Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

World Gastroenterology Organisation Global.14

Download as pdf or txt
Download as pdf or txt
You are on page 1of 15

WGO GUIDELINE

World Gastroenterology Organisation Global Guidelines


Diet and the Gut
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

Govind Makharia, MBBS, MD, DM, DNB,*


Peter R. Gibson, MB, BS(Hons), MD, FRACP,† Julio C. Bai, MD,‡
Tarkan Karakan, MD,§ Yeong Yeh Lee, MD, PhD,∥
Lyndal Collins, BND(Hons),†
Jane Muir, BSc(Hons), PhD, GradDipDietetics,† Nevin Oruc, MD,¶
Eamonn Quigley, MD, FRCP, FACP,#
David S. Sanders, MRCP(UK), MD, FACG,** Caroline Tuck, PhD, APD,††
Cihan Yurdaydin, MD,‡‡ and Anton Le Mair, MD§§

T his guideline was produced in connection with the


World Digestive Health Day (WDHD) held in 2016 on
the theme of “Diet and the Gut.” The Guideline Develop-
theme as well as invited experts, including diet and nutrition
specialists, pharmacists, and primary care physicians.
Given the central role of the digestive tract and its
ment Review Team consisted of experts on the WDHD related organs in the processes of digestion and absorption, it
should come as no surprise that the food we eat has critical
and complex interactions with the gastrointestinal tract and
Received for publication August 15, 2019; accepted May 22, 2021. its contents, including the microbiota. The nature of these
From the *All India Institute of Medical Sciences, Gastroenterology, & interactions is influenced not only by the composition of the
Human Nutrition, New Delhi, Delhi, India; †Department of Gas- diet and the integrity of the gastrointestinal tract but also by
troenterology, Monash University and Alfred Health; ††La Trobe
University, Melbourne, Vic., Australia; ‡University of Salvador and
psychosocial and cultural factors. The general public—and in
Dr. C. Bonorino Udaondo Gastroenterology Hospital, Buenos particular those who suffer from gastrointestinal ailments—
Aires, Argentina; §Gazi University, Ankara; ¶Ege University, Bor- rightly perceive their diet as being a major determinant of
nova; ‡‡Koc University Medical School, Istanbul, Turkey; ∥Uni- such symptoms and seek guidance on optimal dietary regi-
versity of Science, Malaysia, Kota Bharu, Malaysia; #The Meth-
odist Hospital, Houston, TX; **Royal Hallamshire Hospital and
mens. Many medical practitioners, including gastro-
University of Sheffield, Sheffield, UK; and §§Medical Guideline enterologists, are unfortunately often ill-prepared to deal with
Development, ALM Consulting, Amsterdam, The Netherlands. such issues. This is a reflection of the lack of education on the
Review Team: G.M. (Chair, India), P.R.G. (Co-chair, Australia), J.C.B. topic of diet and nutrition in many curricula.
(Argentina), T.K. (Turkey), Y.Y.L. (Malaysia), L.C. (Australia),
J.M. (Australia), N.O. (Turkey), E.Q. (United States), D.S.S. (UK),
Dietary changes have the potential to alleviate symp-
C.T. (Australia), C.Y. (Turkey), A.L.M. (The Netherlands). toms, but they may also result in regimens that are nutri-
P.R.G. has written a recipe/education book on the low FODMAP diet. tionally deficient in 1 or more respects. It is vital, therefore,
Monash University sells a digital application, booklets, and online that whenever possible, the medical practitioner should
education on the low FODMAP diet. C.T., L.C., and J.M. reported
that Monash University sells a digital application and booklets on the
engage the services of a skilled nutritionist/dietitian to
low FODMAP diet, and an online course to train dietitians in how to evaluate a given individual’s nutritional status, instruct the
implement the low FODMAP diet. Funds raised contribute to research patient on new diet plans, and monitor progress. It is also
in the Department of Gastroenterology at Monash University. A.L.M. incumbent on gastroenterologists to become educated on
acts as guidelines development consultant for WGO. The remaining
authors declare that they have nothing to disclose.
modern dietary practices as they relate to gastrointestinal
Address correspondence to: Jim Melberg, World Gastroenterology health and disease. We hope that this guideline will become
Organisation, 555 East Wells Street, Milwaukee, WI 53202 a valuable resource in this regard.
(e-mail: jmelberg@worldgastroenterology.org). Diet, in general, is a very broad subject; we have
Copyright © 2021 World Gastroenterology Organisation. All rights reserved.
DOI: 10.1097/MCG.0000000000001588
therefore decided to be selective and have focused on certain

J Clin Gastroenterol  Volume 56, Number 1, January 2022 www.jcge.com |1


Makharia et al J Clin Gastroenterol  Volume 56, Number 1, January 2022

diets and conditions for which the diet has a real causative
or therapeutic role in adults: celiac disease, dietary fibers, TABLE 2. Cascade of Recommendations on FODMAP
FODMAPs (fermentable oligosaccharides, disaccharides, Extensive resources (gold standard)
monosaccharides, and polyols), carbohydrate intolerance, Clinical evaluation to confirm the diagnosis of IBS, including
and the role of diet in irritable bowel syndrome (IBS). The exclusion of celiac disease
Dietary interview by an expert dietitian to evaluate dietary
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

topic of celiac disease has already been dealt with in the


intake, meal pattern, level of FODMAP consumption
World Gastroenterology Organisation (WGO) guideline on
Dietary instruction with regular follow-up
celiac disease published in 2016, which should be referred to Initial dietary reduction of FODMAP intake for 2-6 wk,
for further details.1,2 providing adequate education on foods to be consumed and to
With WGO “cascades,” the intention is to recognize
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

be avoided, as well as adaptation to suit the patient’s other


differences in disease epidemiology, sociocultural factors, dietary needs (eg, other dietary intolerances, food preferences,
and health care provision that exist in different parts of the religious requirements)
world and the ways in which they preclude, in most Follow-up after 2-6 wk to evaluate the effect of the low
instances, the promulgation of a “one size fits all” or a single FODMAP diet on symptom control
gold-standard approach. Table 10 in this guideline lists When good symptom control has been achieved: strategic
organizations that produce relevant guidelines. This Global rechallenge to assess tolerance to individual FODMAP
subgroups, followed by long-term management planned on the
WGO Guideline includes a set of cascades intended to basis of the response to the rechallenge
provide context-sensitive and resource-sensitive options for When poor symptom control has been achieved: assessment of
the dietary approach to gastrointestinal conditions. Through compliance with dietary recommendations, consideration of
the WGO cascades, the WGO Guidelines program aims to other dietary and nondietary management strategies
provide clinical practice recommendations that are useful in Medium resources
many different environments across the world. Clinical evaluation to confirm the diagnosis of IBS, including
This WGO Guideline on diet and the gut is intended exclusion of celiac disease
for use by health providers, including family care and pri- Dietary interview by a dietitian to evaluate dietary intake
Dietary instruction with semifrequent follow-up
mary care physicians, gastroenterologists, pharmacists, and
Initial dietary reduction of FODMAP intake for 2-6 wk,
nutritionists/dietitians. providing adequate education on foods to be consumed and to
The WGO Guidelines are produced through a sys- be avoided, as well as adaptation to suit the patient’s other
tematic development process for achieving an expert con- dietary needs (eg, other dietary intolerances, food preferences,
sensus on the basis of the medical and scientific literature, religious requirements)
existing practice guidelines, and regional best-practice Follow-up assessment within 3 mo to evaluate the effect of the
standards. All available sources were used to develop this low FODMAP diet on symptom control
guideline. Monthly high-level evidence literature searches in When good symptom control has been achieved: strategic
EMBASE/Medline are delivered to the review team mem- rechallenge to assess tolerance to individual FODMAP
bers as alerts and are scanned by team members to identify subgroups, followed by long-term management planned on the
basis of the response to the rechallenge
new insights and evidence for the next guideline update. When poor symptom control has been achieved: assessment of
compliance with dietary recommendations, consideration of
CASCADES OF DIET OPTIONS other dietary and nondietary management strategies
Limited resources
AND ALTERNATIVES Clinical evaluation to confirm the diagnosis of IBS, including
Tables 1–3 present cascades of resource-sensitive diet exclusion of celiac disease
options and alternatives for countries and regions with dif- Dietary interview by a dietitian, if available, to evaluate dietary
ferent levels of resources, access, culture, and epidemiology. intake
Dietary instruction with semifrequent follow-up, if possible
Initial dietary reduction of FODMAP intake for 2-6 wk
TABLE 1. Cascade of Guidelines On Dietary Fiber Follow-up within 6 mo to evaluate the effect of the low
Individual strategies FODMAP diet on symptom control
Dietary education and/or behavior-change counseling for When good symptom control has been achieved: strategic
individuals with a low-fiber diet or health condition modulated rechallenge to assess tolerance to individual FODMAP
by fiber intake subgroups
Increased consumption of high-fiber foods, including fruit,
FODMAP indicates fermentable oligosaccharides, disaccharides, mon-
vegetables, legumes, and whole grains
osaccharides, and polyols; IBS, irritable bowel syndrome.
Use of fiber supplementation where recommended intake cannot
be met through diet alone, or there is evidence of therapeutic
benefit for a specific health condition
Strategies for governments, international partners, civil society,
nongovernmental organizations, and the private sector FIBER IN THE DIET
Shape healthy environments
Make healthier, high-fiber food options affordable and easily Introduction
accessible to all Dietary fibers are carbohydrates (both natural and
Promote high-fiber food options and increase public awareness of synthetic) that resist digestion in the small intestine of
the health benefits associated with consumption humans and convey a physiological health benefit.3,4 Fiber
Strategies for the food industry adds bulk to the diet, reduces energy density in foods, and
Increase the fiber content of processed foods through changes in may improve glycemic control and prevent or reduce
food-processing practices and/or fortification of highly constipation.3,5 In many countries, a large number of indi-
processed foods
viduals do not consume enough dietary fiber to meet rec-
Increasingly introduce and promote production of innovative,
fiber-rich products ommended targets.3,5 Good dietary fiber sources include:
whole grains, nuts and seeds, vegetables, and fruit.3,5

2 | www.jcge.com Copyright © 2021 World Gastroenterology Organisation. All rights reserved.


