Low FODMAP in 2017: Lessons learned from clinical trials and mechanistic studies.

TLDR: This review article interprets the recent findings reported in this issue of Neurogastroenterology and Motility and summarizes the mechanistic and clinical efficacy data of the low FODMAP diet in IBS patients to date.

Abstract: Given the prevalence of irritable bowel syndrome (IBS) and the suboptimal response to most therapeutic approaches, there has been increasing interest in and adoption of dietary treatment strategies, such as the low Fermentable Oligo-, Di-, & Mono-Saccharides and Polyols (FODMAP) diet. FODMAPs are a diverse group of carbohydrates that exert effects in the gastrointestinal tract not only via fermentation but likely via alterations in the microbiota, metabolome, permeability, and intestinal immunity as well. Clinical evidence for efficacy of this diet is mounting, but there are significant questions regarding short- and long-term safety and effects on the microbiota and nutrition that remain unanswered. This review article interprets the recent findings reported in this issue of Neurogastroenterology and Motility and summarizes the mechanistic and clinical efficacy data of the low FODMAP diet in IBS patients to date.

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Neurogastroenterol Motil. 2017;29:e13055. wileyonlinelibrary.com/journal/nmo 
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https://doi.org/10.1111/nmo.13055
© 2017 John Wiley & Sons Ltd
Received:19January2017
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Accepted:31January2017
DOI: 10.1111/nmo.13055
MINI-REVIEW
Low FODMAP in 2017: Lessons learned from clinical trials and
mechanistic studies
S. Eswaran
Division of Gastroenterology, University of
MichiganHealthSystem,AnnArbor,MI,USA
Correspondence
S. Eswaran, Division of Gastroenterology,
UniversityofMichiganHealthSystem,Ann
Arbor,MI,USA.
Email: seswaran@med.umich.edu
Abstract
Given the prevalence of irritable bowel syndrome (IBS) and the suboptimal response to
most therapeutic approaches, there has been increasing interest in and adoption of
dietary treatment strategies, such as the low Fermentable Oligo- , Di- , & Mono-
SaccharidesandPolyols(FODMAP)diet.FODMAPsareadiversegroupofcarbohy-
drates that exert effects in the gastrointestinal tract not only via fermentation but likely
via alterations in the microbiota, metabolome, permeability, and intestinal immunity as
well. Clinical evidence for efficacy of this diet is mounting, but there are significant
questions regarding short- and long- term safety and effects on the microbiota and
nutrition that remain unanswered. This review article interprets the recent findings
reported in this issue of Neurogastroenterology and Motility and summarizes the mecha-
nisticandclinicalefficacydataofthelowFODMAPdietinIBSpatientstodate.
KEYWORDS
diet, fermentation, irritable bowel syndrome, microbiota
1 | INTRODUCTION
Irritable bowel syndrome (IBS) is a prevalent condition that leads to
considerable morbidity and disability.
1
Despite this, healthcare expen-
ditures for the treatment of organic diseases consume a disproportion-
ate portion of the healthcare pie and leave little for so- called “quality
of life” disorders like IBS. In addition, the heterogeneity inherent to the
phenotype and pathogenesis of IBS has created significant challenges
in drug therapy development for this chronic disease, and the absolute
therapeutic gain from traditional therapies has been marginal, typi-
cally ranging from 7% to 15%.
2
Asaconsequence,providersandIBS
patients are increasingly being forced to find solutions for their symp-
toms that do not involve prescription medications. When one con-
siders that two- thirds of IBS patients associate their symptoms with
eating a meal,
3,4
the importance of finding effective, evidence- based
dietary solutions becomes obvious. Furthermore, IBS patients are de-
manding more “natural,” accessible, cost- effective, and safe options
to treat their disease. Unfortunately, traditional dietary advice for IBS
patients, such as regulating fiber intake or fat content, is not evidence-
based and often has proven ineffective.
