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Irritable bowel syndrome (IBS) is a prevalent disorder of gut–brain interaction (DGBI) with an adverse impact on quality of life. The global consumption of ultra-processed foods (UPF) is rapidly increasing, and UPF intake has recently been linked to a wide range of metabolic and chronic diseases. The potential role of UPF consumption in the onset and symptom generation of IBS is emerging but remains unclear. This narrative review synthesizes epidemiological evidence on the association between UPF consumption and IBS, integrates mechanistic insights from experimental and clinical studies and suggests clinical implications based on the current state of knowledge. Observational studies suggest that higher UPF intake may be associated with increased risk of IBS, although the evidence base is limited and subject to methodological challenges. Mechanistic studies indicate that additives including emulsifiers and non-nutritive sweeteners can alter pathways relevant to IBS symptom generation, such as gut microbiota composition, impair intestinal barrier function and trigger low-grade inflammation. Current evidence supports a possible link between UPF consumption and IBS. Increasing overall dietary quality and reducing UPF intake are promising complementary strategies to established dietary interventions. Future intervention trials may provide insights into relevant biological mechanisms, particularly if such changes co-occur with symptom improvement.

Gut mucosal barrier injury is common following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and associated with poor clinical outcomes. Diet is critical for microbial diversity, but whether nutritional support affects microbiota and outcome after allo-HSCT is unknown. We present a secondary analysis of a randomized controlled nutritional intervention trial during allo-HSCT. We investigated if the intervention influenced gut microbiota, short-chain fatty acids (SCFAs), and markers of gut barrier functions, and if these parameters were associated with clinical outcomes. Fecal specimens were available from 47 recipients, and subjected to 16S rRNA gene sequencing. We found no significant differences between the intervention group and controls in investigated parameters. We observed a major depletion of microbiota, SCFAs, and altered markers of gut barrier function from baseline to 3 weeks post-transplant. One-year mortality was significantly higher in patients with lower diversity at 3 weeks post-HSCT, but not related to diversity at baseline. The relative abundance of Blautia genus at 3 weeks was higher in survivors. Fecal propionic acid was associated with survival. Markers of gut barrier functions were less strongly associated with clinical outcomes. Possibly, other strategies than dietary intervention are needed to prevent negative effects of gut microbiota and clinical outcomes after allo-HSCT. ClinicalTrials.gov (NCT01181076).

Systemic sclerosis (SSc) is an auto-immune, multi organ disease marked by severe gastrointestinal (GI) involvement and gut dysbiosis. Here, we aimed to determine the safety and efficacy of fecal microbiota transplantation (FMT) using commercially-available anaerobic cultivated human intestinal microbiota (ACHIM) in SSc. Ten patients with SSc were randomized to ACHIM (n = 5) or placebo (n = 5) in a double-blind, placebo-controlled 16-week pilot. All patients had mild to severe upper and lower GI symptoms including diarrhea, distention/bloating and/or fecal incontinence at baseline. Gastroduodenoscopy transfer of ACHIM or placebo was performed at weeks 0 and 2. Primary endpoints were safety and clinical efficacy on GI symptoms assessed at weeks 4 and 16. Secondary endpoints included changes in relative abundance of total, immunoglobulin (Ig) A- and IgM-coated fecal bacteria measured by 16s rRNA sequencing. ACHIM side effects were mild and transient. Two placebo controls experienced procedure-related serious adverse events; one developed laryngospasms at week 0 gastroduodenoscopy necessitating study exclusion whilst one encountered duodenal perforation during gastroduodenoscopy at the last study visit (week 16). Decreased bloating, diarrhea and/or fecal incontinence was observed in four of five patients in the FMT group (week 4 or/and 16) and in two of four in the placebo group (week 4 or 16). Relative abundance, richness and diversity of total and IgA-coated and IgM-coated bacteria fluctuated more after FMT, than after placebo. FMT of commercially-available ACHIM is associated with gastroduodenoscopy complications but reduces lower GI symptoms by possibly altering the gut microbiota in patients with SSc.

Clostridium difficile is the leading cause of nosocomial infectious diarrhea. New treatment strategies are needed. In this letter, preliminary data on fecal therapy as primary treatment are assessed.

The short-chain fatty acid (SCFA) butyric acid maintains a healthy gut barrier and vascular endothelium. We aimed to investigate the association between fecal butyric acid, carotid atherosclerosis and risk factors for ischemic stroke. Patients with severe carotid atherosclerosis (i.e. ≥ 50% stenosis) (n = 43) were compared with healthy controls (n = 38). We analyzed fecal SCFAs by gas chromatography, microbiota composition by 16S rRNA sequencing, markers of gut barrier damage and inflammasome activation by immunoassay, and plasma SCFAs by ultra-high performance liquid chromatography-tandem mass spectroscopy. Patients had higher fecal butyric acid level ( p  = 0.024), along with increased functional potential of microbial butyric acid production ( p  = 0.031), compared with controls. Dietary fiber intake was comparable. Patients had higher levels of gut barrier damage markers CCL25 and IFABP, and the inflammasome activation marker IL-18, whereas plasma level of butyric was similar. Increased fecal butyric acid was associated with higher BMI, waist-hip ratio, HbA1c, CRP and leukocyte count. Contrary to our hypothesis, patients with severe carotid atherosclerosis had higher fecal butyric acid level, and increased microbial production, compared with controls. Gut barrier damage in patients might indicate decreased absorption of butyric acid and hence contribute to the higher fecal level.

