Introduction

Ultra-Processed Foods (UPFs) have been associated with chronic diseases such as cancer, obesity and inflammatory bowel diseases (IBD). A typical feature of UPFs is the presence of Advanced Glycation End products (AGEs), including Carboxy-Methyl Lysine (CML), due to thermal treatments.

Aims & Methods

We studied to what extent different cooking methods affect cardiometabolic and inflammatory markers through differential dietary AGE intake.
In a randomized cross-over pilot trial, healthy participants sequentially consumed a diet prepared with cooking methods that generate either low or high amounts of AGEs. Recipes during both periods contained identical ingredients, but simply differed in their cooking methods (grilling and baking vs. steaming and raw foods). Daily food logs were kept using photo documentation and the smartphone application FatSecret during the one-week run-in (baseline diet) and the subsequent two-week intervention periods. Estimated AGEs levels were calculated based on the previously published database of Uribarri et al.¹ Anthropometric measurements and biological samples were taken at baseline and after each intervention period. Blood samples were collected for routine tests, Lipopolysaccharide-Binding Protein (LBP) ELISAs, serum proteomics (Olink Target 96 Inflammation and Cardiometabolic panels), and direct measurement of serum AGEs. Faecal calprotectin, 16S rRNA sequencing, and short chain fatty acids (SCFA) measurements were performed on stool samples. Small intestinal permeability was measured according to a 2-hour Lactulose Mannitol Ratio (LMR) protocol.

Results

Twenty healthy participants with a median age (IQR) of 28 (23.5-38) years, and a median BMI of 23.0 (20.9-25.4) kg/m² were included. The average estimated intake of CML during the high-AGEs diet was comparable to baseline (20,480.5 vs. 19,545 kU CML/day, Wilcoxon signed rank test, p>0.1), but significantly higher than during the low-AGEs period (10,590 kU CML/day, Wilcoxon signed rank test, p=3.8 x 10^-6). Metabolically, total cholesterol values increased (paired Wilcoxon signed rank test, p= 0.04) when changing from a low-to-high AGEs diet. After applying a linear mixed model per protein, eukaryotic initiation factor 4E-binding protein (4E-BP1), increased significantly after consumption of the low-AGEs diet (adjusted p=0.03). The gut microbiota composition was largely unaffected by the diets, as was faecal calprotectin. Importantly, faecal butyrate concentrations increased after the high-AGEs study period in the low-to-high AGEs group (paired Wilcoxon signed rank test, p=0.04). The LMR was increased throughout the study in the high-to-low AGEs group, but not in the low-to-high AGEs group. Serum LBP showed no difference.

Conclusion

By conducting the first randomized cross-over cooking methods trial that focusses on both intestinal and systemic endpoints at a proteomic, gut microbiome and permeability level, we found that cooking methods generating different AGE levels have a differential impact on human and gut microbial metabolism. More specifically, we show a beneficial effect of the low-AGEs diet on lipid profiles and the serum protein 4E-BP1, a protein known to affect lifespan, metabolism, and cancer development. In contrast, the high-AGEs diet was associated with increased faecal butyrate levels, a SCFA that is studied for its beneficial and anti-inflammatory luminal properties. These results are instructive for diet-based interventions in the prevention and treatment of chronic diseases, including the metabolic syndrome and IBD.

References

1. Uribarri J, Woodruff S, Goodman S, et al. AGE’s in Foods and practical ways to reduce them. J Am Diet Assoc. 2010;110(6):911-916.

Disclosure

The authors have no direct conflicts of interest to disclose. However the general COIs can be found below for optimal transparency.