5–8
Thus, the low FODMAP
(Fermentable Oligo- , Di- , & Mono- Saccharides and Polyols) diet has
been gaining popularity for the treatment of this condition. This review
article interprets the recent findings of Hustoft et al.
9
reported in this
issue of Neurogastroenterology and Motility and summarizes the mech-
anisticandclinicalefficacydataofthelowFODMAPdietinIBSpa-
tients to date.
2 | MECHANISTIC INSIGHTS
FODMAPs are a diverse group of poorly absorbed carbohydrates
thought to contribute to gastrointestinal symptoms, likely via mul-
tiple pathways (Figure 1). Conventional thinking has focused on the
cumulativeeffectsofconsumingexcessiveamountsofallFODMAPs.
Undigested,non-absorbedFODMAPscreateanosmoticloadandare
then fermented by small intestinal and colonic bacteria. This leads
to the production of short chain fatty acids and gases (hydrogen,
methane, carbon dioxide), which can trigger symptoms particularly
in patients who have underlying abnormalities in gut motility and
visceral sensation.
10,11
Collectively, these effects can exert primary
and secondary effects on motility, visceral sensation, and the gut mi-
crobiota that may result in symptoms of cramping, bloating, disten-
tion, and flatulence in a subset of IBS patients.
12–14
However, recent
work suggests that the various FODMAPs exert different effects

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along the GI tract parts of the GI tract. Using functional magnetic
resonance imaging (fMRI), investigators from the UK showed differ-
ential effects of fructose and fructans in the small intestine and colon
in healthy volunteers and IBS patients.
15,16
Afterfructoseandinulin
(a fructan) challenges, healthy controls had significantly lower symp-
tom scores after either fructose or inulin consumption than patients
with IBS, despite similar fMRI parameters and breath hydrogen re-
sponses.
16
Fructose led to increased small- bowel water content in
both IBS patients and controls (potentially accelerating small- bowel
transit and peristalsis as well) whereas inulin increased colonic vol-
ume and gas via fermentation by resident bacteria. This indicates
that colonic hypersensitivity, rather than greater gas production or
distension,drivesFODMAP-relatedsymptomsinsomeIBSpatients.
Apart from fermentation effects, FODMAPs may also gen-
erate symptoms via immune activation. Given that wheat prod-
ucts contain high FODMAP content, predominantly fructans and
galacto- oligosaccharides (GOS), studies focusing on non- celiac
wheat sensitivity (NCWS) may be potentially extrapolated to IBS pa-
tients.
17,18
Possible mechanisms for NCWS (and thus a response to a
lowFODMAPdiet) includeincreasedintestinal permeabilityoftight
junctions or stimulation of lamina propria macrophages leading to pro-
inflammatory cytokines.
19,20
Histamine, a signaling molecule known to
underlie IBS symptoms, mayalso be affected by the low FODMAP
diet. McIntosh et al.
21
compared urinary metabolomic profiles of 40
IBSpatientsafter21daysofalow-orhigh-FODMAPdiet.Following
dietary intervention there was a significant separation in urinary me-
tabolomic profiles of patients with IBS in the two diet groups. In the
low FODMAP diet group, urinary histamine level decreased signifi-
cantly after the intervention (P<.05)comparedtothehigh-FODMAP
group. The authors postulate that degranulation of mast cells may
occurdueto directsignaling fromshort chainfattyacids(SCFAs)or
from intestinal distension via fermentation, thereby modulating IBS
symptoms.
3 | EVIDENCE OF CLINICAL BENEFIT
There is a growing body of evidence to support the efficacy of the
low FODMAP diet in patients with IBS symptoms.
22–26
The first
study demonstrating a link between dietary FODMAPs and symp-
tomscomesfromShepherdandGibson’s2008Australianworkdur-
ing which IBS patients were more likely to experience gastrointestinal
symptoms after blinded consumption of escalating doses of fructose
or fructans than after glucose.
