Gastroenterology 2014;146:67–75

CLINICAL—ALIMENTARY TRACT
A Diet Low in FODMAPs Reduces Symptoms of Irritable
Bowel Syndrome1

Department of Medicine, Eastern Health Clinical School, Monash University, Box Hill, Victoria, Australia; 2Department of
Gastroenterology, Central Clinical School, Monash University, Melbourne, Victoria, Australia

See Covering the Cover synopsis on page 1; see
editorial on page 10.
BACKGROUND & AIMS: A diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols(FODMAPs) often is used to manage functional gastrointestinal symptoms in patients with irritable bowel syndrome (IBS), yet there is limited evidence of its efﬁcacy,
compared with a normal Western diet. We investigated theeffects of a diet low in FODMAPs compared with anAustralian diet, in a randomized, controlled, single-blind,cross-over trial of patients with IBS. METHODS: In a studyof 30 patients with IBS and 8 healthy individuals (controls,
matched for demographics and diet), we collected dietarydata from subjects for 1 habitual week. Participants thenrandomly were assigned to groups that received 21 days ofeither a diet low in FODMAPs or a typical Australian diet,followed by a washout period of at least 21 days, before
crossing over to the alternate diet. Daily symptoms wererated using a 0- to 100-mm visual analogue scale. Almost all
food was provided during the interventional diet periods,
with a goal of less than 0.5 g intake of FODMAPs per meal
for the low-FODMAP diet. All stools were collected fromdays 17–21 and assessed for frequency, weight, water content, and King’s Stool Chart rating. RESULTS: Subjects with
IBS had lower overall gastrointestinal symptom scores (22.8;
95% conﬁdence interval, 16.7–28.8 mm) while on a diet low
in FODMAPs, compared with the Australian diet (44.9; 95%
conﬁdence interval, 36.6–53.1 mm; P < .001) and the subjects’ habitual diet. Bloating, pain, and passage of wind also
were reduced while IBS patients were on the low-FODMAP
diet. Symptoms were minimal and unaltered by either dietamong controls. Patients of all IBS subtypes had greater
satisfaction with stool consistency while on the low-FODMAP
diet, but diarrhea-predominant IBS was the only subtype withaltered fecal frequency and King’s Stool Chart scores. CONCLUSIONS: In a controlled, cross-over study of patients with
IBS, a diet low in FODMAPs effectively reduced functional
gastrointestinal symptoms. This high-quality evidence supports its use as a ﬁrst-line therapy. Clinical Trial number:
ACTRN12612001185853.
Keywords: Clinical Trial; Food Intolerance; Abdominal Pain;
Short-Chain Carbohydrates.

Despite irritable bowel syndrome (IBS) being themost common gastrointestinal condition presenting
to gastroenterologists, therapy has been unsatisfactory. The
majority of patients note food as a trigger of symptoms.1,2Diet as a therapy, however, has not been a central platform for management, mainly because the evidence base for
reduction or exclusion of speciﬁc foods such as wheat anddairy3 has been poor.
A diet with increasing evidence of efﬁcacy for the
management of IBS is the low fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) diet.4 FODMAPs5 are poorly absorbed short-chain
carbohydrates including fructose (in excess of glucose),
lactose, polyols, fructans, and galacto-oligosaccharides.
Although individually shown to contribute to IBS
symptoms,6–8 the concept of considering all of these sugars
collectively as a treatment for IBS is relatively new.5 The
potential beneﬁts of restricting a spectrum of FODMAPs in
the diet was ﬁrst shown in a retrospective study thatshowed that 74% of selected patients with both IBS andfructose malabsorption responded well to restriction offructose and fructans (and polyols if the patients noted
symptom induction) of 2–40 months’ duration.9 This thenwas followed up with a randomized, double-blinded, placebo-controlled, rechallenge trial using fructose and fructan, alone and in combination, in selected patients with IBS
and fructose malabsorption who had responded to thediet.10 Symptoms were induced in 4 of 5 study participantson the individual and combined FODMAP solutions
compared with fewer than 1 in 5 with placebo (glucose).
The symptoms were dose-dependent and fructose andfructans had additive effects.10
Understanding of FODMAPs encompasses mechanismsof action, being luminal distension from their osmotic

Abbreviations used in this paper: FODMAP, fermentable oligosaccharides,
disaccharides, monosaccharides, and polyol; FWC, fecal water content;
IBS, irritable bowel syndrome; IBS-C, constipation-predominant irritablebowel syndrome; IBS-D, diarrhea-predominant irritable bowel syndrome;
IBS-M, mixed diarrhea and constipation irritable bowel syndrome; IBS-U,
neither diarrhea nor constipation irritable bowel syndrome; KSC, King’s
Stool Chart; VAS, visual analogue scale.
© 2014 by the AGA Institute0016-5085/$36.00
http://dx.doi.org/10.1053/j.gastro.2013.09.046

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Emma P. Halmos,1,2 Victoria A. Power,1 Susan J. Shepherd,1 Peter R. Gibson,1,2
and Jane G. Muir1,2

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Halmos et al

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effect11 and rapid fermentation preferentially tohydrogen.12 These ﬁndings, together with support ofcontinually expanding food composition analysis, have led
to widespread application of the low FODMAP diet tomanage IBS symptoms throughout Australia and New Zealand, and in some parts of Europe and North America.
In fact, a research center in the United Kingdom found thelow FODMAP diet to be superior to their national guidelines
in IBS management in a nonrandomized, comparative
study.13
Despite the extensive use of this therapy, the only blinded, randomized, controlled trial of efﬁcacy for the low
FODMAP diet in unselected IBS subjects comprised a 2-day
interventional trial comparing low FODMAP with a very
high FODMAP diet in 15 patients with IBS12; few studies
have included healthy controls. There is, therefore, a large
gap in high-quality evidence of the efﬁcacy of the low
FODMAP diet compared with a diet of normal FODMAP
content in unselected patients with IBS.
The present study aimed to ﬁll the major gaps in evidence for the efﬁcacy of the low FODMAP diet by performing a randomized, controlled, cross-over trial. This
trial compared gastrointestinal symptoms over 3 weeks ofa low FODMAP diet with moderate FODMAP intake on a
typical Australian diet in unselected patients with IBS
who had not previously received advice from a dietitian.
As is best practice to investigate the effects of a speciﬁc
dietary manipulation, all food was provided to patients
who were naive to the diet.14 To determine the speciﬁcity
of any observed effects to patients with IBS, a healthy
control population also was included in the interventional
study.

