Throughout the 1980s and 1990s, evidence was building for the role of poorly absorbed, short-chain carbohydrates (lactose, fructose and sorbitol) in the induction of IBS symptoms, with dietary restriction providing symptomatic relief [Goldstein et al. 2000
; Nelis et al. 1990
; Rumessen and Gudmand-Hoyer, 1988
; Symons et al. 1992
]. It was clear, however, that these sugars were not the only answer. Examination of the literature and the biochemistry and physiology of digestion of other carbohydrates suggested involvement of fructo-oligosaccharides (fructans) and galacto-oligosaccharides (GOS) because they are also short-chain carbohydrates and are incompletely absorbed in the human gastrointestinal tract. The incompletely absorbed sugar polyols, sorbitol and mannitol, used as artificial sweeteners but also found naturally in foods, were also potential culprits. Grouping of these poorly absorbed, short-chain carbohydrates according to their chain length resulted in the acronym FODMAP.
In 2005, the first paper describing FODMAPs was published [Gibson and Shepherd, 2005
]. The first research trial confirming the role of a low-FODMAP diet in managing gastrointestinal complaints was a retrospective audit of patients with IBS and fructose malabsorption on a low-fructose/fructan diet [Shepherd and Gibson, 2006
]. A total of 74% of patients reported symptomatic improvement on this dietary regimen. Confirmation of the efficacy of the diet was provided by a follow-up, randomized, placebo-controlled rechallenge trial in patients with IBS with fructose malabsorption [Shepherd et al. 2008
]. All patients improved on a low-fructose/fructan diet, with significant exacerbation of symptoms by rechallenge of fructose or fructans, further exacerbated by a combination of fructose and fructans. Placebo response was minimal. Subsequent study of this dietary approach in the UK has shown it superior to a dietary approach previously considered as best practice [Staudacher et al. 2011
The mechanism by which FODMAPs were exerting their effects was then studied via two separate trials. Using an ileostomy model [Barrett et al. 2010
], it was confirmed that FODMAPs, consumed within meals, are poorly absorbed in the small intestine. Interestingly, delivery of FODMAPs to the stoma, correlated with increased water content of the output, suggesting an osmotic effect of the carbohydrates. This may well be the physiological mechanism that induces diarrhoea in some individuals. The second study [Ong et al. 2010
] involved assessment of breath hydrogen during low- and high-FODMAP diets in patients with IBS and healthy volunteers. Ingestion of a low-FODMAP diet significantly reduced breath hydrogen production in healthy volunteers and patients with IBS with consequential reduction in gastrointestinal symptom scores in the IBS population. This confirms the fermentative nature of the short-chain carbohydrates and their role in the induction of bloating, distension, abdominal pain and excessive flatus.
These mechanistic insights are consistent with current understanding of the pathophysiological mechanisms that underlie IBS. Visceral hypersensitivity, the most important, renders the enteric nervous system to respond to normal distension of the gut by altering motility patterns and sending messages to the brain that may be interpreted as bloating, discomfort and pain. The low-FODMAP diet reduces fermentation and associated gas production, which is likely to minimize the distension induced by food thereby reducing symptom severity. Other potential factors include alterations in the number, composition, function and location of the microbiota. Some patients with IBS may have SIBO with fermentation of malabsorbed carbohydrates occurring in the narrow lumen of the small intestine, the location of which may be associated with abdominal pain and discomfort. They may have more predominant methane-producing bacteria which, when fermenting malabsorbed carbohydrates producing methane gas, is linked to delayed transit and constipation [Chatterjee et al. 2007
; Fiedorek et al. 1990
; Pimentel et al. 2003
Since these initial studies, more details on food composition have become available to fine tune the FODMAP approach. This includes the consideration of a broader range of FODMAPs, including GOS, sorbitol and mannitol, in addition to fructose, lactose and fructans. These six carbohydrates make up the low-FODMAP diet as it is today, with published tables of food composition available on fruits and vegetables and breads and cereals [Biesiekierski et al. 2011
; Muir et al. 2007
]. lists a summary of the richest FODMAP food sources compiled from these published food composition papers. Broader food composition has been completed for the use of the Monash University Comprehensive Nutrition Assessment Questionnaire (CNAQ).This Food Frequency Questionnaire has been validated and will be a useful tool for future investigation of FODMAPs and other dietary components in chronic disease and gastrointestinal disorders [Barrett and Gibson, 2010
FODMAP carbohydrates and their richest food sources.
