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Annual Review of Medicine

Low-FODMAP Diet for
Irritable Bowel Syndrome:
What We Know and What
We Have Yet to Learn
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Jerry Liu,1 William D. Chey,2 Emily Haller,2

and Shanti Eswaran2
1
Department of Internal Medicine, University of Texas Southwestern, Dallas, Texas 75390, USA;
email: jerry.liu@phhs.org
2
Department of Gastroenterology, University of Michigan, Ann Arbor, Michigan 48109, USA;
email: wchey@med.umich.edu, emilyhal@med.umich.edu, seswaran@med.umich.edu

Annu. Rev. Med. 2020. 71:303–14 Keywords

The Annual Review of Medicine is online at
irritable bowel syndrome, IBS, FODMAP, diet, nutrition, functional
med.annualreviews.org

https://doi.org/10.1146/annurev-med-050218- Abstract
013625
Irritable bowel syndrome (IBS) is the most prevalent of gastrointestinal (GI)
Copyright © 2020 by Annual Reviews.
conditions, affecting millions of people worldwide. Given that most IBS pa-
All rights reserved
tients associate their GI symptoms with eating food, specific dietary manipu-
lation has become an attractive treatment strategy. A diet low in FODMAPs
(fermentable oligosaccharides, disaccharides, monosaccharides, and polyols)
has generated the greatest level of scientific and clinical interest. Overall,
52–86% of patients report significant improvement of their IBS symptoms
with elimination of dietary FODMAPs. Patients who experience symptom
improvement with FODMAP elimination should undergo a structured rein-
troduction of foods containing individual FODMAPs to determine sensitiv-
ities and allow for personalization of the diet plan. This review discusses the
literature surrounding the administration of the low-FODMAP diet and its
efficacy in the treatment of IBS.

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INTRODUCTION
Irritable bowel syndrome (IBS) is the most common gastrointestinal (GI) disorder worldwide,
affecting about 15% of the global population (1). Patients with IBS experience abdominal pain
and bowel disturbance, leading to significant negative impact on quality of life and productivity.
In the United States, IBS has an annual burden of care of 3.1 million healthcare visits and an
annual cost of over $20 billion (2, 3). While the majority of IBS patients are women, the female
predominance observed in Western countries is not universally seen in Asia (4).
The pathophysiology of IBS, similar to the clinical presentation, is heterogeneous and likely
driven by both host and environmental factors. Traditionally, research on the pathogenesis of IBS
has focused on host abnormalities in motility, visceral sensation, and brain–gut interactions, but
more recently, the roles of environmental influences such as early adverse life events, prior enteric
infections, and dietary intolerances have been explored. IBS is the consequence of multiple path-
ways converging to produce the clinical symptoms of abdominal pain and altered bowel habits.
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The Rome IV criteria (5) describe the cardinal features of IBS, making this a symptom-based
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disorder diagnosed in the absence of organic diseases, which are typically excluded by a limited
serologic and endoscopic workup (6). IBS patients are subcategorized on the basis of their pre-
dominant stool form: IBS with constipation (IBS-C), IBS with diarrhea (IBS-D), or IBS with a
mixture of constipation and diarrhea (IBS-M) (5). It should be noted that abdominal bloating is
not included in the Rome IV criteria despite being a common and bothersome complaint among
IBS patients (7).
In most patients, IBS is a chronic relapsing disease in which symptoms, exacerbated by mul-
tiple host and environmental factors, may vary over time and sometimes shift between subtypes.
One systematic review demonstrated that 2–18% of IBS cases worsened, 30–50% remained un-
changed, and 12–38% improved over six months to six years of follow-up (8). Predictors of worse
outcomes include previous surgery, longer duration of disease, higher somatic scores, history of
trauma/abuse, pain as the predominant complaint, and comorbid anxiety and depression. Recent
research has shown that a subgroup of sufferers can trace the onset of their IBS symptoms to
an antecedent gastroenteritis. Postinfection IBS appears more likely than other forms of IBS to
improve or spontaneously resolve over time (9, 10).