Materials and Methods
Participants
Patients with IBS according to Rome III criteria15 andhealthy controls without gastrointestinal symptoms wererecruited between April 2009 and June 2011 via advertisements in breath testing centers, community newspapers, andthrough word of mouth. Exclusion criteria comprised exclusion of celiac disease by duodenal biopsy and/or negativeceliac serologic testing while consuming a gluten-rich dietand/or negative HLA-DQ2/DQ8 for IBS patients, previous
abdominal surgery, and comorbid conditions such as diabetes.
All patients must not have previously visited a dietitian for
dietary management of IBS or currently taking any othertherapies for IBS. Patients were not permitted to take pharmacologic agents to alter their symptoms (such as laxatives orantidiarrheal agents). Patients with IBS were assessed by agastroenterologist to ensure inclusion and exclusion criteria
were met and further investigations were performed if
organic disease was implicated. Patients with IBS were
subclassiﬁed further as diarrhea-predominant (IBS-D),
constipation-predominant (IBS-C), those with both diarrhea
and constipation (IBS-M), and those with neither diarrhea nor
constipation (IBS-U).15 Past medical investigations were
documented including results of any breath tests performed
for sugar malabsorptions.

Gastroenterology Vol. 146, No. 1

Study Protocol
During a habitual baseline week, participants recorded theirdietary intake in a food diary and included details about ingredients, brands of foods (if appropriate), cooking methods,
and quantity consumed. Participants recorded their baseline
symptoms daily.
Participants then were randomized according to acomputer-generated order to receive 21 days of a diet low in
FODMAPs or 21 days of a diet containing FODMAP content of atypical Australian diet.16 Participants were blinded to the diets
and almost all food was provided. After this 21-day diet, eachparticipant entered a washout period of at least 21 days inwhich they resumed their usual diet and then crossed-over tothe alternate diet. The second interventional diet was notcommenced until the symptoms had returned to the same level
as during the baseline period, as determined by direct questioning by a study investigator. From days 17 to 21 of bothinterventional periods, participants collected all feces. Participants were instructed to collect each stool in a supplied plastic
container and to avoid urine contamination. The containers
were sealed and immediately stored in a supplied portable -4 C
freezer. Each container was marked with the date and time ofstool passage. The freezers were transported and delivered to
the laboratory within the week after the 5-day collection.
On day 19 of both interventional diets, participants
collected hourly breath samples from 12 midday to 8 PM into
breath collection bags and the content of hydrogen was
analyzed via a Quintron BreathTracker Digital Microlyzer(Quintron Instrument Company, Milwaukee, WI).
All participants provided written informed consent before
commencement of the study. The study protocol was approvedby the Eastern Health and Monash University Human Researchand Ethics Committees. The protocol was registered with theAustralianNew
Zealand
Clinical
TrialsRegistry(ACTRN12612001185853). All authors had access to the study
data and reviewed and approved the ﬁnal manuscript.

Interventional Diets
Almost all food, comprising 3 main meals and 3 snacks
daily, was provided. Detailed meal plans specifying meals andquantities were supplied (Supplementary Table 1 andSupplementary Figure 1). However, participants were instructed to eat to their appetite, and additional food lists were
provided so that they could purchase fresh perishable items
and additional food if participants wanted more. The supplemented foods contained at least one FODMAP for thosefollowing the typical Australian diet or were low FODMAP of 
0.5 g per sitting as previously described on the low FODMAP
diet.10 If participants ate a meal outside of their home orwanted to include foods that were not speciﬁed on the supplied
lists, they contacted the study investigator for guidance.
The study investigator (E.P.H.) and university research chef,
assisted by 2 hospitality students, prepared all food in commercial kitchens. Meals were provided as frozen complete
meals with instructions to thaw and warm either via microwave or oven. They were free of charge and delivered to participants’ homes weekly. All food consumed was recorded infood diaries and adherence to the diet was based on these records. If a participant consumed a high FODMAP meal during
the low FODMAP diet or had a day of no high FODMAP-

containing foods17–19 during the typical Australian diet, thatparticipant was considered noncompliant for that day.
The interventional diets were analyzed for energy, macronutrients, sugars, starch, and ﬁber via FoodWorks (Xyris Software Pty, Ltd, Brisbane, Queensland, Australia). Resistantstarch was estimated from published data20–23 and both diets
contained gluten. A daily average of 3 g psyllium and 5 g
Hi-Maize 220 (National Starch & Chemical Company, Bridgewater, NJ) were mixed in with the meals of the low FODMAP
diet to match the diets for ﬁber and resistant starch, respectively. The meal plans were aimed to provide an average of 8
MJ/day and to meet the recommended servings of all foodgroups according to the Australian dietary guidelines.24 Both
diets also aimed to be low in lactose (<5 g per sitting).25
Because lactose is present in much higher concentrations in
the diet than all other FODMAPs, the presence of lactase deﬁciency and subsequent malabsorption of large loads of lactose
may mask the inﬂuence of the other FODMAPs. Dietary concentrations and absorption of all other FODMAPs is less variable.26 The low FODMAP diet aimed to keep oligosaccharide,fructose in excess of glucose, and polyol content of less than 0.5 geach per sitting based on previously published data,10 and thetypical Australian diet aimed to mimic the FODMAP content
previously estimated by a validated food frequency questionnaire to be typically a daily content of 4.4 g oligosaccharides
and 2.6 g polyols.16 The FODMAP content for all provided foodunderwent FODMAP analysis via high-performance liquid
chromatography and enzymatic assays.

Gastrointestinal Symptoms
Gastrointestinal symptoms were measured daily during thebaseline week and interventional diet periods using a 100-mm
visual analogue scale (VAS), where 0 indicated no symptoms
and 100 represented the worst symptoms ever experienced.
The VAS score was used to measure overall gastrointestinal
symptoms, abdominal pain, bloating, passage of wind, anddissatisfaction with stool consistency as previously applied.10
Differences of 10 mm or more arbitrarily were consideredclinically signiﬁcant.

Fecal Assessment
A single independent observer noted the fecal frequency,
weighed each stool, and rated each stool using the validated
King’s Stool Chart (KSC),27 which considers fecal frequency,
consistency, and weight, and converts it to a daily numericscore. A higher score indicates more frequent, looser, andheavier stools.
To assess fecal water content (FWC), the 5-day fecal samples were defrosted, pooled, and thoroughly mixed, and thentransferred into a small specimen container. Each sample wasweighed and freeze-dried using Operon (Thermo Fisher Scientiﬁc Australia; Scoresby, Victoria, Australia), and thenreweighed, which enabled the calculation of wet weight and dryweight. The FWC was expressed as a percentage.

End Points
The primary end point was the difference in overall
gastrointestinal symptoms on the low FODMAP compared witha typical Australian diet averaged over the last 14 days of each

FODMAPs and IBS

69

of the interventional dietary periods in the IBS cohort
measured by the 100-mm VAS.
Secondary end points included differences in speciﬁc
symptoms of abdominal pain, bloating, passage of wind, anddissatisfaction with stool consistency on the low FODMAP
compared with a typical Australian diet averaged over the last
14 days of each diet in both the IBS and healthy cohorts
measured by the 100-mm VAS; differences in gastrointestinal
symptoms between the baseline and interventional dietary
periods; and differences in fecal frequency, weight, FWC, andKSC score on the last 5 days of the low FODMAP diet comparedwith a typical Australian diet in the IBS and healthy cohorts.

