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doi:10.1111/jgh.13685

REVIEW ARTICLE

History of the low FODMAP diet

Peter R Gibson*
*
Department of Gastroenterology, Monash University and Alfred Hospital, Melbourne, Australia

Key words
carbohydrate malabsorption, fructans, fructose,
galacto-oligosaccharides, lactose intolerance,
sorbitol, xylitol.
Accepted for publication 29 November 2016.
Correspondence
Professor Peter Gibson, Department of
Gastroenterology, Alfred Hospital, 99 Commercial
Road, Melbourne, Victoria 3004, Australia.
Email: peter.gibson@monash.edu
Disclosures: Professor Gibson’s Department fi-
nancially benefits from the sales of a digital appli-
cation and booklets on the low FODMAP diet. He
has published an educational/recipe book on diet.
Abstract
It has long been known that many short-chain carbohydrates can induce abdominal symp-
toms that are similar to those in patients with irritable bowel syndrome (IBS). It was hy-
pothesized that restricting the intake of all short-chain carbohydrates that are either
slowly absorbed or not digested in the small intestine should be considered together be-
cause they all have similar effects on the intestine by distending the lumen. These groups
of carbohydrates were called, Fermentable, Oligosaccharides, Disaccharides and Monosac-
charides and Polyols (FODMAPs), because of the lack of a known collective term. By re-
ducing their dietary intake, it was also hypothesized that abdominal symptoms in patients
with IBS would be alleviated in patients with visceral sensitivity and a low FODMAP diet
was subsequently designed. Over the last 12 years, the mechanisms of action, food content
of FODMAPs and efficacy of the diet, among other aspects have been intensively studied.
In many parts of the world, the low FODMAP diet is now considered a front-line therapy
for IBS.

For a long time, patients have recognized that certain foods can trig-
ger gastrointestinal symptoms (including wind, diarrhea, abdominal
bloating, and discomfort). Recognized food “culprits” have included
milk and other dairy products, legumes and pulses, cruciferous
vegetables, some fruits, and grains, especially wheat and rye. Many
of these foods are known as “gas-producing foods” and were recom-
mended to be avoided in situations of excessive flatulence and
bloating. However, such foods were in lists without any linking of
common components. Consequently, dietary advice pertaining to
such foods was haphazard and without structure.Over the last five
decades, however, advances in science and technology have meant
that the food components that are present in such foods that may
be responsible for these effects can be recognized. As shown in
Figure 1, carbohydrate malabsorption was recognized as a cause
for diarrhea, pain, and bloating and was subsequently implicated as
a cause for symptoms of irritable bowel syndrome (IBS). The early
reports of such carbohydrate malabsorption were as follows:
• Lactose: Congenital alactasia was first reported in 1959,1 but
it was not for another 6 years before acquired hypolactasia in
adults and its causal association with diarrhea was
described.2–4 The use of lactose restriction became common-
place and diagnostic tests such as measurement of lactase ac-
tivity in small intestinal biopsies, blood-based lactose
tolerance tests, and breath hydrogen tests were developed
and applied to confirm lactose malabsorption and intolerance
(i.e. when symptoms developed following ingestion of a test
dose of lactose). Lactose-free diets became a dietary strategy
for patients with IBS, but unfortunately did not have a major
impact on symptoms overall, apart from when they were in
association with ingesting a load of lactose.5
• Fructose and sorbitol: Fructose, the fruit sugar, was impli-
cated in symptom genesis when four patients with long-
standing diarrhea and colic were reported to be cured by a
fructose-free diet.6 In 1983, a breath hydrogen test was used
to demonstrate that a child with diarrhea had fructose malab-
sorption and was helped by dietary fructose reduction.7
“Fruit-juice diarrhoea” was reported in children in 1988.8
There followed reports of good results in patients with IBS
of diets that restricted fructose  sorbitol-free although the
actual diets followed were not described.9–11
• Oligosaccharides: Symptomatic response to fructo-
oligosaccharides that were being used as a sweetener was
reported in 198712 followed by multiple studies. The
induction of gastrointestinal symptoms with galacto-
oligosaccharides (GOS) was reported when GOS was being
evaluated as a prebiotic in 1990.13 This was followed by
multiple studies.
• Polyols: Sugar alcohols such as mannitol and xylitol have
long been used as sweeteners in food manufacturing, and it
was in the 1960s that their ability to induce gut symptoms
was well documented in the Turku sugar studies.14 The
additive effects with fructose and sorbitol (they commonly
exist in foods) on symptoms was first reported in 1982.15
In 2006, the restriction of fructose and fructans in a well-
structured and defined diet specifically for patients with IBS and
fructose malabsorption gave relief for gut symptoms in 76% of
patients in a retrospective study.16 In a subsequent blinded re-
challenge study in patients whose symptoms were well controlled
on that “fructose malabsorption diet”, both fructose and fructans
specifically induced symptoms (and glucose as placebo did not),
and there was some evidence of an additive effect.17 This study
was the first to provide more conclusive support that reduction
of intake of fructose and fructans was the reason for the improve-
ment of symptoms with the diet.

