy model [Barrett et al. intolerance in IBS: the low-FODMAP (fermentable 2010], it was confirmed that FODMAPs, oligosaccharides, disaccharides, monosaccharides consumed within meals, are poorly absorbed and polyols) diet, the elimination diet for food in the small intestine. Interestingly, delivery chemical sensitivity and others including possible of FODMAPs to the stoma, correlated with noncoeliac gluten intolerance. increased water content of the output, suggesting an osmotic effect of the carbohydrates. This may well be the physiological mechanism that induces The low-FODMAP diet diarrhoea in some individuals. The second study Throughout the 1980s and 1990s, evidence [Ong et al. 2010] involved assessment of breath was building for the role of poorly absorbed, hydrogen during low- and high-FODMAP diets short-chain carbohydrates (lactose, fructose and in patients with IBS and healthy volunteers. sorbitol) in the induction of IBS symptoms, with Ingestion of a low-FODMAP diet significantly dietary restriction providing symptomatic relief reduced breath hydrogen production in healthy [Goldstein et al. 2000; Nelis et al. 1990; Rumessen volunteers and patients with IBS with consequen- and Gudmand-Hoyer, 1988; Symons et al. 1992]. tial reduction in gastrointestinal symptom scores It was clear, however, that these sugars were in the IBS population. This confirms the fermen- not the only answer. Examination of the literature tative nature of the short-chain carbohydrates and and the biochemistry and physiology of digestion their role in the induction of bloating, distension, of other carbohydrates suggested involvement abdominal pain and excessive flatus. of fructo-oligosaccharides (fructans) and galacto- oligosaccharides (GOS) because they are also These mechanistic insights are consistent with short-chain carbohydrates and are incompletely current understanding of the pathophysiological absorbed in the human gastrointestinal tract. The mechanisms that underlie IBS. Visceral hypersen- incompletely absorbed sugar polyols, sorbitol and sitivity, the most important, renders the enteric mannitol, used as artificial sweeteners but also nervous system to respond to normal distension found naturally in foods, were also potential of the gut by altering motility patterns and sending culprits. Grouping of these poorly absorbed, messages to the brain that may be interpreted as short-chain carbohydrates according to their bloating, discomfort and pain. The low-FODMAP chain length resulted in the acronym FODMAP. diet reduces fermentation and associated gas pro- duction, which is likely to minimize the distension In 2005, the first paper describing FODMAPs was induced by food thereby reducing symptom published [Gibson and Shepherd, 2005]. The first severity. Other potential factors include altera- research trial confirming the role of a low-FOD- tions in the number, composition, function and MAP diet in managing gastrointestinal complaints location of the microbiota. Some patients with was a retrospective audit of patients with IBS and IBS may have SIBO with fermentation of malab- fructose malabsorption on a low-fructose/fructan sorbed carbohydrates occurring in the narrow diet [Shepherd and Gibson, 2006]. A total of 74% lumen of the small intestine, the location of of patients reported symptomatic improvement on which may be associated with abdominal pain this dietary regimen. Confirmation of the efficacy and discomfort. They may have more predomi- of the diet was provided by a follow-up, rand- nant methane-producing bacteria which, when omized, placebo-controlled rechallenge trial in fermenting malabsorbed carbohydrates produc- patients with IBS with fructose malabsorption ing methane gas, is linked to delayed transit and [Shepherd et al. 2008]. All patients improved on a constipation [Chatterjee et al. 2007; Fiedorek low-fructose/fructan diet, with significant exacer- et al. 1990; Pimentel et al. 2003, 2006]. bation of symptoms by rechallenge of fructose or fructans, further exacerbated by a combination of Since these initial studies, more details on food fructose and fructans. Placebo response was mini- composition have become available to fine tune mal. Subsequent study of this dietary approach in the FODMAP approach. This includes the 262 http://tag.sagepub.com JS Barrett and PR Gibson Table 1. FODMAP carbohydrates and their richest food sources. FODMAP Richest food sources Fructo-oligosaccharides (fructans) Wheat, rye, onions, garlic, artichokes Galacto-oligosaccharides (GOS) Legumes Lactose Milk Fructose Honey, apples, pears, watermelon, mango Sorbitol Apples, pears, stone fruits, sugar-free mints/gums Mannitol Mushrooms, cauliflower, sugar-free mints/gums consideration of a broader range of FODMAPs, 45% and 25% respectively [Barrett et al. 2009]. including GOS, sorbitol and mannitol, in addi- The prevalence of sorbitol, mannitol, fructose tion to fructose, lactose and fructans. These six and lactose malabsorption in healthy people is
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