Statistical Analysis
Power calculations were based on consensus opinion
because previously published data were not suitable. The assumptions made were that the minimum detectable differencein the primary end point was 20 mm on the 100-mm VAS, andthat the variance of that difference was 25 mm for an 80%
power and a P value of .05. According to these assumptions, 27
IBS patients would be required for this positive treatment
cross-over. No power calculations were conducted for healthy
participants. Study recruitment continued until 30 IBS participants completed the study, at which time 8 healthy participantsalso had completed the study. Only participants who attemptedboth the low FODMAP and typical Australian diet were includedin the analysis to enable better representation of the primary
end point of symptom change between the 2 interventional
diets. Symptom data of participants who ceased an interventional diet before the 21-day period were adjusted by carrying
forward the last observation.
All descriptive data, including participant demographics,
were parametric and presented as the mean and 95% conﬁdence interval unless otherwise speciﬁed. A comparison ofsymptoms and fecal characteristics between participant groups
was made by one-way analysis of variance with a post hoc
Tukey multiple comparison analysis, and observations ofdiffering treatment arms within participant groups wereanalyzed by paired t tests. Breath hydrogen data were
nonparametric, summarized by area under the curve, andanalyzed by Wilcoxon signed rank test. All statistical tests wereanalyzed with GraphPad Prism software (version 6; GraphPad
Software, La Jolla, CA). A P value of .05 or less was considered
statistically signiﬁcant.

Results
Participants
Forty-ﬁve participants were recruited for the study.
Seven participants (3 IBS and 4 healthy controls) quit the
study before commencing their second diet and were
excluded from analysis. Six of these 7 participants werefemale, with a median age of 28 years (interquartile range[IQR], 21–29 y), body mass index of 23.6 (IQR, 20.3–25.4),
and none of them had undergone previous breath testing forfructose malabsorption. Five participants exited the study
because the study protocol was too demanding (3 healthy
participants exited after the ﬁrst interventional diet, 1 IBS
subject exited the study after 8 days of the low FODMAP
diet, and 1 IBS subject exited the study after the baseline

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Table 1.Comparison of Subject Demographics and Baseline
Diet Characteristics Between IBS and Healthy
Cohorts

IBS (n ¼ 30)

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Demographics
21 (70%)Femalea41 (29–53)
Age, yb
24 (23–26)
Body mass indexb
Fructose malabsorberc 17/22 (77%)
Baseline dietary intake
Energy, MJ
9.1 [8.4–9.9]
Protein, g93.6 [84.1–103]
Fat, g87.8 [77.9–97.6]
Carbohydrates, g
233 [205–260]
Sugars, g
107 [87.8–127]
Starch, g
138 [123–153]
Fiber, g
24.0 [21.1–26.8]
16.3 [14.1–18.5]
Total FODMAPsd
Oligosaccharides, g
3.8 [3.3–4.3]
Polyols, g
1.7 [1.3–2.1]
Lactose, g
10.8 [8.5–13.1]
18.3 [13.9–22.7]
Fructose,d g
Glucose, g
23.4 [17.4–29.3]
GlutenPresent
Baseline gastrointestinal
symptoms
Overall
36.0 [29.5–42.5]
Bloating
37.6 [29.6–45.6]
Abdominal pain
35.5 [28.2–42.8]
Passage of wind39.0 [31.7–46.3]
Dissatisfaction with35.1 [27.7–42.4]
stool consistency

Healthy
controls(n ¼ 8)Pvalue

6 (75%)
31 (23–60)
24 (23–27)
2/4 (50%)

NS
NS
NS
NS

8.3 [7.2–9.3]
88.0 [74.2–102]
78.8 [63.6–93.8]
208 [158–259]
100 [63.4–137]
116 [86.7–145]
20.6 [16.2–25.0]
16.5 [11.4–21.8]
3.5 [2.7–4.3]
2.0 [0.7–3.3]
11.0 [7.0–15.1]
19.2 [8.6–29.8]
25.3 [13.2–37.4]
Present

NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS

17.8 [4.0–31.7]
18.1 [4.9–31.2]
14.8 [3.2–26.4]
23.1 [10.3–35.9]
21.2 [11.1–31.3]

.012
.022
.008
.041
.068

testing, 1 previously had been referred despite no presenceof IBS, and 2 performed a breath test shortly after study
completion. Of the 30 IBS participants, 10 had IBS-D, 13 had
IBS-C, 5 had IBS-M, and 2 had IBS-U. Participants’ baseline
diets were similar with no obvious differences in any nutrients including energy, ﬁber, or FODMAPs (Table 1). All
participants completed the study diets, except for 6 IBS
participants who could not complete the typical Australian
diet owing to unbearable symptoms. Their symptoms on
exiting the study were carried forward for the remaining
days on the typical Australian diet. In all participants, thelevel of symptoms returned to baseline levels during thewashout period, but 5 participants with IBS extended thisperiod for holidays and 3 for personal reasons. Three IBS
and 1 healthy participant did not collect fecal samples onboth diets, so fecal analysis was not included for theseparticipants.

Interventional Diets
The nutritional composition of the interventional diets isshown in Table 2. The only quantiﬁed difference in nutrient
content of the diets was the average daily intake of
FODMAPs.

Symptoms

NOTE. Data are presented as mean [95% CI] and comparedby unpaired t test except where speciﬁed. Statistically signiﬁcant differences are shown in bold.
an (percentage of total); the Fisher exact analysis was used.
bMedian (IQR).
cn/subjects who undertook breath hydrogen testing afteringestion of 35 g fructose (percentage of total); the Fisher
exact analysis was used.
d
Total FODMAP content does not include fructose in excess
of glucose that cannot be estimated from the FoodWorks
program.

diet), 1 healthy participant had an eating disorder emerge
and exited the typical Australian diet after 12 days, and 1
IBS subject was removed for major protocol violation inwhich the participant did not adhere to the allocated low
FODMAP diet for any of the 7 days that was completed
before withdrawal. Of the remaining 38 participants, 30 had
IBS and 8 were healthy controls. The IBS and healthy
cohorts were well matched for sex, age, and body mass index, and 26 participants had breath hydrogen testing forfructose malabsorption (Table 1). Fourteen of the 22 IBS
participants had performed breath testing before study
enrolment and the remaining 8 participants performed
breath testing shortly after study completion. Of the 4
healthy subjects who had performed fructose breath testing,
1 previously had participated in research involving breath

