FODMAPS, Put simply, FODMAPs are a collection of short-chain carbohydrates (sugars) that aren’t absorbed properly in the gut, which can trigger symptoms in people with IBS. FODMAPs are found naturally in many foods and food additives.

1. Nutrition in the management of gastrointestinal
diseases and disorders: the evidence for the low
FODMAP diet
Shanti Eswaran1
, Jeremy P Farida2
, Jessica Green3
,
Jesse D Miller3
and William D Chey1
A growing interest from both physicians and patients is fueling
research in the interaction of symptoms related to irritable
bowel syndrome (IBS) and diet, particularly the low FODMAP
diet. Recent studies further define the role of these short-chain
fermentable carbohydrates on IBS symptoms and their effects
in different parts of the gastrointestinal tract. Mounting
evidence supports the use of a low FODMAP diet in the clinical
setting, but this dietary approach is not without potential
drawbacks. This review illustrates the mechanisms by which
the low FODMAP diet leads to improvement in IBS symptoms,
summarizes the available clinical evidence, and offers practical
advice regarding implementation of this dietary strategy.
Addresses
1
University of Michigan Health System, Division of Gastroenterology,
Ann Arbor, MI, USA
2
University of Michigan Health System, Department of Internal
Medicine, Ann Arbor, MI, USA
3
NSF International, Ann Arbor, MI, USA
Corresponding author: Eswaran, Shanti (Seswaran@med.umich.edu)
Current Opinion in Pharmacology 2017, 37:151–157
This review comes from a themed issue on Gastrointestinal
Edited by Fedias L Christofi and Adil E Bharucha
For a complete overview see the Issue and the Editorial
Available online 20th November 2017
https://doi.org/10.1016/j.coph.2017.10.008
1471-4892/ã 2017 Elsevier Ltd. All rights reserved.
Introduction
FODMAP is an acronym that stands for fermentable
oligosaccharides, disaccharides, monosaccharides, and
polyols [1]. FODMAPs that are commonly encountered
in the Western diet include lactose, fructose (in excess of
glucose), sugar polyols such as sorbitol and mannitol,
fructans, and galacto-oligosaccharides, which are found
in a number of grains, fruits, vegetables, and dairy, as well
as in beverages, processed food, and food ingredients [2].
FODMAPs are short-chained carbohydrates that share
three main characteristics: poorly absorbed in the small
intestine, osmotically active by virtue of being small, and
rapidly fermentable due to their carbohydrate chain
length [2]. The manner in which the gastrointestinal
(GI) tract responds to the intake of FODMAPs has been
noted as a key factor in triggering the onset of symptoms
and an important differentiator from malabsorption or
intolerance. The data supporting a diet low in FODMAPs
for the treatment of GI diseases are rapidly expanding.
Absorption of FODMAPs
Carbohydrates can be grouped as sugars which include
monosaccharides and disaccharides; polyols, which are
sugar alcohols like sorbitol and xylitol; oligosaccharides
such as galacto-oligosaccharides; and polysaccharides
which account for starches and non-starch carbohydrates
like fructans [3,4]. Absorption of carbohydrates begins
with the breakdown of foods by salivary amylase followed
by pancreatic amylase and other brush border enzymes,
such as lactase and sucrose-isomaltase, to break down
carbohydrates into monosaccharides, which can be
absorbed [3–6]. In addition to hydrolase-dependent
absorption, there are a number of other transport mecha-
nisms which are important in the absorption of individual
short chain carbohydrates.
Lactose is a disaccharide composed of glucose and galac-
tose. It is hydrolyzed in the small intestine by the brush
border enzyme, lactase, to its constituent monosacchar-
ides which are avidly and actively absorbed. In the
absence of lactase, lactose traverses the small bowel
and eventually is utilized as a nutrient source by bacteria
in the distal small bowel and colon [4,5].
Fructose is constructed of a 6-carbon monosaccharide that
is present in the diet in three ways: free fructose, a
substrate of a disaccharide, or as a component of fructans
[1,4]. The small intestine absorption of fructose follows
two different routes: glucose-dependent and glucose-
independent. An important route of fructose absorption
employs the GLUT-2 transporter on the apical mem-
brane on the intestinal epithelium and relies upon the
presence of glucose [7
]. Consumption of glucose and
fructose together in a one to one ratio has shown to
increase the absorptive uptake of fructose in the small
intestine [7
,8,9], and issues of fructose malabsorption
may arise when free fructose is present in the small
intestine in excess of glucose. The second method of
fructose absorption is through carrier-mediated diffusion
via GLUT-5 transporters. The GLUT-5 transport
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2. method has a low-absorptive capacity of approximately
25–50 g of free fructose in healthy persons. Thus, this
system can be easily overwhelmed in the face of excessive
free fructose consumption [7
,8,9].
