EDITORIALS
Diet as a Therapy for Irritable Bowel Syndrome: Progress at Last
See “A diet low in FODMAPs reduces symptoms
of irritable bowel syndrome,” by Halmos EP,
Power VA, Shepherd SJ, et al, on page 67.
P
ostprandial worsening of symptoms, as well as
adverse reactions to one or more foods are common
in patients with irritable bowel syndrome (IBS),1 and selfreported food intolerance in IBS is associated with a high
symptom burden and reduced quality of life.2 In line with
this, approximately two thirds of IBS patients exclude food
items from their diet to improve symptoms.3 Despite this,
there is no evidence suggesting inadequate nutrient intake
in the majority of patients with IBS.4 For patients, identifying the food item/s they do not tolerate is often central
when consulting for their symptoms, and in general guidelines for management of IBS, dietary advice is proposed to
be of major importance.5 However, there are currently no
available evidence-based guidelines for dietetic practice in
IBS, as very few randomized, controlled trials exist on dietary treatment of IBS patients. Instead, the current recommendations are primarily based on studies assessing
physiologic function in relation to dietary components, and
to a lesser degree on research based on randomized, controlled trials examining the role of dietary components in the
therapeutic management of IBS patients.6 Therefore, the
article by Halmos et al7 published in this issue of Gastroenterology is a welcome addition to the existing literature. In
a randomized, controlled trial, they demonstrate that
reducing the intake of poorly absorbed short-chain carbohydrates, or fermentable oligosaccharides, disaccharides,
monosaccharides and polyols (FODMAPs), substantially improves the severity of the key symptoms of IBS.7
The hypothesis that reducing intake of FODMAPs can
improve gastrointestinal (GI) symptoms stems from the
clinical observation that a proportion of patients with IBS
tolerate intake of certain short-chain carbohydrates poorly.8
Moreover, these carbohydrates can be incompletely absorbed in the small intestine due to absent hydrolyzation (eg,
lactose maldigestion, and nondigestible oligosaccharides),
dependence on simultaneous intake of glucose for adequate
absorption (fructose), or passive diffusion (certain monosaccharides and polyols).9 Therefore, the absorption of
short-chain carbohydrates in the small intestine varies
depending on different factors such as presence/absence of
enzymes to digest disaccharides (eg, lactase), small intestinal transit time, dose of the carbohydrate, meal composition,
and also on the presence of mucosal disease.9 If a proportion of the FODMAPs pass unabsorbed through the small
intestine, this increases intestinal luminal water content
through osmosis, and increases gas production via fermentation by gut bacteria, leading to intestinal distension, which
may cause symptoms in susceptible individuals. Moreover,
Gastroenterology 2014;146:10–26
fermentation products such as short-chain fatty acids may also
be involved in symptom generation.10 However, incomplete
absorption of carbohydrates in the small intestine is not
enough to cause symptoms, because not all subjects with, for
example, lactose maldigestion and fructose malabsorption
report symptoms.11,12 Therefore, other factors implicated in
the pathophysiology of IBS such as alterations in gut microbiota composition,13 visceral hypersensitivity,14 GI barrier
defects, and abnormal immune function,15 may serve as cofactors in symptom generation after intake of an excess of
FODMAPs in the diet. Further, symptom experience after
intake of short-chain carbohydrates is also likely to be affected
by central nervous system factors, and therefore directly or
indirectly influenced by anxiety, depression, and stress, but
potentially also by classical conditioning and expectations16
(Figure 1). An important research task is to address the ability of these factors to predict the response to dietary interventions in general, and low-FODMAP diet in particular, as
few predictors for a positive symptomatic response to this diet
exist.9
The scientific evidence supporting a clinically relevant
positive effect of reducing FODMAPs in IBS has so far been
relatively limited, but gradually accumulating over the last
couple of years, and has, besides observational reports,
mainly been based on a randomized single-blinded FODMAP
challenge study,17 a nonrandomized, comparative study,18
and a randomized, controlled trial comparing a low FODMAP diet with the habitual diet in IBS.19 Moreover, a recent
study also demonstrated that a general reduction of FODMAPs in the diet was effective in patients with suspected
nonceliac gluten sensitivity, and no gluten-specific effect
beyond that of the effect of the general FODMAP reduction
could be demonstrated.20 Because few clinical trials in this
area exist, the current study by Halmos et al7 is very
important, because it provides high-quality evidence supporting the effectiveness of a low-FODMAP diet in IBS. By
using a randomized, cross-over design, the authors were
able to demonstrate a convincing reduction of the reported
severity of all the key symptoms of IBS—abdominal pain,
bloating, and bowel habit dissatisfaction—when the patients
were on a low-FODMAP diet compared with when they
received a standard Australian diet. Both diets had a similar
nutritional composition, except for a difference in the
FODMAP content. Moreover, the low FODMAP diet was welltolerated and the nutritional composition met current
nutritional recommendations. The dietary intake was also
strictly controlled as almost all food was provided to the
subjects during the study, which further strengthens the
reliability of the findings, but also begs for future studies to
evaluate how this diet works in clinical practice when the
patient is given dietary advice in an outpatient clinic setting,
without receiving all food from a study center. The clinical
experience is that a substantial proportion of patients find it
difficult to follow strict diets for other than short periods of
EDITORIALS
Figure 1. Proposed mechanisms involved in the
generation
of
gastrointestinal (GI) symptoms
after intake of FODMAPs.