During the baseline period, the overall gastrointestinal
symptoms in the IBS group were 36.0 mm on the VAS[95% CI, 29.5–42.5mm], which were of similar severity topreviously published data.28,29 During the dietary intervention periods, the severity of overall gastrointestinal symptoms diverged, with the greatest difference seen after the ﬁrst
Table 2.The Mean Daily Nutrition Information of Provided
Low and Typical Australian FODMAP Diets
Per day

TypicalAustralian diet

Low
FODMAP diet

P
value

Energy, MJ
8.17 [7.37–8.97] 8.17 [7.09–9.24]
NS
Protein, g
96.1 [84.7–107] 98.1 [83.7–113]
NS
Fat, g71.6 [49.4–93.8] 74.4 [51.9–97.0]
NS
Carbohydrate, g
219 [180–259]
215 [181–249]
NS
Sugars, g
120 [103–137]
122 [106–139]
NS
Starch, g
94.0 [52.8–135] 95.4 [59.7–131]
NS
NSTotal dietary ﬁber,a g 29.7 [23.9–35.7] 30.4 [24.2–36.5]
Fiber, g25.9 [21.3–30.6] 23.4 [18.7–28.2]
NS
Resistant starch, g
3.74 [1.85–5.63] 6.93 [3.56–10.3]
NS
Total FODMAPs, g 23.7 [16.9–30.6] 3.05 [1.86–4.25]<.001
Oligosaccharides, g 5.49 [2.34–8.65] 1.57 [0.47–2.66].009
Polyols, g
4.21 [2.57–5.85] 0.20 [-0.04 to 0.44] .002
Lactose, g
1.35 [0.20–2.49] 0.05 [-0.01 to 0.10] .033b
Fructose in excess 12.7 [8.06–17.3] 1.24 [0.41–2.07].001
of glucose, gGlutenPresent
Present

NOTE. Diets were matched for all nutrients except daily
FODMAPs, indicated in bold (paired t test).
aTotal dietary ﬁber comprises ﬁber and resistant starch.
b
Although there is a signiﬁcant difference in lactose, 5 glactose per sitting is considered well absorbed and tolerated
in the majority of people.25

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71

Stool Analysis
The results of complete fecal samples that were collected
over the last 5 days of each dietary period are shown in
Supplementary Table 2.
Within the IBS group, no differences in the fecal indiceswere found across the subtypes with the exception of the
KSC score, which was higher in the IBS-D group comparedwith the IBS-C group, but only on the typical Australian diet(P ¼ .002). In the IBS-D subgroup, both the KSC score (P <.001) and the FWC (P ¼ .004) were higher compared withhealthy controls, again only on the typical Australian diet(Supplementary Figure 2).
As shown in Supplementary Table 2, the only signiﬁcantdifferences in fecal characteristics were a lower KSC score
and reduced stool frequency on the low FODMAP dietcompared with the typical Australian diet in IBS-D subtype.
No other differences were observed.

Figure 1. Mean overall gastrointestinal symptoms from the(A) IBS cohort and the (B) healthy cohort using a VAS duringbaseline, low FODMAP and typical Australian diets. Symptoms improved signiﬁcantly on low FODMAP compared withbaseline and the typical Australian diet for the IBS cohort. No
differences were observed between any of the diets in thehealthy cohort.

7 days, and thereafter was maintained (Figure 1A). Comparedwith baseline, the overall gastrointestinal symptoms in thelast 14 days of the dietary intervention periods were less on
the low FODMAP diet at 22.8 mm on the VAS [95% CI,
16.7–28.8 mm] (P < .001; repeated-measures analysis
of variance) and greater on the typical Australian diet at
44.9 mm on the VAS [95% CI, 36.6–53.1 mm] (P < .001)(Figure 1A). The difference between the diets was statisticallysigniﬁcant (P < .001). Improvement in overall gastrointestinal symptoms of more than 10 mm was observed in 21 of
30 participants (70%). This observation was of comparable
proportion in IBS subjects with known positive fructose
malabsorption (12 of 17; 70%), no fructose malabsorption (3of 5; 60%), and those with no prior breath testing (6 of 8;75%). Similar results were seen in abdominal pain, bloating,and passage of wind (Figure 2A–C), and dissatisfaction withstool consistency, in which the difference was observed inboth the IBS-D and IBS-C subtypes (Figure 2D and E). The
IBS-M and IBS-U subgroups were too small to analyze. The

Adherence
Adherence to the diets was assessed through recorded
food diaries. The median (range) number of days in which
participants were adherent for the 42 days of the combinedinterventional diets was 41 (33–42) for the IBS and 42(39–42) for the healthy cohort. If adherence for at least 17
days of the 21 days of controlled diet (>81% of the days)
was arbitrarily considered compliant, then all participants
were adherent to the typical Australian diet, and 80% of IBS
participants (24 of 30) and 100% of healthy controls wereadherent to the low FODMAP diet.
Another method of assessing adherence was the hourly
breath tests that were conducted on day 19 of the 2controlled diets (Supplementary Figure 3). The area under
the curve for breath hydrogen on the low FODMAP diet(22.8 IQR, 14.3–44.4 ppm$ 8 h) was less in all participants
than that on the typical Australian diet (80.9 IQR,
46.8–159.8 ppm$ 8 h; P < .001).

Success of Blinding
To assess the blinding of the diets, each participant was
asked to identify the diet that they thought was designed to
manage IBS symptoms on completion of the study. Thirtyone of 38 participants answered the question. In thesubject groups, 17% of the IBS and 71% of the healthy
participants could not correctly identify the low FODMAP
diet. There was also no order effect because the ratio of

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scores for individual symptoms (bloating, abdominal pain,
passage of wind, and dissatisfaction with stool consistency)
as well as composite symptom scores of abdominal pain,
bloating, and dissatisfaction with stool consistency are shownin Table 3.
The healthy subjects had very low scores at baseline foroverall gastrointestinal symptoms 17.0 mm on the VAS[95% CI, 4.0–31.7mm]. During the dietary intervention
arms, there was no evidence of any divergence of symptom
severity between the diets. In fact, no change was observedfor overall or individual symptoms (Figure 1C and Table 3).

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Figure 2. Mean symptomsof(A)
bloating,(B)abdominal pain, and (C)passage of wind from the
IBS cohort using a VAS
while following a typical
Australian and low FODMAP diet. Mean dissatisfaction
with
stool
consistency in (D) IBS-D
and (E) IBS-C after 8–21
days of typical Australianand low FODMAP diets areindicated with a bold line.
Symptoms were signiﬁcantly lower on low FODMAP compared with atypical Australian diet in allmeasured symptoms.

overall gastrointestinal symptoms on the low FODMAP totypical Australian diet was similar when the low FODMAP
diet was given ﬁrst (0.73; [95% CI], 0.41–1.04) comparedwith those participants in which it was given second (0.74;[95% CI], 0.46–1.01).

