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The low fermentable oligosaccharide, disaccharide, monosaccharide and polyol (FODMAP) diet is recommended as a first line therapeutic management strategy for irritable bowel syndrome (IBS)(1). The low FODMAP diet is supported by meta-analytical evidence(2), and demonstrates acceptability and effectiveness for improving symptoms and quality of life (QoL) in 50-75% of individuals with IBS. However, a subset of individuals (25-50%) do not respond to the diet(3). The identification of individual-level predictors of treatment response across all three phases of the low FODMAP diet is currently lacking. The study aims were to assess psychological predictors of symptom and QoL response to the low FODMAP diet in patients with IBS. Adults with IBS underwent a three-phase low FODMAP diet, guided by individualised dietetic education. Predictor variables included levels of depressive, anxiety, and extraintestinal somatic symptoms, stress, treatment beliefs and expectations, behavioural avoidance, and illness perceptions. Symptom severity and QoL were the main outcomes. Questionnaires assessing psychological predictors, symptoms and QoL were administered at five points: pre-dietitian (week 0), post-dietitian, end of elimination (week 5), end of reintroduction (week 13), and end of personalisation (week 25) phases. Latent class growth analysis was used to identify classes of response trajectories for symptoms. Linear mixed models were used to test the effect of baseline psychological scores on symptoms and QoL over time. Cross lagged panel models determined the directional predictive relationship between psychological predictors and symptom severity. 112 participants (89% F) median age 30 ± 17 years were included. There were three classes of symptom response trajectories, including ‘non-improvers’ (21.3% of participants) with high initial symptom severity and minimal improvement, ‘improvers’ (22.5% of participants) with low initial symptom severity and significant improvement, and an ‘intermediate’ group (56.2% of participants) with moderate initial symptom severity and significant improvement. Higher treatment beliefs predicted a stronger initial symptom response (effect on linear slope p = 0.036). Lower gut-specific anxiety, as well as higher levels of personal and treatment control at baseline predicted a stronger reduction in IBS symptom severity and improved QoL from week 0 to week 25. Participants with higher levels of baseline psychological symptoms and negative illness perceptions (i.e., lower emotional representations) predicted a stronger initial and later QoL response (effect on linear (p = 0.006) and quadratic (p = 0.049) slopes). Increased cyclical time beliefs predicted poorer initial and later QoL response (effect on linear (p = 0.015) and quadratic (p = 0.029) slopes). Individuals experiencing lower to mid-range symptom severity at baseline had greater improvement with the low FODMAP diet. Lower anxiety, positive illness views and higher treatment beliefs predict better QoL and symptom response. Personalised strategies are crucial for optimising low FODMAP diet effectiveness in IBS.
A diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) improves functional bowel symptoms and is a second-line dietary management strategy for the treatment of irritable bowel syndrome (IBS). The diet is complex and involves three stages: restriction, reintroduction and personalisation and clinical effectiveness is achieved with dietitian-led education; however, this is not always available. The aim of this review is to provide an update on the evidence for using the low FODMAP diet, with a focus on the impact of FODMAP restriction and reintroduction considering long-term management of IBS in a clinical setting. Randomised controlled trials have assessed symptom response, quality of life, dietary intake and changes to the gut microbiota during FODMAP restriction. Systematic reviews and meta-analyses consistently report that FODMAP restriction has a better symptom response compared with control diets and a network analysis reports the low FODMAP diet is superior to other dietary treatments for IBS. Research focused on FODMAP reintroduction and personalisation is limited and of lower quality, however common dietary triggers include wheat, onion, garlic, pulses and milk. Dietitian-led delivery of the low FODMAP diet is not always available and alternative education delivery methods, e.g. webinars, apps and leaflets, are available but remove the personalised approach and may be less acceptable to patients and may introduce safety concerns in terms of nutritional adequacy. Predicting response to the low FODMAP diet using symptom severity or a biomarker is of great interest. More evidence on less restrictive approaches and non-dietitian-led education delivery methods are needed.
