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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.

FODMAPs: food composition, defining cutoff values and international application

by luciano

Abstract
The low-FODMAP diet is a new dietary therapy for the management of irritable bowel syndrome that is gaining in popularity around the world. Developing the low-FODMAP diet required not only extensive food composition data but also the establishment of “cutoff values” to classify foods as low-FODMAP. These cutoff values relate to each particular FODMAP present in a food, including oligosaccharides (fructans and galacto- oligosaccharides), sugar polyols (mannitol and sorbitol), lactose, and fructose in excess of glucose. Cutoff values were derived by considering the FODMAP levels in typical serving sizes of foods that commonly trigger symptoms in individuals with irritable bowel syndrome, as well as foods that were generally well tolerated. The reliability of these FODMAP cutoff values has been tested in a number of dietary studies. The development of the techniques to quantify the FODMAP content of foods has greatly advanced our understanding of food composition. FODMAP composition is affected by food processing techniques and ingredient selection. In the USA, the use of high-fructose corn syrups may contribute to the higher FODMAP levels detected (via excess fructose) in some processed foods. Because food processing techniques and ingredients can vary between countries, more comprehensive food composition data are needed for this diet to be more easily implemented internationally.

Extrat from the study:
A – “ omissis The Monash University Department of Gastroenterology has performed extensive work for over 10 years to quantify the FODMAP composition of hundreds of foods. Foods tested for FODMAP content represent a range of categories, including fruit and vegetables; grains, cereals, pulses, nuts, and seeds; dairy products and dairy free alternatives; meat, fish, poultry, and eggs; fats and oils; beverages; and condiments and confectionary. Some of these data have been published previously (12 -14) and are summarized in Figs 1 and 2. With growing international interest in the low-FODMAP diet, our program of FODMAP food analysis is expanding to include more international foods. This paper will dis- cuss the criteria for classifying food as low in FODMAPs and the challenges encountered in analysing food for FODMAP content.