J Clin Gastroenterol  Volume 56, Number 1, January 2022 WGO Guideline

TABLE 3. Cascade of Recommendations on Carbohydrate Intolerance


Extensive resources (gold standard)
Lactose intolerance Diagnosis: Challenge with 25 or 50 g lactose and assessment of the hydrogen and methane breath response;
or food challenge with symptom monitoring to identify intolerance
Management: Assessment and education by a dietitian to ensure suitable intake of calcium-rich foods.
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

Reduction of dietary intake of foods high in lactose, with replacement using lactose-free milk and yogurt
products and/or use of oral β-galactosidase
Fructose Fructose intolerance should be considered as a component of the low FODMAP diet (Table 2)
Sucrase-isomaltase Diagnosis: The value of enzyme activity assessment in duodenal/jejunal biopsies has been established in
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

deficiency* children. The value of this test in adults is not yet established
Management: For congenital deficiency, a starch-restricted and sucrose-restricted diet followed by
rechallenge, supervised by a dietitian; sacrosidase enzyme supplementation
Medium resources
Lactose intolerance Diagnosis: Same as above
Management: Same as above, if available
Fructose Same as above
Sucrase-isomaltase Diagnosis: Same as above
deficiency* Management: Consideration should be given to a starch-restricted and sucrose-restricted diet, followed by
rechallenge supervised by a dietitian for congenital enzyme deficiency
Limited resources
Lactose intolerance Diagnosis: Food challenge with symptom monitoring to identify intolerance
Management: Dietary education by a health professional, if available, to ensure suitable intake of calcium-
rich foods. Reduction of dietary intake of foods high in lactose, with replacement using lactose-free milk
and yogurt products and/or use of oral β-galactosidase, if available
Fructose Fructose intolerance should be considered as a component of the low FODMAP diet
Sucrase-isomaltase Diagnosis: In the absence of clinical testing, consideration should be given to the clinical picture: symptom
deficiency* types and response to treatment in children with suspected congenital deficiency only
Management: Consideration should be given to a starch-restricted and sucrose-restricted diet with
instruction from a dietitian, if available, and only in children with suspected congenital deficiency
*To avoid invasive biopsies, diagnostic surrogate markers are currently used (based on the exhalation of gases produced by the enzymatic degradation of the
substrate); the development of genetic methods is in progress.
FODMAP indicates fermentable oligosaccharides, disaccharides, monosaccharides, and polyols.

A greater intake of dietary fiber has been associated with a solubility of fiber was once thought to determine its phys-
lower risk of several chronic diseases, including car- iological effect, more recent studies suggest that other
diovascular disease and diabetes, and it may reduce the risk properties of fiber, especially fermentability and viscosity,
of all-cause mortality.5–9 Dietary fiber may be included in are more important, and plant components (such as anti-
the nutrition panel on food labels, and it is typically listed as oxidant compounds) associated with dietary fiber may also
a subset of total carbohydrates (Table 4). contribute to reduced disease risk.5,13

Types of Dietary Fiber Beneficial Effects of Dietary Fibers


Food naturally contains a mixture of soluble and For a summary of the physical characteristics and
insoluble fibers, and both types have important health physiological benefits of naturally occurring fibers, please
benefits in the context of a high-fiber diet.3,5 Although the refer to Table 5 in the WGO online version of this guideline

TABLE 4. Definitions
Concept Definition
Dietary fiber10,11 The edible parts of plants or analogous carbohydrates that are resistant to digestion and absorption in the
human small intestine, with complete or partial fermentation in the large intestine. Dietary fiber includes
polysaccharides, oligosaccharides, lignin, and associated plant substances. Dietary fibers promote beneficial
physiological effects including laxation, and/or blood cholesterol attenuation, and/or blood glucose
attenuation
Fibers that are incorporated into foods as additives should demonstrate functional human health outcomes to
receive a fiber classification
A database has been developed, listing studies that test fiber and physiological health outcomes identified by
experts at the Ninth Vahouny Conference12
Diet and the gut Clinical diet, intended to treat (part of) the disease or disorder, or to correct excess or deficiency in relation to
selected gastrointestinal disorders
“Fiber-rich” 3 g or more of fiber per labeled serving
“High in fiber” on food Must contain at least 5 g per serving
label
Energy density Relationship of calories to the weight of food (calories per gram)
Fiber density Fiber content in a specified amount of a food or diet, usually per 100 g of food, and for comparing diets usually
per 1000 kcal intake

Copyright © 2021 World Gastroenterology Organisation. All rights reserved. www.jcge.com |3


Makharia et al J Clin Gastroenterol  Volume 56, Number 1, January 2022

TABLE 5. Clinical Management Flowchart for Using the Low FODMAP Diet
Family physician (general practitioner) and/or gastroenterologist
Medical investigation
Appropriate exclusion of other gastrointestinal Referral to dietitian
disorders
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

A clinical diagnosis of IBS


Dietitian
Assessment of usual diet and symptoms Symptom improvement
Low FODMAP diet trial for 2-6 wk Dietary rechallenge
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

Assessment of dietary adherence Individual dietary triggers identified: “individual modified low FODMAP
diet” established
Poor response
Reintroduce high FODMAP foods
Consider other triggers/therapies:
Food chemicals
Stress
Small intestinal bacterial overgrowth
FODMAP indicates fermentable oligosaccharides, disaccharides, monosaccharides, and polyols; IBS, irritable bowel syndrome.
Source: Tuck et al.14

(www.worldgastroenterology.org/guidelines/global-guidelines). Role of Dietary Fiber in Gastrointestinal


The following is a list of well-established beneficial physio- Conditions
logical effects associated with the consumption of a high-fiber
diet with whole foods in general12: Constipation in Adults
 Reduction in blood total and/or low-density lipoprotein
(LDL) cholesterol.  Increasing fiber in the diet has long been considered a
 Reduction in postprandial blood glucose and/or insulin levels. first-line treatment for constipation.3,18,19
 Increased stool bulk and/or decreased transit time.  Increasing fluid in the diet has long been considered a
 Increased production of short-chain fatty acids (SCFAs) first-line treatment for constipation3,18,19; the evidence to
due to fermentation by the colonic microbiota. support this is mixed.
In addition, the following physiological effects of  Improvements in bowel movement frequency and consis-
dietary fibers are considered probable, but require further tency may be observed by gradually increasing dietary fiber
scientific substantiation12: (or by adding fiber supplements) to a target dose of 20 to
 Reduced blood pressure. 30 g of total dietary and/or supplementary fiber per day.
 Increased satiety. Fiber should be introduced gradually into the diet over
 Weight loss/reduction in obesity. weeks rather than days to allow the body to adjust.19,20
 Positive modulation of colonic microbiota.  Stool frequency is thought to be improved by soluble
Please refer to Table 5 in the WGO online version of fiber through an increase in stool bulk and weight and by
this guideline (www.worldgastroenterology.org/guidelines/ insoluble fiber through the acceleration of intestinal
global-guidelines) for a summary of the physiological effects transit time; for both, however, and especially for
of different types of fiber (adapted from Eswaran et al15). insoluble fibers, high-quality evidence is lacking.15
 The best evidence for fiber supplementation is for
psyllium in the management of chronic constipation.19
Interaction of Dietary Fibers With the Gut  Evidence for the efficacy of fiber is particularly lacking for
Microbiota individual constipation subtypes: metabolic, neurological, diet-
Ingested fiber may influence fecal microbiota profiles, cause related, myogenic, drug-related, and pelvic floor dysfunction.15
changes in the complex gastrointestinal environment, and pro-  In patients with obstructive diseases of the intestine, a
mote the growth of bacteria in general and potentially beneficial high-fiber diet should be avoided.
bacteria in particular.15–17 Oligosaccharides, including fructo-  Delayed colon transit or dyssynergic defecation may be
oligosaccharides and galacto-oligosaccharides (GOS), inulin, and present when patients experience marked worsening of
possibly other soluble fibers, are therefore regarded as prebiotics their constipation-related symptoms with fiber.18,21,22
that may stimulate the preferential growth of lactobacilli, bifi- Recommendations: A high-fiber diet may be protective
dobacteria, and other health-promoting bacteria in the against, and therapeutically useful in the treatment of, con-
colon.3,15–17 The gut microbiota are thought to play a crucial stipation. A gradual increase in fiber intake through diet and/or
role in human health and prevention of disease through a variety supplementation to 20 to 30 g/d with adequate fluid is recom-
of mechanisms, including the production of SCFA, which are mended. In addition, psyllium supplementation may be appro-
important for maintaining gut homeostasis and optimal immune priate in the management of chronic constipation. The role of
function.3,15–17 Changes in the gut microenvironment have been fiber in other forms of constipation is limited, and a high-fiber
associated with many common conditions, including IBS, obe- diet may exacerbate symptoms in some individuals.
sity, cardiovascular disease, and asthma.16,17 The relationship
between the gut microbiota, dietary fiber, and health outcomes is IBS
an area of rapidly growing interest, but well-controlled human
trials are required to confirm the emerging links noted in animal  The effect of fiber on IBS symptoms is variable and
and epidemiological studies.16,17 specific to fiber type.15,23,24

4 | www.jcge.com Copyright © 2021 World Gastroenterology Organisation. All rights reserved.


J Clin Gastroenterol  Volume 56, Number 1, January 2022 WGO Guideline

 Soluble fiber supplements—including linseed, methylcel- Recommendations: Consumption of a high-fiber diet


lulose, partially hydrolyzed guar gum, and psyllium— may be protective against the development of diverticular
have demonstrated therapeutic benefit in a number of disease, and the risk of complications (diverticulitis) may be
clinical trials, particularly for patients with constipation- higher in those on a low-fiber diet. Short-term use of a low-
predominant IBS (IBS-C).3,15,23,24 fiber diet may be indicated in the case of diverticulitis.
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

 Highly fermentable fibers, such as oligosaccharides and However, all of these recommendations are supported by
wheat bran fiber (by virtue of its oligosaccharide content), limited evidence and expert opinion only.
may contribute to increased gas production, thus
exacerbating symptoms of bloating, flatus, and gastro- Colorectal Cancer
intestinal discomfort in IBS.15,23,24
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