• JW reports no conflict of interest.
• EV reports no conflict of interest.
• AD reports no conflict of interest.
• SH received consultancy fees from Ferring, Takeda.
• Julie Vanderstappen received consultancy fees from Ferring, Janssen.
• Joke Verbeke reports no conflict of interest to disclose.
• RV is a clinical investigator for Bayer, Eli Lilly, Boehringer Ingelheim, Novo Nordisk; he reports speaker’s fees from Boehringer Ingelheim, Eli Lilly, Goodlife Pharma, Novo Nordisk, Prowell, Sanofi; consultancy fees from Boehringer Ingelheim, Eli Lilly, Sanofi; Financial compensation for these activities has been received by the institution (UZ/KU Leuven).
• BV reports having received Research support from AbbVie, Biora Therapeutics, Landos, Pfizer, Sossei Heptares and Takeda. Speaker’s fees from Abbvie, Biogen, Bristol Myers Squibb, Celltrion, Chiesi, Falk, Ferring, Galapagos, Janssen, Lily, MSD, Pfizer, R-Biopharm, Sandoz, Takeda, Tillots Pharma, Truvion and Viatris. Consultancy fees from Abbvie, Alimentiv, Applied Strategic, Atheneum, BenevolentAI, Biora Therapeutics, Bristol Myers Squibb, Galapagos, Guidepont, Landos, Lily, Mylan, Inotrem, Ipsos, Janssen, Pfizer, Progenity, Sandoz, Santa Ana Bio, Sosei Heptares, Takeda, Tillots Pharma and Viatris.
• MF reports to have received research grants from AbbVie, Amgen, Biogen, EG, Janssen, Pfizer, Takeda, and Viatris; consultancy fees from AbbVie, Agomab Therapeutics, Boehringer Ingelheim, Celltrion, Eli Lilly, Janssen-Cilag, Medtronic, MRM Health, MSD, Pfizer, Regeneron, Samsung Bioepis, Sandoz, Takeda, and Thermo Fisher; and speakers’ fees from AbbVie, Amgen, Biogen, Boehringer Ingelheim, Falk, Ferring, Janssen-Cilag, Lamepro, MSD, Mylan, Pfizer, Samsung Bioepis, Sandoz, Takeda, and Truvion Healthcare.
• CM is chair of the KU Leuven Fund ‘Nutrition’, a donation-based fund to stimulate research on nutrition. Recipient of travel/accommodation expenses and small participation fee (<100€/meeting) as member of working groups of the Belgian Superior Health Council and Belgian Federal Agency of the Safety of the Food Chain. Recipient of travel/accommodation expenses as member of the scientific advisory body of the EU Joint Programme Initiative Healthy Diet, Healthy Life, as co-chair ILSI Europe Task Force Dietary Intake and Exposure, as member ILSI Europe Task Force Nutrient Intake Optimisation. Recipient of honoraria (<500€/year) as active member of the advisory board of NutriNews (Belgian Nutrition Information Center). Recipient of honoraria as jury-member of nutrition-related awards and reviewing EU-grants. Recipient of royalties form a textbook (Handboek Voeding, ACCO). Honoraria are used to support research of PhD Students.
• JR reports grants from Beneo, Cargill, Colruyt group, Danone, DSM, J&J, MRM/Prodigest, Nestle Pfizer, and Takeda; and has received consulting and/or speaking fees from Aphea, Biofortis, DSM, Ferring, GSK, Janssen Pharmaceuticals, Metagenics, MSD, MRM/Prodigest, Nutricia, Takeda, Tsumura
• KV receives travel /accommodation expenses as co-chair of the ILSI Europe Prebiotic Task Force and travel expenses and a participation fee as a member of a working group of the Belgian Superior Health Council. Recipient of honoraria and travel/accommodation expenses as a reviewer of grants (NWO (The Netherlands), ANR (France) and EU grants). Recipient of speakers’fees from Yakult and Kintu.
• SV received financial support for research from AbbVie, J&J, Pfizer, Takeda and Galapagos and receives speakers’ and/or consultancy fees from AbbVie, Abivax, AbolerISPharma, AgomAb, Alimentiv, Arena Pharmaceuticals, AstraZeneca, BMS, Boehringer Ingelheim, Celgene, Cytoki Pharma, Dr Falk Pharma, Ferring, Galapagos, Genentech-Roche, Gilead, GSK, Hospira, Imidomics, Janssen, J&J, Lilly, Materia Prima, Mestag Therapeutics, MiroBio, Morphic, MrMHealth, Mundipharma, MSD, Pfizer, Prodigest, Progenity, Prometheus, Robarts Clinical Trials, Surrozen, Takeda, Theravance, Tillots Pharma AG, VectivBio, Ventyx, Zealand Pharma.
• JS reports speaker’s fees from Pfizer, Abbvie, Ferring, Falk, Takeda, Janssen, Fresenius, and Galapagos; consultancy fees from Janssen, Ferring, Fresenius, Abbvie, Galapagos, Celltrion, Pharmacosmos, and Pharmanovia; and research support from Galapagos and Viatris.