Several factors affect the
absorption of these shortchain carbohydrates in the
small intestine. Incomplete
absorption of FODMAPs
leads to increased water
retention through their osmotic activity and to gas
production due to fermentation by gas bacteria. This
leads to intestinal distension, which together
with peripheral and central
predisposing factors can
generate GI symptoms.
time, and as can be expected adherence to the low-FODMAP
diet has been found to be an important predictor for the
outcome.21 The authors also assessed the effect on stool
parameters objectively, by collection of feces, and here the
effect of the diet was modest, despite the fact that the effect
on bowel habit dissatisfaction was striking, further highlighting the complex nature of symptom reporting in IBS
patients.
As the authors rightfully acknowledge in their discussion, there were of course some limitations with the present
study. Due to the logistic complexity of the study a relatively
limited number of patients (n ¼ 30) was included, which
limits the possibility of finding predictors for a favorable
response, which is a clinically important question, as not all
patients respond favorably to this treatment alternative.
Further, a relatively short treatment period (3 weeks) was
used and currently no scientific guidance exists on how this
diet works in the long run or if gradual reintroduction of
excluded food items can be done without worsening of
symptoms. Moreover, the use of a cross-over design carries
a risk of carry-over effects, but the authors used a relatively
long wash-out period to reduce this risk, and also performed
several additional analyses to secure the absence of a relevant carry-over effect. In the present study, no further
mechanistic insight into the mechanism behind symptom
improvement was provided, as for instance the results from
breath testing or stool parameters did not predict symptom
response. However, based on the current convincing data,
clearly demonstrating an excellent short-term response of
low-FODMAP diet in a substantial proportion of IBS
patients,7 future studies can address the remaining research
questions, such as how to identify the right patients for this
therapy and also to determine how strict the diet needs to be to
yield a sufficiently favorable long-term response. Moreover, so
far no study has demonstrated that this diet therapy is superior to the dietetic practice that has been used for patients with
IBS before a low-FODMAP diet was suggested as a treatment
alternative for IBS, that is, to encourage a regular meal pattern
and a “healthy eating,” to avoid large meals, reduce intake of
fat, discourage excessive fiber intake (especially soluble fibers), reduce caffeine, and avoid gas-producing foods, such as
beans, cabbage, and onions.6
To conclude, with the study from Halmos et al,7 we now
have solid scientific data supporting that a low-FODMAP
diet is efficient in reducing GI symptoms in IBS, at least in
the short term. Long-term studies are now needed, as well
as investigations finding clinically useful predictors that can
help clinicians in selecting patients who are likely to
respond to this relatively cumbersome form of therapy, for
which access to expert dieticians are needed. Moreover,
high-quality, head-to-head comparisons with other dietary
strategies used in the management of patients with IBS will
be helpful for practicing dieticians and gastroenterologists,
as well as evaluation of ways to facilitate dissemination of
dietary information to large groups of patients, such as
group education and web-based tools. For the benefit of our
patients, some progress has been made finally regarding
diet as a therapy for IBS, but as always, a nice study always
raises further questions that need to be addressed in future
studies!
11
EDITORIALS
MAGNUS SIMRÉN
Department of Internal Medicine and Clinical Nutrition
Institute of Medicine and
University of Gothenburg Centre for Person-Centred Care
Sahlgrenska Academy
University of Gothenburg
Gothenburg, Sweden
References
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intolerance in subjects with irritable bowel syndrome:
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Reprint requests
Address requests for reprints to: Professor Magnus Simrén, Department of
Internal Medicine & Clinical Nutrition, Institute of Medicine, Sahlgrenska
Academy, University of Gothenburg, 41345 Gothenburg, Sweden. e-mail:
[email protected].
Conflicts of interest
The author discloses the following: Magnus Simrén has received unrestricted
research grants from Danone and AstraZeneca, served as a Consultant/
Advisory Board member for Danone, Novartis, Almirall, Albireo, and Shire,
and been on the Speaker’s bureau for Almirall, Danone, Shire, Menarini,
Abbvie, MSD, Tillotts and Vifor Pharma.
© 2014 by the AGA Institute
0016-5085/$36.00
http://dx.doi.org/10.1053/j.gastro.2013.11.027