 Reducing the intake of highly fermentable fibers, as part  Evidence that fiber decreases the risk of colorectal cancers
of a low FODMAP dietary approach (see the “The low is mixed, and further research is needed.30
FODMAP diet” section below), is recommended for the  A 2012 analysis from the European Prospective Inves-
management of IBS and provides symptomatic relief in tigation into Cancer and Nutrition (EPIC) study showed
∼75% of patients.15,23 that total dietary fiber was inversely associated with
Recommendations: Highly fermentable fibers, including colorectal cancer risk, with similar results for colon and
oligosaccharides and inulin, and also wheat bran, may rectal cancers. Dietary fiber sources from cereals, fruits,
exacerbate symptoms of IBS. The best evidence indicates and vegetables were similarly associated with a reduced
that reducing the intake of these fermentable fibers as part of risk of colon cancer.31 Only cereal fiber was associated
a low FODMAP dietary approach (see the “The low with a decreased risk of rectal cancer.31
FODMAP diet” section below) is effective in managing  There is no evidence from randomized controlled trials
symptoms in the majority of IBS patients. Conversely, (RCTs) to suggest that increased dietary fiber intake will
soluble fiber supplements including psyllium, linseed, and reduce the incidence or recurrence of adenomatous
methylcellulose may be of therapeutic benefit, particularly polyps within a 2- to 8-year period.32 Longer term trials
in IBS-C. with higher dietary fiber levels are needed to evaluate this
further.32
Inflammatory Bowel Disease (IBD) Recommendations: Evidence from cohort studies gen-
erally indicates a protective effect of a high-fiber diet against
 Evidence for a therapeutic effect of dietary fiber in IBD is colorectal cancer; however, it is not certain whether this
lacking. However, due to the potential anti-inflammatory relationship is based on cause and effect. Further high-
and immune-modulating effects of fiber, this warrants quality studies are required to elucidate the relationship and
further investigation.25 identify potential mechanisms of action.
 Restriction of dietary fiber in IBD is unnecessary except
in the case of significant intestinal stenosis.25 Clinical Indications for a Low-fiber Diet
 Reducing the intake of highly fermentable fibers, as part
of a low FODMAP dietary approach, may be useful in  Ingestion of low-fiber foods may help decrease diarrhea,
the symptomatic management of IBD patients who have gas, and bloating by slowing bowel movements and
coexisting IBS (see the “The low FODMAP diet” section reducing colonic fermentation.33
below).26,27  Short-term use of a low-fiber diet (< 10 g/d) may be
Recommendations: There is currently a paucity of evi- recommended for bowel cleansing purposes in the days
dence supporting a therapeutic role of dietary fiber in IBD. before diagnostic procedures such as colonoscopy,
Further high-quality studies are therefore required. The colonography, and laparoscopic gynecologic surgery. In
intake of dietary fiber should not be restricted in IBD comparison with traditional bowel preparation regimens
patients, except in the case of intestinal obstruction. IBD (clear fluid diet with the use of cathartic agents), studies
patients with coexisting IBS may benefit from reducing their have shown that a low-fiber diet approach may be better
intake of highly fermentable fibers as part of a low FOD- tolerated, have fewer side effects, and permit a reduction
MAP dietary approach. in the dosage of cathartic agents required without
compromising the quality of bowel preparation.33,34
Diverticular Disease  A low-fiber diet is often recommended temporarily after a
flare-up of diverticulitis, Crohn’s disease or ulcerative
 Higher intakes of dietary fiber may be associated with a colitis, or following gastrointestinal surgery. However,
reduced risk of diverticular disease.28,29 more studies are required to clarify whether this is of any
 It is not clear whether a high-fiber diet is beneficial in therapeutic benefit.33 Despite this, short-term use poses a
patients with diverticulosis, as its pathogenesis is little nutritional risk, especially if delivered under the
probably multifactorial and complex. More studies are guidance of a dietitian,33 and reintroduction of fiber
needed to evaluate the role of fiber in the pathogenesis occurs in the long term.
and treatment of diverticular disease.28,29  Dietary advice regarding a low-fiber diet may include the
 A few poor-quality studies have suggested that fiber may following: avoiding nuts and seeds, using more refined
improve symptoms associated with uncomplicated diver- breads and cereals, reducing the intake of fruits and
ticulosis and decrease the risk of diverticulitis. However, vegetables where possible, and peeling fruits and vegeta-
high-quality evidence is lacking.28,29 bles when consumed.33
 During an episode of acute diverticulitis, a low-fiber diet  In some cases, fiber is not the only dietary factor to be
is often recommended to minimize bowel irritation.28,29 considered when a low-fiber diet is recommended. Diet-
However, there is limited evidence to support this ary advice for patients with bloating, pain, and other IBS-
strategy. like symptoms may include avoidance of spicy foods,

Copyright © 2021 World Gastroenterology Organisation. All rights reserved. www.jcge.com |5


Makharia et al J Clin Gastroenterol  Volume 56, Number 1, January 2022

Addressing the “Fiber Gap”


TABLE 6. Three-step Process for Implementing the Low
FODMAP Diet
Adequate dietary fiber intake can be achieved by
increasing variety in daily food patterns.5 Eating at least
Phase 1 —Initial assessment by a dietitian to evaluate symptoms 400 g or 5 portions of fruit and vegetables per day reduces
and FODMAP intake the risk of chronic disease and helps ensure an adequate
—The dietitian provides education on the low FODMAP
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

daily intake of dietary fiber.11,36 Dietary messages about


diet
Phase 2 —The dietitian reviews the patient’s response to dietary increasing consumption of high-fiber foods such as whole
modification grains, legumes, fruit, and vegetables should be broadly
—FODMAP rechallenges are started supported by food and nutrition professionals.5,36
—The dietitian reviews the response to FODMAP Although consumers are also turning to fiber supple-
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

Phase 3
challenges ments and bulk laxatives as additional fiber sources, the best
—The challenges are interpreted advice is to consume fiber in foods. Few fiber supplements
have been studied for physiological effectiveness.5 Increas-
FODMAP indicates fermentable oligosaccharides, disaccharides, mon-
osaccharides, and polyols. ing fiber in the diet too quickly can lead to symptoms such
as gas, bloating, and abdominal cramping, so a gradual
increase in the intake should always be recommended.5
fatty foods, gut irritants (such as alcohol and caffeinated Good sources of dietary fiber include: whole-grain
beverages), and individual foods that are poorly products, fruit, vegetables, beans, peas and legumes, and
tolerated.20 nuts and seeds. Foods labeled “high in fiber” typically
Recommendations: Please refer to Table 11 in the WGO contain at least 5 g of fiber per serving. However, food-
online version of this guideline (www.worldgastroenterology. labeling requirements vary across countries.4,5
org/guidelines/global-guidelines) for clinical symptoms and Examples of common high-fiber foods include37:
pathophysiology of lactose intolerance. There is limited evi-  ½ cup red kidney beans, cooked (6.5 g fiber).
dence to support the therapeutic use of a low-fiber diet in the  ½ cup wheat bran cereal (9.1 g fiber).
context of gastrointestinal disease and surgery. However, this  1 cup butternut squash, baked (6.6 g fiber).
is common in clinical practice, and short-term use presents a  1 large orange (7.2 g fiber).
little nutritional risk. A low-fiber diet may be useful in the  1 cup raspberries (8.0 g fiber).
context of bowel preparation for diagnostic procedures and  1 cup whole-wheat spaghetti, cooked (5.9 g fiber).
may improve patient satisfaction and compliance.  1 cup broccoli, boiled (5.5 g fiber).
Consumers have an interest in increasing fiber intake,
but compliance and cost pose a challenge. Dietary change
Fiber Intake and Recommendations requires alterations in long-term habits and is difficult to
Targets for recommended dietary fiber intake vary achieve, despite the reported benefits. Maintaining dietary
globally (please refer to Table 6 in the WGO online version of change requires motivation, behavioral skills, and a sup-
this guideline at www.worldgastroenterology.org/guidelines/ portive social and also political environment (please refer to
global-guidelines for the recommended and actual fiber intake Table 7 in the WGO online version of this guideline at:
in different countries).4,35 However, guidelines typically rec- www.worldgastroenterology.org/guidelines/global-guidelines
ommend an intake of > 20 g/d.4,5 Actual dietary fiber intake for a list of possible barriers to dietary change and
falls below recommendations in many countries worldwide, solutions).5,39
but it is notably higher in regions with predominantly plant- Many factors and complex interactions influence the
based diets such as sub-Saharan Africa (please refer to Fig. 1 in evolution and shape of individual dietary patterns over time:
the WGO online version of this guideline) (www. income, food prices (the availability and affordability of
worldgastroenterology.org/guidelines/global-guidelines).3–5 healthy foods), individual preferences and beliefs, cultural

TABLE 7. Food Sources of FODMAPs and Suitable Alternatives


Food Group Richest Sources of FODMAPs Suitable Alternatives
Fruit Apples, apricots, cherries, blackberries, boysenberries, Banana, blueberry, cantaloupe, grapefruit, grapes, lemon,
mango, nashi pears, nectarines, peaches, pears, lime, mandarin, orange, passion fruit, raspberry,
persimmon, plums, watermelon rhubarb, strawberry
Vegetables Artichokes, asparagus, cauliflower, garlic, mushrooms, Carrot, chili, chives, cucumber, eggplant, ginger, green
onion, shallots, snow peas, spring onion (white part) beans, lettuce, olives, parsnips, peppers, potato,
spinach, tomato, zucchini
Protein sources Legumes/pulses All fresh beef, chicken, lamb, pork, veal
Pistachio nuts Macadamia, peanut, walnut, and pine nuts
Cashews Eggs, tempeh, tofu
Breads and Wheat, rye, barley Buckwheat, corn, oats, polenta, quinoa, rice, spelt
cereals
Dairy Condensed or evaporated milk, cottage or ricotta cheese, Butter, lactose-free milk, lactose-free yogurt, other
custard, ice cream, milk, yogurt cheeses, rice milk
Other Honey, sorbitol or mannitol, high-fructose corn syrup, Golden syrup, maple syrup, regular sugar (sucrose),
fructose glucose
FODMAP indicates fermentable oligosaccharides, disaccharides, monosaccharides, and polyols.
Source: Barrett.38

6 | www.jcge.com Copyright © 2021 World Gastroenterology Organisation. All rights reserved.


