Review article: biological mechanisms for symptom causation by individual FODMAP subgroups – the case for a more personalised approach to dietary restriction.

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Wang XJ, Camilleri M, Vanner S, Tuck C

Aliment Pharmacol Ther 2019 DOI: 10.1111/apt.15419


This literature review aimed to examine the biological plausibility and mechanisms by which foods high in FODMAP subgroups cause symptoms, and to use this information to explore the possibility of targeting select dietary components to allow for a more personalised approach to dietary adjustment. In doing so, the authors pondered and discussed the use of a ‘bottom up’ rather than a ‘top down’ approach to the low FODMAP diet.


Disaccharide – lactose

Lactose cannot be absorbed in the small intestine when lactase is absent. Unabsorbed lactose creates osmotic action in the small intestine, increasing water delivery into the lumen. Unabsorbed lactose is subsequently fermented by colonic bacteria resulting in gas production. Distension created by water and gas results in symptom generation.

Approximately 65% of the population has a reduced ability to digest lactose after infancy. Lactose malabsorption in adulthood is most prevalent in people of East Asian descent, affecting more than 90% of adults in some communities. Lactose malabsorption can be measured using breath testing. However, only when lactose malabsorption results in symptoms of lactose intolerance should dietary modifications be considered.  Symptoms include diarrhoea, abdominal pain, bloating and gas. In addition to ethnicity, a key clinical consideration is the dose of lactose consumed by the individual. An intake of 12-15g/day or less (240ml milk) is likely to produce negligible symptoms. How the lactose is consumed may also alter symptom response. Consumption of lactose with other foods will slow gastric emptying and small intestinal transit, allowing more time for hydrolysis and absorption, resulting in reduced symptom generation.

Monosaccharide – excess fructose

Absorption of excess fructose occurs in te small intestine via 2 transporters. Rapidly via GLUT-2 (the sodium-dependent active transport mechanism) in conjunction with glucose, and slowly via GLUT-5 (using carrier-mediated facilitated diffusion). In the absence of equal concentrations of glucose, the slow absorption via GLUT-5 allows fructose to have an osmotic effect, increasing water delivery to the lumen. The proportion that is malabsorbed is then fermented by colonic bacteria to produce gas. Distension created by water and gas results in symptom generation.

Whilst the osmotic effects of excess fructose have been shown experimentally using MRI imaging, it is unclear whether the results of fructose administration alone, either in MRI experiments or in a standard fructose-hydrogen breath tests (during which 35g fructose solution is given to a fasting patient), realistically reflects the way in which dietary fructose is normally consumed. Under normal circumstances, fructose is consumed as part of solid food and therefore does not reach the colon for at least 2 hours. In addition the concomitant ingestion of glucose in the same food helps to increase fructose absorption via GLUT-2, whilst the presence of fibre slows gut transit. The amount of fructose reaching the colon for bacterial fermentation is critical but unknown. Unfortunately the applicability of breath testing to assess fructose malabsorption is particularly flawed – the dosage used does not reflect a normal diet, the test also has poor predictive value (especially for a low fructose diet). It is still unproven that the same dose of fructose administered in real food actually causes symptoms compared to a 35g clinical testing dose administered in aqueous solution (35g = 2 pears, 2 apples & 16oz glass of apple juice). The degree to which dietary fructose causes symptoms and the threshold dose required to produce fermentation in the colon, and whether this is a mechanism for symptom generation, is still unknown. For sensitive individuals management may include reduced intake of foods including apples and pears and fruit juices known to have high levels of excess fructose.

Polyols – mannitol and sorbitol

Absorption occurs along the length of the small intestine by slow passive diffusion. Osmotic action increases water delivery into the lumen during transit through the small intestine and the proportion that is malabsorbed is fermented by colonic bacteria. Distension created by water and gas results in symptom generation.