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 (Pgroup < 0·001) and class Erysipelotrichia (Pgroup = 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 (Pinteraction ≤ 0·009). No differences were found in faecal bacterial α-diversity (Pgroup ≥ 0·20) or in faecal neutrophil gelatinase-associated lipocalin (ELISA), a biomarker of gut integrity and inflammation (Pgroup = 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).
Observational studies suggest a correlation between post-traumatic stress disorder (PTSD) and gastrointestinal tract (GIT) disorders. However, the genetic overlap, causal relationships, and underlining mechanisms between PTSD and GIT disorders were absent.
Methods
We obtained genome-wide association study statistics for PTSD (23 212 cases, 151 447 controls), peptic ulcer disease (PUD; 16 666 cases, 439 661 controls), gastroesophageal reflux disease (GORD; 54 854 cases, 401 473 controls), PUD and/or GORD and/or medications (PGM; 90 175 cases, 366 152 controls), irritable bowel syndrome (IBS; 28 518 cases, 426 803 controls), and inflammatory bowel disease (IBD; 7045 cases, 449 282 controls). We quantified genetic correlations, identified pleiotropic loci, and performed multi-marker analysis of genomic annotation, fast gene-based association analysis, transcriptome-wide association study analysis, and bidirectional Mendelian randomization analysis.
Results
PTSD globally correlates with PUD (rg = 0.526, p = 9.355 × 10−7), GORD (rg = 0.398, p = 5.223 × 10−9), PGM (rg = 0.524, p = 1.251 × 10−15), and IBS (rg = 0.419, p = 8.825 × 10−6). Cross-trait meta-analyses identify seven genome-wide significant loci between PTSD and PGM (rs13107325, rs1632855, rs1800628, rs2188100, rs3129953, rs6973700, and rs73154693); three between PTSD and GORD (rs13107325, rs1632855, and rs3132450); one between PTSD and IBS/IBD (rs4937872 and rs114969413, respectively). Proximal pleiotropic genes are mainly enriched in immune response regulatory pathways, and in brain, digestive, and immune systems. Gene-level analyses identify five candidates: ABT1, BTN3A2, HIST1H3J, ZKSCAN4, and ZKSCAN8. We found significant causal effects of GORD, PGM, IBS, and IBD on PTSD. We observed no reverse causality of PTSD with GIT disorders, except for GORD.
Conclusions
PTSD and GIT disorders share common genetic architectures. Our work offers insights into the biological mechanisms, and provides genetic basis for translational research studies.
The study aimed to assess the total prevalence of functional gastrointestinal disorders (FGID), and separately, irritable bowel syndrome (IBS) among adults and to determine their potential association with fructose consumption. Data from the Hellenic National Nutrition and Health Survey were included (3798 adults; 58·9 % females). Information regarding FGID symptomatology was assessed using self-reported physician diagnosis questionnaires the reliability of which were screened using the ROME III, in a sample of the population. Fructose intake was estimated from 24 h recalls, and the MedDiet score was used to assess adherence to the Mediterranean diet. The prevalence of FGID symptomatology was 20·2 %, while 8·2 % had IBS (representing 40·2 % of total FGID). The likelihood of FGID was 28 % higher (95 %CI: 1·03–1·6) and of IBS 49 % (95 %CI: 1·08–2·05) in individuals with higher fructose intake than with lower intake (3rd tertile compared with 1st). When area of residence was accounted for, individuals residing in the Greek islands had a significantly lower probability of FGID and IBS compared with those residing in Mainland and the main Metropolitan areas, with Islanders also achieving a higher MedDiet score and lower added sugar intake, comparatively to inhabitants of the main metropolitan areas. FGID and IBS symptomatology was most prominent among individuals with higher fructose consumption, and this was most conspicuous in areas with a lower Mediterranean diet adherence, suggesting that the dietary source of fructose rather than total fructose should be examined in relation to FGID.