J Clin Gastroenterol  Volume 56, Number 1, January 2022 WGO Guideline

traditions, as well as geographical, environmental, social, How to Implement a Low FODMAP Diet:
and economic factors.36 Reintroduction and Problems/Limitations
The low FODMAP diet is best implemented with the
Cascade Guidelines—Dietary Fiber assistance of an experienced dietitian. Table 5 provides a
Please see Table 1 above. clinical management overview, including the roles of the
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

family physician (general practitioner) or gastroenterologist


and the dietitian. The diet can be implemented in a 3-step
THE LOW FODMAP DIET process (Table 6).
First, patients should be identified as having functional
Introduction
bowel symptoms and should have other conditions such as
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

What is the Low FODMAP Diet? celiac disease adequately excluded before their diet is
The low FODMAP diet was developed by researchers changed. This is important, as dietary modifications may
at Monash University in Melbourne, Australia, to assist affect the accuracy of tests such as those for celiac disease.
patients with IBS.40–42 Research worldwide has now con- Patients should then be educated on ways of reducing high
firmed that the diet is effective in managing the symptoms of FODMAP foods in the diet, usually for a period of 2 to 6
IBS.43–47 While the evidence for efficacy in the first phase of weeks.59 The primary aim of this initial phase is to improve
the FODMAP diet (see Table 6 below) was rated as very symptom control. Patients are best educated by an experi-
low (due to heterogeneity of studies and risk of bias in enced dietitian on the FODMAP content of foods to ensure
RCTs) by the American College of Gastroenterology, the that they understand which foods to avoid—and impor-
Canadian Association of Gastroenterology, and the Korean tantly, which foods to include during the initial phase. No
Society of Neurogastroenterology and Motility, these entire food groups should be excluded; instead, mod-
organizations recommend that the diet should be used early ifications should be made to the types of food chosen in
in the management of patients with IBS.48–50 each food group. For example, consumption of apples,
“FODMAP” is an acronym that stands for: ferment- which have a high FODMAP content, might be changed to
able oligosaccharides, disaccharides, monosaccharides, and intake of oranges, which have a low FODMAP content.
polyols. This is important for maintaining nutritional adequacy.59
The acronym groups together specific types of short- Patients should understand the mechanisms of FODMAPs
chain carbohydrates that are slowly absorbed or not and the effect of dose so that they can grasp the dietary
digested in the small intestine. Because of their small process.
molecular size, they increase the water content of the small The second phase is the rechallenge phase, the aim of
intestine through an osmotic effect, and because they are which is to identify specific dietary triggers in each indi-
readily fermented by bacteria, their delivery to the large vidual. It is unlikely that all high FODMAP foods cause
bowel results in gas production.40,41,51 FODMAPs can thus symptoms for every individual, and strategic challenges are
distend (or stretch) the bowel. In patients with IBS who are therefore used to identify tolerance levels for each FOD-
hypersensitive to this stretching, symptoms occur such as MAP subgroup.60 Guidance from a dietitian helps the
abdominal pain, bloating, excessive flatulence, and changes patient test each FODMAP subgroup, including dose-
in bowel habits (constipation and/or diarrhea).52 Please refer response, frequency of consumption, and the additive effect
to Figure 2 in the WGO online version of this guideline of multiple high FODMAP foods.60 Individual tolerance for
(www.worldgastroenterology.org/guidelines/global-guidelines) FODMAPs varies widely. Tolerance within an individual
for classification of indigestible and slowly absorbed carbo- can also vary depending on other factors, including stress
hydrates according to their functional properties.53 levels.
The low FODMAP diet includes reducing dietary The final phase is the maintenance phase. The aim of
intake of the 5 main subgroups of carbohydrates: the maintenance phase is for the patient to reintroduce as
 Fructose in excess of glucose—for example, many high FODMAP foods back into the diet as tolerated
honey, mango. while still maintaining good symptom control. Any foods
 Lactose (when hypolactasia is present)—for example, that are well tolerated should be reintroduced into the diet.
milk, yogurt. Foods that are moderately tolerated may be reintroduced on
 Sugar polyols (including sorbitol and mannitol)—for an occasional basis, while foods that are poorly tolerated
example, avocado, mushrooms. should continue to be avoided.60 In the long term, patients
 Fructans—for example, wheat, onion, garlic. are encouraged to continue to challenge themselves with
 GOS—for example, legumes, soy milk. poorly tolerated foods from time to time to reassess their
The aims of the low FODMAP diet are to help patients tolerance.
control their symptoms and subsequently to identify specific  List of high FODMAP foods and low FODMAP
food triggers. This is done through an initial dietary alternatives: due to continuing and rapidly progressing
reduction of all FODMAPs, followed by strategic rechal- research into the low FODMAP diet, many food lists that
lenges. Patients are then able to follow their own modified are available—both printed and online—are unfortu-
version of the diet. It is not suggested that the strict low nately outdated and hence have inaccuracies.61 Table 7
FODMAP diet should be followed over the longer term. lists rich sources of FODMAPs and suitable low FOD-
The FODMAP content of a wide range of foods has MAP alternatives.38 The Monash University smartphone
been analyzed by the Department of Gastroenterology at application for the low FODMAP diet is the most useful
Monash University, with findings published in a number of tool, as it is regularly updated.58 The app costs US$10
research articles.54–57 The complete list of the FODMAP with no other fees, including all updates.
content of foods—classified as low, moderate, and high—is  Potential adverse effects of the low FODMAP diet: Any
available to the public through a smartphone application major change to dietary intake carries risks of unwanted
developed by the university.58 effects such as reduced dietary fiber or an increased risk

Copyright © 2021 World Gastroenterology Organisation. All rights reserved. www.jcge.com |7


Makharia et al J Clin Gastroenterol  Volume 56, Number 1, January 2022

of nutritional inadequacy in general. The effect of dietary belching, epigastric pain, and discomfort. Many patients
modification on quality of life must also be considered. In experience both FD and IBS simultaneously. Although data
addition, what is eaten is a major factor in defining the are limited for the effect of the low FODMAP diet specifi-
gastrointestinal microbiota.62 There is, therefore, a cally for FD, there are anecdotal reports that it can be used
potential that restricting FODMAPs, including prebiotic to manage symptoms.73 Further data are required to assess
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

fructans and GOS, could have marked effects on the the effects of the low FODMAP diet in patients with FD.
composition of the microbiota.63
 To date, there are only limited published data on the
nutritional adequacy of patients’ intake while on the short- Cascade Guidelines—FODMAP
term low FODMAP diet or in the long term following the Please refer to Table 2 above.
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

reintroduction of FODMAPs for tolerance. However, it is


thought that with appropriate dietary counseling, the diet
can be applied in a nutritionally adequate way. The effect of
the diet on nutritional adequacy when self-implemented is
CARBOHYDRATE INTOLERANCE
not known.63 Studies to date suggest that total energy, Lactose Intolerance/Lactase Deficiency
carbohydrate, and calcium intake may be reduced in the
short term, although fiber intake does not appear to be Definition of Terms
altered. Due to the potential of the diet to cause alterations
to nutritional intake, body weight and dietary intake should  Lactose: A disaccharide that is commonly found in dairy
be monitored throughout the duration of the therapy.63 products, with the highest concentrations in milk and
A low FODMAP diet can potentially improve or yogurt.
worsen an individual’s quality of life; however, most data  Lactase: A brush-border enzyme required for cleaving
suggest that the low FODMAP diet does not lead to a lactose (a disaccharide) into the monosaccharides glucose
deterioration in the quality of life and may even improve and galactose.
it.64 A recently published placebo-controlled study in  Lactase deficiency: brush-border lactase activity that is
patients with IBS reported that a low FODMAP diet was markedly reduced relative to the activity observed in
associated with adequate symptom relief and significantly infants.
reduced symptom scores in comparison with a placebo.65  Lactose malabsorption: Occurs when a substantial
Because of these potentially detrimental effects of amount of lactose is not absorbed in the small intestine.
dietary modification, long-term adherence to the low  Lactose intolerance: Occurs when lactose malabsorption
FODMAP diet is recommended only for those who have induces gastrointestinal symptoms.74
severe symptoms and require ongoing restriction for symp-
tom control. A program of reintroduction of high FOD-
MAP-containing foods to identify the patient’s tolerance Lactose Intolerance in Perspective: When Is It
threshold is therefore encouraged. Relevant?
The expression of lactase is down-regulated in ∼ 65% to
Gastrointestinal Conditions and the Low 75% of the human population after weaning. Lactose mal-
FODMAP Diet absorption is more prevalent in populations in Asia, South
America, and Africa.75 Lactase persistence (continued lac-
Indications for Low FODMAP Diet tase production in adult life) is a genetically determined trait
Most of the evidence for the use of the low FODMAP and occurs most frequently in European and some African,
diet is for patients with IBS. As mentioned above, it is Middle Eastern, and Southern Asian populations.76
important for patients to have received a clinical diagnosis The rate at which lactase activity is lost varies
of IBS, with the exclusion of other diseases, before a low depending on ethnicity. Chinese and Japanese lose 80% to
FODMAP diet is implemented. 90% of lactase activity within 3 to 4 years of weaning, in
There is evidence regarding the use of the low FOD- comparison with 7 years after weaning in Jews and 18 to
MAP diet in patients with IBD (Crohn’s disease and 20 years after weaning in Northern Europeans.77
ulcerative colitis).27,66–68 In patients with IBD, it is common Secondary lactose intolerance can be caused by dam-
to have IBS-type symptoms. The use of the low FODMAP age to the small intestine, as in untreated celiac disease or
diet in IBD is therefore targeted at controlling the IBS-type viral gastroenteritis. Secondary lactose intolerance is usually
symptoms rather than inflammation related to the disease reversible once the primary condition has been treated.75
itself. This may also apply to patients with celiac disease. As distinct from lactose intolerance, cow’s milk allergy
The use of the low FODMAP diet in cases of infantile is an inflammatory response to milk proteins. There are
colic (a dietary recommendation for lactating mothers) is overlapping symptoms between lactose intolerance and
supported by a RCT.69 The diet is also being investigated cow’s milk allergy, and misdiagnosis is therefore possible.
for other conditions such as endometriosis,70 functional Cow’s milk protein allergy occurs in 2% to 6% of infants and
dyspepsia (FD), fibromyalgia,71 scleroderma, chronic fati- 0.1% to 0.5% of adults.78 In addition to gastrointestinal
gue syndrome, and gastrointestinal symptoms in athletes.72 symptoms, cow’s milk protein allergy can lead to skin
However, the evidence for the use of the diet in these con- symptoms (erythema, pruritus) and respiratory system
ditions is minimal, and it is therefore not recommended for manifestations (wheezing, breathlessness), and even to
use in connection with them at this stage. anaphylaxis.78 Due to the similarity of some symptoms, it is
important for health professionals to be aware of the dif-
The Low FODMAP Diet, FD, and IBS ferences between the 2. Cow’s milk allergy can also be
There is a considerable overlap of symptoms between induced by dairy products with minimal lactose content
IBS and FD. FD is characterized by symptoms of bloating, (such as hard cheeses).

8 | www.jcge.com Copyright © 2021 World Gastroenterology Organisation. All rights reserved.