23
This approach was novel because
until this time, dietary strategies focused on the elimination of a sin-
gle carbohydrate type (ie, lactose, sorbitol, fructose) rather than entire
groups of carbohydrates. Subsequent retrospective and randomized
studies of dietary FODMAP restriction have reported symptomatic
improvement in 52%–76% of IBS patients.
11,24,27–29
Many studies in-
volving diet for IBS suffer from placebo effect, limited duration, lack of
rigorous endpoints, lack of randomization/blinding, and limited dietary
assessment to confirm adherence.
Theresults ofrandomized controlled trials for the lowFODMAP
diet in IBS patients in IBS patients have not been uniformly positive, es-
pecially when compared with active interventions in a more “real world”
setting where food was not supplied to subjects.
30,31
Bohn et al.
31
FIGURE1 Mechanisms by which
Fermentable Oligo- , Di- , & Mono-
Saccharides and Polyols s may cause
Gastrointestinalsymptoms.Adapted
from Spencer M, et al. Current treatment
Options in Gastroenterology. 2014;
12:424- 440
FODMAPs
Osmotic effects
Trophic
effects
Luminal pH
Increased
osmotic load
Microbiome
changes
Increased
biomass
Acceleration of
transit time
Effects on:
• Motility
• Visceral sensation
• Immune activation
• Permeability
• Mast cell activation
GI symptoms
• Pain
• Gas/bloating
• Altered bowel movements
Bacterial fermentation
SCFA
(Butyrate, propionate,
acetate)
Gas production
(CH
4
, H
2
, CO
2
)
Cognitive and
emotional factors
Key Points
• TherearelikelymultiplemechanismsbywhichFODMAPs
exert their effects along the GI tract.
• AlowFODMAPdietislikelyhelpfulintreatingIBSsymp-
toms, but the evidence is not entirely supportive of this
approach.
• ThelowFODMAPdiethaspotentiallimitations,including
effects on the intestinal microbiota and metabolome.

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comparedthelowFODMAPdiettostandarddietaryadviceandfound
that about half of each group improved with the intervention, with no
significant difference between the two groups after 4 weeks. Each
group received dietitian counseling, and all IBS subtypes were included.
Similar improvements in each group were noted for most individual
symptoms as well (bloating, abdominal pain). Our group recently com-
pleted the first US comparative effectiveness trial comparing the low
FODMAPdietvsusualdietaryrecommendationsinIBSpatientswith
diarrhea (IBS- D) using a similar study design in 92 patients.
30
There was
no significant difference between the interventions for the primary
endpointofadequaterelief(52%withalowFODMAPdietvs41%with
usual dietary recommendations. However, a significantly greater pro-
portioninlowFODMAPdietgroupthantheusualdietaryrecommen-
dation group experienced improvement in abdominal pain and bloating,
two of the most bothersome complaints associated with IBS. In addi-
tion, significant improvements were seen in stool consistency, stool fre-
quency, and urgency compared to usual dietary recommendations for
IBS. Significant improvements in quality of life measures, as well as anx-
ietywereseeninthelowFODMAPdietcomparedtousualdietaryrec-
ommendations for IBS.
32
The primary endpoints were negative in both
trials that utilized an active comparator and dietitian- directed dietary
interventions,highlightingsomeofthelimitationsofthelowFODMAP
diet in the clinical setting (see below). However, the results for the
secondary endpoints differed, likely explained by intrinsic differences
in genetics, microbiome, diet, and cultural issues between the study
populations, in addition to variation in dietary advice and IBS subtype.
4 | DIET LIMITATIONS
Althoughthepopularity of this dietary approachhasprogressively in-
creasedworldwide,thelowFODMAPdiethasanumberofimportant
shortcomings. This approach, while clinically effective, is highly restric-
tive and may be confusing to administer, leading to potential problems
withadherence.Anotherissueisthatthefulleliminationphaseisnot in-
tended to be continued indefinitely; if a patient improves during the full
elimination phase, providing tailored dietary counseling to re- introduce
FODMAPcontainingfoodgroupstoarriveateachindividual’sversion
ofthelowFODMAPdietisrecommended.Thedurationofthefulllow
FODMAP diet has potential long-term implications considering that
fermentable carbohydrates such as FODMAPs provide substrates for
“healthy” GI bacteria. Indeed, several studies comparing the effects of
alowFODMAPdiettoahabitualdietdemonstratedareductioninthe
proportion and concentration of Bifidobacteria.