Major depressive disorder (MDD) is clinically documented to co-occur with multiple gastrointestinal disorders (GID), but the potential causal relationship between them remains unclear. We aimed to evaluate the potential causal relationship of MDD with 4 GID [gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), peptic ulcer disease (PUD), and non-alcoholic fatty liver disease (NAFLD)] using a two-sample Mendelian randomization (MR) design.
Methods
We obtained genome-wide association data for MDD from a meta-analysis (N = 480 359), and for GID from the UK Biobank (N ranges: 332 601–486 601) and FinnGen (N ranges: 187 028–218 792) among individuals of European ancestry. Our primary method was inverse-variance weighted (IVW) MR, with a series of sensitivity analyses to test the hypothesis of MR. Individual study estimates were pooled using fixed-effect meta-analysis.
Results
Meta-analyses IVW MR found evidence that genetically predicted MDD may increase the risk of GERD, IBS, PUD and NAFLD. Additionally, reverse MR found evidence of genetically predicted GERD or IBS may increase the risk of MDD.
Conclusions
Genetically predicted MDD may increase the risk of GERD, IBS, PUD and NAFLD. Genetically predicted GERD or IBS may increase the risk of MDD. The findings may help elucidate the mechanisms underlying the co-morbidity of MDD and GID. Focusing on GID symptoms in patients with MDD and emotional problems in patients with GID is important for the clinical management.
The 10th International Yakult Symposium was held in Milan, Italy, on 13–14 October 2022. Two keynote lectures covered the crewed journey to space and its implications for the human microbiome, and how current regulatory systems can be adapted and updated to ensure the safety of microorganisms used as probiotics or food processing ingredients. The remaining lectures were split into sections entitled “Chances” and “Challenges.” The “Chances” section explored opportunities for the science of probiotics and fermented foods to contribute to diverse areas of health such as irritable bowel syndrome, major depression, Parkinson’s disease, immune dysfunction, infant colic, intensive care, respiratory infections, and promoting healthy longevity. The “Challenges” section included selecting appropriate clinical trial participants and methodologies to minimise heterogeneity in responses, how to view probiotics in the context of One Health, adapting regulatory frameworks, and understanding how substances of bacterial origin can cross the blood–brain barrier. The symposium provided evidence from cutting-edge research that gut eubiosis is vital for human health and, like space, the microbiota deserves further exploration of its vast potential.
Wheat was first cultivated in the Fertile Crescent (South Western Asia) with a farming expansion that lasted from around 9000 BC to 4000 BC. Whilst humans have been exposed to wheat for around the last 10 000 years, humans have existed for greater than 2·5 million years. Therefore, wheat (and thereby gluten) are relatively new introductions to our diet! By the end of the 20th century, global wheat output had expanded by 5-fold, with a corresponding increase in the prevalence of gluten-related disorders. Coeliac disease (CD) is a state of heightened immunological responsiveness to ingested gluten in genetically susceptible individuals. CD now affects 1 % or more of all adults, for which the management is a strict lifelong gluten-free diet (GFD). However, there is a growing body of evidence to show that a far greater proportion of individuals without CD are self-initiating a GFD. This includes individuals initiating a GFD as a lifestyle choice, people with irritable bowel-type symptoms and those diagnosed with non-coeliac gluten (or wheat) sensitivity. Despite a greater recognition of gluten-related disorders, gaps still remain in our understanding of both their aetiology and management. This article explores the role of the gluten-free diet in gluten-related disorders, along with current uncertainties.
Functional constipation is a significant health issue impacting the lives of an estimated 14 % of the global population. Non-pharmaceutical treatment advice for cases with no underlying medical conditions focuses on exercise, hydration and an increase in dietary fibre intake. An alteration in the composition of the gut microbiota is thought to play a role in constipation. Prebiotics are non-digestible food ingredients that selectively stimulate the growth of a limited number of bacteria in the colon with a benefit for host health. Various types of dietary fibre, though not all, can act as a prebiotic. Short-chain fatty acids produced by these microbes play a critical role as signalling molecules in a range of metabolic and physiological processes including laxation, although details are unclear. Prebiotics have a history of safe use in the food industry spanning several decades and are increasingly used as supplements to alleviate constipation. Most scientific research on the effects of prebiotics and gut microbiota has focussed on inflammatory bowel disease rather than functional constipation. Very few clinical studies evaluated the efficacy of prebiotics in the management of constipation and their effect on the microbiota, with highly variable designs and conflicting results. Despite this, broad health claims are made by manufacturers of prebiotic supplements. This narrative review provides an overview of the literature on the interaction of prebiotics with the gut microbiota and their potential clinical role in the alleviation of functional constipation.
Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder, affecting about 20% of people worldwide. This complex and multifaceted disorder has been proposed as a system disease involving not only individual systems including the nervous, endocrine, imune, digestive, microbiota and the environment but also the interactions of these systems. The aetiology of IBS is complex and incompletely understood and this disease are frequently associated with a comorbid psychiatric disease. Current treatment is symptom-directed, rather than based on underlying pathophysiological mechanisms.
Objectives
The authors elaborate a narrative literature review to identify the pathophysiology and therapeutic approach of IBS.
Methods
Pubmed databased searched using the therms “psychiatry”, “irritable bowel syndrome” and “treatment”.
Results
The IBS is the most common and best described of the functional bowel disorders, which represents a considerable therapeutic challenge. Studies looked at the efficacy of fibre, antispasmodics and peppermint oil in the treatment of IBS found moderately effectiveness in the treatment of global symptoms. Elimination diets are helpful in improving IBS. There is evidence that a low-FODMAP diet can have a favorable impact on IBS symptoms, especially abdominal pain, bloating and diarrhea with improved irritable bowel syndrome symptoms and quality of life. Among the currently available classes of drugs for the treatment of IBS, antidepressants such as selective serotonin releasing inhibitors and tricyclic antidepressants are useful because of their analgesic properties, independent of their mood-improving effects.
Conclusions
Evidence suggest that antidepressants might be useful for treatment symptom of IBS however further investigation is required.
Irritable bowel syndrome (IBS) is a disorder of gut–brain interaction with a complex pathophysiology. Growing evidence suggests that alterations of the gut microenvironment, including microbiota composition and function, may be involved in symptom generation. Therefore, attempts to modulate the gut microenvironment have provided promising results as an indirect approach for IBS management. Antibiotics, probiotics, prebiotics, food and faecal microbiota transplantation are the main strategies for alleviating IBS symptom severity by modulating gut microbiota composition and function (eg. metabolism), gut barrier integrity and immune activity, although with varying efficacy. In this narrative review, we aim to provide an overview of the current approaches targeting the gut microenvironment in order to indirectly manage IBS symptoms.
This study evaluated the association between dietary patterns, gas-related symptoms (GRS) and their impact on quality of life (QoL) in a representative sample (n 936) of the French adult population. During the 2018–2019 ‘Comportements et Consommations Alimentaires en France’ survey (Behaviors and Food Consumption in France), online evaluation of GRS in adult participants was performed using the validated Intestinal Gas Questionnaire (IGQ), which captures the perception of GRS and their impact on QoL via six symptom dimensions scores (range 0–100; 100 = worse) and a global score (mean of the sum of the six symptom dimensions scores). Socio-demographics, lifestyle parameters and dietary habits (7-d e-food diary) were also collected online. Quality of diet was determined using the Nutrient-Rich Food 9.3 (NRF9.3) score (range 0–900; 900 = best). Univariate and multivariate linear regression models were applied to identify factors associated with IGQ global score. K-means was used to identify clusters of subjects based on their dietary records. Data from 936 adults who completed both the IGQ and the food diary showed a mean IGQ global score of 11·9 (sd 11·2). Younger age and female sex were associated with a higher IGQ global score. Only 7 % of subjects reported no symptom at all and nearly 30 % of study participants reported a high impact of GRS on their QoL. Two dietary clusters were identified: cluster 1, characterised by a higher consumption of fruits and vegetables, lower sugars intake and higher NRF9.3 score and cluster 2, characterised by higher intake of sugars, lower intake in dietary fibres and lower NRF9.3 score. The IGQ global score was lower in cluster 1 and higher in cluster 2 v. the total sample average (P < 0·001). The prevalence of GRS in the French adult population is high and is associated with impaired QoL and dietary patterns. A change in food habits towards healthier patterns could help reducing the burden of GRS.
