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Background Almonds contain lipid, fiber, and polyphenols and possess physicochemical properties that affect nutrient bioaccessibility, which are hypothesized to affect gut physiology and microbiota. Objectives To investigate the impact of whole almonds and ground almonds (almond flour) on fecal bifidobacteria (primary outcome), gut microbiota composition, and gut transit time. Methods Healthy adults (n  = 87) participated in a parallel, 3-arm randomized controlled trial. Participants received whole almonds (56 g/d), ground almonds (56 g/d), or an isocaloric control in place of habitual snacks for 4 wk. Gut microbiota composition and diversity (16S rRNA gene sequencing), SCFAs (GC), volatile organic compounds (GC-MS), gut transit time (wireless motility capsule), stool output and gut symptoms (7-d diary) were measured at baseline and endpoint. The impact of almond form on particle size distribution (PSD) and predicted lipid release was measured (n  = 31). Results Modified intention-to-treat analysis was performed on 79 participants. There were no significant differences in mean ± SD abundance of fecal bifidobacteria after consumption of whole almonds (8.7% ± 7.7%), ground almonds (7.8% ± 6.9%), or control (13.0% ± 10.2%; q  = 0.613). Consumption of almonds (whole and ground pooled) resulted in higher mean ± SD butyrate (24.1 ± 15.0 μmol/g) than control (18.2 ± 9.1 μmol/g; P  = 0.046). There was no effect of almonds on gut microbiota at the phylum level or diversity, gut transit time, stool consistency, or gut symptoms. Almond form (whole compared with ground) had no effect on study outcomes. Ground almonds resulted in significantly smaller PSD and higher mean ± SD predicted lipid release (10.4% ± 1.8%) than whole almonds (9.3% ± 2.0%; P  = 0.017). Conclusions Almond consumption has limited impact on microbiota composition but increases butyrate in adults, suggesting positive alterations to microbiota functionality. Almonds can be incorporated into the diet to increase fiber consumption without gut symptoms. This trial was registered at clinicaltrials.gov as NCT03581812. [ABSTRACT FROM AUTHOR]

Background: Short‐term trials demonstrate the low FODMAP diet improves symptoms of irritable bowel syndrome (IBS) but impacts nutrient intake and the gastrointestinal microbiota. The aim of this study was to investigate clinical symptoms, nutrient intake, and microbiota of patients with IBS 12 months after starting a low FODMAP diet. Methods: Participants enrolled in a previous short‐term clinical trial and who had been through structured FODMAP restriction, reintroduction, and personalization were invited to participate in a follow‐up study at one time point at 12 months. Gastrointestinal symptoms, stool output, dietary intake, and quality of life were recorded. Stool samples were collected and analyzed for microbiota (qPCR) and short‐chain fatty acids (SCFA). Data were compared with baseline (prior to any intervention in the original clinical trial) using non‐parametric statistics. Key Results: Eighteen participants were included in the study. Adequate relief of symptoms occurred in 5/18 (28%) at baseline and increased to 12/18 (67%) following long‐term personalized low FODMAP diet (p = 0.039). There was a reduction in IBS‐SSS total score between baseline (median 227, IQR 99) and long term (154, 89; p < 0.001). Bifidobacteria abundance was not different between baseline (median 9.29 log10 rRNA genes/g, IQR 1.45) and long term (9.20 log10 rRNA genes/g, 1.41; p = 0.766, q = 0.906); however, there were lower concentrations of total SCFA, acetate, propionate, and butyrate. Conclusions: In this long‐term analysis, two thirds of patients reported adequate relief of symptoms after 12 months of personalized low FODMAP diet that did not result in differences from baseline in Bifidobacteria. FODMAP reintroduction and personalization may normalize some of the effects of short‐term FODMAP restriction. [ABSTRACT FROM AUTHOR]

The global burden of inflammatory bowel disease [IBD] has increased over the 21st century. Despite multiple studies investigating the pathogenesis of IBD, the causative mechanisms pertaining to its increased prevalence remain unclear. There is growing evidence that aspects of a 'Western diet' increase the risk of developing IBD. More recently, evidence implicating dietary emulsifiers has accumulated, with ecological studies showing a positive correlation between inflammatory bowel disease and emulsifier consumption. Further to these, cell and animal studies have demonstrated plausible mechanisms by which dietary emulsifiers may contribute to IBD pathogenesis through mechanisms including: promotion of pro-inflammatory intestinal microbiota; disruption of mucus architecture; increased intestinal permeability; activation of inflammatory pathways; and disruption of the cell cycle. This review critically analyses the current evidence for these mechanisms that may be of pathological relevance to IBD, evaluates recent dietary trials, acknowledges the challenges of dietary intervention studies, and gives an overview of ongoing and future clinical trials in this important area. [ABSTRACT FROM AUTHOR]