Polyols (e.g. sorbitol, mannitol, xylitol, and others) are
absorbed via passive diffusion, and similar to other FOD-
MAPs, they may be partially absorbed in the gut lumen.
Unlike their counterparts, however, their absorption may
be more affected by varying molecular sizes, the presence
of any luminal abnormalities, or a combination of both
[5,10]. The 6-carbon chain polyols, sorbitol and mannitol,
are partially absorbed in the small intestine. Yao and
colleagues [10] reported that symptom induction result-
ing from sorbitol and mannitol were more dependent
upon their osmotic properties than malabsorption. They
also found that dosing and co-administering with fructose
increased symptoms in healthy volunteers and IBS
patients. On the other hand, the 4-carbon polyol, erythri-
tol, is relatively well-absorbed in the small intestine,
demonstrating the differential absorptive capacities of
the small intestine for polyols of various molecular sizes.
The abundance of polyols in whole and processed foods
underscores the need for research to better define
expected tolerances of dietary intake in IBS patients.
A number of carbohydrates cannot be digested or
absorbed by the human small intestine. For example,
the human small intestine lacks the enzyme needed to
break down oligosaccharides, which contain fructosyl-
fructose glycoside bonds such as inulin-type fructans
and galacto-oligosaccharides, found in popular foods such
as onions, chicory (inulin), garlic, and legumes. This
ensures that they are delivered to the colon intact where
they are fermented, serving as an important nutrient
source for colonic bacteria [3–5,7
].
How do FODMAPs cause GI symptoms?
The structure of FODMAPs plays an important role in
their likelihood to induce GI symptoms. In general,
shorter chain length and smaller molecules are more
fermentable and osmotically active [11]. Fermentation
of FODMAPs by colonic bacteria produces short chain
fatty acids such as acetic, butyric and propionic acids and
gases including carbon dioxide, methane and hydrogen
[7,10]. The resultant changes in the luminal microenvi-
ronment, luminal distension, and colonic transit [12] are
thought to underpin the development of symptoms in
IBS patients, who have underlying abnormalities in motil-
ity and visceral sensation. In addition, changes in the
luminal microenvironment, including the microbiome
and metabolome, may exert additional, as yet unproven,
effects on barrier function, mucosal immune system
activation, and bile acid metabolism (Figure 1) [13,14].
Though it has been proposed that symptoms in IBS
patients result from the cumulative consumption of the
five different types of dietary FODMAPs, clinical expe-
rience suggests that individuals may be more or less
sensitive to a particular FODMAP over another [1,14].
Recent research has made clear that different FODMAPs
exert differential effects in particular parts of the GI tract.
In a study by Murray and colleagues using magnetic
resonance imaging (MRI) in sixteen healthy volunteers,
the monosaccharide fructose led to increased small bowel
water secretion, while the longer chain fructan, inulin, did
not. On the other hand, while fructose had minimal effect
in the colon, inulin led to increased colonic water secre-
tion and gas production [15
]. In a follow-up study in IBS
patients, the same group found that while MRI changes in
the small bowel and colon in response to FODMAP
challenges were similar in IBS patients and healthy
volunteers, only the IBS patients developed symptoms.
This suggests that abnormal visceral sensation rather than
altered fermentation is important to the development of
symptoms in IBS patients.
A low FODMAP diet may also affect immune regulation.
Hustoft and colleagues recently reported that along with
improved IBS symptoms, a low FODMAP diet led
to lower levels of pro-inflammatory cytokines (IL-6 and
IL-8) [16]. Similarly, urinary histamine (a signaling mol-
ecule known to underlie IBS symptoms) has been shown
to decrease after a low FODMAP diet [17], again suggest-
ing that a low FODMAP diet may have effects on
immune function in patients with IBS.
It would be anticipated that restricting dietary intake of
oligosaccharides (fructans and GOS) which are important
prebiotics in the colon, could have effects on the colonic
microbiome [18]. A recent review identified five studies
which investigated the effects of the low FODMAP diet
on the fecal microbiome in IBS patients. A fifty percent
decrease in total FODMAP consumption was associated
with a 6-fold reduction in Bifidobacteria compared to the
control group consuming FODMAPs alongside their nor-
mal diet. Similar changes were not observed for total
bacteria count or with other bacteria such as Lactobacillus
or Faecalbacterium prauznitzii, both of which are felt to be
favorable colonic bacteria [18].