Functional somatic disorders (FSD) feature medical symptoms of unclear etiology. Attempts to clarify their origin have been hampered by a lack of rigorous research designs. We sought to clarify the etiology of the FSD by examining the genetic risk patterns for FSD and other related disorders.
Methods
This study was performed in 5 829 186 individuals from Swedish national registers. We quantified familial genetic risk for FSD, internalizing disorders, and somatic disorders in cases of chronic fatigue syndrome (CFS), fibromyalgia (FM), and irritable bowel syndrome (IBS), using a novel method based on aggregate risk in first to fifth degree relatives, adjusting for cohabitation. We compared these profiles with those of a prototypic internalizing psychiatric – major depression (MD) – and a somatic/autoimmune disorder: rheumatoid arthritis (RA).
Results
Patients with FM carry substantial genetic risks not only for FM, but also for pain syndromes and internalizing, autoimmune and sleep disorders. The genetic risk profiles for IBS and CFS are also widely distributed although with lower average risks. By contrast, genetic risk profiles of MD and RA are much more restricted to related conditions.
Conclusion
Patients with FM have a relatively unique family genetic risk score profile with elevated genetic risk across a range of disorders that differs markedly from the profiles of a classic autoimmune disorder (RA) and internalizing disorder (MD). A similar less marked pattern of genetic risks was seen for IBS and CFS. FSD arise from a distinctive pattern of genetic liability for a diversity of psychiatric, autoimmune, pain, sleep, and functional somatic disorders.
Resistant starch 2 (RS2) may offer therapeutic value to irritable bowel syndrome (IBS) patients particularly in combination with minimally fermented fibre, but tolerability data are lacking. The present study evaluated the tolerability of RS2, sugarcane bagasse and their combination in IBS patients and healthy controls. Following baseline, participants consumed the fibres in escalating doses lasting 3 d each: RS2 (10, 15 and 20 g/d); sugarcane bagasse (5, 10 and 15 g/d); and their combination (20, 25 and 30 g/d). Gastrointestinal symptoms were assessed daily. Six IBS patients and five controls were recruited. No differences in overall symptoms from baseline were found across the fibre doses (IBS, P = 0⋅586; controls, P = 0⋅687). For IBS patients, all RS2 doses led to increased bloating. One IBS patient did not tolerate the low combination dose and another the high sugarcane bagasse dose. Supplementation of RS2 ≤ 20 g/d caused mild symptoms and was generally tolerated in IBS patients even when combined with minimally fermented fibre.
Pulses are healthy and sustainable but induce gut symptoms in people with a sensitive gut. Oats, on the contrary, have no fermentable oligo- di-, monosaccharides and polyols compounds and are known for the health effects of their fibres. This 4-day cross-over trial investigated the effects of oat and rice flour ingested with pulses on gut symptoms and exhaled gases (4th day only) in subjects with a sensitive gut or IBS (n 21) and controls (n 21). The sensitive group perceived more symptoms after both meals than controls (P = 0·001, P = 0·001). Frequency, intensity or quality of the symptoms did not differ between meals during the first 3 d in either group. More breath hydrogen was produced after an oat than rice containing meal in both groups (AUC, P = 0·001, P = 0·001). No between-group difference was seen in breath gases. During day 4, both sensitive and control groups perceived more symptoms after the oat flour meal (P = 0·001, P = 0·0104, respectively) as mainly mild flatulence. No difference in moderate or severe symptoms was detected. Increased hydrogen production correlated to a higher amount of perceived flatulence after the oat flour meal in both the sensitive and the control groups (P = 0·042, P = 0·003, respectively). In summary, ingestion of oat flour with pulses increases breath hydrogen levels compared with rice flour, but gastrointestinal symptoms of subjects sensitive to pulses were not explained by breath hydrogen levels. Additionally, consumer mindsets towards pulse consumption and pulse-related gut symptoms were assessed by an online survey, which implied that perceived gut symptoms hinder the use of pulses in sensitive subjects.
