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FODMAP: Food Composition and Definition of Tolerable Cutoff Values

by luciano

Abstract

The low-FODMAP diet represents an established dietary strategy for the management of irritable bowel syndrome (IBS). However, it should be considered an evidence-based strategy for symptom control rather than a curative therapy for the disease. In recent years, numerous clinical studies, systematic reviews and meta-analyses have confirmed the effectiveness of this approach in reducing gastrointestinal symptoms and improving patients’ quality of life.

The dietary approach is based on limiting poorly absorbed fermentable carbohydrates (FODMAPs), including oligosaccharides (fructans and galacto-oligosaccharides), disaccharides (lactose), monosaccharides (fructose in excess of glucose), and polyols (sorbitol and mannitol).

The development of the low-FODMAP diet required not only detailed data on food composition but also the definition of cutoff values to classify foods as low in FODMAPs. In recent years, the expansion of food composition databases and the analysis of new industrial and regional products have improved the international standardization of the diet.

Recent studies indicate that approximately half, and in some cases up to two-thirds of patients with IBS experience improvement in symptoms after applying the low-FODMAP diet, particularly abdominal pain, bloating and abdominal distension [1,2,3]. However, the modern approach to the diet emphasizes a temporary restriction followed by a phase of food reintroduction and personalization.

1. Food Composition and Classification of FODMAPs

FODMAPs (Fermentable Oligo-, Di-, Mono-saccharides And Polyols) include short-chain carbohydrates that are poorly absorbed in the small intestine and easily fermented in the colon.

These molecules present two main characteristics:

  1. Poor intestinal absorption

  2. High fermentability by the intestinal microbiota

Fermentation produces gas and osmotic compounds that can cause intestinal distension, pain, and alterations in intestinal motility [7].

The main categories of FODMAPs include:

1 – oligosaccharides (fructans and galacto-oligosaccharides)

2 – disaccharides (lactose)

3 – monosaccharides (fructose in excess of glucose)

4 -polyols (sorbitol and mannitol)

These carbohydrates are widely present in commonly consumed foods, including fruit, vegetables, cereals, dairy products and legumes [5]. Recent studies indicate that the average daily intake of FODMAPs in the general population is approximately 20 g per day, without substantial differences between healthy individuals and patients with functional gastrointestinal disorders [4].

2. Definition of FODMAP Cutoff Values

To apply the low-FODMAP diet it is necessary to define threshold values useful for classifying foods as low (“low FODMAP”) or high (“high FODMAP”) in fermentable carbohydrates.

In the initial development of the diet, these values were established considering several factors:

the specific FODMAP content in foods typical portion sizes consumed in a single meal
clinical observations of the frequency with which certain foods induced symptoms in patients with irritable bowel syndrome (IBS).

Based on these criteria, conservative threshold values were proposed with the aim of allowing the combined consumption of several foods classified as low-FODMAP within the same meal without exceeding levels generally associated with the onset of symptoms.

In early controlled dietary studies on the low-FODMAP diet it was suggested that a total intake of approximately 0.5 g of FODMAPs per meal (excluding lactose) was generally well tolerated during the initial restriction phase.

However, in more recent clinical applications this value should be interpreted as an operational reference derived from experimental studies rather than as a universally applicable threshold, since individual tolerance to FODMAPs may vary significantly among patients.

More recent clinical evidence nevertheless supports the overall effectiveness of the low-FODMAP approach. Numerous systematic reviews and meta-analyses of randomized trials have shown that the low-FODMAP diet significantly reduces the severity of IBS symptoms, particularly abdominal pain, bloating and distension, and contributes to improving patients’ quality of life [1,2].

In a review of meta-analyses including more than 3,700 patients with IBS, the low-FODMAP diet showed a significant reduction in the severity of gastrointestinal symptoms compared with other dietary interventions or standard dietary recommendations [1].

These results confirm that defining cutoff values of FODMAPs in foods represents a useful tool for designing the diet, although flexible and personalized application is required in clinical practice.