Food additive intakes have increased with the increase in "ultra-processed" food consumption. Food additive emulsifiers have received particular research attention in recent years due to preliminary evidence of adverse gastrointestinal and metabolic health effects. In this review, the use of emulsifiers as food additives is discussed, and the current estimations of exposure to, and safety of, emulsifiers are critically assessed. Food additive emulsifier research is complicated by heterogeneity in additives considered to be emulsifiers and labelling of them on foods globally. Major limitations exist in estimating food additive emulsifier exposure, relating predominantly to a lack of available food occurrence and concentration data. Development of brand-specific food additive emulsifier databases are crucial to accurately estimating emulsifier exposure. Current research on the health effects of food additive emulsifiers are limited to in vitro and murine studies and small, acute studies in humans, and future research should focus on controlled human trials of longer duration. [ABSTRACT FROM AUTHOR]

Background: Clinical guidelines provide limited and conflicting recommendations regarding dietary fiber supplementation in irritable bowel syndrome (IBS). Nopal (Opuntia ficus‐indica) is a cactus plant fiber containing both insoluble and soluble fibers that may have therapeutic potential in IBS. Our aim was to evaluate the dose–response effect of extracted nopal fiber powder on symptoms in IBS. Methods: We performed a 4‐arm, double‐blind, parallel, randomized controlled trial in 60 patients fulfilling Rome IV criteria for IBS. Patients were randomized and blindly allocated to receive either nopal fiber (10, 20, or 30 g/day) or placebo (30 g/day dextrose) for one week and to keep their usual diet. Symptom severity (Global Symptom Question, IBS‐SSS, Gastrointestinal Symptom Rating Scale), stool frequency and consistency (Bristol Stool Form Scale), breath hydrogen response, and stool short‐chain fatty acids (SCFA) were measured at baseline and follow‐up. Key results: Significantly more patients reported adequate relief of symptoms after 20 g/day (87%, p = 0.008) and 30 g/day (80%, p = 0.025) of nopal fiber compared to placebo (33%). More patients receiving 20 g/day nopal fiber (67%) had a > 50% reduction in IBS‐SSS compared to placebo (20%, p = 0.027), whereas the 30 g/day dose induced more loose stools (p = 0.027). Response rates were similar among IBS subtypes. There were no differences in breath hydrogen or stool SCFA between groups. Conclusions and inferences: Nopal fiber supplementation at doses of 20 and 30 g/day was associated with short‐term improvement in IBS symptoms, warranting a fully powered clinical trial of longer duration with symptomatic, physiological, and microbiological endpoints. [ABSTRACT FROM AUTHOR]

INTRODUCTION: The low FODMAP diet (LFD) reduces symptoms and bifidobacteria in irritable bowel syndrome (IBS). [beta]-galactooligosaccharides (B-GOS) may reduce the symptoms and increase bifidobacteria in IBS. We investigated whether B-GOS supplementation alongside the LFD improves IBS symptoms while preventing the decline in bifidobacteria. METHODS: We performed a randomized, placebo-controlled, 3-arm trial of 69 Rome III adult patients with IBS from secondary care in the United Kingdom. Patients were randomized to a sham diet with placebo supplement (control) or LFD supplemented with either placebo (LFD) or 1.4 g/d B-GOS (LFD/B-GOS) for 4 weeks. Gastrointestinal symptoms, fecal microbiota (fluorescent in situ hybridization and 16S rRNA sequencing), fecal short-chain fatty acids (gas-liquid chromatography) and pH (probe), and urine metabolites (1H NMR) were analyzed. RESULTS: At 4 weeks, adequate symptom relief was higher in the LFD/B-GOS group (16/24, 67%) than in the control group (7/23, 30%) (odds ratio 4.6, 95% confidence interval: 1.3-15.6; P = 0.015); Bifidobacterium concentrations (log10 cells/g dry weight) were not different between LFD and LFD/B-GOS but were lower in the LFD/B-GOS (9.49 [0.73]) than in the control (9.77 [0.41], P = 0.018). A proportion of Actinobacteria was lower in LFD (1.9%, P = 0.003) and LFD/B-GOS (1.8%, P < 0.001) groups than in the control group (4.2%). Fecal butyrate was lower in the LFD (387.3, P = 0.028) and LFD/B-GOS (346.0, P = 0.007) groups than in the control group (609.2). DISCUSSION: The LFD combined with B-GOS prebiotic produced a greater symptom response than the sham diet plus placebo, but addition of 1.4 g/d B-GOS did not prevent the reduction of bifidobacteria. The LFD reduces fecal Actinobacteria and butyrate thus strict long-term use should not be advised. [ABSTRACT FROM AUTHOR]