CURRENT TREATMENT STRATEGIES

A respectful patient–physician relationship is the cornerstone of successful IBS treatment, and es-
tablishing a secure and confident diagnosis of IBS is crucial to patient acceptance of the diagnosis.
Goals of treatment include improving quality of life and reducing stress, in addition to control-
ling IBS symptoms. The treatment of IBS can be just as varied as the causes of the condition, and
strategies can be symptom-based or globally focused. First-line therapies, typically consisting of
lifestyle modifications and over-the-counter medications, generally target bowel symptoms (di-
arrhea or constipation) but offer only a marginal benefit for abdominal symptoms such as pain
and bloating. When these strategies fail, prescription medications (6) are often utilized. Further-
more, about half of patients with IBS utilize complementary and alternative approaches either in
addition to or instead of conventional medical therapy (11).
Dietary factors are central for patients with IBS, and >80% of IBS patients link their symptoms
to eating or to specific foods. In fact, postprandial IBS symptoms are associated with decreased
quality of life and increased disease severity (12). This apparent cause-and-effect relationship of-
ten prompts patients to attribute their IBS to a food allergy or specific food intolerance (12, 13).
There are, however, many potential explanations for postprandial exacerbation of GI symptoms
other than a true allergy (14). Given the primary function of the gut, it should come as no surprise

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that food ingestion is the most potent stimulus of GI functions, including motility and secretion.
Postprandial symptoms in IBS patients can arise as a consequence of triggering exaggerated phys-
iologic responses, such as a hyperactive gastrocolic response, with or without amplified sensory
responses to the normal or exaggerated physiology (15). These abnormalities should be viewed
within the context of IBS pathophysiology, particularly disordered gut–brain signaling. Part of this
reaction to food may be explained by food–microbiota interactions as well, since gut microbes play
an important role in the digestion of dietary components, resulting in metabolites that may di-
rectly or indirectly contribute to IBS symptoms.
Given the heterogeneous factors contributing to the pathophysiology, there currently exists no
single universal truth in regard to treatment of IBS. Patients are most likely to experience benefit
with tailored, individualized, multifaceted treatment plans, and this has led to a focus on dietary
manipulation as a primary strategy to improve symptom severity and quality of life. The optimal
dietary strategy for IBS patients would ideally be clinically effective, nutritionally balanced, and
safe.
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MECHANISMS OF THE LOW-FODMAP DIET

Specifically, a diet low in FODMAPs (fermentable oligosaccharides, disaccharides, monosaccha-
rides, and polyols) has been shown to be effective and safe in the IBS population. FODMAPs are
a diverse family of osmotically active carbohydrates thought to contribute to GI symptoms, likely
via multiple mechanisms (Figure 1). These short-chain carbohydrates feature increased concen-
tration of fructose in excess of glucose (apples, pears), lactose (dairy products), fructans (wheat,
onions), polyols (artificial sweeteners and sorbitol), and galacto-oligosaccharides (legumes,

FODMAPs

Osmotic Bacterial fermentation

effects

SCFA Gas production

(Butyrate, proprionate, acetate) (CH4, H2, CO2)

Trophic Decreased Increased

effects luminal pH osmotic load

Microbiome Increased Effects on:

changes biomass • Motility
• Visceral sensation
Acceleration of • Immune activation
transit time • Permeability

GI symptoms
• Pain
• Gas/bloating
• Altered bowel movements

Figure 1
Mechanisms by which FODMAPs cause gastrointestinal symptoms. Abbreviations: FODMAPs, fermentable
oligosaccharides, disaccharides, monosaccharides, and polyols; GI, gastrointestinal; SCFA, short-chain fatty
acid. Adapted from Reference 17 with permission.

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Table 1 Examples of low- and high-FODMAP foodsa

Dairy/
FODMAPb plant-based
content Grains Fruits Vegetables alternatives Proteins Beverages
High wheat apples/apple artichoke coconut milk most high-fructose-
rye juice asparagus (in the beans/legumes containing
barley apricots cauliflower carton) processed sodas and
blackberries garlic ice cream meatsc juices
cherries leeks milk rum
dates mushrooms cheese (soft) teas: chamomile,
grapefruits (button, soy milk oolong, fennel,
mangos portabella) yogurt and chai
pears onions/shallots
watermelons sugar snap peas
Low corn tortillas/ bananas bok choy almond milkc edamame alcohol: wine
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chips (unripe) broccoli cheese (most) lentils (most), beer,