3. Coexistence of Gluten and FODMAPs in Cereal Foods

Many foods containing gluten also contain high levels of FODMAPs, particularly fructans. Consequently, the reduction in symptoms observed in patients who eliminate gluten may in fact be attributable to reduced FODMAP intake rather than to the removal of gluten itself. Recent studies indicate that the low-FODMAP diet often proves more effective than a simple gluten-free diet in controlling IBS symptoms [6]. However, not all gluten-free products are necessarily low in FODMAPs. Their final composition depends on:

1 -the ingredients used
2 -industrial food processing techniques.

4. Effect of Food Processing Technologies

The final FODMAP content of foods can be significantly modified by technological processing.

Among the processes that most influence FODMAP levels are:

1 – fermentation
2 – cooking
3 – hydration and thermal treatment
4 -lactic fermentation.

A relevant example is sourdough bread, in which lactic acid bacteria metabolize part of the fructans present in flour, reducing the final FODMAP content. Similarly, some processing techniques can reduce the galacto-oligosaccharide content in legumes. These findings highlight that the FODMAP composition of foods depends not only on the raw ingredient but also on the technological processing used.

5. Recent Developments in Low-FODMAP Diet Research

In recent years the low-FODMAP diet has been the subject of numerous clinical studies and meta-analyses.

Recent evidence indicates that:

1 – the low-FODMAP diet is one of the most effective dietary interventions for IBS [2]
2 – approximately 50–70% of patients experience symptom improvement [7]
3 – the main effects concern abdominal pain, bloating and distension [3].

In a network meta-analysis of randomized trials, the low-FODMAP diet was identified as the most effective dietary strategy for the overall control of IBS symptoms [2].

6. Effects on the Intestinal Microbiota

A topic of considerable interest in recent years concerns the impact of the low-FODMAP diet on the intestinal microbiota. A meta-analysis of randomized clinical studies showed that the diet may lead to a reduction in the abundance of bifidobacteria, without significantly altering the overall diversity of the intestinal microbiota [3]. This observation has led to the recommendation that the restrictive phase of the diet should be limited in time and followed by a controlled reintroduction phase.

7. Evolution of the Dietary Model: Restriction, Reintroduction and Personalization

The modern approach to the low-FODMAP diet is based on three phases:

  1. restriction phase (2–6 weeks)

  2. reintroduction phase of individual FODMAP groups

  3. long-term personalization phase.

The goal is not the permanent elimination of FODMAPs but the identification of the specific categories that trigger symptoms in individual patients [9]. This approach allows patients to maintain a more varied and nutritionally balanced diet.

Conclusions

In recent years the low-FODMAP diet has become one of the most effective dietary approaches for the management of irritable bowel syndrome. Progress in the characterization of food composition, the expansion of international databases, and new clinical evidence have improved the understanding of the pathophysiological mechanisms associated with FODMAPs.

Recent evidence also highlights the importance of:

1 – applying the diet under professional supervision
2 – limiting the restrictive phase
3 – progressively personalizing dietary intake.

Main High-FODMAP Foods (to be reduced):

  1. Fruit: Apples, pears, apricots, cherries, peaches, watermelon, plums.

  2. Vegetables: Garlic, onion, asparagus, broccoli, cauliflower, mushrooms, artichokes.

  3. Dairy: Milk, yogurt, and fresh cheeses containing lactose.

  4. Legumes: Chickpeas, lentils, beans.

  5. Grains: Wheat, rye, barley.

  6. Sweeteners: Honey, high-fructose corn syrup, sorbitol, mannitol.

Veronesi Foundation

Main Low-FODMAP Foods (allowed):

  1. Fruit: Bananas, blueberries, strawberries, kiwi, grapes, oranges, melon.

  2. Vegetables: Carrots, green beans, cucumbers, lettuce, zucchini, potatoes, tomatoes.

  3. Dairy: Lactose-free dairy products, aged cheeses (such as Parmesan).

  4. Grains: Rice, oats, corn, quinoa, gluten-free pasta/bread.

  5. Proteins: Meat, fish, eggs.

Bibliografia scientifica recente

[1] Black C.J., Staudacher H.M., Ford A.C.
Efficacy of a Low-FODMAP Diet in Irritable Bowel Syndrome: Systematic Review and Network Meta-analysis.
Gut. 2022;71(6):1117-1126.
DOI: 10.1136/gutjnl-2021-325214