J Clin Gastroenterol  Volume 56, Number 1, January 2022 WGO Guideline

Symptoms of Lactose Intolerance plasma glucose should increase by at least 1.4 mmol/L
Typical symptoms of lactose intolerance include (25.2 mg/dL); its failure to do so indicates lactose
abdominal pain, bloating, flatulence, diarrhea, and bor- malabsorption. The test’s sensitivity and specificity for
borygmi. It may also result in nausea and vomiting, lactase deficiency are high (both > 90%).
although these are less frequent.75  Genetic test.80 The genetic test identifies single nucleotide
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

In patients with common adult-type hypolactasia, the polymorphisms associated with lactase persistence/non-
amount of ingested lactose required to produce symptoms persistence. For example, genotype CC correlates with
varies from 12 to 18 g or 8 to 12 ounces of milk. Ingestion of hypolactasia, while the TT genotype correlates with
small to moderate amounts of lactose usually produces lactase persistence. Not everyone with the CC genotype
bloating, cramps, and flatulence, but not diarrhea. Ingestion will develop symptoms of lactose malabsorption. How-
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

of larger amounts of lactose, faster gastric emptying times, ever, the relevant mutations depend on the ethnicity of
and faster intestinal transit times all contribute to more the population studied.
severe symptoms. Several factors determine the onset of  Intestinal biopsy. A jejunal biopsy can be used to assess
symptoms of lactose intolerance, such as lactose content in lactase activity, but it is less sensitive and more invasive
the diet, gut transit time, fermentation capacity of the gut than the lactose breath test. This test is not recommended
microbiome, visceral hypersensitivity,79 and (possibly) neu- in clinical practice.
ropsychological factors.80  Food challenge. A dietary challenge may be sufficient to
Please refer to Table 11 in the WGO online version of identify lactose malabsorption in many cases. The food
this guideline (www.worldgastroenterology.org/guidelines/ used for the challenge should be relevant to the
global-guidelines) for clinical symptoms and pathophysio- individual’s needs and food preferences. A standard
logy of lactose intolerance. challenge involves consuming 1 cup (250 mL) of skimmed
milk (since some persons are intolerant of dairy fat/
How to Diagnose: in Resource-limited triacylglycerol) in one sitting, with individual monitoring
and Well-resourced Settings of the symptom response. However, this should be
The diagnosis of lactose intolerance is based on self- adapted to the individual. For example, if a particular
reporting of symptoms after lactose ingestion.14 Determin- person rarely consumes this quantity of milk and would
ing the dose of lactose that persons with lactose intolerance rather challenge with 200 g of yogurt, then skimmed milk
can tolerate is critical in determining its implications for yogurt should be used for the food challenge.60
health.74 The presence of malabsorption of lactose is com-
monly not associated with symptoms. It is only when lactose How to Treat
malabsorption induces symptoms that “lactose intolerance” There are 2 key ways of treating lactose intolerance:
can be diagnosed. either through dietary avoidance of foods that contain sig-
 Lactose hydrogen breath testing. Lactose hydrogen breath nificant amounts of lactose (Table 8) or by using β-gal-
testing is currently considered to be the most cost- actosidase to hydrolyze the lactose content of foods.
effective, noninvasive, and reliable measure of lactose  Dietary modification—reduction of large quantities of
malabsorption.75 The breath test usually involves con- lactose. Most individuals with lactose intolerance can
sumption of 25 or 50 g of lactose, followed by measure- tolerate 12 to 15 g of lactose without gastrointestinal
ment of breath hydrogen and methane over the following symptoms being triggered.74 An average dairy-based meal
3 to 4 hours. Although diagnostic guidelines vary, an contains ∼ 12 g of lactose81; hence small quantities of
increase in breath hydrogen by 20 ppm (parts per million) lactose are likely to be well tolerated even in those with
above baseline or in methane by 10 ppm above baseline lactose intolerance. Consideration of the dosage of lactose
suggests lactose malabsorption.75 consumption is imperative for the management of lactose
 Lactose “tolerance” test.80 This is a blood test for lactase intolerance. Dairy products such as hard cheese, an
deficiency, and the traditional term “tolerance” test is a excellent source of calcium, contain <1 g of lactose and
misnomer. The patient consumes 50 g of lactose dissolved should therefore be included in the diet of those with lactose
in water. Samples of capillary blood are obtained to test intolerance. Appropriate education is imperative to ensure
the plasma glucose concentration at −5, 0, 15, 30, 45, and adequate intake of calcium-rich foods.
60 minutes. When lactose malabsorption is present, the Consideration should be given to reducing the intake of
blood sugar will not rise after lactose ingestion; normally, large quantities of lactose. This can be done by reducing the

TABLE 8. Food Items That Are Restricted or Allowed in Individuals With Lactose Intolerance
Food Items to Be Avoided Food Items That Are Allowed
All kinds of milk: whole, low-fat, nonfat, cream, powdered, condensed, All fruits, vegetables, legumes
and evaporated
Chocolate containing milk All cereals
Cottage cheese, ice cream, creamy/cheesy sauces, cream cheeses, soft cheese, All meat, fish, and eggs
and mozzarella
Milk and creamer All vegetable fats
Lactose-free milk and soy milk
Hard cheeses and other lactose-free dairy products
Yogurts, unless unfermented milk is added back in
Kefir
Source: WGO Handbook on Diet and the Gut, 2016.80

Copyright © 2021 World Gastroenterology Organisation. All rights reserved. www.jcge.com |9


Makharia et al J Clin Gastroenterol  Volume 56, Number 1, January 2022

intake of products that are high in lactose and/or by using Intake of Fructose
lactose-free products. Dairy products such as cow’s milk Estimates of fructose consumption suggest that total
and yogurt can be preincubated with β-galactosidase to fructose intake has increased in recent years, largely due to
hydrolyze the lactose content. There is an increasing the increased use of high-fructose corn syrups. A study in
demand for lactose-free products in some countries, the United States that compared intake in the periods 1977-
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

resulting in the availability of lactose-free milk, yogurt, 1978 and 1999-2004 found only a 1% increase in fructose
cheese, cream, and ice cream. However, the need for consumption as a percentage of energy intake, in compar-
products such as lactose-free cheese and cream is ques- ison with a 41% increase in total carbohydrate intake80,87—
tionable in view of their minimal lactose content.14 suggesting that the increase in fructose consumption is not
 Enzyme supplementation. An alternative treatment for as significant as thought. Fruit and fruit products were the
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

lactose intolerance is supplementation with lactase (β- main source of dietary fructose in 1999-2004.87
galactosidase) enzyme, which can be taken orally
together with food. Studies have shown that this is Use of Dietary Modification
effective in reducing breath hydrogen and in achieving Early studies investigating the effect of excess fructose
symptomatic improvement,82–84 although higher doses of on gastrointestinal symptoms focused on fructose alone or
lactose, such as 50 g, appeared to overwhelm the fructose in combination with sorbitol. However, these
enzyme’s capacity.83 fructose-restricted diets were poorly described. Since excess
fructose is often consumed together with other short-chain
Fructose Intolerance carbohydrates that have similar effects on the bowel (ie,
Definition of Terms FODMAPs), it is the combined role of these specific car-
bohydrates in the pathogenesis of gastrointestinal symp-
 Fructose: A monosaccharide commonly found in honey, toms, as opposed to their effects individually54–56 that
mango, apple, pear, and high-fructose corn syrup. results in symptoms. The grouping of these fermentable
 Excess fructose: Fructose and glucose commonly coexist carbohydrates as part of the low FODMAP diet has been
in foods; excess fructose is defined as the presence of associated with symptom improvement in up to three
fructose in excess of glucose (also termed “free fructose”). quarters of patients with functional gastrointestinal
The absorption of excess fructose relies on low-capacity disorders.42,43,46,88
absorptive pathways that appear to be present along the
length of the small intestine. In this situation, fructose Recommendations
molecules are likely to remain in the small intestinal
lumen for longer and exert their osmotic effects over  Fructose ingestion (in excess of glucose) is modified as a
much of its length, with or without “spill-over” into the component of the low FODMAP diet. Reduction of all
colon (ie, fructose malabsorption).14,51 The fructose that dietary FODMAPs, rather than fructose alone, has a more
reaches the large intestine is then available for colonic beneficial effect on reducing gastrointestinal symptoms.
fermentation, creating by-products of hydrogen and  “Fructose malabsorption” is neither a diagnosis nor a
methane that can be measured in expired air. condition. Rather, dietary fructose may trigger IBS-like
 Fructose malabsorption: Incomplete absorption of a given gastrointestinal symptoms, and its effects should be
dose of fructose in the small intestine, resulting in “spill- considered along with the effects of the other dietary
over” into the large intestine. Fructose malabsorption has FODMAPs (see the “The low FODMAP diet” section
been shown to be a normal phenomenon, occurring in above).
∼35% of healthy individuals.85  The clinical value of breath tests for identifying fructose
 Fructose intolerance: This occurs when the consumption malabsorption is limited.
of fructose induces gastrointestinal symptoms.  For food items that should be avoided, please refer to the
FODMAP composition table (Table 7).
Proposed Mechanisms
Sucrase-Isomaltase Deficiency
 Fructose has been shown to have an osmotic effect, Sucrase-isomaltase deficiency (also known as sucrose
increasing luminal water content in the small intestine and intolerance) usually manifests early in life and can result in
leading to distension (stretching) of the intestinal wall. If this carbohydrate malabsorption, causing symptoms of diarrhea,
is marked, or if visceral hypersensitivity is present, it may bloating, and abdominal pain, similar to the symptoms of
result in abdominal pain, bloating, and sometimes diarrhea. diarrhea-predominant IBS. The cause of sucrase-isomaltase
This effect has been found to occur regardless of the degree deficiency is reduced small intestinal activity of an enzyme
of fructose absorption in the small intestine.51 It is, known as glucosidase. The enzyme is normally involved in
therefore, not the presence of malabsorption but rather the digestion of starch and sugars. With reduced glucosidase
the presence of visceral hypersensitivity such as that seen in activity, carbohydrates—particularly sucrose—then behave
functional gastrointestinal disorders that is likely to cause as FODMAPs, with increased osmotic activity and fermen-
the symptoms after fructose consumption.52 tation in the bowel, potentially leading to symptoms of IBS.89
 Breath hydrogen testing used to be a popular tool to help in A role for sucrose-isomaltase deficiency in later-onset IBS is
targeting dietary therapy; it was thought that patients who poorly established.
had a negative fructose breath test did not require fructose
restriction. However, symptoms may occur regardless of the Congenital Sucrase-Isomaltase Deficiency
presence of malabsorption based on breath hydrogen or In congenital sucrase-isomaltase deficiency, mutations
methane production due to the effects of fructose on the in the sucrase-isomaltase (SI) gene lead to severe symptoms.
small intestine. Breath hydrogen testing is therefore no This is a rare condition. However, recent studies have
longer recommended for assessing fructose absorption.86 identified multiple variations of the SI gene with reduced

10 | www.jcge.com Copyright © 2021 World Gastroenterology Organisation. All rights reserved.