Epilepsy is one of the most common neurological disorders worldwide characterized by unpredictable and recurrent seizures, resulting from abnormal brain activity, accompanied by loss of consciousness and control of bowel or bladder function.
Objectives
A higher risk of comorbid disorders in epilepsy has been reported for psychiatric affective conditions (i.e., depression and schizophrenia), sleep alterations, as well as some gastrointestinal disorders (inflammatory bowel disease and constipation), and lately there is an interest to determine and explain a putative association between functional gastrointestinal disorders (FGID) such as Irritable bowel syndrome (IBS) and epilepsy.
Methods
In this way, we decided to review the current aspects of the gastrointestinal functional impairments and epilepsy by searching in the literature possible connection mechanisms.
Results
A handful of studies have only recently reported an increased prevalence of IBS in epilepsy in children, in adults, and conversely a higher incidence of epilepsy in IBS patients at the populational level. Paroxysmal abdominal complaints resulting from seizure activity are present in the abdominal epilepsy syndrome and the link between constipation and seizures has been demonstrated in animal models. Currently, there is no data to directly address the cellular and molecular connections between epilepsy and FGID, but these would probably involve the bidirectional dysregulation of the brain-gut axis with increased afferent processing of visceral nociceptive signals and subsequent hyperalgesia.
Conclusions
Thus, intestinal dysbiosis may play a role in triggering inflammatory and immune-related mechanisms reported in IBS manifestations and epilepsy, while vagal neuroimunomodulation issues are likely to be involved in both pathologies as well.
Conflict of interest
The authors are currently supported by a Young Research Teams supporting research grant PN-III-P1-1.1-TE2016-1210, named ”Complex study on oxidative stress status, inflammatory processes and neurological manifestations correlations in irritable bowel synd
This review intends to act as an overview of fructose malabsorption (FM) and its role in the aetiology of diseases including, but not limited to, irritable bowel syndrome (IBS) and infantile colic and the relationship between fructose absorption and the propagation of some cancers. IBS results in a variety of symptoms including stomach pains, cramps and bloating. Patients can be categorised into two groups, depending on whether the patients’ experiences either constipation (IBS-C) or diarrhoea (IBS-D). FM has been proposed as a potential cause of IBS-D and other diseases, such as infantile colic. However, our knowledge of FM is limited by our understanding of the biochemistry related to the absorption of fructose in the small intestine and FM’s relationship with small intestinal bacterial overgrowth. It is important to consider the dietary effects on FM and most importantly, the quantity of excess free fructose consumed. The diagnosis of FM is difficult and often requires indirect means that may result in false positives. Current treatments of FM include dietary intervention, such as low fermentable oligo-, di-, monosaccharides and polyols diets and enzymatic treatments, such as the use of xylose isomerase. More research is needed to accurately diagnose and effectively treat FM. This review is designed with the goal of providing a detailed outline of the issues regarding the causes, diagnosis and treatment of FM.