Background Individuals with non-celiac gluten/wheat sensitivity (NCGWS) experience improvement in gastrointestinal symptoms following a gluten-free diet. Although previous results have indicated that fructo-oligosaccharides (FOS), a type of short-chain fructans, were more likely to induce symptoms than gluten in self-reported NCGWS patients, the underlying mechanisms are unresolved. Methods Our main objective was therefore to investigate whether FOS-fructans and gluten affect the composition and diversity of the faecal microbiota (16S rRNA gene sequencing), faecal metabolites of microbial fermentation (short-chain fatty acids [SCFA]; gas chromatography with flame ionization detector), and a faecal biomarker of gut inflammation (neutrophil gelatinase-associated lipocalin, also known as lipocalin 2, NGAL/LCN2; ELISA). In the randomised double-blind placebo-controlled crossover study, 59 participants with self-reported NCGWS underwent three different 7-day diet challenges with gluten (5.7 g/day), FOS-fructans (2.1 g/day), and placebo separately (three periods, six challenge sequences). Results The relative abundances of certain bacterial taxa were affected differently by the diet challenges. After the FOS-fructan challenge, Fusicatenibacter increased, while Eubacterium ( E. ) coprostanoligenes group , Anaerotruncus , and unknown Ruminococcaceae genera decreased. The gluten challenge was primarily characterized by increased abundance of Eubacterium xylanophilum group . However, no differences were found for bacterial diversity (α-diversity), overall bacterial community structure (β-diversity), faecal metabolites (SCFA), or NGAL/LCN2. Furthermore, gastrointestinal symptoms in response to FOS-fructans were generally not linked to substantial shifts in the gut bacterial community. However, the reduction in E. coprostanoligenes group following the FOS-fructan challenge was associated with increased gastrointestinal pain. Finally, correlation analysis revealed that changes in gastrointestinal symptoms following the FOS-fructan and gluten challenges were linked to varying bacterial abundances at baseline. Conclusions In conclusion, while FOS-fructans induced more gastrointestinal symptoms than gluten in the NCGWS patients, we did not find that substantial shifts in the composition nor function of the faecal microbiota could explain these differences in the current study. However, our results indicate that individual variations in baseline bacterial composition/function may influence the gastrointestinal symptom response to both FOS-fructans and gluten. Additionally, the change in E. coprostanoligenes group , which was associated with increased symptoms, implies that attention should be given to these bacteria in future trials investigating the impact of dietary treatments on gastrointestinal symptoms. Trial registration Clinicaltrials.gov as NCT02464150.

Individuals with coeliac disease (CeD) often experience gastrointestinal symptoms despite adherence to a gluten-free diet (GFD). While we recently showed that a diet low in fermentable oligo-, di-, monosaccharides and polyols (FODMAP) successfully provided symptom relief in GFD-treated CeD patients, there have been concerns that the low FODMAP diet (LFD) could adversely affect the gut microbiota. Our main objective was therefore to investigate whether the LFD affects the faecal microbiota and related variables of gut health. In a randomised controlled trial GFD-treated CeD adults, having persistent gastrointestinal symptoms, were randomised to either consume a combined LFD and GFD (n 39) for 4 weeks or continue with GFD (controls, n 36). Compared with the control group, the LFD group displayed greater changes in the overall faecal microbiota profile (16S rRNA gene sequencing) from baseline to follow-up (within-subject β-diversity, P < 0·001), characterised by lower and higher follow-up abundances (%) of genus Anaerostipes (P group < 0·001) and class Erysipelotrichia (P group = 0·02), respectively. Compared with the control group, the LFD led to lower follow-up concentrations of faecal propionic and valeric acid (GC-FID) in participants with high concentrations at baseline (P interaction ≤ 0·009). No differences were found in faecal bacterial α-diversity (P group ≥ 0·20) or in faecal neutrophil gelatinase-associated lipocalin (ELISA), a biomarker of gut integrity and inflammation (P group = 0·74), between the groups at follow-up. The modest effects of the LFD on the gut microbiota and related variables in the CeD patients of the present study are encouraging given the beneficial effects of the LFD strategy to treat functional GI symptoms (Registered at clinicaltrials.gov as NCT03678935).

