Sociocultural determinants such as cultural norms, diet, and environmental factors, along with their effects on the gastrointestinal microbiome, can modify the risk to develop disorders of gut-brain interaction (DGBI). These factors also shape symptom perception and health care-seeking behaviors, and how society and health care providers respond to patients with DGBI. This document summarizes the knowledge about the role of sociocultural factors in the manifestation of DGBI and the management of these patients. Symptom expression and societal response to DGBI varies across different cultural settings, influencing individual patient outcomes and the overall societal burden of disease. Patients with DGBI are often stigmatized, leading to a bias toward conditions with visible abnormalities and underfunded services for DGBI. Recognizing the role of sociocultural factors for DGBI outcomes presents an opportunity to refine pathophysiologic concepts and improve patient outcomes. This calls for greater awareness and equitable resource allocation for DGBI research and treatment.

ABSTRACT Small intestinal bacterial overgrowth (SIBO) has evolved from a severe debilitating illness to a clinical spectrum associated with abnormalities of microbial populations in the small intestine. It is best described as a pathophysiological state that may contribute to symptoms or other pathology in a wide range of gastrointestinal conditions that include disorders of gut‐brain interaction, inflammatory bowel disease, and chronic liver disease. The controversy surrounding SIBO largely rests on diagnostic limitations of currently widely used diagnostic tests. The gold standard test of bacterial culture of proximal small intestinal fluid will miss the majority of bacteria, has severe methodological limitations, and is clinically uncommonly used. Breath‐hydrogen testing after oral glucose or lactulose ingestion is associated with falsely positive and negative results, due largely to the inability to accurately define where in the gastrointestinal tract the hydrogen is being generated. Such performance characteristics raise concerns regarding its application to clinical decision‐making in the individual patient. Therapies such as antibiotics can normalize breath test findings and ameliorate symptoms, but whether this is due to an action on the small intestinal microbiota is uncertain. It is proposed that conceptual modifications that include the assessment of the mucosa‐associated microbiota in biopsies obtained with minimal contamination, molecular and functional characterization of the microbiota, rather than purely culture‐based density of bacteria, and expansion of the definition of SIBO to small intestinal dysbiosis will facilitate more precision and resolve the controversial place of SIBO in clinical practice.

BACKGROUND AND AIMS:Increased risk of alcohol dependence is recognised following bariatric surgery. Modified gastrointestinal anatomy and neurohormonal profiles lead to altered alcohol metabolism, peak blood alcohol concentrations and enhanced reward circuits and cravings. For patients with metabolic associated fatty liver disease, bariatric surgery has been shown to reduce liver fibrosis; however, the impact of bariatric surgery on alcohol consumption and consequent liver fibrosis has not been well-characterised using validated measures. This study examined the changes in alcohol consumption patterns, alcohol dependence and validated liver fibrosis measures before and after bariatric surgery. DESIGN, SETTING AND PARTICIPANTS:A retrospective cohort study assessing patients seeking treatment for alcohol problems with a history of gastric sleeve (GS) or Roux-en-Y Gastric Bypass (RYGB) in a quaternary hospital in Brisbane, Australia. MEASUREMENTS:Validated measures of alcohol dependence [Alcohol Use Disorders Identification Test (AUDIT) and brief Michigan Alcohol Screening Test (bMAST)] and non-invasive liver fibrosis (FIB4 and APRI) were compared pre- and post-surgery. FINDINGS:Twenty patients were identified with prior GS and 10 patients with RYGB. Following bariatric surgery, body mass index was reduced by 14.5 (±9.39) kg/m2. Metabolic co-morbidities were less frequent post-surgery. Pre-surgery, the mean AUDIT score was 10.2 ± 8.9, with 9 patients having scores indicative of alcohol dependence. Mean AUDIT increased statistically significantly post-surgery (18.1, standard deviation ±11.4; P < 0.001) with 29 patients meeting criteria for alcohol dependence. AUDIT components relating to both consumption (volume, frequency) and harmful consequences of alcohol increased following surgery. Despite surgery lowering metabolic liver fibrosis risk, worsened liver fibrosis was observed [mean FIB4 (0.98 ± 1.8) and APRI (0.41 ± 0.83) increased; P < 0.05]. CONCLUSION:Within a cohort of adults seeking treatment for alcohol problems, increases in alcohol consumption and alcohol-related harm were observed following bariatric surgery. Despite improvement in risk factors for metabolic-associated fatty liver disease after surgery, non-invasive markers for hepatic fibrosis worsened, likely in the setting of harmful alcohol intake and associated liver injury. This supports the role of bariatric surgery pre-operative assessment and post-operative follow-up to identify and manage alcohol-related problems and associated liver disease risk.

BACKGROUND:Disorders of Gut-Brain Interaction (DGBI) impact as many as one in three individuals at some stage of their lives. Clinically, patients with DGBI may present with meal-related symptoms that progressively lead to altered food intake behaviors, resulting in subsequent weight loss and nutritional deficiencies. These patients often experience psychological distress and multi-system co-morbidities. This distinct subgroup can be referred to as DGBI-induced altered food intake behavior (DGBI-AFIB) and needs to be differentiated from the eating disorder defined in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition: Avoidant/Restrictive Food Intake Behavior. PURPOSE:There is currently no expert consensus on the management of DGBI-AFIB. To address this gap, a multidisciplinary, multi-society expert panel employed a Delphi process to develop evidence-based management guidelines for DGBI-AFIB. The group formulated and evaluated 23 statements using the GRADE system. Experts agreed that a diagnosis of DGBI-AFIB should be considered when gastrointestinal symptoms meet the Rome criteria for DGBI, are aggravated by food intake, and subsequently result in altered (reduced) food intake, leading to a significant (unintended) reduction in body weight. To establish a positive diagnosis of DGBI-AFIB, relevant differential diagnoses need consideration, including organic causes/eating disorders. A multidisciplinary team approach is key to management. Treatment must align with established DGBI principles and consider each patient's specific challenges. Enteral or parenteral feeding should only be pursued in patients with life-threatening nutritional deficiencies after all oral nutrition approaches have failed. Future research is essential to elucidate the epidemiological characteristics and risk factors for DGBI-AFIB, thereby enhancing long-term management.