[2] Whelan K., Martin L.D., Staudacher H.M., Lomer M.C.E.
The Low FODMAP Diet in the Management of Irritable Bowel Syndrome: Recent Advances and Clinical Applications.
Current Opinion in Gastroenterology. 2022;38(2):101-108.
DOI: 10.1097/MOG.0000000000000786

[3] So D., Staudacher H.M., Lomer M.C.E., Whelan K.
Effects of a Low-FODMAP Diet on the Colonic Microbiome in Irritable Bowel Syndrome: A Systematic Review and Meta-analysis.
American Journal of Clinical Nutrition. 2022;116(1):225-236.
DOI: 10.1093/ajcn/nqac164

[4] Zanzer Y.C., Whelan K., Staudacher H.M.
Habitual FODMAP Intake and Dietary Patterns: A Systematic Review and Meta-analysis.
Journal of Functional Foods. 2023;100:105914.
DOI: 10.1016/j.jff.2023.105914

[5] Skodje G.I., Sarna V.K., Minelle I.H. et al.
Fructan, Rather Than Gluten, Induces Symptoms in Patients With Self-Reported Non-Celiac Gluten Sensitivity.
Gastroenterology. 2018;154(3):529-539.
DOI: 10.1053/j.gastro.2017.10.040

[6] Loponen J., Gänzle M.G.
Use of Sourdough Fermentation to Reduce FODMAP Content in Wheat-Based Products.
Food Microbiology. 2018;72:93-101.
DOI: 10.1016/j.fm.2017.07.003

[7] Staudacher H.M., Whelan K.
Mechanisms and Efficacy of Dietary FODMAP Restriction in Irritable Bowel Syndrome.
Nature Reviews Gastroenterology & Hepatology. 2023;20(3):165-182.
DOI: 10.1038/s41575-023-00742-9

[8] Varney J., Muir J.G., Gibson P.R.
Twenty Years of FODMAP Research: Progress and Future Directions.
Journal of Gastroenterology and Hepatology. 2024.
DOI: 10.1111/jgh.16523

[9] Halmos E.P., Gibson P.R.
Dietary FODMAP Reduction and Gastrointestinal Symptoms in Irritable Bowel Syndrome: Updated Evidence.
Clinical Gastroenterology and Hepatology. 2024.
DOI: 10.1016/j.cgh.2024.02.012

[10] Bogdanowska-Charkiewicz D., et al.
Low-FODMAP Diet in Irritable Bowel Syndrome: Umbrella Review of Meta-analyses.
Nutrients. 2025;17:1545.
DOI: 10.3390/nu17091545

Studi fondamentali del gruppo Monash

[11] Halmos E.P., Power V.A., Shepherd S.J., Gibson P.R., Muir J.G.

A Diet Low in FODMAPs Reduces Symptoms of Irritable Bowel Syndrome.
Gastroenterology. 2014;146(1):67-75.
DOI: 10.1053/j.gastro.2013.09.046

Abstract (summary)

  1. Randomized controlled trial conducted by the Monash group comparing a typical Australian diet with a low-FODMAP diet in patients with IBS.

  2. The results demonstrated a significant reduction in gastrointestinal symptoms, particularly abdominal pain, bloating, and flatulence, in patients following the low-FODMAP diet.

  3. This study represents one of the most frequently cited clinical trials supporting the effectiveness of the diet.

[12] Varney J., Barrett J., Scarlata K., Catsos P., Gibson P., Muir J.

FODMAPs: Food Composition, Defining Cutoff Values and International Application.
Journal of Gastroenterology and Hepatology. 2017;32(S1):53-61.
DOI: 10.1111/jgh.13698

Abstract (summary)

  1. Landmark article describing the development of methodologies for analyzing the FODMAP composition of foods and defining the threshold values used to classify foods as low-FODMAP.

  2. The paper also discusses the implications of differences between national food systems and the importance of updated databases for the international application of the diet.

Final note

  1. These two studies are among the most cited in the FODMAP literature.

  2. Halmos 2014 → fundamental clinical trial.

  3. Varney 2017 → definition of cutoff values and food composition.

Almost all recent reviews (including those from 2023–2024) continue to cite them.