9,24
 Another study did
not demonstrate a decrease in Bifidobacteria, but did show a decrease
in total bacteria abundance,
33
the consequences of which have not been
well characterized. In addition to changing the microbiota, fermenta-
tion creates by-products such as SCFAs, including butyrate, providing
nutrients and other benefits for the colonic mucosa and playing a criti-
cal role in the luminal microenvironment (Figure 1).
34
Thus, while the
low FODMAP diet may improve GI symptoms, long-term avoidance
of FODMAPs may have potentially harmful effects on colon health.
StudiesinvestigatingtheeffectsofthelowFODMAPdietonthecolon
metabolome are conflicting. Halmos etal. found no change in SFCA
concentrationbetweenthelowFODMAPdietandahabitualAustralian
diet,
33
whileothershave observedadecreaseinSCFA comparedtoa
habitual diet.
9
In this issue, Hustoft et al.
9
report the results of a crossover study
designed to investigate the importance of fructo- oligosaccharides
(FOS) in symptom generation in IBS patients. After 3weeks of a low
FODMAP diet, 20 patients with non-constipated IBS received either
10 days of FOS or placebo supplements, followed by a washout period
of 3 weeks, followed by another 10- day cross- over period. The authors
analyzedinflammatorycytokinesthroughoutthestudy,andSCFAsand
gut microbiota composition were analyzed as well. Most patients had
severe IBS symptoms as measured by IBS- SSS. Interestingly, all patients
improvedwiththe lowFODMAPdiet(definedas reductioninat least
50 points IBS- SSS) and all patients completed the trial. When the FOS
supplement was introduced, significantly fewer subjects reported control
of IBS symptoms compared to placebo, with no order effect observed
(80% vs 30%). There was a large inter- subject variability in the responses
to FODMAPprovocation (FOSvs placebo) as compared to FODMAP
reduction. Levels of IL-6 and Il-8 (but not TNF-α) both decreased sig-
nificantlyafter 3weeksofa lowFODMAPdiet,with a medianreduc-
tion of 0.065 pg/mL and of 2.95 pg/mL, respectively. Cytokine levels did
not change in response to FOS supplementation, however. F.prausnitzii,
Actinobacteria, and Bifidobacterium abundance were significantly altered
inbothdietaryinterventions(decreasedinlowFODMAPdiet,increased
againwith FOS supplementation). Levelsoftotal SCFAsandn-butyric
acid both decreased significantly following a low FODMAP diet as
comparedtobaseline,butSCFAlevelswereotherwisenotsignificantly
altered when comparing values from samples obtained at baseline, fol-
lowingalowFODMAPdiet,andafterFOSsupplementation.
This manuscript from Norway addresses several unanswered ques-
tionsaboutthelowFODMAPdiet.Becauseofitscross-overdesign
and lack of worsening symptoms with the maltodextrin placebo, it is
clear that a placebo response is not entirely responsible for the effect
of the diet. In addition, although IBS symptoms significantly worsened
in response to FOS, the severity was not comparable to the symptom
level observed at baseline. This lends weight to the belief that while
individualFODMAPrestrictionmaybe partiallybeneficial,collective
FODMAP restriction (at least in this patient population) maybe re-
quired to achieve maximum symptom response. There was however
a larger inter- subject variability in response to the two supplements,
supportingtheviewthateachpatient’sthreshold/FODMAPsensitiv-
ity is specific and may be individualized.