Not all FODMAPs will be symptom triggers for all patients. Only those that are malabsorbed are likely to play a role. Importantly, fructans and GOS are always malabsorbed and fermented by intestinal microflora [Macfarlane et al. 2008
; Rumessen and Gudmand-Hoyer, 1998
; Saunders and Wiggins, 1981
]. This results in gas production and associated flatulence in healthy people; however, with altered gut flora, motility disorders and hypersensitivity in IBS, the outcome can induce symptoms [Ong et al. 2010
]. The remaining FODMAP carbohydrates will only induce symptoms in the proportion of patients with IBS that malabsorb them. The sugar polyols, sorbitol and mannitol, are incompletely absorbed [Evans et al. 1998
; Fernandez-Banares et al. 1991
; Langkilde et al. 1994
]. The small levels found naturally in foods and in sugar-free products and medications can be well absorbed in most people. Hydrogen breath testing at a dose of 10 g of sorbitol and mannitol in patients with IBS suggests malabsorption in 57% and 20% of patients respectively [Yao et al. 2011
]. The prevalence of fructose and lactose in white patients with IBS is 45% and 25% respectively [Barrett et al. 2009
]. The prevalence of sorbitol, mannitol, fructose and lactose malabsorption in healthy people is greater than 18% for all sugars [Barrett et al. 2009
; Yao et al. 2011
]. A lack of symptoms in these people despite malabsorption is again explained by the absence of altered gut microflora and gut hypersensitivity.
Breath testing is a useful addition to the low-FODMAP diet application. In most areas of food intolerance, diagnosis is not possible. Breath testing provides a reliable measure of absorption of a test sugar by assessment of breath hydrogen levels. A significant rise in breath hydrogen following ingestion of the test sugar (e.g. fructose) demonstrates poor absorption with subsequent fermentation by intestinal microflora. In the presence of IBS, this may well contribute to symptoms, with restriction of the sugar useful in the management of gastrointestinal symptoms. Negative breath tests demonstrating complete absorption of the sugar suggests that the patient can continue to consume this sugar without impacting on their symptoms. Routinely, the breath tests that are offered to detect for FODMAP intolerances are fructose, lactose and sorbitol. It is vital to remember that, regardless of breath test results, there are three other FODMAP carbohydrates that need to be considered as potential triggers. Fructans and GOS are not breath tested as they are always malabsorbed. They are always fermented and should be considered as triggers in all patients with IBS. Mannitol is rarely offered as a breath test because it is not found widely in the diet and can be investigated as a trigger through simple dietary elimination and rechallenge.
When breath tests are undertaken, a low-FODMAP diet can be implemented without restricting sugars shown to be well absorbed. This individualizes the diet and avoids unnecessary restrictions. If breath testing is unavailable, a trial of a full low FODMAP diet can be conducted. This is usually recommended for 4–6 weeks, following which, rechallenge of any of the potentially well absorbed carbohydrates can be undertaken, that is, fructose, lactose, sorbitol and mannitol. Tolerance to fructans and GOS can then be tested. In large amounts these carbohydrates will always contribute to gas-associated symptoms. In extreme amounts this may even occur in healthy people [Ong et al. 2010
]. However, small amounts of fructans and GOS may be tested to assess the level of tolerance of the patient. This is particularly important for vegetarians (legumes), but may also highlight to a patient that they can cope with garlic as a minor ingredient, or wheat products occasionally. This assists the nutritional composition of the diet longer term, as well as removing some of the social inhibitions that a special diet can endure. In addition, FODMAPs have prebiotic effects due to the production of short-chain fatty acids after fermentation. Therefore, all patients are encouraged to try and reintroduce FODMAPs to a level that they can comfortably tolerate.