Clinical efficacy and implementation
Since the first study demonstrating potential clinical
benefits of the low FODMAP diet was published in
2008 [19], practitioners have been utilizing this dietary
approach to treat patients with IBS. The low FODMAP
diet is composed of three distinct phases: elimination,
reintroduction, and maintenance (Figure 2). Thus far, the
entirety of research supporting the low FODMAP diet
has focused on the elimination phase, which typically
lasts about 2–4 weeks, after which symptom improvement
is determined. If a therapeutic response is achieved,
patients then undergo a structured reintroduction phase
(optimally with the help of a dietitian), finally arriving at
152 Gastrointestinal
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3. one’s personal version of a modified low FODMAP diet
(maintenance phase).
In the last ten years, retrospective and randomized stud-
ies of dietary FODMAP restriction have reported symp-
tomatic improvement in 52–76% of IBS patients (Table 1)
[17,20–22
,23
,24–26], leading to widespread adoption of
this approach in clinical practice. However, the results of
randomized, controlled trials in IBS patients have not
been consistently supportive, especially when compared
with other diet interventions (rather than placebo com-
parisons) and when dietary intake was not directly pro-
vided to subjects [21,22
]. Bohn et al. [21] compared the
low FODMAP diet to standard dietary advice in IBS
patients (all subtypes) and found that about half of each
group experienced overall symptom improvement with
the intervention, with no significant difference between
the two groups after 4 weeks. Additionally, treatment
responses for individual IBS symptoms (bloating, abdom-
inal pain) were similar with the low FODMAP diet and
standard dietary recommendations.
Another randomized, controlled trial compared the low
FODMAP diet to usual dietary recommendations for IBS
in 92 American IBS-D subjects over a 4-week period.
Though there was a therapeutic gain of 11% favoring the
low FODMAP diet for the primary end-point of adequate
relief, this difference failed to reach statistical significance
(52% versus 41%, P = 0.31). However, in the low FOD-
MAP group, there were significant improvements in
several key IBS symptoms including pain, bloating,
Evidence for the low FODMAP diet in IBS Eswaran et al. 153
Figure 1
FODMAPs
Bacterial fermentation
Gas production
(CH4, H2, CO2)
Increased
osmotic load
Effects on:
Luminal pH
Trophic
effects
Osmotic
Effects
Microbiome
changes
Increased
biomass •Motility
•Visceral sensation
•Immune activation
•Permeability
Acceleration of
transit time
GI Symptoms
•Pain
•Gas / bloating
•Altered bowel movements
SCFA
(Butyrate, propionate,
acetate)
Current Opinion in Pharmacology
Proposed mechanisms by which FODMAPs result in GI symptoms.
Adapted from Spencer et al. [13].
Figure 2
Elimination
phase
Reintroduction
phase
Maintenance
phase
2-4 weeks
Symptom
Improvement?
• Elimination: Identify FODMAP
sensitive patients.
• Reintroduction: Diversification
to enhance adherence avoid
potential risk of a low FODMAP
diet
• Maintenance: Using
reintroduction to develop a
personalized version of low
FODMAP diet
6-8 weeks
Symptom Relapse?
Indefinite?
Current Opinion in Pharmacology
The low FODMAP diet is comprised of three distinct phases.
www.sciencedirect.com Current Opinion in Pharmacology 2017, 37:151–157

4. and frequency of bowel movements, which were not seen
in the group randomized to usual dietary advice. Further,
the low FODMAP diet led to significantly greater
improvements in disease specific quality of life and
anxiety than usual dietary recommendations for IBS [27].