Introduction

Behaviours such as supra-gastric belching, gastric belching, and aerophagia, often identified during oesophageal physiology studies (e.g., 24-hour pH and impedance study), are known to exacerbate symptoms like reflux, bloating, and regurgitation. These behaviours are frequently misunderstood and may lead to unnecessary referrals to specialists or invasive interventions. Upper GI biofeedback (UGI BFB) therapy offers a tailored, non-invasive approach to help patients manage these behaviours. By teaching specific techniques such as diaphragmatic breathing, open-mouth posture, and the multiple rapid swallow technique, patients are empowered to take control of their symptoms, improve their quality of life, and reduce reliance on surgical or gastroenterology pathways.

Aims & Methods

• Participants: Between December 2022 and December 2024, 35 patients were referred for UGI BFB therapy. Most referrals (n=31) came after oesophageal physiology studies, with additional referrals from gastroenterologists for belching and bloating (n=2) and from clinical endoscopists for persistent hiccups and audible wheezing (n=2).
• Intervention: Patients attended a one-hour education session in the Gastrointestinal (GI) Physiology unit. This included a review of diagnostic findings and practical training in diaphragmatic breathing, open-mouth posture, and the multiple rapid swallow technique. A follow-up telephone consultation at 6–8 weeks allowed for monitoring progress. For cases of poor oesophageal clearance, referring clinicians were advised to consider prokinetics. For frequent gastric belching, small intestinal bacterial overgrowth (SIBO) breath testing was recommended to assess any additional contributing factors.

Results

• Supra-gastric belching episodes were reduced by 50% (mean: 24 episodes pre-therapy to 12 post-therapy; p<0.001).
• GERD-HRQL scores improved by 45%, indicating significant quality-of-life improvements (mean: 22 pre-therapy to 12 post-therapy; p<0.001).
• 75% of patients reported substantial reductions in belching, bloating, and reflux-like symptoms.
• Half of the patients (50%) no longer required specialist referrals, as symptoms were successfully managed with therapy or GP-led interventions, including prokinetics or medications for hypersensitivity.
• Stress emerged as a critical factor for most patients. Relaxation techniques, mindfulness, and stress management strategies played an important role in symptom control. One patient, who became a mental health first aider at work, reported long-term symptom relief due to stress reduction efforts.

Conclusion

Upper GI biofeedback therapy is a valuable approach for addressing behavioural contributors to symptoms like air swallowing, belching, and bloating. A multidisciplinary approach, involving cognitive behavioural therapy or hypnotherapy alongside UGI BFB, can be highly beneficial. The GI Physiology team also recognises its limitations and has found that referrals to Speech and Language Therapy can be instrumental when patients are unable to engage fully with the therapy. This collaborative, patient-centred approach ensures that UGI BFB therapy not only reduces the need for invasive procedures and specialist consultations but also empowers patients to adopt long-lasting lifestyle and behavioural changes.