Irritable Bowel Syndrome (IBS) and Intestinal Permeability

by luciano

Abstract
Irritable bowel syndrome (IBS) is a complex and multifactorial disorder that cannot be explained by a single pathogenic mechanism. In recent years, increased intestinal permeability (“leaky gut”) has received considerable attention as a potential contributor to IBS pathophysiology. However, current scientific evidence indicates that barrier dysfunction affects only a subset of patients rather than representing a universal feature of the condition. Increased intestinal permeability is more frequently observed in diarrhea-predominant IBS (IBS-D) and post-infectious IBS (PI-IBS), whereas many patients exhibit a structurally intact intestinal barrier. In these cases, symptoms are more accurately attributed to alterations in the gut–brain axis, visceral hypersensitivity, disordered intestinal motility, and gut microbiota dysbiosis. An integrated understanding of these mechanisms is essential to move beyond reductionist models and to guide personalized therapeutic strategies.

Keywords
irritable bowel syndrome, IBS, intestinal permeability, leaky gut, IBS-D, post-infectious IBS, gut barrier, tight junctions, gut-brain axis, visceral hypersensitivity, gut microbiota, functional gastrointestinal disorders, chronic abdominal pain, low-grade inflammation, personalized IBS treatment

1. Introduction
Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, characterized by recurrent abdominal pain associated with changes in bowel habits, in the absence of identifiable structural abnormalities. Over the past two decades, the traditional view of IBS as a purely “functional” disorder has been progressively replaced by a more comprehensive model that integrates neurobiological, immune, microbial, and mucosal barrier factors.
Within this evolving framework, increased intestinal permeability—commonly referred to as “leaky gut”—has been proposed as a central mechanism in IBS pathogenesis. While this hypothesis has gained substantial attention, accumulating evidence suggests a more nuanced reality: increased permeability is present only in a subset of IBS patients and does not constitute a defining feature of the syndrome as a whole.

2. Evidence of Altered Intestinal Permeability in IBS
Numerous clinical and experimental studies have assessed intestinal barrier function in IBS using permeability tests (e.g., lactulose/mannitol ratio), urinary and plasma biomarkers, mucosal biopsies, and molecular analyses of tight junction proteins.
Collectively, these studies demonstrate that:
A significant but non-majority proportion of IBS patients exhibits increased intestinal permeability;
Barrier dysfunction is more commonly observed in the colon, although small intestinal involvement may occur in specific subgroups;
Increased permeability is not stable over time and may fluctuate in response to prior infections, dietary factors, psychological stress, and microbiota composition.
These findings indicate that intestinal barrier dysfunction represents an important pathogenic mechanism in IBS, but not an exclusive or universal one.

3. Differences Among IBS Subtypes
The heterogeneity of IBS becomes particularly evident when examining its clinical subtypes:
IBS-D (diarrhea-predominant IBS): This subtype is most frequently associated with increased intestinal permeability. Alterations in tight junction proteins and enhanced immune exposure to luminal antigens have been consistently reported.
Post-infectious IBS (PI-IBS): PI-IBS represents one of the strongest models linking IBS to barrier dysfunction. Following acute gastroenteritis, some patients develop chronic symptoms associated with increased permeability, low-grade mucosal inflammation, and mast cell activation.
IBS-C (constipation-predominant IBS): In most studies, intestinal permeability in IBS-C patients is comparable to that of healthy controls.
IBS-M (mixed subtype): Barrier function appears most consistently preserved in this group.
These differences underscore the absence of a single biological phenotype underlying IBS.

4. Molecular Mechanisms of Barrier Dysfunction
In IBS patients with increased permeability, several structural and functional alterations of the intestinal epithelial barrier have been documented, including:
Reduced expression or disorganization of tight junction proteins such as ZO-1, occludin, and claudins;
Increased paracellular passage of luminal molecules and antigens;
A correlation between the degree of barrier impairment and the severity of abdominal pain.
Loss of epithelial integrity facilitates contact between luminal antigens (bacterial or dietary) and the mucosal immune system, contributing to low-grade inflammatory responses.