J Clin Gastroenterol  Volume 56, Number 1, January 2022 WGO Guideline

function. About 2% to 9% of persons of North American  WGO Global Guidelines: Celiac Disease (2016).1 The
and European descent may be affected, suggesting that it is 2017 update of this WGO Global Guideline has been
possibly an underrecognized condition.90 However, it has published in the Journal of Clinical Gastroenterology.2
yet to be shown whether it is pathogenetically involved with Several uncontrolled studies have shown that a pro-
symptom induction in patients with functional gastro- portion of patients who meet the criteria for IBS will
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

intestinal disorders. respond to a GFD.95–98 The controversy lies in whether the


offending food components are gluten, nongluten wheat
Secondary or Acquired Sucrase-Isomaltase Deficiency proteins, or fructans. There is a cohort of patients with IBS
Secondary or acquired sucrase-isomaltase deficiency or other functional gut symptoms, often with extraintestinal
can also theoretically occur, but it is usually transient. symptoms, who self-report that they are gluten-sensitive.
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

Animal studies have shown that villous atrophy, such as However, gluten has yet to be implicated as the causative
that occurring in untreated celiac disease, may result in a molecule in such patients. A subgroup who have an
sucrase-isomaltase deficiency. This should be reversible with increased density of intraepithelial lymphocytes and eosi-
healing of the villous atrophy.90 nophils in the small-bowel and often large bowel mucosae
have been shown to develop gastrointestinal symptoms after
Diagnosis double-blind placebo-controlled challenges to wheat and
A diagnosis of sucrose-isomaltase deficiency can be other proteins.99 Dietary restriction guided by the results of
established using duodenal or jejunal biopsies in children for such challenges has led to long-term symptomatic benefits in
assessment of sucrase, lactase, isomaltase, and maltase these patients.100 Further research in other centers is
activity.90 However, the biopsy samples must be immediately required to assess the generalizability of these findings.
frozen, and due to the complex freeze/thaw process required In the majority of individuals who do not have the
for sample analysis, inaccurate results may occur.91 Other above-mentioned histopathologic changes, GFD may be
methods of diagnosis are available, such as sucrose breath effective, but whether the patient needs to be gluten-free or
testing, but performing hydrogen breath testing in young whether gluten is a marker for other molecules contained in
children is problematic.91 More recently, genetic sequencing wheat, such as fructans, remains controversial. A recent
has become available to identify forms of congenital sucrase- study in Norway provided evidence that fructans, but not
isomaltase deficiency,90 although these results should be con- gluten or wheat protein, were the culprits in patients with
sidered in combination with the clinical picture. There are few self-reported gluten sensitivity.101
data on the value of performing such tests in adults. So-called “nonceliac” gluten sensitivity (NCGS) is
likely to represent a heterogenous group of patients, often
Treatment with IBS, and may include a proportion with non–
Limited evidence is available for the treatment of immunoglobulin E-mediated wheat protein sensitivity. The
sucrase-isomaltase deficiency. Treatment options include majority of these patients will have no evidence that they are
dietary restriction of sugars and starch, although this has intolerant of gluten itself—as consistently shown in RCTs
been poorly studied. Patients undertake an initial restrictive using double-blind placebo-controlled cross-over food
phase, followed by gradual reintroduction to determine challenges.102
tolerance. However, such dietary restrictions are difficult,  There are currently no biomarkers of gluten sensitivity.
and patients are often noncompliant.91 An alternative to Determining HLA-DQ2/8 as a predictive marker for
dietary modification is enzyme replacement with sacrosi- wheat sensitivity cannot be recommended.97
dase, which has shown good effect in studies with small  In the absence of biomarkers for NCGS, a double-blind
sample sizes.91,92 However, enzyme supplementation is placebo-controlled trial (DBPCT) to assess gluten-
costly and may not be available worldwide. induced symptoms has been considered in clinical
practice to be the best method of detecting NCGS after
Cascade Guidelines excluding celiac disease and wheat allergy. This approach
Please refer to Table 3. has been utilized in some areas of Europe but has been
seldom used in the rest of the world. However, a recent
OTHER DIETARY INTERVENTIONS IN IBS European study103 revealed the limitations of this test,
Certain food items trigger the symptoms experienced
by IBS patients, including foods that are rich in FODMAPs.
TABLE 9. Abbreviations Used in This WGO Guideline
See the “The low FODMAP diet” section above for
FODMAP diets in IBS. DBPCT Double-blind placebo-controlled trial
Among other dietary approaches, few have good- FD Functional dyspepsia
quality evidence of efficacy, safety, and nutritional ade- FODMAP Fermentable oligosaccharides, disaccharides,
quacy. The exception is the gluten-free diet (GFD), which monosaccharides, and polyols
GFD Gluten-free diet
has been widely initiated by IBS sufferers in the United GOS Galacto-oligosaccharide
States without any input from health care professionals. IBD Inflammatory bowel disease
Reference may also be made to the following WGO IBS Irritable bowel syndrome
Global Guidelines93: IBS-C Constipation-predominant irritable bowel syndrome
 Irritable Bowel Syndrome: a Global Perspective (2015), for IBS-D Diarrhea-predominant irritable bowel syndrome
clinical recommendations on IBS diagnosis and manage- LDL Low-density lipoprotein
ment, including WGO cascade options—since neither the NCGS Nonceliac gluten sensitivity
epidemiology nor the clinical presentation of the condition, RCT Randomized controlled trial
nor the availability of diagnostic and therapeutic resources, SCFA Short-chain fatty acid
WDHD World Digestive Health Day
are sufficiently uniform throughout the world to support the WGO World Gastroenterology Organisation
provision of a single, gold-standard approach.94

Copyright © 2021 World Gastroenterology Organisation. All rights reserved. www.jcge.com | 11


Makharia et al J Clin Gastroenterol  Volume 56, Number 1, January 2022

TABLE 10. Organizations Publishing Relevant Guidelines


World Health Organization (WHO) guidelines on nutrition108 (www.who.int/publications/guidelines/nutrition/en/)
American College of Gastroenterology (ACG) guidelines (eg, nutrition therapy in the adult hospitalized patient)109 (https://doi.org/10.1038/
ajg.2016.28)
British Society of Gastroenterology (BSG) guidelines (eg, celiac disease)110 (www.bsg.org.uk/clinical/bsg-guidelines.html and http://gut.bmj.
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

com/content/63/8/1210)
National Institute for Health and Care Excellence (NICE) guidelines (eg, diet, nutrition and obesity)111 (www.nice.org.uk/sharedlearning/
lifestyle-and-wellbeing/diet–nutrition-and-obesity)
North American/European Societies for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN/ESPGHAN) guidelines (for
children)112 (www.naspghan.org/content/55/en/Nutrition-and-Obesity)
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

World Gastroenterology Organisation (WGO) guideline: Coping with common gastrointestinal symptoms20 (https://journals.lww.com/jcge/
Fulltext/2014/08000/Coping_With_Common_Gastrointestinal_Symptoms_in.4.aspx and www.worldgastroenterology.org/guidelines/global-
guidelines/common-gi-symptoms)
World Gastroenterology Organisation (WGO) guideline on celiac disease2 (www.worldgastroenterology.org/guidelines/global-guidelines/
celiac-disease)
British Dietetic Association (BDA): Dietary management of irritable bowel syndrome in adults23 (https://doi.org/10.1111/jhn.12385)

suggesting that gluten is not the source of these patients’ 5. Slavin JL. Position of the American Dietetic Association:
symptoms, that a DBPCT is inadequate to determine health implications of dietary fiber. J Am Diet Assoc. 2008;108:
whether gluten is causing the symptoms and that the 1716–1731.
DBPCT is not a satisfactory method of detecting gluten- 6. Kim Y, Je Y. Dietary fiber intake and total mortality: a meta-
analysis of prospective cohort studies. Am J Epidemiol.
induced symptoms in individual patients without celiac 2014;180:565–573.
disease. However, a standardized and rigorous method- 7. Threapleton DE, Greenwood DC, Evans CEL, et al. Dietary
ology for assessing NCGS, once developed, may fibre intake and risk of cardiovascular disease: systematic
have merit. review and meta-analysis. BMJ. 2013;347:f6879.
 Many patients who suffer from IBS-like symptoms self- 8. Yang Y, Zhao L-G, Wu Q-J, et al. Association between
report “gluten sensitivity,” and their symptoms may dietary fiber and lower risk of all-cause mortality: a meta-
improve on a GFD.98 According to a recently published analysis of cohort studies. Am J Epidemiol. 2015;181:83–91.
study in Norway,101 this improvement is probably due to 9. Yao B, Fang H, Xu W, et al. Dietary fiber intake and risk of
a reduction in fructans rather than gluten or nongluten type 2 diabetes: a dose-response analysis of prospective
studies. Eur J Epidemiol. 2014;29:79–88.
wheat proteins. 10. American Association of Cereal Chemists. The definition of
 The benefits of a low FODMAP diet may outweigh the dietary fiber. Report of the Dietary Fiber Definition
benefits of a GFD.104 Committee to the Board of Directors of the American
 The ultimate role of diet in different IBS subtypes needs Association of Cereal Chemists. Cereal Foods World. 2001;46:
further research.105 112–126.
Despite uncertainty regarding the role of gluten, spe- 11. Livingston KA, Chung M, Sawicki CM, et al. Development of
cifically, in the genesis of symptoms in IBS, a trial of GFD is a publicly available, comprehensive database of fiber and
a reasonable intervention for people who feel that their health outcomes: rationale and methods. PLoS One. 2016;11:
symptoms become worse with gluten-containing foods. e0156961.
12. Howlett JF, Betteridge VA, Champ M, et al. The definition of
 IBS patients with pain or bloating as the predominant dietary fiber—discussions at the Ninth Vahouny Fiber
symptom106 and patients with diarrhea-predominant IBS Symposium: building scientific agreement. Food Nutr Res.
(IBS-D) or mixed IBS may benefit most. 2010;54:1–9.
 A GFD is difficult to implement and maintain, and it is 13. McRorie JW, McKeown NM. So D, Gibson PR, Muir JG, et al.
not inexpensive.107 Dietary fibres and IBS: translating functional characteristics to
 The involvement of a trained registered dietitian is clinical value in the era of personalised medicine. Gut. 2021;20:
recommended. gutjnl-2021-324891.
14. Tuck CJ, Muir JG, Barrett JS, et al. Fermentable oligosac-
charides, disaccharides, monosaccharides and polyols: role in
Abbreviations irritable bowel syndrome. Expert Rev Gastroenterol Hepatol.
Table 9. 2014;8:819–834.
15. Eswaran S, Muir J, Chey WD. Fiber and functional gastro-
intestinal disorders. Am J Gastroenterol. 2013;108:718–727.
Organizations Publishing Relevant Guidelines 16. Maslowski KM, Mackay CR. Diet, gut microbiota and
immune responses. Nat Immunol. 2011;12:5–9.
Table 10. 17. Slavin J. Fiber and prebiotics: mechanisms and health benefits.
Nutrients. 2013;5:1417–1435.
REFERENCES 18. Christodoulides S, Dimidi E, Fragkos KC, et al. Systematic
1. Bai JC, Ciacci C. Celiac disease. World Gastroenterology review with meta-analysis: effect of fibre supplementation on
Organisation global guidelines online version. 2016;1–35. chronic idiopathic constipation in adults. Aliment Pharmacol
Available at: http://www.worldgastroenterology.org/guideli Ther. 2016;44:103–116.
nes/global-guidelines/celiacdisease/celiac-disease-english. 19. Lindberg G, Hamid SS, Malfertheiner P, et al. World Gastro-
2. Bai JC, Ciacci C. World Gastroenterology Organisation global enterology Organisation global guideline: Constipation—a global
guidelines: celiac disease. J Clin Gastroenterol. 2017;51:755–768. perspective. J Clin Gastroenterol. 2011;45:483–487.
3. Anderson JW, Baird P, Davis RH, et al. Health benefits of 20. Hunt R, Quigley E, Abbas Z, et al. Coping with common
dietary fiber. Nutr Rev. 2009;67:188–205. gastrointestinal symptoms in the community: a global perspective
4. Jones JM. CODEX-aligned dietary fiber definitions help to on heartburn, constipation, bloating, and abdominal pain/
bridge the “fiber gap”. Nutr J. 2014;13:34. discomfort. May 2013. J Clin Gastroenterol. 2014;48:567–578.