Clinical Case Summary

Non celiac gluten wheat sensitivity (NCGWS) is a syndrome whose symptoms are strictly related to gluten ingestion and presents with both intestinal and extraintestinal manifestations. However a liver involvement has never been shown. We report one case of NCGWS presenting with altered bowel habits, a persistent raise of alanine aminotransferase (ALT), aspartate aminotransferase (AST) since childhood and migraines. Gamma GT, alcaline phosphatase, bilirubin, were all within the range of normality over multiple testing. Viral serology (HAV, HBV, HCV), markers for autoimmune hepatitis (ANA, anti-smooth muscle and liver kidney microsome), protein electrophoresis, iron metabolism markers, urinary and blood copper were normal. Abdominal ultrasound reported liver size within the range of normality, regular structure and without focal lesions. No gallstones nor biliary tract dilation. Hepatic elastography was normal. Patient denied alcohol consumption at the time. Coeliac screening was negative (total IgA, IgA tTg-2 and IgA anti-endomysium). She performed a gastroscopy which showed regular macroscopic features of both stomach and duodenum. The histology showed non-specific signs of inflammation (Marsh 0). We found a rise of native IgG anti gliadin (AGA) >100 U/ml and serum zonulin (47,4 ng/ml, ULN <38). Therefore, we proposed a possible diagnosis of NCGWS following Salerno criteria and a gluten free diet (GFD) was recommended to the patient. The adherence to a GFD normalised bowel habits, migraines and the levels of liver enzymes. The pathogenesis of the liver damage in NCGWS is unclear. We hypothesized that the gut barrier dysfunction led to a translocation of toxins and antigens to the liver, therefore creating damage and a mild raise of hepatic transaminase. To date, this case is the first reporting a relation between altered liver enzymes and NCGWS. Further evidence is needed to better establish the link between these two conditions.

References

Hollon J, Puppa EL, Greenwald B, Goldberg E, Guerrerio A, Fasano A. Effect of Gliadin on Permeability of Intestinal Biopsy Explants from Celiac Disease Patients and Patients with Non-Celiac Gluten Sensitivity. Nutrients. 2015 Mar;7(3):1565–76.
Tripathi A, Debelius J, Brenner DA, Karin M, Loomba R, Schnabl B, et al. The gut-liver axis and the intersection with the microbiome. Nat Rev Gastroenterol Hepatol. 2018 Jul;15(7):397–411.
​Garcia-Mazcorro JF, Rivera-Gutierrez X, Cobos-Quevedo ODJ, Grube-Pagola P, Meixueiro-Daza A, Hernandez-Flores K, et al. First Insights into the Gut Microbiota of Mexican Patients with Celiac Disease and Non-Celiac Gluten Sensitivity. Nutrients. 2018 Nov;10(11):1641.

Introduction

Hepatocellular carcinoma (HCC) is an end stage liver disease with increasing morbidity and mortality worldwide. Development of the disease is dependent on various genetic, dietary and environmental factors. While alcohol-related liver disease (ALD/MetALD) remains a major contributor, metabolic dysfunction-associated steatotic liver disease (MASLD) is becoming increasingly relevant in clinical practice. There is increasing evidence for the role of bacteria, for instance, such as Bifidobacterium and Blautia, which were considered protective, while Streptococcus has been associated with disease progression. However, little is known about the alteration of microRNAs (miRNAs) in liver diseases and its interrelationship with microbial environment in view of etiological factors.

Aims & Methods

This study aimed to elucidate gastrointestinal miRNA alterations and explore their relationship with microbiome composition in patients with different stages of liver disease in terms of disease etiology. Multi-omics analyses were performed in a subset of well characterized patients (n=59) with liver disease and healthy controls. Systematic characterization included clinical, laboratory, demographic and imaging characterization and dietary preferences. Patients subclassification included fibrosis stage (no fibrosis, fibrosis, liver cirrhosis(LC)) and etiology (MetALD/ALD vs. MASLD). Fecal miRNAs were extracted using the Qiagen miRNeasy Kit and profiled via Agilent miRNA microarray. Microbiome analyses were performed amplifying the V1-V2 region of the 16S rRNA gene following Illumina sequencing.