Discussion
Despite the growing popularity of the low FODMAP diet,
efﬁcacy data in unselected patients with IBS in which theeffect of the diet on gastrointestinal symptoms is comparedin a randomized, blinded manner with that of diet containing typical amounts of FODMAPs has been lacking. The
results of the current study provide high-quality data to ﬁllthat gap. As highlighted by Figure 1, symptoms were morethan halved in IBS subjects and all measured symptoms

were reduced to a level that arguably is considered good
symptom control. The difference in symptoms between the
2 controlled diets was seen immediately and the greatest
symptom control was achieved and maintained after 7 daysof the low FODMAP diet. Interestingly, of the 70% of subjects who felt better on the low FODMAP diet, this encompassed subjects across all 4 subtypes of IBS. The presence offructose malabsorption also had no bearing on the beneﬁt of
the low FODMAP diet. Because the interventional diets were
provided and matched for all nutrients including ﬁber andresistant starch, results reﬂect the true inﬂuence ofrestricting dietary FODMAPs without confounding variablesfrom other dietary components.
On evaluation of FODMAP intake on healthy controls, nodifference was observed between the subjects’ baseline dietand either of the controlled diets. Earlier studies have used

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FODMAPs and IBS

73

Table 3.Bloating, Abdominal Pain, Dissatisfaction With Stool Consistency, and Composite Scores of All Three Symptoms in
IBS and Healthy Participants While Following Low FODMAP and Typical Australian Diets

Subject
group

Diet

Abdominal pain
VAS (0–100 mm)

Dissatisfaction withstool consistency

CompositescoresVAS(0–300 mm)

IBS (n ¼ 30) Typical45.1 (35.1–55.0) P < .001 43.8 (35.0–52.5) P < .001 47.8 (37.6–57.9) P < .001 137 (110–163) P < .001
AustralianLow
24.2 (17.1–31.2)
22.5 (16.3–28.6)
25.9 (18.9–32.9)
73.1 (54.0–92.1)
FODMAP
Healthy
Typical11.8 (5.9–17.8) P ¼ .742 9.6 (5.1–14.4) P ¼ .742 17.7 (7.5–27.9) P ¼ .547 38.7 (19.4–57.9) P ¼ .304
controls
Australian(n ¼ 8)Low
10.4 (5.4–15.4)
9.1 (4.6–13.7)
10.1 (4.9–15.2)
29.6 (14.9–44.4)
FODMAP

NOTE. Data from the last 14 days of the interventional diets were analyzed using repeated-measures analysis of variance.
Statistically signiﬁcant differences are shown in bold.

very high FODMAP diets or rechallenge solutions in comparison with a low FODMAP diet.8,10,12 However, it is
known that FODMAPs will exert a laxative effect and increase gastrointestinal symptoms in the general population
if taken in large enough doses.30 Previous studies may haveshown a biased beneﬁt of the low FODMAP diet by exaggerating symptoms induced on the high FODMAP comparison.10,12 The typical Australian diet used in this study was
designed to represent a usual dietary intake of FODMAPs,
and, as such, was comparable with previously publisheddata on the intake of healthy Australians.16 The importanceof including healthy controls in this study was to ensure thetypical Australian diet used did not induce symptoms in thegeneral population. Indeed, symptoms remained low andwere unaffected by the interventional study diets. In thesubjects with IBS, symptoms still were greater on the
typical Australian diet compared with participants on thebaseline diet. This probably is because the oligosaccharide
and polyol content of the diet fed to the patients was higher
than their estimated intake on their baseline diet. This wasa limitation of the present study and despite efforts todesign a diet typical of the habitual intake of the recruited
population, the oligosaccharide and polyol content wasoverestimated. Nevertheless, the FODMAP content of thetypical Australian dietary arm was still much less than inprevious studies in which high FODMAP intake was up to 4fold greater,10,12 and the low FODMAP diet led to signiﬁcantly lower levels of symptoms than observed during thebaseline period. This reduction suggests that even if the
FODMAP content of the typical Australian diet was overestimated, there was still a therapeutic beneﬁt of the low
FODMAP diet compared with their habitual diet in the patients studied.
Despite the signiﬁcantly lower severity of gastrointestinal symptoms on the low FODMAP diet, little effect wasseen on fecal indices. In fact, there was no clear impact of
the low FODMAP compared with typical Australian diet on
fecal frequency, weight, KSC score, or FWC, except in the
IBS-D subjects, who had reduced fecal frequency and KSC

score on the low FODMAP diet. Unexpectedly, the score forsubjective scoring of dissatisfaction of stool consistency was
lower on the low FODMAP diet in all subtypes of IBS,
despite the stool consistency being unchanged by altering
FODMAP intake when assessed by the less subjective
indices of FWC. This discrepancy may reﬂect differing
perception of stool consistency when other symptoms, suchas abdominal pain and bloating, were improved.
The strengths of the study included the comparison of
the degree of symptom beneﬁt of the low FODMAP dietcompared with a typical Australian FODMAP intake, rather
than high FODMAP intake. The measures put in place tominimize biased results such as recruiting FODMAP-naive
patients and blinding participants to the provided diets
also adds strength to the ﬁndings. In fact, assessment ofblinding by questioning healthy subjects after the study andthe lack of an order effect supported that the blinding was
successful. The former method could not be applied to thepatients with IBS because they were inﬂuenced by changes
in symptoms. Despite no overt knowledge of the low FODMAP diet on enrolment questioning, it may be that the 14
IBS participants who had undergone breath testing before
study enrolment had some prior knowledge because thebreath testing protocol prescribes a diet low in FODMAPs
and ﬁber for the day before testing. This may have been apoint of reference for dietary identiﬁcation. No differenceswere apparent in overall gastrointestinal symptoms in theinterventional diets of IBS participants with prior breath
testing compared with those with no prior breath testing.
Baseline symptoms were also similar between those who
had undergone breath testing and those who had not (datanot shown).
Providing almost all food to participants facilitated ahigh degree of adherence to the study diets and the tightly
controlled food consumption of the participants facilitatedthe accurate assessment of the inﬂuence of dietary FODMAPs rather than confounding factors on symptoms andfecal characteristics. The cross-over study design enabled agreater power of the study, particularly because each