grits grapes carrots coconut yogurt canned/rinsed spirits (most)
gluten-free kiwifruits chives hemp milkc chickpeas coffee
pastas, lemons cucumbers lactose-free ice beef sucrose-
crackers, and limes eggplants cream, milk, chicken sweetened
breads mandarin kale yogurt,c eggs or diet soft
oatmealc oranges lettuce cottage fish/seafood drinks
potatoes oranges mushrooms cheese pork teas (except those
popcorn papayas (oyster) turkey listed above)
rice pineapples olives tempehc water
sourdough radishes tofu (firm)
bread spinach
quinoa tomatoes

a
Not a complete list of foods. Portion size matters; several foods have a specific serving size in which they would be high versus low in FODMAPs.
b
Abbreviation: FODMAPs, fermentable oligosaccharides, disaccharides, monosaccharides, and polyols.
c
Read labels of packaged foods to ensure they do not have added high-FODMAP ingredients (e.g., high-fructose corn syrup, wheat, onion, garlic).

cabbage), all of which are poorly absorbed from the GI lumen (Table 1) (16). By reducing
consumption of these short-chain carbohydrates, symptoms of abdominal pain, bloating, and
flatus production, in particular, may be alleviated. More recently, improvement in disease-specific
quality of life has also been demonstrated, improving the acceptance of the low-FODMAP diet
in the treatment of IBS (18).
Conventional thinking has focused on the fact that FODMAPs are poorly absorbed or nonab-
sorbed in the small intestine. Some FODMAPs exert direct osmotic effects that draw water into
the intestinal and/or colonic lumen. FODMAPs that reach the distal ileum and colon undergo
fermentation to short-chain fatty acids and gases (hydrogen, methane, carbon dioxide), which can
trigger symptoms, particularly in patients who have underlying abnormalities in gut motility and
visceral sensation (19, 20).
Previous studies reporting alterations in the gut microbiota and fermentation patterns suggest
that physiological responses to FODMAPs, such as luminal water secretion or gas production,
might differ between IBS patients and healthy volunteers (21, 22). However, recent work from the
United Kingdom argues otherwise and suggests that different FODMAPs exert different effects
along the GI tract. Using functional magnetic resonance imaging (fMRI), a recent study showed
differential effects of fructose and fructans in the small intestine and colon in healthy volunteers

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and IBS patients (23, 24). After fructose or inulin (a fructan) challenges, healthy controls reported
significantly lower symptom scores than patients with IBS, despite similar fMRI parameters
and breath hydrogen responses. Fructose led to increased small-bowel water content in both
IBS patients and controls (potentially accelerating small-bowel transit and peristalsis as well),
whereas inulin increased colonic volume and gas via fermentation by resident bacteria. Thus, the
physiologic responses to FODMAP intake do not seem to differ between patients with IBS and
healthy controls, suggesting that visceral hypersensitivity, rather than alterations in fermentation
patterns and gas production, may be the primary driver of FODMAP-related symptoms in IBS
patients.
Aside from osmotic and fermentation effects, FODMAPs may also generate symptoms via im-
mune activation. McIntosh et al. (25) compared urinary metabolomic profiles of 40 IBS patients
after 21 days of a low- or high-FODMAP diet. Following dietary intervention, there was a sig-
nificant separation in urinary metabolomic profiles of patients with IBS in the two diet groups.
In the low-FODMAP diet group, the urinary histamine level of a single postintervention sample
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showed a marginal decrease (p < 0.05) compared to the high-FODMAP group. Another study
reported a decrease in inflammatory cytokines interleukin (IL)-6 and IL-8 in IBS patients on a
low-FODMAP diet (26). Regarding gut microbiota, a low-FODMAP diet does lead to measurable
changes in the fecal microbiota composition (and metabolome composition), including a decrease
in gut microbes generally associated with health, such as Bifidobacteria, which may seem counter-
intuitive (25–27). However, the relevance of such changes in the gut luminal microenvironment
and changes in symptoms remain unclear.