Results

For miRNA analysis stringent criteria were applied to identify high quality miRNA targets. From approximately 4,000 candidates filtering resulted in selection of 202 high-quality miRNAs with reliably measurable concentrations. 28 of these miRNAs showed significantly positive alterations in concentration in patients with liver disease and 7 miRNAs significant negative alterations. Specifically, miR-642a-3p, miR-5006, miR-6781, and miR-6849 were elevated in feces in patients with LC. In contrast, miR-6869, miR-4467, and miR-5001 were present in lower concentration in LC patients. Notably, miR-4467 also showed strong negative associations with liver-specific laboratory markers, including gamma-glutamyl transferase (GGT) (r=-0.34; p=0.026) and M65, a marker of apoptosis (r=-0.42; p=0.005). Cross-sectional comparison of miRNA and microbiome data revealed miRNA alterations associated with specific microbial signatures. MiR-6795-5p, which was associated with liver stiffness (r = 0.39, p = 0.01), also correlated positively with the abundance of Streptococcus, a genus linked to disease progression (r=0.29; p=0.047). Conversely, miR-6869, miR-4467, and miR-5001 showed positive correlations with the potentially protective genera Blautia and Bifidobacterium (miR-6869: r_{Bifidobacterium}=0.35; p_{Bifidobacterium}=0.012; r_Blautia=0.37; p_Blautia=0.008; miR-4467: r_Blautia=0.41; p_Blautia=0.002; miR-5001: r_Blautia=0.38; p_Blautia=0.006).

Conclusion

Multi-omics analysis reveals distinct alterations in fecal miRNAs and gut microbiota across different stages of liver disease. Changes in microbial composition were associated with shifts in miRNA profiles, suggesting a functional link in maintaining intestinal homeostasis. These findings highlight the potential of integrated microbiome–miRNA signatures as novel diagnostic and therapeutic targets. Further studies are warranted to validate these associations and explore their clinical applications.

Introduction

Fructans or fructooligosaccharides are included in the spectrum of FODMAP (fermented) sugars, which are relevant in the induction of symptoms in patients with disorders of gut-brain interaction (DGBI) and in non-coeliac gluten sensitivity (1). Fructans have been shown to induce visceral hypersensitivity, an increase in mucosal mast cells, and changes in the colonic mucosal barrier in mice, and hypersensitivity associated with an altered gut microbiome in humans (2-5). Breath tests are used in the assessment of intolerances to several FODMAPs, but the test is poorly standardised for fructans (6).

Aims & Methods

A standardised breath test with fructans (10g Orafti^®HSI) was performed afer a 24-hour low-FODMAP diet and >8-hour fast. Exhaled hydrogen and methane concentrations were measured every 30 minutes until 5h, and synchronised symptom assessments performed for 24h (composite symptom index score, SI, 7) in 600 successive male (33%) and female patients of average age 41 years referred to our gastroenterology practice with DGBI (irritable bowel syndrome and/or functional dyspepsia, Rome 4 criteria). Breath gas concentration thresholds of >20ppm and >8ppm above baseline were used for hydrogen and methane, respectively.

Results

The SI was positive in 61.2% (n=367) of patients within 24 hours of fructan ingestion. The SI peaked in the first 3 hours in 17.5% (n=105) and in the first 5 hours in 42.5% (n=255) of patients. Suprathreshold increases in hydrogen and methane concentrations within 5 hours were seen in 62.7% and 14.9% of patients, respectively. Discordant SI and breath gas results were obtained in 35.1% (hydrogen) and 57.8% (methane) of patients. A negative SI with a suprathreshold hydrogen or methane result occurred in 18.2% and 5.2%, respectively. A positive SI with a subthreshold hydrogen or methane result occurred in 16.9% and 52.6%, respectively. Suprathreshold concentrations in methane and not in hydrogen were apparent in 4.5%. Main symptoms during tests were excessive flatulence (58.8%), bloating (50.3%), abdominal fullness (49.3%), abdominal cramps (29.0%), nausea (26.7%), GORD (26.7%), diarrhoea (9%) and extra-GI symptoms (16.2%).