CLINICAL AT

Bloating

74

Halmos et al

CLINICAL AT

participant acted as his/her own control, minimizing manypotentially confounding variables. The application of such adesign has been criticized in patients with IBS because to
the uncertainties regarding a carry-over effect and the potential for patients withdrawing from the study substantially affecting the results.31 In the present study, the latterissue was not a major issue because only 3 patients in the
IBS cohort dropped out after commencing the ﬁrst dietaryinterventional arm. Furthermore, a carry-over effect on theseverity of symptoms was not evident because symptoms
appeared to return to the baseline level before crossingover to the alternative diet within the planned washout
period. However, potential changes in microbiota after theﬁrst diet and the possible unblinding of subjects when thesecond comparative diet was received both may haveinﬂuenced the symptomatic response on the second diet. In
addition, no formal protocol was in place to ensure symptoms returned to baseline severity. It was reassuring that noevidence of an order effect was identiﬁed.
A potential weakness was the way in which participants
who stopped a dietary arm because of intolerable symptoms
were handled. The assumed ﬁxed symptom level that was
carried forward from the 6 participants who ceased thetypical Australian diet prematurely may inﬂate the mean
symptom scores of this diet. Four of these 6 participantsreceived the low FODMAP diet ﬁrst, which again may
accentuate the differences in symptoms between thecontrolled diets.
Although providing such a controlled diet is a strength in
examining the role of FODMAPs in IBS, such a study design
is not representative of reality. In life, the low FODMAP dietis dietitian-taught. Dietary restriction would have morevarying degrees of compliance and depend on the patients’degree of understanding, food choices, and motivation foraltering dietary habits, as well as the dietitians’ advice onlevel of FODMAP restriction required. Furthermore, dietaryﬁber, including resistant starch, readily is found in high
FODMAP foods such as wheat, rye, and legumes,20 and,
therefore, are at risk of being reduced on a low FODMAP
diet if not supplemented. Dietary ﬁber accelerates transit
and promotes laxation through contribution to fecal
weight.32,33 A reduced ﬁber diet is likely to inﬂuence fecal
characteristics and confound these study ﬁndings.
Because wheat, rye, and barley are FODMAP-containing
grains, gluten, which also is present in these grains, inevitably also is reduced.34 In the only studies to have examined
gluten’s effects independently of those of FODMAPs, symptoms induced were more severe in high vs zero gluten
intake in one small parallel group study,35 but no evidenceof gluten-speciﬁc induction of symptoms (whether in highor low dose) was evident in a subsequent cross-over study
in patients who believed themselves to be gluten-sensitive.28 Nonetheless, because gluten could not be matched in
the interventional diets, it could be a possible confounding
factor.
In conclusion, the results of this study provide highquality evidence that the low FODMAP diet is efﬁcacious
for treatment of functional gastrointestinal symptoms in
unselected IBS with symptoms being halved compared with

Gastroenterology Vol. 146, No. 1

a typical Australian diet. Furthermore, the symptomatic
beneﬁts of the low FODMAP diet are unlikely to benonspeciﬁc because varying the intake of FODMAPs had no
symptomatic effect on healthy controls. Self-assessed satisfaction with stool consistency also was improved in both
IBS-D and IBS-C subgroups, although more objective
markers were altered only in subjects with IBS-D. These
results support the notion that the low FODMAP diet has
efﬁcacy in the vast majority of patients with IBS and support
its use as a ﬁrst-line therapy.

Supplementary Material
Note: To access the supplementary material accompanying
this article, visit the online version of Gastroenterology at
www.gastrojournal.org, and at http://dx.doi.org/10.1053/
j.gastro.2013.09.046.

References
1. Bohn L, Storsrud S, Tornblom H, et al. Self-reported
food-related gastrointestinal symptoms in ibs are common and associated with more severe symptoms andreduced quality of life. Am J Gastroenterol 2013;
108:634–641.
2. Hayes P, Corish C, O’Mahony E, et al. A dietary survey ofpatients with irritable bowel syndrome. J Hum Nutr Diet
2013. Epub ahead of print.
3. Atkinson W, Sheldon TA, Shaath N, et al. Food elimination based on IgG antibodies in irritable bowel syndrome:a randomised controlled trial. Gut 2004;53:1459–1464.
4. Gibson PR, Shepherd SJ. Evidence-based dietary management of functional gastrointestinal symptoms: the
FODMAP approach. J Gastroenterol Hepatol 2010;
25:252–258.
5. Gibson PR, Shepherd SJ. Personal view: food forthought–western lifestyle and susceptibility to Crohn’sdisease. The FODMAP hypothesis. Aliment Pharmacol
Ther 2005;21:1399–1409.
6. Fernández-Bañares F, Rosinach M, Esteve M, et al.
Sugar malabsorption in functional abdominal bloating: apilot study on the long-term effect of dietary treatment.
Clin Nutr 2006;25:824–831.
7. Goldstein R, Braverman D, Stankiewicz H. Carbohydrate
malabsorption and the effect of dietary restriction on
symptoms of irritable bowel syndrome and functional
bowel complaints. Isr Med Assoc J 2000;2:583–587.
8. Yao C, Tan HL, Gibson PR, et al. Discordant absorptionof mannitol and sorbitol in patients with irritable bowel
syndrome - a reﬂection of possible epithelial abnormalities? J Gastroenterol Hepatol 2010;25:A104.
9. Shepherd SJ, Gibson PR. Fructose malabsorption andsymptoms of irritable bowel syndrome: guidelines for
effective dietary management. J Am Diet Assoc 2006;
106:1631–1639.
10. Shepherd SJ, Parker FC, Muir JG, et al. Dietary triggers
of abdominal symptoms in patients with irritable bowel
syndrome: randomized placebo-controlled evidence.
Clin Gastroenterol Hepatol 2008;6:765–771.

11. Barrett JS, Gearry RB, Muir JG, et al. Dietary poorly
absorbed, short-chain carbohydrates increase delivery ofwater and fermentable substrates to the proximal colon.
Aliment Pharmacol Ther 2010;31:874–882.
12. Ong DK, Mitchell SB, Barrett JS, et al. Manipulation of
dietary short chain carbohydrates alters the pattern ofgas production and genesis of symptoms in irritablebowel syndrome. J Gastroenterol Hepatol 2010;
25:1366–1373.
13. Staudacher HM, Whelan K, Irving PM, et al. Comparisonof symptom response following advice for a diet low infermentable carbohydrates (FODMAPs) versus standard
dietary advice in patients with irritable bowel syndrome.
J Hum Nutr Diet 2011;24:487–495.
14. Yao CK, Gibson PR, Shepherd SJ. Design of clinical trials
evaluating dietary interventions in patients with functional
gastrointestinal disorders. Am J Gastroenterol 2013;
108:748–758.
15. Rome. Guidelines–Rome III diagnostic criteria for functional gastrointestinal disorders. J Gastrointestin Liver
Dis 2006;15:307–312.
16. Barrett JS, Gibson PR. Development and validation of acomprehensive semi-quantitative food frequency questionnaire that includes FODMAP intake and glycemic
index. J Am Diet Assoc 2010;110:1469–1476.
17. Biesiekierski JR, Rosella O, Rose R, et al. Quantiﬁcationof fructans, galacto-oligosacharides and other shortchain carbohydrates in processed grains and cereals.
J Hum Nutr Diet 2011;24:154–176.
18. Muir JG, Rose R, Rosella O, et al. Measurement of shortchain carbohydrates in common australian vegetables
and fruits by high-performance liquid chromatography(HPLC). J Agric Food Chem 2009;57:554–565.
19. Muir JG, Shepherd SJ, Rosella O, et al. Fructan and freefructose content of common Australian vegetables andfruit. J Agric Food Chem 2007;55:6619–6627.
20. Englyst KN, Liu S, Englyst HN. Nutritional characterization and measurement of dietary carbohydrates. Eur J
Clin Nutr 2007;61(Suppl 1):S19–S39.
21. Murphy MM, Douglass JS, Birkett A. Resistant starch
intakes in the United States. J Am Diet Assoc 2008;
108:67–78.
22. Roberts J, Jones GP, Rutishauser IHE, et al. Resistantstarch in the Australian diet. Nutr Diet 2004;61:98–104.
23. Sambucetti ME, Zuleta A. Resistant starch in dietary ﬁbervalues measured by the AOAC method in different cereals. Anal Tech Instr 1996;73:759–761.
24. NHMRC. Dietary guidelines for Australian adults.
Australian Government 2003.
25. Gudmand Hoyer E, Simony K. Individual sensitivity tolactose in lactose malabsorption. Am J Dig Dis 1977;
22:177–181.
26. Barrett JS, Irving PM, Shepherd SJ, et al. Comparison of
the prevalence of fructose and lactose malabsorption
across chronic intestinal disorders. Aliment Pharmacol
Ther 2009;30:165–174.
27. Whelan K, Judd PA, Preedy VR, et al. Covert assessment of concurrent and construct validity of a chart to