5. Interaction Between Intestinal Permeability, Immune System, and Microbiota
In IBS subgroups characterized by barrier dysfunction, increased permeability may initiate a pathogenic cascade involving:
Activation of mast cells and other immune cells within the lamina propria;
Release of inflammatory and neuroactive mediators;
Sensitization of enteric nerve endings.
The gut microbiota plays a central role in this process. Qualitative and functional alterations of microbial communities can both contribute to barrier dysfunction and amplify immune and neural responses. Nevertheless, these mechanisms are not present in all IBS patients, reinforcing the concept of biological heterogeneity.

6. IBS Without Increased Intestinal Permeability
A crucial and often underestimated aspect of IBS is that many patients exhibit a structurally intact intestinal barrier. This is well documented in IBS-C and IBS-M subtypes, but also applies to a proportion of IBS-D patients.
In such cases, the leaky gut model alone is insufficient to explain symptom generation.

7. Alternative Mechanisms Independent of Permeability
7.1 Gut–Brain Axis Dysfunction
IBS is currently classified as a disorder of gut–brain interaction. Altered bidirectional communication between the enteric nervous system and the central nervous system can generate pain, urgency, and bowel habit changes in the absence of mucosal damage.
7.2 Visceral Hypersensitivity
Many IBS patients exhibit a reduced pain threshold to physiological intestinal stimuli. This phenomenon is attributed to:
Peripheral neural sensitization;
Central amplification of nociceptive signaling.
7.3 Altered Intestinal Motility
Disruptions in intestinal motor patterns may account for diarrhea, constipation, or alternating bowel habits without involving epithelial barrier dysfunction.
7.4 Dysbiosis Independent of Barrier Damage
Gut microbiota alterations may influence fermentation, gas production, bile acid metabolism, and neuroendocrine signaling even when intestinal permeability remains normal.

8. Clinical and Therapeutic Implications
Recognizing the heterogeneity of IBS has important clinical consequences:
In IBS-D and PI-IBS patients with documented increased permeability, interventions targeting barrier function (e.g., low-FODMAP diet, microbiota modulation, mucosal protective strategies) may be particularly beneficial;
In patients with normal permeability, therapeutic approaches focused on the gut–brain axis, visceral sensitivity modulation, and stress management are likely more appropriate.
A personalized approach is therefore essential.

9. Conclusions
IBS is a multifactorial and biologically heterogeneous condition. Increased intestinal permeability represents a documented and clinically relevant pathogenic mechanism, but it is not universal. In many patients, symptoms arise from neurofunctional, motor, or microbial alterations in the presence of an intact intestinal barrier.
An integrated perspective allows clinicians and researchers to move beyond reductionist models and to develop more effective diagnostic and therapeutic strategies.
The inflammatory, neurofunctional, microbial, and barrier-related mechanisms discussed here are explored in greater detail in the related articles referenced below.

Commented Bibliographic References (for Further Reading)
1. Camilleri M. et al. – Review on IBS and intestinal barrier function
A critical analysis of permeability alterations across IBS subtypes, emphasizing their non-universality.
2. Bischoff S.C. et al. – Intestinal permeability: mechanisms and clinical relevance
A foundational reference on molecular mechanisms of barrier function and clinical implications.
3. Spiller R., Garsed K. – Post-infectious IBS . Describes PI-IBS as a key model linking low-grade inflammation and increased permeability.
4. Barbara G. et al. – Mast cells and IBS. Seminal work on mast cell involvement in visceral pain and hypersensitivity.
5. Ford A.C. et al. – Systematic reviews on IBS pathophysiology
Integrated overview of microbiota, motility, and gut–brain axis mechanisms.
6. Drossman D.A. – Disorders of gut–brain interaction. A cornerstone reference framing IBS within modern gut–brain interaction paradigms.

The different mechanisms discussed—inflammatory, neuro-functional, microbial, and barrier-related—are examined separately in the related articles.