Conclusion

Standardised oral provocation with fructans resulted in familiar clinical symptoms in a majority of patients with DGBI, suggesting a high prevalence of fructan intolerance. Due to the slow fermentation of intestinal fructans and the associated delayed symptoms, prolonged data collection over at least 12, preferably 24 hours is recommended. The test duration of 3 hours currently commonly used in test centres is inadequate. Symptom and breath gas concentration results are often divergent, as is known from other FODMAP breath tests, and validation against clinical outcome results is required. Fructans are of interest in DGBI as the current literature suggests they have both protective as well as detrimental effects on intestinal physiology, which may be dependent on the resident microbiota.

References

1. Gry I et al. Gastroenterology 2018;154:529–539
2. Kamphuis JBJ et al. Gastroenterology 2020;158:652-663
3. Chen BR et al. World J Gastroenterol 2017;23:8321-8333
4. Kamphuis JBJ et al. FASEB J. 2022;36:e22297
5. Chumpitazi BP et al. Aliment Pharmacol Ther 2021;53:499-509
6. Fedewa A et al. Curr Gastroenterol Rep 2014;16:370
7. Wilder-Smith CH et al. Aliment Pharmacol Ther 2013;37:1074-83

Introduction

Gut transit time is a key modulator of host-microbiome interactions, influencing gut microbiota composition and fecal metabolites concentrations. Prolonged colonic transit time is associated with greater microbial diversity, increased proteolytic fermentation activity and reduced concentrations of short-chain fatty acids (SCFAs). Metabolites derived from protein fermentation (such as ammonia, indole, p-cresol, and hydrogen sulfide) can impair epithelial integrity, while SCFAs, produced from nondigestible carbohydrates, support mucosal health through anti-inflammatory and antineoplastic effects. An imbalance between these metabolites may compromise colonic homeostasis, predisposing colonocytes to aberrant proliferation and increasing the risk of neoplastic transformation. These early alterations can be clinically detected through the presence of adenomatous polyps during colonoscopy, marking a critical window for preventive strategies.

Aims & Methods

The aim was to evaluate the role of gut transit time in shaping gut microbiota composition and fecal levels of bacterial-derived metabolites in individuals with a history of colorectal polyps. Thirty-three individuals who had undergone a colonoscopy were recruited and categorized based on gut transit time, assessed using the blue dye method. Fecal samples were collected and cocentrations of SCFAs, ammonium and indole were quantified using gas chromatography, a fluorometric assay and a colorimetric assay, respectively. The V3–V4 region of the 16S rRNA gene was sequenced using the Illumina NovaSeq platform. Sequence variant inference, quality filtering, chimera removal, and paired-end read merging were performed using the DADA2 pipeline in R, followed by taxonomic assignment with the Silva reference database. Alpha diversity was assessed by measuring richness (number of operational taxonomic units) and diversity (Shannon index). Beta diversity was analyzed using Canonical Correspondence Analysis (CCA) based on Bray–Curtis distances, with group differences tested via PERMANOVA. Linear discriminant analysis with an LDA score threshold >2 was applied to identify differentially abundant taxa.

Results

Alpha-diversity did not differ between groups with different gut transit times. Regarding Beta diversity, CCA based on Bray–Curtis distance showed a non-significant trend (p=0.095), whereas PERMANOVA analysis revealed a statistically significant effect (p=0.038), indicating that gut transit time explains a significant portion of the variance in microbial composition. Individuals with slow transit time exhibited an enrichment of several bacterial families from the phyla Actinobacteria (Micrococcaceae, Actinomycetaceae, Eggerthellaceae) and Firmicutes (Christensenellaceae, Ruminococcaceae, Lachnospiraceae, Peptostreptococcaceae and Veillonellaceae). A trend toward lower fecal SCFAs concentrations was observed in slow transit group compared to individuals with normal transit (69.2 ± 43.2 vs. 98.6 ± 34 umol/gr, p=0.087). No significant differences in fecal ammonium or indole concentrations were detected between groups. Multinomial logistic regression analysis indicated that higher levels of SCFA were linked to a lower likelihood of being in the slow transit group (p = 0.055). No differences were found in the frequency of polyp diagnosis according to transit time classification (p=0.495).