EFFICACY OF THE LOW-FODMAP DIET

Since its efficacy was first hypothesized in the early 2000s (28), numerous randomized controlled
trials (RCTs) and observational studies have reported that the majority of IBS patients (ranging
from 52% to 86% of patients) experience significant improvement in their GI symptoms with
the low-FODMAP diet (29–31). In the seminal feeding trial, Halmos et al. (32) compared the
low-FODMAP diet to a general Australian diet in a single-blind, crossover RCT. Thirty IBS pa-
tients were randomized into the low-FODMAP diet group or a general Australian diet group for
21 days. The primary endpoint was overall GI symptoms measured by the 100-mm Visual Analog
Scale with secondary endpoints of abdominal pain, bloating, and flatus. The study found that
overall GI symptom scores were lower on the low-FODMAP diet than a general diet (22.8 versus
44.9, p < 0.001) and that individual symptoms of bloating, flatus, and abdominal pain also signif-
icantly improved. While this study sparked much interest in the low-FODMAP diet, the small
sample size and highly homogeneous study population were limitations. Furthermore, the provi-
sion of all of the subjects’ food, which contributed to the scientific rigor of the study, opened the
door to questions about the practical application of the low-FODMAP diet in real-world clinical
practice.

Low-FODMAP Diet Compared to Other Active Diet Interventions

Given the difficulties with blinding and implementing a true placebo in dietary studies, most
larger-scale trials have compared the low-FODMAP diet to another active diet intervention rather
than placebo. Standard dietary advice for IBS, which includes the National Institute for Health and
Care Excellence (NICE) guidelines and advice from the British Dietetic Association, recommends
patients eat regular, small meals; avoid caffeine and alcohol; and limit their fiber intake. Studies
comparing the low-FODMAP diet to this standard dietary advice have demonstrated mixed re-
sults. In a retrospective study by Staudacher et al. (29), a greater number of patients reported

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improvement in a GI composite symptoms score (which assessed bloating, diarrhea, abdominal

pain, and flatulence) with the low-FODMAP diet compared to the NICE guidelines (86% versus
49%, p < 0.001). Patients were also more satisfied with the results of the low-FODMAP diet than
standard dietary advice (76% versus 54%, p = 0.038). Similarly, a single-blind trial from Iran con-
cluded that there was a significantly greater decrease in the Irritable Bowel Syndrome Severity
Scoring System (IBS-SSS) scores (n = 110, score 108 versus 149.75, p < 0.001), abdominal pain,
and abdominal distention for those with IBS-D on a low-FODMAP diet as opposed to standard
advice, although both interventions resulted in symptom improvement from baseline (33).
A multicenter, single-blind RCT in Sweden compared a dietitian-led low-FODMAP diet ver-
sus standard dietary advice over four weeks in 75 IBS patients. Investigators found no difference
in the number of patients reporting symptom reduction between the two diets for the primary
endpoint of a reduction in IBS-SSS score of ≥50 (p = 0.62) (34). An American single-center RCT
in 84 IBS-D patients found no statistically significant difference in primary outcome of adequate
relief of GI symptoms between four weeks of a dietitian-led low-FODMAP diet or a diet based
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upon modified NICE guidelines (foods containing FODMAPs were not excluded in the modified
NICE guideline group). Interestingly, the low-FODMAP diet did achieve a therapeutic gain
over the modified NICE diet of 11% (52% for low-FODMAP diet and 41% for modified NICE,
p = 0.31), raising questions about whether this study was adequately powered for the primary
endpoint (30). In this study, the low-FODMAP diet led to significant improvements in abdominal
pain, bloating, and stool frequency scores compared to the modified NICE diet. In a secondary
analysis from this study, the low-FODMAP diet was more than twice as likely as the modified
NICE diet to achieve a clinically meaningful improvement in disease-specific quality of life (52%
versus 21%, p < 0.001) (18).

Low-FODMAP Diet Compared to Placebo/Sham Diet

Given the powerful placebo response already present in functional GI disease, controlling for
the nocebo response in dietary trials is particularly important to minimize patient bias, as the
clinical outcome to a dietary change is invariably influenced by patient expectations (both positive
and negative). The development of a true sham diet of comparable feasibility and complexity,
however, can be challenging (36). The only true placebo-controlled trial was performed in the
United Kingdom and utilized a bespoke sham diet of similar complexity, intensity, and fiber/energy
content as a low-FODMAP diet (37). Although the percentage of participants reporting adequate
symptom relief in the intention-to-treat analysis did not reach statistical significance (57% in the
low-FODMAP group versus 38% in the sham diet group, p = 0.051), the difference was significant
in the per-protocol analysis (61% versus 39%, p = 0.042). In addition, the IBS-SSS score for
the low-FODMAP group was also significantly lower than for the sham group (173 in the low-
FODMAP group versus 224 in the sham diet group, p = 0.001). The totality of clinical outcomes
pointed toward the clinical efficacy of the low-FODMAP diet over a true placebo, and was the
first to do so using dietary advice, making it directly relevant to clinical practice.