Sensitivity to wheat, gluten and FODMAPs in IBS: facts or fiction?

by luciano

 

ABSTRACT
IBS is one of the most common types of functional bowel disorder. Increasing attention has been paid to the causative role of food in IBS. Food ingestion precipitates or exacerbates symptoms, such as abdominal pain and bloating in patients with IBS through different hypothesised mechanisms including immune and mast cell activation, mechanoreceptor stimulation and chemosensory activation. Wheat is regarded as one of the most relevant IBS triggers, although which component(s) of this cereal is/are involved remain(s) unknown. Gluten, other wheat proteins, for example, amylase-trypsin inhibitors, and fructans (the latter belonging to fermentable oligo-di-mono-saccharides and polyols (FODMAPs)), have been identified as possible factors for symptom generation/exacerbation. This uncertainty on the true culprit(s) opened a scenario of semantic definitions favoured by the discordant results of double-blind placebo-controlled trials, which have generated various terms ranging from non-coeliac gluten sensitivity to the broader one of non-coeliac wheat or wheat protein sensitivity or, even, FODMAP sensitivity. The role of FODMAPs in eliciting the clinical picture of IBS goes further since these short-chain carbohydrates are found in many other dietary components, including vegetables and fruits. In this review, we assessed current literature in order to unravel whether gluten/wheat/FODMAP sensitivity represent ‘facts’ and not ‘fiction’ in IBS symptoms. This knowledge is expected to promote standardisation in dietary strategies (gluten/wheat-free and low FODMAP) as effective measures for the management of IBS symptoms.

Extract from study:

WHEAT SENSITIVITY
Wheat is considered one of the foods known to evoke IBS symptoms. However, which component(s) of wheat is/are actually responsible for these clinical effects still remain(s) an unsettled issue. The two parts of wheat that are thought to have a mechanistic effect comprise proteins (primarily, but not exclusively, gluten) and carbohydrates (primarily indigestible short-chain components, FODMAPs). Two distinct views characterise the clinical debate: one line identifies wheat proteins as a precipitating/perpetuating factor leading to symptoms, while the other believes that FODMAPs are the major trigger for IBS.

The controversy over nomenclature
If gluten is a major trigger for IBS, it expands the gluten-related disorders by adding a new entity now referred to as non-coeliac gluten sensitivity (NCGS). Indeed, coeliac disease-like abnormalities were reported in a subgroup of patients with IBS many years ago. A recent expert group of researchers reached unanimous consensus attesting the existence of a syndrome triggered by gluten ingestion. This syndrome recognises a wide spectrum of symptoms and manifestations including an IBS-like phenotype, along with an extra-intestinal phenotype, that is, malaise, fatigue, headache, numbness, mental confusion (‘brain fog’), anxiety, sleep abnormalities, fibromyalgia-like symptoms and skin rash. In addition, other possible clinical features include gastroesophageal reflux disease, aphthous stomatitis, anaemia, depression, asthma and rhinitis. Symptoms or other manifestations occur shortly after gluten consumption and disappear or recur in a few hours (or days) after gluten withdrawal or challenge. A fundamental prerequisite for suspecting NCGS is to rule out all the established gluten/wheat disorders, comprising coeliac disease (CD), gluten ataxia, dermatitis herpetiformis and wheat allergy. The major issue not addressed by the consensus opinion was that gluten is only one protein contained within wheat. Other proteins, such as amylase-trypsin inhibitors (ATIs), are strong activators of innate immune responses in monocytes, macrophages and dendritic cells. Furthermore, wheat germ agglutinin, which has epithelial-damaging and immune effects at very low doses at least in vitro, might also contribute to both intestinal and extraintestinal manifestations of NCGS. Consequently, a further development of this research field led to suggestions of a broader term, non-coeliac wheat sensitivity (NCWS). The problems with this term are twofold. First, rye and barley may be inappropriately excluded. Second, the term will refer to any wheat component that might be causally related to induction of symptoms and, therefore, will also include fructans (FODMAPs). It will then have a very nonspecific connotation in IBS. A more correct term would then be non-coeliac wheat protein sensitivity (NCWPS) since this does not attribute effects to gluten without evidence of such specificity, eliminates the issue of fructan-induced symptoms and avoids the unknown contribution of rye and barley proteins to the symptoms. Both NCGS, the currently accepted term, and NCWPS will be used subsequently in this paper.