Based on this and other studies,
21,24,33
it seems clear that the low
FODMAPdiethaseffectsonthemicrobiotaandmetabolome,decreas-
ingSCFAsandbacteria thoughttopromoteGIhealth.The factthat
the abundance of several bacteria (F. prausnitzii,Actinobacteria, and
Bifidobacterium) rebounded after 10 days of FOS supplementation is
reassuring, that the effect of dietary change is temporary. However
after FOS supplementation, both cytokine levels and SCFA levels
were unchanged. Reasons for this are not clear—perhaps 10 days of
FOS supplementation is not of sufficient duration, or that alternate
FODMAPsaredrivingthosechanges.

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5 | UNANSWERED QUESTIONS
TheefficacyofalowFODMAPdietforIBSisbecomingincreasingly
obvious but several areas remain to be clarified: (i) the mechanism(s)
by which FODMAP restriction improves symptoms, (ii) long-term
effects/safety in terms of gut microbiota and potential nutritional
deficiencies, (iii) standardization of a reintroduction protocol, (iv)
whether or not complete exclusion of all FODMAPs is necessary
for full clinical benefit, and (v) improving patient selection to enrich
symptom response. These questions are linked, and as we deter-
minethemechanism(s)bywhichFODMAPexclusionalleviatesIBS
symptoms, the answers to the remaining questions will become more
apparent.
If an IBS patient improves with the full elimination of dietary
FODMAPs,areintroductionphasebeginstodetermineanindividual
patient’sFODMAPintolerances.Givenboththeconcernsaboutlong-
term effectsof the low FODMAPdiet on the microbiotaand over-
all nutrition, as well as the restrictive nature of the diet, the full low
FODMAPdiet isnotmeantto serveasalong-termsolution forpa-
tientswithIBS.ThecurrentmeansbywhichFODMAPreintroduction
is conducted varies dramatically from center to center and is driven by
the biases and clinical experiences of providers rather than evidence. It
is a poorly defined trial- and- error process which is clearly suboptimal
and may expose patients to prolonged or even unnecessary suffer-
ingastheytrytoidentifytheirpersonalFODMAPtriggers.Thereare
currently little scientifically rigorous data to allow an evidence- based
approachto FODMAPreintroductionand consequently,thereis no
widely accepted protocol for this process. This leaves providers to de-
velop their own non- evidence based protocols to address the com-
plexities surrounding (i) specific foods used to challenge patients, (ii)
FODMAPdose,and(iii)durationofexposure.Generatingastructured
reintroduction protocol for clinical practice would serve as a construct
for clinicians worldwide to guide dietitians and patients during this
process. In addition, further investigative efforts should be made to
determine if the observed changes in the microbiota mitigated by the
lowFODMAPdietremainoncecertainFODMAPsarere-introduced
to tolerance.
One could image a future where it may then be possible to con-
structalessrestrictiveversionofthelowFODMAPdiet,whichoffers
similar clinical benefits to most IBS patients. Determining a less re-
strictiveversionofthelowFODMAPdietcouldimproveadherence,
create wider appeal, and ease the financial and logistic burden for this
dietary approach. Facebook, Netflix, and Google currently curate user
content based on our demographics, past purchases, and search his-
tories. There is no reason then that we as clinicians cannot grasp the
tools to do the same for our patients: to curate their care based on
their preferences, symptoms, and biomarker data including stool and
metabolomic profiles.
CONFLICT OF INTERESTS
The author has no competing interests.
AUTHOR CONTRIBUTION
SE wrote the entire manuscript.
REFERENCES
1. Chey WD, Kurlander J, Eswaran S. Irritable bowel syndrome: a clinical
review. JAMA. 2015;313:949-958.
2. Jailwala J, Imperiale TF, Kroenke K. Pharmacologic treatment of the
irritable bowel syndrome: a systematic review of randomized, con-
trolled trials. Ann Intern Med. 2000;133:136-147.
 3. Simrén M, Månsson A, Langkilde AM, et al. Food-related gastro-
intestinal symptoms in the irritable bowel syndrome. Digestion.