12 | www.jcge.com Copyright © 2021 World Gastroenterology Organisation. All rights reserved.


J Clin Gastroenterol  Volume 56, Number 1, January 2022 WGO Guideline

21. Rao SSC, Patcharatrakul T. Diagnosis and treatment of 41. Barrett JS, Gearry RB, Muir JG, et al. Dietary poorly
dyssynergic defecation. J Neurogastroenterol Motil. 2016;22: absorbed, short-chain carbohydrates increase delivery of water
423–435. and fermentable substrates to the proximal colon. Aliment
22. Suares NC, Ford AC. Systematic review: the effects of fibre in Pharmacol Ther. 2010;31:874–882.
the management of chronic idiopathic constipation. Aliment 42. Halmos EP, Power VA, Shepherd SJ, et al. A diet low in
Pharmacol Ther. 2011;33:895–901. FODMAPs reduces symptoms of irritable bowel syndrome.
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

23. McKenzie YA, Bowyer RK, Leach H, et al. British Dietetic Gastroenterology. 2014;146:67.e5–75.e5.
Association systematic review and evidence-based practice 43. Eswaran SL, Chey WD, Han-Markey T, et al. A randomized
guidelines for the dietary management of irritable bowel controlled trial comparing the low FODMAP diet vs.
syndrome in adults (2016 update). J Hum Nutr Diet. 2016;29: modified NICE guidelines in US adults with IBS-D. Am J
549–575. Gastroenterol. 2016;111:1824–1832.
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

24. Nagarajan N, Morden A, Bischof D, et al. The role of fiber 44. Staudacher HM, Lomer MCE, Anderson JL, et al. Ferment-
supplementation in the treatment of irritable bowel syndrome: able carbohydrate restriction reduces luminal bifidobacteria
a systematic review and meta-analysis. Eur J Gastroenterol and gastrointestinal symptoms in patients with irritable bowel
Hepatol. 2015;27:1002–1010. syndrome. J Nutr. 2012;142:1510–1518.
25. Wedlake L, Slack N, Andreyev HJN, et al. Fiber in the 45. McIntosh K, Reed DE, Schneider T, et al. FODMAPs alter
treatment and maintenance of inflammatory bowel disease: a symptoms and the metabolome of patients with IBS: a
systematic review of randomized controlled trials. Inflamm randomised controlled trial. Gut. 2016;66:1241–1251.
Bowel Dis. 2014;20:576–586. 46. de Roest RH, Dobbs BR, Chapman BA, et al. The low
26. Gibson PR. Use of the low-FODMAP diet in inflammatory FODMAP diet improves gastrointestinal symptoms in
bowel disease. J Gastroenterol Hepatol. 2017;32(suppl 1): patients with irritable bowel syndrome: a prospective study.
40–42. Int J Clin Pract. 2013;67:895–903.
27. Gearry RB, Irving PM, Barrett JS, et al. Reduction of dietary 47. Pedersen N, Vegh Z, Burisch J, et al. Ehealth monitoring in irritable
poorly absorbed short-chain carbohydrates (FODMAPs) bowel syndrome patients treated with low fermentable oligo-, di-,
improves abdominal symptoms in patients with inflammatory mono-saccharides and polyols diet. World J Gastroenterol.
bowel disease—a pilot study. J Crohns Colitis. 2009;3:8–14. 2014;20:6680–6684.
28. Böhm SK. Risk factors for diverticulosis, diverticulitis, 48. Ford AC, Moayyedi P, Chey WD, et al. American College of
diverticular perforation, and bleeding: a plea for more subtle Gastroenterology monograph on management of irritable
history taking. Viszeralmedizin. 2015;31:84–94. bowel syndrome. Am J Gastroenterol. 2018;113(suppl 2):
29. Carabotti M, Annibale B, Severi C, et al. Role of fiber in 1–18.
symptomatic uncomplicated diverticular disease: a systematic 49. Moayyedi P, Andrews CN, MacQueen G, et al. Canadian
review. Nutrients. 2017;9:161. Association of Gastroenterology clinical practice guideline for
30. Asano T, McLeod RS. Dietary fibre for the prevention of the management of irritable bowel syndrome (IBS). J Can
colorectal adenomas and carcinomas. Cochrane Database Syst Assoc Gastroenterol. 2019;2:6–29.
Rev. 2002;2:CD003430. 50. Song KH, Jung H-K, Kim HJ, et al. Clinical practice
31. Murphy N, Norat T, Ferrari P, et al. Dietary fibre intake and guidelines for irritable bowel syndrome in Korea, 2017 revised
risks of cancers of the colon and rectum in the European edition. J Neurogastroenterol Motil. 2018;24:197–215.
Prospective Investigation into Cancer and Nutrition (EPIC). 51. Murray K, Wilkinson-Smith V, Hoad C, et al. Differential
PLoS One. 2012;7:e39361. effects of FODMAPs (fermentable oligo-, di-, mono-saccharides
32. Yao Y, Suo T, Andersson R, et al. Dietary fibre for the and polyols) on small and large intestinal contents in healthy
prevention of recurrent colorectal adenomas and carcinomas. subjects shown by MRI. Am J Gastroenterol. 2014;109:
Cochrane Database Syst Rev. 2017;1:CD003430. 110–119.
33. Vanhauwaert E, Matthys C, Verdonck L, et al. Low-residue 52. Major G, Pritchard S, Murray K, et al. Colon hypersensitivity
and low-fiber diets in gastrointestinal disease management. to distension, rather than excessive gas production,
Adv Nutr. 2015;6:820–827. produces carbohydrate-related symptoms in individuals with
34. Butt J, Bunn C, Paul E, et al. The White Diet is preferred, irritable bowel syndrome. Gastroenterology. 2017;152:124.
better tolerated, and non-inferior to a clear-fluid diet for bowel e2–133.e2.
preparation: a randomized controlled trial. J Gastroenterol 53. Gibson PR, Varney J, Malakar S, et al. Food components and
Hepatol. 2016;31:355–363. irritable bowel syndrome. Gastroenterology. 2015;148:1158.
35. Global Nutrition and Policy Consortium. Dietary intake of e4–1174.e4.
major foods by region, 1990; 2017. Available at: www. 54. Muir JG, Shepherd SJ, Rosella O, et al. Fructan and free
globaldietarydatabase.org/dietary-data-by-region.html. Accessed fructose content of common Australian vegetables and fruit. J
April 22, 2017. Agric Food Chem. 2007;55:6619–6627.
36. World Health Organization. Healthy diet; 2017. Available at: 55. Muir JG, Rose R, Rosella O, et al. Measurement of short-
www.who.int/mediacentre/factsheets/fs394/en/. Accessed Januray chain carbohydrates in common Australian vegetables and
18, 2017. fruits by high-performance liquid chromatography (HPLC). J
37. United States Department of Agriculture. Agricultural Agric Food Chem. 2009;57:554–565.
Research Service. USDA food composition databases; 2017. 56. Biesiekierski JR, Rosella O, Rose R, et al. Quantification of
Available at: https://ndb.nal.usda.gov/ndb/nutrients/index. fructans, galacto-oligosacharides and other short-chain carbohy-
Accessed April 21, 2017. drates in processed grains and cereals. J Hum Nutr Diet. 2011;24:
38. Barrett JS. Extending our knowledge of fermentable, short- 154–176.
chain carbohydrates for managing gastrointestinal symptoms. 57. Yao CK, Tan H-L, van Langenberg DR, et al. Dietary
Nutr Clin Pract. 2013;28:300–306. sorbitol and mannitol: food content and distinct absorption
39. European Food Information Council (EUFIC). Why we eat patterns between healthy individuals and patients with
what we eat: the barriers to dietary and lifestyle change; 2004. irritable bowel syndrome. J Hum Nutr Diet. 2014;27(suppl 2):
Available at: www.eufic.org/en/healthy-living/article/why-we- 263–275.
eat-what-we-eat-the-barriers-to-dietary-and-lifestyle-change. 58. Monash University. Download the low FODMAP diet app for
Accessed May 19, 2018. on-the-go IBS support; 2017. Available at: www.med.monash.
40. Ong DK, Mitchell SB, Barrett JS, et al. Manipulation of edu/cecs/gastro/fodmap/iphone-app.html. Accessed April
dietary short chain carbohydrates alters the pattern of gas 21, 2017.
production and genesis of symptoms in irritable bowel 59. Barrett JS. How to institute the low-FODMAP diet. J
syndrome. J Gastroenterol Hepatol. 2010;25:1366–1373. Gastroenterol Hepatol. 2017;32(suppl 1):8–10.

