Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) share common culprit foods and potential pathophysiological factors. However, how diet may contribute to disease course and whether this differs between both entities is unclear. We therefore investigated the association of dietary indices with intestinal inflammation and gastrointestinal symptoms in both IBD and IBS patients. Food frequency questionnaires from 238 IBD, 261 IBS and 195 healthy controls (HC) were available to calculate the overall diet quality by the Dutch Healthy Diet-Index 2015 (DHD-2015) and its inflammatory potential by the Adapted Dietary Inflammatory Index (ADII). Intestinal inflammation and symptoms were evaluated by faecal calprotectin and the Gastrointestinal Symptom Rating Scale, respectively. The DHD-2015 was lower in IBD and IBS versus HC (p < 0.001), being associated with calprotectin levels in IBD (b = −4.009, p = 0.006), and with abdominal pain (b = −0.012, p = 0.023) and reflux syndrome (b = −0.016, p = 0.004) in IBS. ADII scores were comparable between groups and were only associated with abdominal pain in IBD (b = 0.194, p = 0.004). In this side-by-side comparison, we found a lower diet quality that was differentially associated with disease characteristics in IBD versus IBS patients. Longitudinal studies are needed to further investigate the role of dietary factors in the development of flares and predominant symptoms.

A Western diet comprises high levels of dicarbonyls and advanced glycation endproducts (AGEs), which may contribute to flares and symptoms in inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). We therefore investigated the intake of dietary dicarbonyls and AGEs in IBD and IBS patients as part of the habitual diet, and their association with intestinal inflammation. Food frequency questionnaires from 238 IBD, 261 IBS as well as 195 healthy control (HC) subjects were used to calculate the intake of dicarbonyls methylglyoxal, glyoxal, and 3-deoxyglucosone, and of the AGEs Nε-(carboxymethyl)lysine, Nε-(1-carboxyethyl)lysine and methylglyoxal-derived hydroimidazolone-1. Intestinal inflammation was assessed using faecal calprotectin. The absolute dietary intake of all dicarbonyls and AGEs was higher in IBD and HC as compared to IBS (all p < 0.05). However, after energy-adjustment, only glyoxal was lower in IBD versus IBS and HC (p < 0.05). Faecal calprotectin was not significantly associated with dietary dicarbonyls and AGEs in either of the subgroups. The absolute intake of methylglyoxal was significantly higher in patients with low (<15 μg/g) compared to moderate calprotectin levels (15–<50 μg/g, p = 0.031). The concentrations of dietary dicarbonyls and AGEs generally present in the diet of Dutch patients with IBD or IBS are not associated with intestinal inflammation, although potential harmful effects might be counteracted by anti-inflammatory components in the food matrix.

Many individuals reduce their bread intake because they believe wheat causes their gastrointestinal (GI) symptoms. Different wheat species and processing methods may affect these responses. We investigated the effects of six different bread types (prepared from three wheat species and two fermentation conditions) on GI symptoms in individuals with self-reported non-coeliac wheat sensitivity (NCWS). Two parallel, randomised, double-blind, crossover, multicentre studies were conducted. NCWS individuals, in whom coeliac disease and wheat allergy were ruled out, received five slices of yeast fermented (YF) (study A, n=20) or sourdough fermented (SF) (study B, n=20) bread made of bread wheat, spelt, or emmer in a randomised order on three separate test days. Each test day was preceded by a run-in period of 3 days of a symptom-free diet and separated by a wash-out period of ≥7 days. GI symptoms were evaluated by change in symptom score (test day minus average of the 3-day run-in period) on a 0-100mm visual analogue scale (ΔVAS), comparing medians using the Friedman test. Responders were defined as an increase in ΔVAS of ≥15mm for overall GI symptoms, abdominal discomfort, abdominal pain, bloating and/or flatulence. GI symptoms did not differ significantly between breads of different grains (YF bread wheat median ΔVAS 10.4mm [interquartile range 0.0-17.8mm], spelt 4.9mm [-7.6-9.4mm], emmer 11.0mm [0.0-21.3mm], p=0.267; SF bread wheat 10.5mm [-3.1-31.5mm], spelt 11.3mm [0.0-15.3mm], emmer 4.0mm [-2.9-9.3mm], p=0.144). The number of responders was also comparable for both YF (6 to wheat, 5 to spelt, and 7 to emmer, p=0.761) and SF breads (9 to wheat, 7 to spelt, and 8 to emmer, p=0.761). The majority of NCWS individuals experienced some GI symptoms for at least one of the breads, but on a group level, no differences were found between different grains for either YF or SF breads. ClinicalTrials.gov, NCT04084470(https://classic. gov/ct2/show/NCT04084470).

Certain dietary factors with anti-inflammatory and/or anti-cancer properties would be a promising preventive strategy for inflammatory bowel disease (IBD) patients against developing colitis-associated colorectal cancer (CAC). In this study, fecal water (FW) was obtained from 80 IBD patients and 20 healthy controls (HCs). The comet assay was applied to determine the DNA damage induced by FW, and the protective potential of FW against hydrogen peroxide (H₂O₂) induced DNA damage in Caco-2 cells. Information on diet was obtained via food frequency questionnaires. The results showed that FW from IBD patients, especially patients with flares, induced higher levels of direct DNA damage in Caco-2 cells and showed less protection against H₂O₂-induced DNA damage, when compared to HCs. The DNA damage induced by FW was positively associated with consumption of processed meat and sugary foods, and nutrient intakes including heme iron and added sugars, whereas negatively correlated to intakes of soy products, and a dietary pattern characterized by high consumption of potatoes, white meat, nuts and seeds, eggs, legumes and soy products. FW from subjects with high coffee consumption protected against H₂O₂-induced DNA damage. These results can help to develop potential preventive strategies for IBD patients to reduce the CAC risk.

Irritable bowel syndrome (IBS) is heterogenous disorder of gut-brain interaction, with a key role for the dysregulated host-gut microbiota interplay. IBS subtyping is based only on symptoms of bowel habits, reflecting limited insight into underlying biological mechanisms. This study aimed to define microbiota-based IBS phenotypes and to compare these to traditional stool-based subtyping. The study utilized data from the Maastricht IBS cohort. Gut microbiota composition was analysed using shotgun metagenomic sequencing. Faecal volatile organic compounds (VOCs) were measured by gas chromatography mass spectrometry. Dietary intake and gastrointestinal and mental health symptoms were assessed using a food frequency questionnaire, the Dutch Healthy Diet-15 index, the gastrointestinal symptom rating scale, and hospital anxiety and depression scores, respectively. Machine-learning approaches were applied to identify microbiota-based phenotypical clusters, which were compared with established Rome III subtypes, and associated with faecal VOCs, gastrointestinal symptom severity, diet and mental health. 178 IBS patients and 134 healthy controls were included. Gut microbiota composition distinguished IBS patients from healthy controls with an AUCROC 0 · 8. This discriminatory profile was not associated with Rome III subtypes, while statistically significant associations were found with faecal VOCs profiles (i.e. R = 0 · 67, p = 4 · 46e-4) and symptom severity scores of abdominal pain ( p = 0 · 05), reflux ( p = 0 · 03), diarrhoea ( p = 0 · 01) and depression ( p < 0 · 001). Dietary associations varied across clusters. These results suggest that gut microbiota profiling might provide a basis to define relevant IBS endotypes. Further exploration and validation efforts into this direction are needed using longitudinal studies to refine IBS patient stratification ultimately.