2001;63:108-115.
4. Chey WD. The role of food in the functional gastrointestinal dis-
orders: introduction to a manuscript series. Am J Gastroenterol.
2013;108:694-697.
5. Bohn L, Storsrud S, Simren M. Nutrient intake in patients with ir-
ritable bowel syndrome compared with the general population.
Neurogastroenterol Motil. 2013;25(23–30):e21.
6. Heizer WD, Southern S, McGovern S. The role of diet in symptoms of
irritable bowel syndrome in adults: a narrative review. J Am Diet Assoc.
2009;109:1204-1214.
7. Eswaran S, Muir J, Chey WD. Fiber and functional gastrointestinal dis-
orders. Am J Gastroenterol. 2013;108:718-727.
 8. FordAC,TalleyNJ,SpiegelBM,etal.Effectoffibre,antispasmodics,
and peppermint oil in the treatment of irritable bowel syndrome: sys-
tematic review and meta- analysis. BMJ. 2008;337:a2313.
9. Hustoft TN, Hausken T, Ystad SO, et al. Effects of varying dietary con-
tent of fermentable short- chain carbohydrates on symptoms, fecal mi-
croenvironment, and cytokine profiles in patients with irritable bowel
syndrome [published online October 16 2016]. Neurogastroenterol
Motil. 2016. doi: 10.1111/nmo.12969
10. Ong DK, Mitchell SB, Barrett JS, et al. Manipulation of dietary short
chain carbohydrates alters the pattern of gas production and gene-
sis of symptoms in irritable bowel syndrome. J Gastroenterol Hepatol.
2010;25:1366-1373.
11. Shepherd SJ, Lomer MC, Gibson PR. Short- chain carbohydrates
and functional gastrointestinal disorders. Am J Gastroenterol.
2013;108:707-717.
12. Gibson PR, Newnham E, Barrett JS, Shepherd SJ, Muir JG. Review arti-
cle: fructose malabsorption and the bigger picture. Aliment Pharmacol
Ther. 2007;25:349-363.
13. Brighenti F, Casiraghi MC, Pellegrini N, Riso P, Simonetti P, Testolin
G. Comparison of lactulose and inulin as reference standard for the
study of resistant starch fermentation using hydrogen breath test. Ital
J Gastroenterol. 1995;27:122-128.
14. TazoeH,OtomoY,KajiI,TanakaR,KarakiSI,KuwaharaA.Rolesof
short- chain fatty acids receptors, GPR41 and GPR43 on colonic func-
tions. J Physiol Pharmacol. 2008;59(suppl 2):251-262.
15. Murray K, Wilkinson-Smith V, Hoad C, et al. Differential effects of
FODMAPs(fermentableoligo-,di-,mono-saccharidesandpolyols)on
small and large intestinal contents in healthy subjects shown by MRI.
Am J Gastroenterol. 2014;109:110-119.
16. Major G, Pritchard S, Murray K, et al. Colon hypersensitivity to disten-
sion, rather than excessive gas production, produces carbohydrate-
related symptoms in individuals with irritable bowel syndrome.
Gastroenterology. 2017;152:124-133 e122.
17. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson
PR. No effects of gluten in patients with self- reported non- celiac gluten
sensitivity after dietary reduction of fermentable, poorly absorbed, short-
chain carbohydrates. Gastroenterology. 2013;145(320–328):e321-e323.
18. Biesiekierski JR, Iven J. Non- coeliac gluten sensitivity: piecing the
puzzle together. United European Gastroenterol J. 2015;3:160-165.

|
5 of 5
ESWARAN
19. VerduEF,ArmstrongD,MurrayJA.Betweenceliacdiseaseandirri-
table bowel syndrome: the “no man’s land” of gluten sensitivity. Am J
Gastroenterol. 2009;104:1587-1594.