Journal of Gastroenterology and Hepatology 2017; 32 (Suppl. 1): 5–7 5

© 2017 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd

History of the low FODMAP diet
Figure 2 The multiple lines of investigations that have arisen from the
development of the Fermentable, Oligosaccharides, Disaccharides and
Monosaccharides and Polyols (FODMAP) concept.
There were flaws in the logic that such dietary restriction should
be restricted to patients with fructose malabsorption, especially be-
cause fructans that are indigestible in all people-induced symp-
toms. It was hypothesized that the reason for the improvement
was related to a common physiological effect—distension of the
intestinal lumen by water and/or gas production. In fact, additive
effects of fructose and sorbitol, and of fructan and lactose15,18
had previously been documented. Limiting such an effect to
fructose and fructan was questioned and, consequently, all short-
chain carbohydrates that are slowly absorbed or indigestible in
the small intestine were included as they all had similar, physio-
logical effects. It was also argued that, if they were all restricted
together, then the effect would be more reliable and greater in
many. Broad restriction would improve the ability of the “elimina-
tion” phase of the diet to define those sensitive to such intestinal
distension; it was hypothesized that this would represent visceral
hypersensitivity. Hence, GOS, lactose (in hypolactasic individuals)
and polyols were added to the carbohydrates to be restricted and
6 Journal of Gastroenterology and Hepatology 2017; 32 (Suppl. 1): 5–7
© 2017 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd
14401746, 2017, S1, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jgh.13685 by CochraneItalia, Wiley Online Library on [13/02/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
PR Gibson
Figure 1 The history of the development of the
Fermentable Oligosaccharides, Disaccharides and
Monosaccharides and Polyols (FODMAP) concept.
The dates shown represent the first reports that in-
dividual FODMAPs may induce abdominal
symptoms.
the dietary description was extended considerably. This represented
a “top-down” approach.
The creation of an acronym to describe these short-chain carbo-
hydrates was needed because there was no collective term that
encompassed them, and there was a need to focus thinking on
the spectrum sugars, not on fructose (as was fashionable at the
time). In 2004, the Monash group agreed on the term, Fermentable
Oligosaccharides, Disaccharides and Monosaccharides and
Polyols (“FODMAP”). The next challenge was to get the term in
the published arena because it was likely to be some time before
studies using the “low FODMAP diet” that had been designed
could be finished. The solution was to develop a serious hypothe-
sis for the pathogenesis of Crohn’s disease (the FODMAP hypoth-
esis). It was published in Alimentary Pharmacology and
Therapeutics in 2005.19 That paper continues to be one of the most
downloaded papers from the journal.
An intensive program of research was then planned (Fig. 2).
This involved several aspects and many of these are outlined in
other articles in this Supplement. These include confirmation of
the mode of action of FODMAPs, comprehensive food analysis,
development of the cut-off levels that define what is low
FODMAP, tools for assessing the intake of FODMAPs, namely
the Complete Nutritional Assessment Questionnaire (CNAQ),
proof of efficacy for the low FODMAP diet, identification poten-
tial risks of the low FODMAP diet, applications to situations
other than IBS, such inflammatory bowel disease and functional
dyspepsia and in pediatric populations. The internationalization
of the low FODMAP diet was facilitated by seeding of expertise
from the Monash group to Christchurch, New Zealand, by
Richard Gearry and to King’s College London, UK, by Peter
Irving and Heidi Staudacher. Insightful champions across the
world risked their credibility by supporting the concept, and
these included William Chey (USA), Pia Monkholm
(Denmark), Victoria Tan (Hong Kong), Knut Lundin (Norway)
and Clive Wilder-Smith (Switzerland). Many enthusiastic dietitians
in clinical practice such as Kate Scalata and Patsy Catsos (USA)
and Miranda Lomer and Kevin Whelan (UK) who also evaluated
the diet with high-quality research studies. Good and bad publicity,

PR Gibson
as well as favorable responses in clinical practice also helped
spread the ideas.
There are multiple reasons why, over a period of 12 years, the
low FODMAP diet has become well known and widely practiced.
First, it is biologically feasible with well-defined modes of action
that are readily understood. Secondly, the dietary principles are
well structured and clearly defined, something that many diets in
the past (and present) cannot claim. Thirdly, the diet is underpinned
with an extensive database of food composition analysis. Fourthly,
the evidence base for efficacy is strong. Finally, the implementation
of the diet to the world has been greatly facilitated by the provision
of accurate and regularly-updated information on food composition
and dietary principles by the innovative use of a digital smartphone
application, thanks to the insight and work of Jane Muir.
In conclusion, the low FODMAP diet has had a rapid develop-
ment from converting apparently disparate known physiological
effects into a well-structured overarching concept through the in-
novation and hard work of a team of researchers, initially at
Monash University and now across the world.
References
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