Copyright © 2021 World Gastroenterology Organisation. All rights reserved. www.jcge.com | 13


Makharia et al J Clin Gastroenterol  Volume 56, Number 1, January 2022

60. Tuck C, Barrett J. Re-challenging FODMAPs: the low Health Day (WDHD)—May 29, 2016. Milwaukee, WI: World
FODMAP diet phase two. J Gastroenterol Hepatol. 2017;32 Gastroenterology Organisation and WGO Foundation; 2016:1–60.
(suppl 1):11–15. 81. O’Connell S, Walsh G. Physicochemical characteristics of commer-
61. McMeans AR, King KL, Chumpitazi BP. Low FODMAP cial lactases relevant to their application in the alleviation of lactose
dietary food lists are often discordant. Am J Gastroenterol. intolerance. Appl Biochem Biotechnol. 2006;134:179–191.
2017;112:655–656. 82. Montalto M, Nucera G, Santoro L, et al. Effect of exogenous
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

62. Payne AN, Chassard C, Lacroix C. Gut microbial adaptation beta-galactosidase in patients with lactose malabsorption and
to dietary consumption of fructose, artificial sweeteners and intolerance: a crossover double-blind placebo-controlled
sugar alcohols: implications for host-microbe interactions study. Eur J Clin Nutr. 2005;59:489–493.
contributing to obesity. Obes Rev. 2012;13:799–809. 83. Lin MY, Dipalma JA, Martini MC, et al. Comparative effects
63. Staudacher HM. Nutritional, microbiological and psychoso- of exogenous lactase (beta-galactosidase) preparations on
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

cial implications of the low FODMAP diet. J Gastroenterol in vivo lactose digestion. Dig Dis Sci. 1993;38:2022–2027.
Hepatol. 2017;32(suppl 1):16–19. 84. Rosado JL, Solomons NW, Lisker R, et al. Enzyme replace-
64. Ostgaard H, Hausken T, Gundersen D, et al. Diet and effects of ment therapy for primary adult lactase deficiency. Effective
diet management on quality of life and symptoms in patients reduction of lactose malabsorption and milk intolerance by
with irritable bowel syndrome. Mol Med Rep. 2012;5:1382–1390. direct addition of beta-galactosidase to milk at mealtime.
65. Staudacher HM, Lomer MCE, Farquharson FM, et al. A diet low Gastroenterology. 1984;87:1072–1082.
in FODMAPs reduces symptoms in patients with irritable bowel 85. Barrett JS, Gibson PR. Fructose and lactose testing. Aust Fam
syndrome and a probiotic restores bifidobacterium species: a Physician. 2012;41:293–296.
randomized controlled trial. Gastroenterology. 2017;153: 86. Yao CK, Tuck CJ, Barrett JS, et al. Poor reproducibility of breath
936–947. hydrogen testing: implications for its application in functional
66. Prince AC, Myers CE, Joyce T, et al. Fermentable carbohydrate bowel disorders. United European Gastroenterol J. 2017;5:284–292.
restriction (low FODMAP diet) in clinical practice improves 87. Marriott BP, Cole N, Lee E. National estimates of dietary
functional gastrointestinal symptoms in patients with inflamma- fructose intake increased from 1977 to 2004 in the United
tory bowel disease. Inflamm Bowel Dis. 2016;22:1129–1136. States. J Nutr. 2009;139:1228S–1235S.
67. Halmos EP, Christophersen CT, Bird AR, et al. Consistent 88. Staudacher HM, Whelan K, Irving PM, et al. Comparison of
prebiotic effect on gut microbiota with altered FODMAP intake in symptom response following advice for a diet low in
patients with Crohn’s disease: a randomised, controlled cross-over fermentable carbohydrates (FODMAPs) versus standard
trial of well-defined diets. Clin Transl Gastroenterol. 2016;7:e164. dietary advice in patients with irritable bowel syndrome. J
68. Cox SR, Lindsay JO, Fromentin S, et al. Effects of low FODMAP Hum Nutr Diet. 2011;24:487–495.
diet on symptoms, fecal microbiome, and markers of inflammation 89. Henström M, Diekmann L, Bonfiglio F, et al. Functional
in patients with quiescent inflammatory bowel disease in a variants in the sucrase-isomaltase gene associate with
randomized trial. Gastroenterology. 2019;158:176.e7–188.e7. increased risk of irritable bowel syndrome. Gut. 2018;67:
69. Iacovou M, Craig SS, Yelland GW, et al. Randomised clinical 263–270.
trial: reducing the intake of dietary FODMAPs of breastfeed- 90. Cohen SA. The clinical consequences of sucrase–isomaltase
ing mothers is associated with a greater improvement of the deficiency. Mol Cell Pediatr. 2016;3:5.
symptoms of infantile colic than for a typical diet. Aliment 91. Puntis JWL, Zamvar V. Congenital sucrase-isomaltase defi-
Pharmacol Ther. 2018;48:1061–1073. ciency: diagnostic challenges and response to enzyme replace-
70. Moore JS, Gibson PR, Perry RE, et al. Endometriosis in ment therapy. Arch Dis Child. 2015;100:869–871.
patients with irritable bowel syndrome: specific symptomatic 92. Harms H-K, Bertele-Harms R-M, Bruer-Kleis D. Enzyme-
and demographic profile, and response to the low FODMAP substitution therapy with the yeast Saccharomyces cerevisiae in
diet. Aust N Z J Obstet Gynaecol. 2017;57:201–205. congenital sucrase–isomaltase deficiency. N Engl J Med. 1987;316:
71. Marum AP, Moreira C, Saraiva F, et al. A low fermentable 1306–1309.
oligo-di-mono saccharides and polyols (FODMAP) diet 93. World Gastroenterology Organisation. Global guidelines; 2018.
reduced pain and improved daily life in fibromyalgia patients. Available at: www.worldgastroenterology.org/guidelines/global-
Scand J Pain. 2016;13:166–172. guidelines. Accessed May 19, 2018.
72. Lis DM. Exit gluten-free and enter low FODMAPs: a novel 94. Quigley EMM, Fried M, Gwee K-A, et al. World Gastro-
dietary strategy to reduce gastrointestinal symptoms in enterology Organisation global guidelines. Irritable bowel
athletes. Sports Med. 2019;49(suppl 1):87–97. syndrome: a global perspective. Update September 2015. J
73. Tan VP. The low-FODMAP diet in the management of Clin Gastroenterol. 2016;50:704–713.
functional dyspepsia in East and Southeast Asia. J Gastro- 95. Shahbazkhani B, Sadeghi A, Malekzadeh R, et al. Non-celiac
enterol Hepatol. 2017;32(suppl 1):46–52. gluten sensitivity has narrowed the spectrum of irritable bowel
74. Shaukat A, Levitt MD, Taylor BC, et al. Systematic review: syndrome: a double-blind randomized placebo-controlled
effective management strategies for lactose intolerance. Ann trial. Nutrients. 2015;7:4542–4554.
Intern Med. 2010;152:797–803. 96. Eswaran S, Goel A, Chey WD. What role does wheat play in
75. Lomer MCE, Parkes GC, Sanderson JD. Review article: the symptoms of irritable bowel syndrome? Gastroenterol
lactose intolerance in clinical practice—myths and realities. Hepatol. 2013;9:85–91.
Aliment Pharmacol Ther. 2008;27:93–103. 97. Barmeyer C, Schumann M, Meyer T, et al. Long-term response
76. Itan Y, Jones BL, Ingram CJ, et al. A worldwide correlation of to gluten-free diet as evidence for non-celiac wheat sensitivity in
lactase persistence phenotype and genotypes. BMC Evol Biol. one third of patients with diarrhea-dominant and mixed-type
2010;10:36. irritable bowel syndrome. Int J Colorectal Dis. 2017;32:29–39.
77. Matthews SB, Waud JP, Roberts AG, et al. Systemic lactose 98. Aziz I, Trott N, Briggs R, et al. Efficacy of a gluten-free diet in
intolerance: a new perspective on an old problem. Postgrad subjects with irritable bowel syndrome–diarrhea unaware of
Med J. 2005;81:167–173. their HLA-DQ2/8 genotype. Clin Gastroenterol Hepatol.
78. Crittenden RG, Bennett LE. Cow’s milk allergy: a complex 2016;14:696.e1–703.e1.
disorder. J Am Coll Nutr. 2005;24(suppl):582S–591S. 99. Carroccio A, Mansueto P, Iacono G, et al. Non-celiac wheat
79. Zhu Y, Zheng X, Cong Y, et al. Bloating and distention in sensitivity diagnosed by double-blind placebo-controlled
irritable bowel syndrome: the role of gas production and challenge: exploring a new clinical entity. Am J Gastroenterol.
visceral sensation after lactose ingestion in a population with 2012;107:1898–1906.
lactase deficiency. Am J Gastroenterol. 2013;108:1516–1525. 100. Carroccio A, D’Alcamo A, Iacono G, et al. Persistence of
80. World Gastroenterology Organisation. WGO handbook on diet nonceliac wheat sensitivity, based on long-term follow-up.
and the gut. In: Makharia GK, Sanders DS, eds. World Digestive Gastroenterology. 2017;153:56.e3–58.e3.

14 | www.jcge.com Copyright © 2021 World Gastroenterology Organisation. All rights reserved.


J Clin Gastroenterol  Volume 56, Number 1, January 2022 WGO Guideline

101. Skodje GI, Sarna VK, Minelle IH, et al. Fructan, rather 107. Moayyedi P, Quigley EMM, Lacy BE, et al. The effect of
than gluten, induces symptoms in patients with self-reported dietary intervention on irritable bowel syndrome: a systematic
non-celiac gluten sensitivity. Gastroenterology. 2018;154:529. review. Clin Transl Gastroenterol. 2015;6:e107.
e2–539.e2. 108. World Health Organization. WHO Guidelines on Nutrition.
102. Gibson PR, Skodje GI, Lundin KEA. Non-coeliac gluten Geneva, Switzerland: WHO; 2018.
sensitivity. J Gastroenterol Hepatol. 2017;32(suppl 1): 109. McClave SA, DiBaise JK, Mullin GE, et al. ACG clinical
Downloaded from http://journals.lww.com/jcge by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AW

86–89. guideline: nutrition therapy in the adult hospitalized patient.


103. Molina-Infante J, Carroccio A. Suspected nonceliac gluten Am J Gastroenterol. 2016;111:315–334.
sensitivity confirmed in few patients after gluten challenge in 110. Ludvigsson JF, Bai JC, Biagi F, et al. Diagnosis and
double-blind, placebo-controlled trials. Clin Gastroenterol management of adult coeliac disease: guidelines from the
Hepatol. 2017;15:339–348. British Society of Gastroenterology. Gut. 2014;63:1210–1228.
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 03/19/2024

104. Lacy BE. The science, evidence, and practice of dietary 111. National Institute for Health and Care Excellence (NICE). Diet,
interventions in irritable bowel syndrome. Clin Gastroenterol nutrition and obesity; 2018. Available at: www.nice.org.uk/
Hepatol. 2015;13:1899–1906. resources/lifestyle-and-wellbeing/diet–nutrition-and-obesity.
105. Portincasa P, Bonfrate L, de Bari O, et al. Irritable bowel Accessed May 19, 2018.
syndrome and diet. Gastroenterol Rep. 2017;5:11–19. 112. North American Society for Pediatric Gastroenterology,
106. Bhat K, Harper A, Gorard DA. Perceived food and drug Hepatology and Nutrition (NASPGHAN). Nutrition &
allergies in functional and organic gastrointestinal disorders. obesity; 2016. Available at: www.naspghan.org/content/55/
Aliment Pharmacol Ther. 2002;16:969–973. en/Nutrition-and-Obesity. Accessed May 19, 2018.

Copyright © 2021 World Gastroenterology Organisation. All rights reserved. www.jcge.com | 15

You might also like