20. Vazquez-RoqueMI,Camilleri M,SmyrkT, etal.Acontrolledtrialof
gluten- free diet in patients with irritable bowel syndrome- diarrhea:
effects on bowel frequency and intestinal function. Gastroenterology.
2013;144:903-911.
21. McIntoshK,ReedDE,SchneiderT,etal.FODMAPsaltersymptoms
and the metabolome of patients with IBS: a randomised controlled
trial. Gut [published online March 14 2016]. 2016. doi: 10.1136/
gutjnl-2015-311339
22. Eswaran S, Tack J, Chey WD. Food: the forgotten factor in the irritable
bowel syndrome. Gastroenterol Clin North Am. 2011;40:141-162.
23. Shepherd SJ, Parker FC, Muir JG, Gibson PR. Dietary triggers of ab-
dominal symptoms in patients with irritable bowel syndrome: ran-
domized placebo- controlled evidence. Clin Gastroenterol Hepatol.
2008;6:765-771.
24. StaudacherHM, LomerMC,AndersonJL,etal.Fermentablecarbo-
hydrate restriction reduces luminal bifidobacteria and gastrointes-
tinal symptoms in patients with irritable bowel syndrome. J Nutr.
2012;142:1510-1518.
25. Staudacher HM, Whelan K, Irving PM, Lomer MC. Comparison of
symptom response following advice for a diet low in fermentable
carbohydrates(FODMAPs)versusstandarddietaryadviceinpatients
with irritable bowel syndrome. J Hum Nutr Diet. 2011;24:487-495.
26. Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG. A diet
low in FODMAPs reduces symptoms of irritable bowel syndrome.
Gastroenterology. 2014;146:67-75.
27. Shepherd SJ, Gibson PR. Fructose malabsorption and symptoms of ir-
ritable bowel syndrome: guidelines for effective dietary management.
J Am Diet Assoc. 2006;106:1631-1639.
28. Staudacher HM, Whelan K, Irving PM, Lomer MC. Comparison
of symptom response following advice for a diet low in
fermentable carbohydrates (FODMAPs) versus standard dietary
advice in patients with irritable bowel syndrome. J Hum Nutr Diet.
2011;24:487-495.
29. deRoestRH,DobbsBR,ChapmanBA,etal.ThelowFODMAPdiet
improves gastrointestinal symptoms in patients with irritable bowel
syndrome: a prospective study. Int J Clin Pract. 2013;67:895-903.
30. EswaranSL,CheyWD,Han-MarkeyT,BallS,JacksonK.Arandom-
ized controlled trial comparing the low FODMAP diet vs. modi-
fied NICE guidelines in US adults with IBS- D. Am J Gastroenterol.
2016;111:1824-1832.
31. BohnL, StorsrudS, Liljebo T, et al. Diet lowin FODMAPs reduces
symptoms of irritable bowel syndrome as well as traditional di-
etary advice: a randomized controlled trial. Gastroenterology.
2015;149(1399–1407):e1392.
32. Eswaran S, Chey W, Jackson K, Pillai S, Chey S, Han-Markey T. A
lowFODMAPdiet improves qualityof life, reducesactivity impair-
ment, and improves sleep quality in patients with irritable bowel syn-
drome and diarrhea: results from a U.S. randomized, controlled trial.
Gastroenterology. 2016;150:S172.
33. HalmosEP,ChristophersenCT,BirdAR,ShepherdSJ,GibsonPR,Muir
JG.DietsthatdifferintheirFODMAPcontentalterthecoloniclumi-
nal microenvironment. Gut. 2015;64:93-100.
34. Hamer HM, Jonkers D, Venema K, Vanhoutvin S, Troost FJ, Brummer
RJ. Review article: the role of butyrate on colonic function. Aliment
Pharmacol Ther. 2008;27:104-119.
How to cite this article:EswaranS.LowFODMAPin2017:
Lessons learned from clinical trials and mechanistic studies.
Neurogastroenterol Motil. 2017;29:e13055. https://doi.
org/10.1111/nmo.13055