INTRODUCTION:Disorders of gut-brain interaction (DGBI) are frequently encountered among patients with eating disorders (ED). Underlying both ED and DGBI may be psychological comorbidities, but it is uncertain how often psychological disorder explains the development of either disorder. We hypothesized a DGBI may predispose to a new onset ED. We aimed to determine the associations and chronological presentation of DGBI, ED, and psychological comorbidities. METHODS:Data were collected from a retrospective cohort of n = 1,256,331 patients attending general practices in the UK; 1,018 patients diagnosed with both a DGBI and an ED were included, with 777 also having data on anxiety and/or depression. Timing of order of onset and potential moderators of the sequence of occurrence were considered. Clinical significance level was set at P < 0.01 and odds ratio (OR) ≥ 2.0. RESULTS:Prevalence of any ED was 0.7%. Chronic constipation was associated with anorexia nervosa (OR = 2.12; 95% confidence interval 1.84-2.45) and any ED (OR = 2.06; 95% confidence interval 1.79-2.36). Irritable bowel syndrome and functional dyspepsia were significantly associated with one or more ED. More patients in primary care were diagnosed with an ED (59.5%, n = 606) preceding a DGBI than vice versa (40.5%, n = 412, P < 0.001). Independent predictors of having a diagnosed DGBI preceding an ED were younger age at first diagnosis of DGBI ( P < 0.001), antecedent depression ( P < 0.003), and antecedent proton pump inhibitor use ( P < 0.001). DISCUSSION:Psychological disorders, ED, and DGBI overlap. ED more frequently preceded the onset of a DGBI diagnosis; younger age, antecedent depression, and proton pump inhibitor use were independently associated with a DGBI predicting an ED.

ABSTRACT Background Green kiwifruit ( Actinidia deliciosa var Hayward ) extract improves constipation. This study aimed to determine its efficacy in patients with constipation‐predominant irritable bowel syndrome (IBS‐C). Methods A randomized, multicenter, double‐blind, parallel‐group, placebo‐controlled trial was conducted in 186 IBS‐C patients (Rome III criteria). Patients received either placebo or kiwifruit extract (575 mg twice daily for 4 weeks, followed by 575 mg daily for 4 weeks). Outcomes included measures of bowel movement frequency, Bristol Stool Scores, and abdominal pain and related measures (100 mm visual analog scale). The primary efficacy end point was the combined improvement of the number of complete spontaneous bowel movements and reduction of weekly average abdominal pain symptom score by at least 30% for at least half of the weeks during treatment. Results On kiwifruit extract, the proportion of subjects with increased frequency of spontaneous bowel movements (54% vs. 36%, p = 0.012), improved Bristol Stool Score (87 vs. 73%, p = 0.014), and abdominal pain (74% vs. 59%, p = 0.023) was greater than in controls. However, no difference was observed in the combined two‐variable primary end point (24% vs. 26%; p = 0.798). In post hoc analyses of 49 subjects with severe pain (≥ 50 mm), kiwifruit extract improved the primary end point (33% vs. 8%, p = 0.028) and normalized or maintained normal bowel actions with kiwifruit extract (44% vs. 24%, p = 0.005). Conclusions In patients with IBS‐C, kiwifruit extract improves bowel habits and abdominal pain. The predefined end point for the whole study population was not met because the 30% or greater improvement of pain only occurred in patients with more pain. Trial Registration Australian Clinical Trial Research Network (ACTRN 12613001222730)

BACKGROUND:The gut-brain axis is a bidirectional communication pathway connecting the gastrointestinal tract and the brain. Disorders of gut-brain interaction (DGBI) manifest as highly prevalent gastrointestinal disorders such as irritable bowel syndrome (IBS) or functional dyspepsia (FD). SUMMARY:The initial focus of DGBI research was on the effects of psychological stress on digestive functions like gastrointestinal motility, or secretion of gastric acid and pancreatic enzymes. Concepts related to DGBI have expanded in recent decades. Activation of mucosal or systemic immune functions has been observed in DGBI, and it is established that the gastrointestinal microbiome can alter mucosal integrity and permeability, leading to pro-inflammatory cytokine release that affects brain function. Pharmacologic treatments (e.g., tricyclic antidepressants) and non-pharmacologic interventions (e.g., cognitive behavioral therapy) are now standard for DGBI patients. Advances in culture-independent methods to study gastrointestinal microbes reveal new insights into DGBI and gut microbiota appear to play a crucial role in modulating the gut-brain axis and regulating various bodily functions. KEY MESSAGES:DGBI are highly prevalent. Research in this field has evolved from studying the effects of psychological stress to recognizing the significant role of the gut microbiome and its metabolites in mucosal integrity and immune responses.