Comparative Effectiveness of the Low-FODMAP Diet

and Nondietary Interventions
In addition to other diets, comparative studies between the low-FODMAP diet and other forms of
nonpharmacologic treatments have been conducted. A 2016 Australian study compared the low-
FODMAP diet, gut hypnotherapy, and the combination of the two in 74 patients (38). Improve-
ment from baseline was observed in all three groups (71%, 72%, and 73% of patients, respectively)

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at both six weeks and six months. However, there was no statistically significant difference between
the groups at six weeks (p = 0.67), suggesting individual benefits for the low-FODMAP diet and
hypnotherapy, but no additive benefit.
Another mind–body practice, yoga, has also been compared to the low-FODMAP diet. A
single-blind study in 59 IBS patients compared twice-weekly yoga sessions to the low-FODMAP
diet over 12 weeks. Both groups demonstrated improvement in IBS-SSS from baseline, with no
difference found between groups at 12 weeks [ = 31.80; 95% confidence interval (CI) = −11.90,
75.50; p = 0.151] (39). Combination therapy was not assessed in this study.
These preliminary studies punctuate the growing trend toward nonpharmacologic, multimodal
treatment of IBS. Though they are quite promising, further studies are needed to explore this
approach to IBS therapy.

Limitations of the Low-FODMAP Diet

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Despite the widespread adoption of the low-FODMAP diet for IBS patients in clinical practice,
several concerns have been raised regarding potential effects of prolonged FODMAP elimination
on nutritional status and the gut microbiome. A decrease in calcium intake with a low-FODMAP
diet has been demonstrated (37); however, a similar study found that this decrease was no longer
significant after correcting for calorie-adjusted nutrient intake (40). Furthermore, a modified low-
FODMAP diet (after reintroduction to determine sensitivities) is likely nutritionally adequate as
assessed by a longer-term study of dietary intake utilizing postal questionnaires (41). Fiber intake
may also decrease during the elimination phase of the low-FODMAP diet. Like calcium intake,
this issue can be addressed during FODMAP reintroduction (42). Additional research to more
fully understand the effects of the low-FODMAP diet on nutrition and energy status is clearly
needed, particularly in patients already susceptible to nutritional deficiencies such as those with
inflammatory bowel disease.
Diet is perhaps the most important influence on the human gut microbiome (43, 44). Thus, it
should come as no surprise that restricting dietary FODMAPs exerts measurable effects on the gut
microbiome. Several investigators have reported a relative decrease in total bacterial abundance
(45) and bacteria thought to be beneficial to the GI tract (18, 21, 22). For example, some studies
have found reduced Bifidobacterium species (25, 26, 37) and increases in potentially harmful species
such as Porphyromonadaceae (25). Whether these changes are associated with long-term effects—
bad, good, or indifferent—remains to be determined. Some of these changes may be reversible
with the reintroduction of FODMAPs (26) and/or with probiotic use (37).
Additionally, questions have been raised about the generalizability of the available data from
clinical research to real-world practice. Almost all of the current research has assessed the effi-
cacy or effectiveness of the elimination phase of the low-FODMAP diet plan. There are almost
no data regarding the other two phases of the diet plan: reintroduction of foods containing in-
dividual FODMAPs and personalization of the diet for more long-term use. Given that IBS is a
chronic condition, the short-term duration of most of the research studies raises questions about
the durability of the clinical benefits of the low-FODMAP diet. Most RCTs only followed patients
for several weeks, with the longest duration being six months. Retrospective trials have had longer
follow-up times, up to 16 months (31, 46). Finally, initial reactions from patients and providers are
that the low-FODMAP diet is prohibitively restrictive and confusing. Ultimately, however, stud-
ies have not supported this impression and have demonstrated that patients generally have good
comprehension and adherence when treatment is administered under the guidance of a dietitian
(31, 32, 47).