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characterize fecal output and diarrhea in patients receiving
enteral nutrition. JPEN J Parenter Enteral Nutr 2008;
32:160–168.
28. Biesiekierski JR, Peters SL, Newnham ED, et al. 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.
29. Francis CY, Morris J, Whorwell PJ. The irritable bowel
severity scoring system: a simple method of monitoring
irritable bowel syndrome and its progress. Aliment
Pharmacol Ther 1997;11:395–402.
30. Clausen MR, Jorgensen J, Mortensen PB. Comparisonof diarrhea induced by ingestion of fructooligosaccharide
idolax and disaccharide lactulose: role of osmolarity
versus fermentation of malabsorbed carbohydrate. Dig
Dis Sci 1998;43:2696–2707.
31. Triantafyllou K. Problems and challenges in the design ofirritable bowel syndrome clinical trials. Focusing on the
future with the experience from the past. Ann Gastroenterol 2002;15:263–270.
32. Grabitske HA, Slavin JL. Gastrointestinal effects of lowdigestible carbohydrates. Crit Rev Food Sci Nutr 2009;49:327–360.
33. Topping DL, Clifton PM. Short-chain fatty acids andhuman colonic function: roles of resistant starch andnonstarch polysaccharides. Physiol Rev 2001;81:1031–1064.
34. Gibson PR, Muir JG. Not all effects of a gluten-free dietare due to removal of gluten. Gastroenterol 2013. Epubahead of print.
35. Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten
causes gastrointestinal symptoms in subjects withoutcoeliac disease: a double blind randomised placebo
controlled trial. Am J Gastroenterol 2011;106:508–514.

Author names in bold designate shared co-ﬁrst authorship.
Received June 1, 2013. Accepted September 18, 2013.
Reprint requests
Address requests for reprints to: Emma P. Halmos, Department of
Gastroenterology, Central Clinical School, Monash University, Level 6 The
Alfred Centre, 99 Commercial Road, Melbourne Victoria 3004, Australia.
e-mail: Emma.Halmos@monash.edu; fax: (þ61) 3-9903-0556.
Acknowledgments
The authors thank Gina Dimitrakopoulos and Debbie King (Monash University)
for their assistance with food preparation and packaging; Kelly Liels, Ourania
Rosella, and Rosemary Rose (Monash University) for analysis of FODMAP
content of meals; Alicia Moltzen (Monash University) for analysis of breath
samples; and Minfeng Deng and Chu Kion Yao (Monash University) for
statistical analysis.
Conﬂicts of interest
These authors disclose the following: Susan Shepherd has published a bookon food intolerances and several cookbooks related to the topic of thearticle, and Peter Gibson has published a book on food intolerances. The
remaining authors disclose no conﬂicts.
Funding
This study was supported by the National Health and Medical ResearchCouncil of Australia, the Eva and Les Erdi Foundation, and by a scholarshipfrom the Faculty of Medicine, Nursing and Health Sciences, Monash
University (E.P.H.).

CLINICAL AT

January 2014

75.e1 Halmos et al

Gastroenterology Vol. 146, No. 1

Supplementary Figure 1. Photographs of example meals provided.

January 2014

FODMAPs and IBS 75.e2

Supplementary Figure 2. Effects of dietary change on moreobjective markers of fecal characteristics across diseasegroups and IBS subtypes. (A) FWC was higher in the IBS-D
cohorts compared with the healthy controls (HC) while
following a typical Australian diet. (B) KSC scores weresigniﬁcantly higher in IBS-D participants compared with both
IBS-C and healthy controls, indicating more frequent, looser,
and heavier stools.

Supplementary Figure 3. Median breath hydrogen from 12
midday until 8 PM taken at hourly intervals following a typical
Australian diet and low FODMAP diet in all participants (n ¼28). The area under the curve indicates that less breathhydrogen was produced on the low FODMAP diet (median,22.8 ppm; IQR, 14.3–44.4 ppm; 8 h) compared with thetypical Australian diet (median, 80.9 ppm; IQR, 46.8–159.8
ppm; 8 h; P < .001; Wilcoxon signed rank test).

MealsMondayTypical Australian diet
Breakfast2 wheat biscuittype cereal with
1/2 cup lactosefree milk, 2 slices
wheat toast withspread (listprovided)Morning tea
Apple, drink (listprovided)

Lunch

Vegetable frittata, 1/2
cup apple juice

Afternoon tea

Mufﬁn, drink (listprovided)

DinnerSalmon withvegetables andcouscous

Supper

Lunch

Vegetable frittata,
cup cordial

Afternoon tea

Mufﬁn, drink (listprovided)WednesdayThursdayFridaySaturday

Sunday1/3 cup muesli with
1/2 cup lactosefree milk,
lactose-freeyogurtCup wheat ﬂakes
and dried fruit
cereal with 1/2
cup lactose-freemilk, 1 cup
lactose-free milk

Cup wheat ﬂakes
and dried fruit
cereal with 1/2
cup lactose-freemilk, packaged
peaches

Apple quick oatswith 1/2 cup
lactose-freemilk, 1 cup
lactose-free milk

Honey quick oatswith 1/2 cup
lactose-freemilk, packaged
peaches

1 slicewatermelon,
drink (listprovided)
Chicken risotto, 1/2
cup apple juice

Apple, drink (listprovided)2 wheat biscuittype cereal with
1/2 cup lactosefree milk, 2 slices
wheat toast withspread (listprovided)Pear, drink (listprovided)