The therapeutic value of specific fibres is partly dependent on their fermentation characteristics. Some fibres are rapidly degraded with the generation of gases that induce symptoms in patients with irritable bowel syndrome (IBS), while more slowly or non-fermentable fibres may be more suitable. More work is needed to profile a comprehensive range of fibres to determine suitability for IBS. Using a rapid in vitro fermentation model, gas production and metabolite profiles of a range of established and novel fibres were compared. Fibre substrates (n 15) were added to faecal slurries from three healthy donors for 4 h with gas production measured using real-time headspace sampling. Concentrations of SCFA and ammonia were analysed using GC and enzymatic assay, respectively. Gas production followed three patterns: rapid (≥60 ml/g over 4 h) for fructans, carrot fibre and maize-derived xylo-oligosaccharide (XOS); mild (30–60 ml/g) for partially hydrolysed guar gum, almond shell-derived XOS and one type of high-amylose resistant starch 2 (RS2) and minimal (no differences with blank controls) for methylcellulose, another high-amylose RS2, acetylated or butyrylated RS2, RS4, acacia gum and sugarcane bagasse. Gas production correlated positively with total SCFA (r 0·80, P < 0·001) and negatively with ammonia concentrations (r –0·68, P < 0·001). Proportions of specific SCFA varied: fermentation of carrot fibre, XOS and acetylated RS2 favoured acetate, while fructans favoured butyrate. Gas production and metabolite profiles differed between fibre types and within fibre classes over a physiologically relevant 4-h time course. Several fibres resisted rapid fermentation and may be candidates for clinical trials in IBS patients.
The relationship between daily meal and snack frequency with irritable bowel syndrome (IBS) was less investigated in the literature. We aimed to evaluate this association with IBS symptoms.
Design:
A cross-sectional study.
Setting:
This investigation was performed in Isfahan, a large province in the centre of Iran. Individuals were asked to complete a self-administered questionnaire to quantify the numbers of daily main meals (one, two or three), snacks (never, 1–2, 3–5 or >5) and the total of them (<3, 3–5, 6–7 or ≥8). IBS and its subtypes were diagnosed according to Rome Ш criteria.
Participants:
General adults (n 4669, 2063 men and 2606 women).
Results:
The prevalence of IBS was 18·6 % in males and 24·1 % in females. Individuals consuming three main meals had 30 % decreased risk of IBS (OR 0·70, 95 % CI 0·52, 0·94) compared with those with one main meal in the crude model. After adjustments for all potential confounders this relation disappeared (OR 0·67, 95 % CI 0·43, 1·03). Gender-specified analysis revealed that women consuming three main meals per day had 32 % decreased likelihood of having IBS symptoms compared with one daily main meal takers (OR 0·68, 95 % CI 0·47, 0·99). This relation remained significant after adjustment for potential confounders (OR 0·56, 95 % CI 0·36, 0·89). A decreased likelihood of IBS in the highest category of main meal consumption compared with the lowest one was found in obese or overweight subjects (OR 0·54, 95 % CI 0·32, 0·91), after adjustment for all confounders.
Conclusions:
Our findings suggested that there was no significant relation between main meal or snack frequency and IBS in Iranian adults, but a small inverse association was found among females and overweight/obese individuals in subgroup analysis. Further prospective studies are needed confirming these associations.
It has been claimed that functional somatic syndromes share a common etiology. This prospective population-based study assessed whether the same variables predict new onsets of irritable bowel syndrome (IBS), chronic fatigue syndrome (CFS) and fibromyalgia (FM).
Methods
The study included 152 180 adults in the Dutch Lifelines study who reported the presence/absence of relevant syndromes at baseline and follow-up. They were screened at baseline for physical and psychological disorders, socio-demographic, psycho-social and behavioral variables. At follow-up (mean 2.4 years) new onsets of each syndrome were identified by self-report. We performed separate analyses for the three syndromes including participants free of the relevant syndrome or its key symptom at baseline. LASSO logistic regressions were applied to identify which of the 102 baseline variables predicted new onsets of each syndrome.
Results
There were 1595 (1.2%), 296 (0.2%) and 692 (0.5%) new onsets of IBS, CFS, and FM, respectively. LASSO logistic regression selected 26, 7 and 19 predictors for IBS, CFS and FM, respectively. Four predictors were shared by all three syndromes, four predicted IBS and FM and two predicted IBS and CFS but 28 predictors were specific to a single syndrome. CFS was more distinct from IBS and FM, which predicted each other.
Conclusions
Syndrome-specific predictors were more common than shared ones and these predictors might form a better starting point to unravel the heterogeneous etiologies of these syndromes than the current approach based on symptom patterns. The close relationship between IBS and FM is striking and requires further research.