In the most recently published randomized controlled
trial, Staudacher et al. reported their results of a
2 Â 2 factorial design utilizing sham dietary advice versus
the low FODMAP diet with or without probiotic supple-
mentation (VSL#3, CD Investments VSL Pharmaceuti-
cals Inc., Rome, Italy) in 104 non-constipated IBS
patients [23
]. Blinding in dietary advice trials is notori-
ously difficult and therefore, the sham diet was rigorously
designed to be similarly challenging and restrictive. Sim-
ilar to the US trial, though there was a difference in the
154 Gastrointestinal
Table 1
Summary table of trials of the low FODMAP diet in IBS patients. LFD (low FODMAP diet), IBS (irritable bowel syndrome), IBS-D (IBS-
diarrhea), NC-IBS (non-constipated IBS), IBS-SSS (IBS Symptom Severity Scale), HFD (high FODMAP diet), mNICE (modified National
Institute for Health and Care Excellence), FOS (fructo-oligosaccarides)
Authors Design Participants Length Results
Halmos et al. [20]
2014
Randomized, single-blinded,
placebo-controlled, crossover
30 IBS patients 21 days Endpoints:
Overall gastrointestinal symptoms
on visual analogue scale in last
14 days: LFD (22.8 mm) versus
typical Australian diet (44.9 mm),
P 0.001
LFD group had lower scores on
visual analogue scale for bloating
(P 0.001), pain (P 0.001), and
dissatisfaction with stool
consistency (P 0.001)
Bohn et al. [21]
2015
Randomized, single-blinded 75 IBS patients
LFD versus traditional IBS
diet
4 weeks Endpoints:
IBS-SSS reduction !50%: LFD
(50%) versus traditional IBS diet
(46%), P = 0.72
McIntosh et al. [17]
2016
Randomized, single-blinded 40 IBS patients
LFD versus HFD
3 weeks Endpoints:
IBS symptom reduction !50%: LFD
(72%) versus HFD (21%), P 0.009
Abdominal pain scores: LFD (52%
reduction), P 0.01; HFD had more
days in pain, P 0.05
Peters et al. [29]
2016
Randomized 74 IBS patients
LFD versus hypnotherapy
versus combination
6 weeks Endpoints:
Improvement of overall symptoms:
LFD (71%) versus hypnotherapy
(72%) versus combination (72%),
P = 0.67
Eswaran et al. [22]
2016
Randomized, single-blinded 84 IBS-D patients
LFD versus mNICE diet
4 weeks Endpoints:
Adequate relief of symptoms !50%
of last 2 weeks: LFD (52%) versus
mNICE (41%), P = 0.31
Composite end point: LFD (27%)
versus mNICE (13%), P = 0.13
Bloating responder: LFD (52%)
versus mNICE (26%), P = 0.013
Abdominal pain response: LFD
(51%) versus mNICE (23%),
P = 0.008
Staudacher et al. [23]
2017
Randomized, single blinded 104 NC-IBS patients
LFD versus Sham diet with or
without probiotic
supplementation
4 weeks Endpoints:
Adequate relief of symptoms in past
7 days: LFD total (57%) versus sham
diet total (38%), P = 0.051; per
protocol analysis — LFD total (61%)
versus sham diet total (39%),
P = 0.042
Reduction in total IBS-SSS by
!50%: LFD total (73%) versus sham
diet total (42%), P = 0.0017
Current Opinion in Pharmacology 2017, 37:151–157 www.sciencedirect.com

5. intention-to-treat response rates favoring the low FOD-
MAP diet versus the sham diet for the primary endpoint
of adequate relief of IBS symptoms, this difference failed
to reach statistical significance (57% versus 38%,
P = 0.051). On the other hand, there was a significant
benefit for the low FODMAP diet versus sham diet in
the per protocol analysis (61% versus 39%, P = 0.043).
Additionally, there was an overall decrease in the IBS-
SSS score (mean 173 in low FODMAP v 224 in the sham
diet, P = 0.001) and a significant reduction in key individ-
ual symptom sub-scores. There was no difference when
accounting for probiotic supplementation. The totality of
the reported outcomes pointed toward the clinical effec-
tiveness of the low FODMAP diet over and above placebo.
While the popularity of this diet is increasing, several
shortcomings regarding the quality of evidence have been
raised. Recently, Krogsgaard et al. [28
] conducted a
systematic review highlighting several limitations includ-
ing short duration (no studies longer than 6 weeks despite
the chronic nature of IBS), high degree of performance
bias (eight out of the nine trials), difficulty with blinding,
small sample size, and high risk of design bias. Addition-
ally, there are few comparative efficacy trials comparing
the low FODMAP diet to existing IBS therapies [29],
making it difficult to determine if this approach should be
used as first line therapy.
This approach to the treatment of IBS has been regarded
as highly restrictive, confusing to administer, and associ-
ated with greater costs than a habitual diet. Additionally,
several studies have reported an association with the low
FODMAP diet and decreases in certain fecal bacteria and
short-chain fatty acids thought to be associated with gut
health [16,23
,26,30]. However, it is important to
remember that the elimination phase of this diet is not
meant to be a long-term solution; indeed, if an IBS patient
improves during the elimination phase, the goal is to
systematically reintroduce individual FODMAPs to
determine each patient’s intolerances and tolerances.