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E limination Determination of S ensitivities P ersonalization

Diagnose FODMAP Challenge with foods containing Find each patient’s
sensitivity individual FODMAPs low-FODMAP diet

Figure 2
Three phases of the low-FODMAP diet: elimination, determination of sensitivities, and personalization.
Elimination is the beginning, not the end! Abbreviation: FODMAPs, fermentable oligosaccharides,
disaccharides, monosaccharides, and polyols.

DELIVERY OF THE LOW-FODMAP DIET

The low-FODMAP diet is composed of three distinct phases for which we have created the
acronym ESP: elimination; reintroduction of foods containing individual FODMAPs to deter-
mine a person’s sensitivities; and personalization (Figure 2) (48, 49). The elimination phase, which
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typically lasts about 2–6 weeks, should be viewed as a diagnostic test to determine if a patient is
sensitive to FODMAPs. If there is no response, the diet should be discontinued. If a therapeutic
response is achieved, patients should undergo the reintroduction phase to determine their sensi-
tivities and tolerances. This information can then be used to create a personalized version of the
low-FODMAP diet for long-term use.
Given the complexity of low-FODMAP meal planning and education, counseling is best pro-
vided by a properly trained dietitian. It is worth pointing out that nearly all of the RCTs assessing
the low-FODMAP diet have utilized one-on-one instruction with a registered dietitian. However,
there is evidence that group education may achieve similar outcomes to individual counseling. A
UK study that looked at the clinical effectiveness and cost of group versus one-on-one counseling
demonstrated no difference in IBS symptom reduction between study arms (54% for group versus
60% for individual, p = 0.271), but cost savings significantly favored the group-education arm of
the study (50). Internet- or app-based instructions may be a useful adjunct, but research currently
supports having a dietitian lead the education in either a group or individual setting. The reality,
however, is that many patients receive little or no formal instruction on the low-FODMAP diet
and may find a plethora of anecdotes, testimonials, and inaccurate information online. A list of
trustworthy sources about IBS and FODMAPs for patients and providers is included in Table 2.

FUTURE DIRECTIONS AND CONCLUDING REMARKS

The low-FODMAP diet has become a key component in the management of IBS and reinvigo-
rated discussions around the role of diet in the pathophysiology and treatment of IBS patients. It
has also laid bare the inadequacies of the “medicine first” strategy that dominated the treatment
of IBS for decades. The low-FODMAP diet has helped to usher in a new age of IBS management
which recognizes that outcomes are maximized when providers and patients embrace an integra-
tive, holistic clinical care model—one that considers diet, behavior/lifestyle, and exercise, along
with medications. One size does not fit all when it comes to IBS.
That same logic should be more generally applied to the emerging role of diet therapies for IBS.
The low-FODMAP diet has validated the importance of food to the pathogenesis and treatment
of IBS. However, just as the elimination phase should be viewed as the beginning, not the end, of
the low-FODMAP diet plan, the low-FODMAP diet should be viewed as the beginning, not the
end, of our quest for effective diet interventions for IBS patients. Future research should focus on
the identification of biomarkers to assist providers to identify IBS patients who are more likely
to benefit from the low-FODMAP diet. Preliminary research suggests that “precision nutrition”

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Table 2 Best easy-to-use resources to implement the low-FODMAP diet

Resource Details
My Nutrition Health A comprehensive website for both patients and providers explaining
http://myginutrition.com the low-FODMAP diet, complete with videos, recipes, and
frequently asked questions
University of Michigan gastrointestinal Pinterest Page Pinterest account from University of Michigan dietitians with
http://www.pinterest.com/UMGIdietitians up-to-date low-FODMAP products that are suitable for the
low-FODMAP diet elimination phase as well as low-FODMAP
recipes. Great for visual learners and for making grocery shopping
easier
Monash University website and phone app Researchers at Monash University developed the low-FODMAP diet
http://www.monashfodmap.com and a corresponding smartphone app to assist patients and providers
in implementing the diet. Additionally, they maintain an informative
and up-to-date low-FODMAP blog
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Kate Scarlata website and books Kate Scarlata, registered dietitian, is a low-FODMAP diet expert who
http://www.katescarlata.com has low-FODMAP diet resources, recipes, and blog articles available
on her website. Her book The Low-FODMAP Diet: Step by Step is a
great resource for patients and providers (57)
Patsy Catsos website and books Patsy Catsos, registered dietitian, is a low-FODMAP diet expert who
http://www.ibsfree.net has low-FODMAP diet resources, recipes, and blog articles available
on her website. Her book The IBS Elimination Diet and Cookbook is a
great resource for patients and providers (58)
FODMAP Everyday Website with low-FODMAP recipes, products, and diet guidance as
http://www.fodmapeveryday.com well as resources and support