Abstract Background Distinguishing irritable bowel syndrome (IBS) from inflammatory bowel disease (IBD) flare-ups is challenging. This study used objective remission markers to accurately determine IBS prevalence in a population-based cohort of patients with IBD. Methods Adults with ulcerative colitis and Crohn’s disease were recruited from the IBD in South-Eastern Norway III cohort study. Irritable bowel-like symptoms were assessed using the Rome IV criteria for patients in remission from IBD at 1- and 3-year follow-ups. Remission was defined objectively using the biochemical marker fecal calprotectin (FC) ≤ 250 µg/g, and comparisons to remission based on endoscopic indices were made at 1-year follow-up. Results Among patients with FC ≤ 250 µg/g, IBS prevalences were 21.9% (n = 62/283) and 16.1% (n = 49/304) at the 1- and 3-year follow-ups, respectively, which were higher than that in the Norwegian population (9.5%; P < .005). Of patients in endoscopic remission at 1-year follow-up, 19.2% (n = 43/224) reported IBS-like symptoms, which was not significantly different from IBS prevalence for patients with FC ≤ 250 µg/g. Irritable bowel syndrome was independently associated with substantial fatigue (odds ratio: 3.05 [95% CI, 1.48-6.27]) and female sex (odds ratio: 2.67 [95% CI, 1.34-5.32]) at the 1-year follow-up. Patients with IBS reported significantly reduced health-related quality of life (HRQoL) scores. Conclusions The prevalence of IBS among patients in remission from IBD was approximately twice as common as that in the Norwegian population. Irritable bowel syndrome was independently associated with substantial fatigue, female sex, and reduced HRQoL. Lay Summary In this prospective cohort of newly diagnosed patients with inflammatory bowel disease (IBD), patients in remission from IBD reported irritable bowel-like symptoms 2 to 3 times more frequently than the general Norwegian population at both the 1- and 3-year follow-ups. Graphical Abstract Graphical Abstract

Abstract Introduction We aimed to determine the diagnostic and prognostic potential of baseline microbiome profiling in inflammatory bowel disease (IBD). Methods Participants with ulcerative colitis (UC), Crohn’s disease (CD), suspected IBD, and non-IBD symptomatic controls were included in the prospective population-based cohort Inflammatory Bowel Disease in South-Eastern Norway III (third iteration) based on suspicion of IBD. The participants donated fecal samples that were analyzed with 16S rRNA sequencing. Disease course severity was evaluated at the 1-year follow-up. A stringent statistical consensus approach for differential abundance analysis with 3 different tools was applied, together with machine learning modeling. Results A total of 1404 individuals were included, where n = 1229 samples from adults were used in the main analyses (n = 658 UC, n = 324 CD, n = 36 IBD-U, n = 67 suspected IBD, and n = 144 non-IBD symptomatic controls). Microbiome profiles were compared with biochemical markers in machine learning models to differentiate IBD from non-IBD symptomatic controls (area under the receiver operating curve [AUC] 0.75-0.79). For UC vs controls, integrating microbiome data with biochemical markers like fecal calprotectin mildly improved classification (AUC 0.83 to 0.86, P < .0001). Extensive differences in microbiome composition between UC and CD were identified, which could be quantified as an index of differentially abundant genera. This index was validated across published datasets from 3 continents. The UC-CD index discriminated between ileal and colonic CD (linear regression, P = .008) and between colonic CD and UC (P = .005), suggesting a location-dependent gradient. Microbiome profiles outperformed biochemical markers in predicting a severe disease course in UC (AUC 0.72 vs 0.65, P < .0001), even in those with a mild disease at baseline (AUC 0.66 vs 0.59, P < .0001). Conclusions Fecal microbiome profiling at baseline held limited potential to diagnose IBD from non-IBD compared with standard-of-care. However, microbiome shows promise for predicting future disease courses in UC. Lay Summary This study assessed the diagnostic and prognostic potential of baseline microbiome profiling in IBD. The microbiome holds the potential to differentiate IBD from controls and enhanced predictive capacity for UC severity. A UC-CD microbial index distinguished disease types and was validated with a global cohort.

The gut microbiota and their metabolites, e.g., short-chain fatty acids (SCFA), are associated with obesity. The primary aims were to study faecal SCFA levels and the changes in SCFA levels after weight-loss interventions in subjects with obesity, and secondarily, to study factors associated with the faecal SCFA levels. In total, 90 subjects (men / women: 15/75) with a mean age of 44.4 (SD 8.4) years, BMI 41.7 (SD 3.7) kg/m2 and morbid obesity (BMI > 40 or > 35 kg/m2 with obesity-related complications) were included. Faecal SCFA and other variables were measured at inclusion and after a six-month conservative weight-loss intervention followed by bariatric surgery (Roux-en-Y gastric bypass or gastric sleeve). Six months after surgery, the total amount of SCFA was reduced, the total and relative amounts of the main straight SCFA (acetic-, propionic-, and butyric- acids) were reduced, and the total and relative amounts of branched SCFA (isobutyric-, isovaleric-, and isocaproic- acids) were increased. The changes indicate a shift toward a proteolytic fermentation pattern with unfavorable health effects. The amount of SCFA was associated with the diet but not with metabolic markers or makers of the faecal microbiota composition. Dietary interventions could counteract the unfavorable effects.