Indeed, many of the changes to the microbiome, which
occur with full FODMAP elimination, appear to be
reversible with reintroduction of foods containing FOD-
MAPs [16]. Unfortunately, the current means by which
FODMAP reintroduction is conducted lacks standardiza-
tion and is driven more by the biases and experiences of
providers and patients than by evidence. A standardized,
scientifically validated and structured reintroduction pro-
tocol is needed to guide practitioners and patients
through this phase in terms of optimal dose, duration,
and type of food as FODMAPs are reintroduced to the
level of tolerance.
In general, the use of a registered dietitian with expertise
in GI diseases and the low FODMAP diet is incredibly
Evidence for the low FODMAP diet in IBS Eswaran et al. 155
Table 2
Low FODMAP resources for patients: education, blogs, tips, diet plans, and recipes
Resources Author
Website:
http://www.myginutrition.com/
Pinterest page: https://www.pinterest.com/UMGIdietitians/
University of Michigan
Comprehensive Website
Website:
http://fodmapmonash.blogspot.com.au/
Application for Android and iPhone:
http://www.med.monash.edu/cecs/gastro/fodmap/iphone-app.html
Monash University
Website:
http://blog.katescarlata.com/
Application:
https://itunes.apple.com/us/app/fodmap-grocery-guide/id1220227921?mt=8ign-mpt=uo%3D4
Kate Scarlata, RD, LDH
Website:
http://www.daniellecapalino.com/
Book:
Healthy Gut, Flat Stomach: The Fast and Easy Low-FODMAP Diet Plan
Danielle Capalino, MSPH, RD
Website:
http://www.ibsfree.net/
Pinterest page: http://www.pinterest.com/pcatsos/
Book:
The IBS Elimination Diet and Cookbook: The Proven Low-FODMAP Plan for Eating Well and Feeling
Patsy Catsos, MS, RD, LD
Book:
A Teen’s Guide to Gut Health: The Low-FODMAP Way to Tame IBS, Crohn’s, Colitis, and Other
Digestive Disorders
Rachel Melzer Warren, MS, RD
www.sciencedirect.com Current Opinion in Pharmacology 2017, 37:151–157

6. helpful for patients and will translate directly to higher
adherence and therefore symptom improvement [31]. If a
dietitian is not available, a one-page handout is not
sufficient, but there are several books, applications, and
internet tools available that can help in administering the
low FODMAP diet (Table 2). After teaching, a 2–4 week
elimination phase is generally sufficient to gauge clinical
response though some patients can require up to a 6-week
trial. If symptoms do not improve (and adherence is not a
concern), patients should be instructed to liberalize their
diet. If symptoms improve, then reintroduction can begin,
adding back small amounts of individual FODMAPs to
the level of symptom tolerance. This allows for dietary
diversification, improved adherence, and avoids the
potential for adverse effects of a long-term dietary FOD-
MAP restriction (micronutrient deficiencies, changes to
the microbiome).
It would be beneficial to identify biomarkers which might
target IBS patients more likely to respond to the low
FODMAP diet, given that only a subset of IBS patients
improves, as well as the theoretical concerns regarding
effects on the colonic microbiome and operational/cost-
related issues. Recent work suggests that the gut micro-
biome [32,33], metabolome [17,34], and genetic factors
[35] might provide a means by which to enrich the
likelihood of response to the low FODMAP diet. Given
the high prevalence of IBS and its significant impact on
quality of life, our patients deserve our ongoing efforts
to turn this blunt instrument into a precise tool that
would enable us to engineer a personalized approach to
treatment.
Concluding remarks
The recent shift in IBS treatment to include dietary
modification has been driven not just by physicians
and researchers, but by patients themselves, as they
demand more holistic and integrated approaches for their
symptoms. Given the present limitations of available
pharmaceutical options to treat IBS, diet-based strategies
are especially attractive for functional GI diseases like
IBS. While this approach is gaining popularity amongst
both providers and patients, several areas require refine-
ment: further elucidation of the positive and negative
effects of the elimination phase, standardization of the
reintroduction phase, clarification of mechanisms of ben-
efit, identification of biomarkers which predict response,
and determination of the optimal way to administer this
diet plan in a medically responsible manner. These
comments make clear that the flurry of medical research
in support of the low FODMAP diet, while encouraging,
should be viewed as the beginning, not the end of what
could be a transformative and exciting journey.
Conflict of interest statement
William Chey is a consultant for Nestle Health Sciences.
He receives research funding from Nestle Health
Sciences and True Self Foods. There were no other
conflicts of interest reported by the authors.
References and recommended reading
Papers of particular interest, published within the period of review,
have been highlighted as:
of special interest
of outstanding interest
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