Conclusion

This study confirms that gut transit time influences both microbiota composition and SCFA levels. These findings highlight the relevance of gut transit modulation as a preventive target in individuals at risk of colorectal neoplasia.

Introduction

Patients with Disorders of Gut-Brain Interaction (DGBI) often experience meal-related symptoms, potentially due to carbohydrate intolerances like fructose and/or lactose. While breath tests are common for exploring carbohydrate malabsorption, assessing intolerances, defined by the onset of gastrointestinal (GI) symptoms after a defined load of carbohydrates, is valuable. The adult carbohydrate perception questionnaire (aCPQ) can be used for detecting carbohydrate intolerances (1).

Aims & Methods

We aimed to determine lactose and fructose intolerance prevalence in DGBI and characterize these patients. DGBI patients who underwent fructose (25g) and lactose (25g) breath tests alongside the aCPQ in our tertiary center between May 2022 and December 2023 were included. Carbohydrate intolerance was a 20 mm increase in any of the five Visual Analog Scales (VAS) scores (for abdominal pain, nausea, diarrhea, bloating, and flatulence) in aCPQ. An increase from baseline of ≥20 ppm in exhaled H2 or ≥10 ppm of CH4 (≥20 ppm for fructose) indicated malabsorption. Patients completed questionnaires on irritable bowel syndrome (IBS) symptom severity (IBS-SSS), somatic symptoms (PHQ-15), quality of life (QOL)(GIQLI), anxiety, and depression (HAD).

Results

We included 314 DGBI patients, among them, 124 were lactose intolerant, 138 were fructose intolerant, and 77 were intolerant to both carbohydrates. Lactose intolerant patients were younger (42± 15.9 vs 46 ± 15.3; p=0.022), and more likely to have lactose malabsorption and fructose intolerance, while fructose intolerant patients were more likely to have fructose malabsorption, lactose intolerance, and higher anxiety/depression levels. Both intolerant groups were more likely to be female (81.5% vs 61.6%; p<0.0001 for lactose, 77.5% vs 63.1%; p=0.006 for fructose), with 2 DGBI or more (63.1% vs 40.7%; p<0.0001 for lactose, 57.4% vs 43.5%; p=0.021 for fructose), to have a reduced QOL, higher levels of GI symptoms, and somatic symptoms (table). Logistic regressions showed independent associations of female sex, fructose intolerance, and lactose malabsorption with the lactose intolerance variable, and IBS symptom severity, lactose intolerance, and fructose malabsorption with the fructose intolerance variable.

Table: Comparison of DGBI patients with and without lactose and fructose intolerance

Conclusion

DGBI patients with lactose and fructose intolerance exhibit severe IBS symptoms and reduced QOL. Interestingly, intolerance to one carbohydrate is associated with malabsorption of this specific carbohydrate and the coexistence of intolerance to the other carbohydrate.

References

1. Hammer, Johann et al. European journal of gastroenterology & hepatology 2021, doi:10.1097/MEG.0000000000001880

Disclosure

CM has served as a consultant/advisory board member for KyowaKirin, Norgine, Biocodex, Mayoly Spindler, Tillots, Ipsen, Nestlé HealthScience and Viatris.
FM has served as a consultant/speaker for Laborie, Medtronic, Dr Falk Pharma.
GG has served as a consultant/speaker for Laborie, Medtronic, Kyowa Kirin, Lilly and Enterra medical.