Malabsorption of sorbitol has been suggested to occur in 67% of healthy controls and 60% of IBS patients. Mannitol malabsorption is similar to that of sorbitol in healthy controls, but only 20% in IBS patients. There appears to be poor correlation between polyol malabsorption and GI symptoms, with both sorbitol and mannitol increasing symptoms independent of the degree of malabsorption. Breath hydrogen studies to monitor polyol malabsorption have used 5-20g sorbitol/ mannitol, however the average intake of polyols from a single meal is just 1.9g, with average daily intake 3.5g. Therefore it is unclear whether such malabsorption testing is clinically relevant. Restrictions should be targeted to patients consuming larger quantities of artificial sugars in hard candies (which may contain up to 5.7g sorbitol), chewing gums and mints, as well as certain fruits which contain sources of multiple polyols or multiple FODMAP groups, e.g peaches contain both 1.3g sorbitol and 0.7g mannitol, whilst pears contain 3.8g sorbitol and 6.2g excess fructose per piece. As with fructose, the degree of restriction may need to be individualised in the absence of robust data from which to draw recommendations.

Oligosaccharides – fructans and galacto-oligosaccharides (GOS)

This is a subgroup of FODMAPs on which there should be little controversy. Humans lack the small intestinal hydrolases to target oligosaccharides and hence they are not absorbed in the small intestine. Once reaching the large intestine, colonic bacteria ferment the undigested oligosaccharides creating gas and distension. This is a normal process in humans, however hypersensitivity to distension in IBS results in symptom generation.

While prevalence of sensitivity to fructans in IBS in largely unknown, sensitivity to GOS has been shown to occur in around 68% of patients with IBS. Specific symptoms associated with a high oligosaccharide intake include abdominal pain, bloating, nausea, gas and fatigue. Restriction of oligosaccharides should be targeted to the individual’s usual diet, with those consuming regular servings of rye, wheat, onion and garlic more likely to benefit from fructan restriction, and those consuming legumes and nuts likely to benefit from GOS restriction.

The traditional ‘top-down’ approach to the Low FODMAP diet

The low FODMAP diet is a 3-phase approach, commencing with restriction of all FODMAP subgroups for 6-8 weeks, followed by strategic re-challenge of subgroups to test tolerance, and finally an individualised long-term maintenance phase. As such, it may be described as a ‘top-down’ approach. The potential advantages of this approach are more rapid symptom relief, and ease of identification of trigger foods following symptom improvement in the initial phase. However, potential disadvantages are a more restrictive diet in the initial phase, which may continue to impact upon microbiota and nutritional status if phases 2 and 3 are not implemented correctly. Therefore, this approach may be best suited to those with more severe symptoms and lack of identifiable patterns for symptoms generation. 

A hypothetical model for a ‘bottom-up’ approach

The bottom-up approach starts with a more liberalised diet and only restricts a few specific foods or FODMAP subgroups thought to cause symptoms, based on a thorough diet history and patient-reported triggers. A first approach may include a lactose-restricted diet, for example in a patient of Asian background who has not previously restricted dairy. Evidence suggests that low lactose intakes are tolerable and total restriction may be burdensome and unnecessary. Beyond this, restrictions may be tailored to patients usual food intake and possible triggers, e.g a patient with abdominal pain and gas who is consuming large amounts of wheat, onion and garlic may be likely to benefit from just fructan restriction. Following the initial restriction of just 1 or 2 foods/ subgroups for approximately 2 weeks, symptoms can be re-evaluated and if improved, no further restriction is necessary. Additional foods/ subgroups can be added if symptoms persist, until symptoms resolve or no response is noted. Patients who are likely to benefit most from this approach are those with milder symptoms or those already at risk of nutritional deficiencies. Although this approach has not been studied, likely advantages are a more acceptable and achievable dietary prescription and reduced risk of nutritional deficiencies, however a re-challenge phase will still be important to minimise impact on nutritional status.


While some of the compenents of a low FODMAP diet have strong biological plausibility for symptom generation (lactose, fructans, GOS), others such as excess fructose and polyols may only cause symptoms in specific individuals when consumed in high doses, however clinical data to prove this is lacking. The authors of this study suggest that clinicians consider a tailored, personalised ‘bottom-up’ approach to the low FODMAP diet for some patients. This will allow for individualisation of dietary recommendations based on factors such as ethnicity, symptom profile, prior experience with specific foods and usual dietary intake.