might be possible by leveraging characteristics of the gut microbiome (51, 52), metabolome (25,
53), or genetics (54). We should also remember that not all IBS patients with symptoms related to
eating respond to the low-FODMAP diet. This likely reflects the heterogeneity that is inherent to
the pathophysiology of IBS and should motivate researchers and clinicians alike to remain curious
and open to the possibility of other effective diet interventions for our IBS patients. We should also
broaden our focus beyond dietary exclusion; supplementation rather than restriction may provide
an as yet largely untapped treatment approach (55, 56). Through education and practical advice
based upon sound science, our collective goal should be to transition IBS patients from viewing
food as a source of pain and misery to something closer to how the rest of us view food—a source
of sustenance, nutrition, and joy.

DISCLOSURE STATEMENT
The authors are not aware of any affiliations, memberships, funding, or financial holdings that
might be perceived as affecting the objectivity of this review.

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nal diseases. Gastroenterology 136(3):741–54
3. Agarwal N, Spiegel BM. 2011. The effect of irritable bowel syndrome on health-related quality of life
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Annual Review of
Medicine

Contents Volume 71, 2020

Bariatric Surgery as a Long-Term Treatment for Type 2

Diabetes/Metabolic Syndrome
Zubaidah Nor Hanipah and Philip R. Schauer p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 1
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Sex Hormones and Prostate Cancer
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CD40 Agonist Antibodies in Cancer Immunotherapy
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Fecal DNA Testing for Colorectal Cancer Screening
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The Clinical Spectrum of PTEN Mutations
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Precision Management of Advanced Non–Small Cell Lung Cancer
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Microbiome Anomalies in Allogeneic Hematopoietic Cell
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A Crucial Role for Diet in the Relationship Between Gut Microbiota
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Omics and Cardiometabolic Disease Risk Prediction
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Ablation Therapy for Refractory Ventricular Arrhythmias
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Atherosclerosis: Making a U Turn

Ira J. Goldberg, Gaurav Sharma, and Edward A. Fisher p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 191
Cardiac Amyloidosis: Overlooked, Underappreciated, and Treatable
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Contemporary Application of Cardiovascular Magnetic Resonance
Imaging
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Postural Orthostatic Tachycardia Syndrome: Mechanisms and New
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Transcatheter Mitral Valve Replacement: Rationale and Current Status
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Hiding in Plain Sight: Interleukin-11 Emerges as a Master Regulator
of Fibrosis, Tissue Integrity, and Stromal Inflammation
Stuart A. Cook and Sebastian Schafer p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 263
New Frontiers in Osteoporosis Therapy
Cheng Cheng, Kelly Wentworth, and Dolores M. Shoback p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 277
New Therapies for Emerging Endotypes of Asthma
Geoffrey Lowell Chupp, Ravdeep Kaur, and Anne Mainardi p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 289
Low-FODMAP Diet for Irritable Bowel Syndrome: What We Know
and What We Have Yet to Learn
Jerry Liu, William D. Chey, Emily Haller, and Shanti Eswaran p p p p p p p p p p p p p p p p p p p p p p p 303
Is a Universal Influenza Virus Vaccine Possible?
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Broadly Neutralizing Antibodies for HIV Prevention
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Prevention of HIV Transmission and the HPTN 052 Study
Myron S. Cohen, Theresa Gamble, and Marybeth McCauley p p p p p p p p p p p p p p p p p p p p p p p p p p p p 347
Topical Microbicides in HIV Prevention: State of the Promise
Jared M. Baeten, Craig W. Hendrix, and Sharon L. Hillier p p p p p p p p p p p p p p p p p p p p p p p p p p p p 361

Indexes

Cumulative Index of Contributing Authors, Volumes 67–71 p p p p p p p p p p p p p p p p p p p p p p p p p p p 379

Cumulative Index of Article Titles, Volumes 67–71 p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p 383

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