2 rye crackers withcheese, drink(list provided)

Pear, drink (listprovided)

Lactose-free yogurt,
drink (listprovided)

Mini pizza, 1/2 cup
apple juice

Tomato roulade, 1/2
cup apple juice

Chicken crepe, 1/2
cup apple juice

2 chocolate
biscuits, drink(list provided)
Chicken stir-fry with
1/2 packet
noodles

Apple, drink (listprovided)

1 slicewatermelon,
drink (listprovided)

Chocolate brownie,
drink (listprovided)

2 rye crackers andcheese, drink(list provided)
Chicken kebabs,
beetroot salad(recipeprovided)
1 slicewatermelon,
drink (listprovided)

Wheat sandwich(ﬁllings list
provided), cupapple juice
Pear, drink (listprovided)

Cup corn ﬂakes with
1/2 cup lactosefree milk, 2 slices
spelt toast withspread (listprovided)Orange drink (listprovided)Cup rice bubbles
with 1/2 cup
lactose-freemilk, 2 kiwi fruit

Plain quick oats with
1/2 cup lactosefree milk, 1 cup
lactose-free milk

Brown sugar andcinnamon quickoats with 1/2 cup
lactose-freemilk, 2 kiwi fruit

2 rice cakes withcheese, drink(list provided)
Tomato roulade, 1/2
cup cordial

Banana, drink (listprovided)Orange drink (listprovided)

2 rice cakes withcheese, cupcordial

Lactose-free yogurt,
drink (listprovided)
Spelt sandwich(ﬁllings list
provided), cupcordialBanana, drink (listprovided)

1/2 cup cherries,
drink (listprovided)

Wheat sandwich(ﬁllings list
provided), 1/2
cup apple juice
Flavored potato
chips, drink (listprovided)
Shepherd’s pie,
beetroot salad(recipeprovided)
1/2 mango,
lactose-freeyogurtPlain quick oats with
1/2 cup lactosefree milk,
lactose-freeyogurtCup rice bubbles
with 1/2 cup
lactose-freemilk, 1 cup
lactose-free milk

1 slice cantaloupe,
drink (listprovided)
Chicken risotto, cupcordialBanana, drink (listprovided)

2 chocolate
biscuits, drink(list provided)
Ratatouille with 100
g pasta

2 gluten-freechocolatebiscuits, drink(list provided)

Spelt sandwich(ﬁllings list
provided), cupcordialPotato chips, drink(list provided)

Mini-pizza, cupcordial2 gluten-freechocolatebiscuits, cupcordialSoy and ginger ﬁshwith vegetables

Chicken crepe, cupcordialBraised lambshanks withvegetables
Apple sorbet, drink(list provided)

Gastroenterology Vol. 146, No. 1

1 slicewatermelon,
drink (listprovided)
Low FODMAP diet
Breakfast
Cup corn ﬂakes with
1/2 cup lactosefree milk, 2 slices
spelt toast withspread (listprovided)Morning tea
Orange drink (listprovided)

Tuesday

75.e3 Halmos et al

Supplementary Table 1.Weekly Meal Plans Detailing Meals and Quantities to Be Consumed for the Typical Australian Diet and Low FODMAP Diet

MealsMondayTuesday

DinnerSalmon withvegetables andquinoaRatatouille with 150 ggluten-free pasta

Supper

1 slice cantaloupe,
drink (listprovided)Cup grapes, drink(list provided)

WednesdayThursdayFridaySaturdayShepherd’s pie,
Greek salad(recipeprovided)

Chicken stir fry with
1/2 packet rice

Soy and ginger ﬁshwith vegetables

1/2 cupstrawberries,
lactose-freeyogurt1 slice cantaloupe,
drink (listprovided)

Chocolate brownie,
drink (listprovided)

Chicken kebabs
with potato,
Greek salad(recipeprovided)
1 slice cantaloupe,
drink (listprovided)

SundayBraised lambshanks withvegetables

January 2014

Supplementary Table 1. Continued

Raspberry sorbet,
drink (listprovided)

NOTE. Meal plans were provided with all speciﬁed food, except where indicated in bold, and delivered to IBS and healthy participants weekly. Meal plans were repeated 3
times each over the interventional period.

FODMAPs and IBS 75.e4

Fecal frequency: stools/day
Subject group
IBS (n ¼ 27)
IBS-D (n ¼ 8)
IBS-C (n ¼ 12)
IBS-M (n ¼ 5)
IBS-U (n ¼ 2)
Healthy controls(n ¼ 7)

Diet

0

1–2

3–4

Australian
Low FODMAP
Australian
Low FODMAP
Australian
Low FODMAP
Australian
Low FODMAP
Australian
Low FODMAP
Australian
Low FODMAP

0
2
0
0
0
2
0
0
0
0
2
1

26
24
7
8
12
9
5
5
2
2
5
6

1
1
1
0
0
1
0
0
0
0
0
0

Fecal weight, g/day
P ¼ .108
P [ .018
P ¼ .120P ¼ .136
P ¼ .157
P ¼ .088

123 (104–149)
118 (96–157)
164 (121–207)
152 (114–191)
126 (112–141)
122 (99–145)
106 (66–146)
123 (74–172)
106 (-97 to 309)
99 (-149 to 346)
132 (107–158)
135 (92–179)

P ¼ .449
P ¼ .641
P ¼ .224
P ¼ .438
P ¼ .278
P ¼ .813

FWC, % of total weight73.3 (71.4–75.2)
73.5 (71.2–75.8)
75.7 (72.9–78.5)
74.7 (71.0–78.3)
71.4 (67.7–75.1)
72.3 (67.4–77.2)
73.5 (69.9–77.2)
74.0 (70.2–77.9)
74.4 (69.5–79.3)
75.0 (18.8–131)
66.3 (60.7–71.8)
67.8 (61.8–73.8)

P ¼ .628
P ¼ .633
P ¼ .639
P ¼ .668
P ¼ .902
P ¼ .688

KSC score27
5.2 (4.0–6.4)
4.7 (3.5–5.8)
7.2 (5.4–9.1)
6.1 (4.2–7.9)
3.3 (2.1–4.5)
4.4 (2.4–6.3)
6.3 (1.3–11.3)
3.8 (-0.4 to 8.0)
4.3 (-22.4 to 31.0)
2.6 (-2.5 to 7.7)
1.9 (0.7–3.2)
2.2 (1.1–3.3)

P ¼ .396

75.e5 Halmos et al

Supplementary Table 2.Daily Fecal Frequency, Weight, KSC Score, and FWC in IBS and Healthy Participants After Following a Low FODMAP and Typical Australian Diet
for 17 to 21 Days

P [ .034
P ¼ .094
P ¼ .223
P ¼ .500
P ¼ .172

NOTE. Statistically signiﬁcant differences are shown in bold.

Gastroenterology Vol. 146, No. 1