Background: Disorders of gut–brain interaction (DGBIs) have a complex pathophysiology that is often characterized by a relationship between food ingestion and triggering of symptoms. Understanding of the underlying mechanisms and the role of nutrients as a therapeutic target are rapidly evolving. Aims and methods: We performed a narrative review of the literature using the following keywords, their acronyms, and their associations: nutrients, disorders of gut–brain interaction; functional dyspepsia; malabsorption; irritable bowel syndrome; diarrhea; constipation. Results: Functional dyspepsia displayed a significant correlation between volume, fat and/or wheat abundance, chemical composition of ingested food and symptoms of early satiety, fullness and weight loss. Carbohydrate malabsorption is related to enzyme deficiency throughout the GI tract. Food composition and richness in soluble vs. non-soluble fibers is related to constipation and diarrhea. The elimination of fermentable oligo-, di-, monosaccharides and polyols (FODMAPs) has a significant and non-unidirectional impact on irritable bowel syndrome (IBS) symptoms. Conclusions: Food volume, nutritive and chemical composition, and its malabsorption are associated with symptom generation in DGBIs. Further multicenter, randomized-controlled clinical trials are needed to clarify the underlying pathophysiology.

Background: The SARS-COV 2 pandemic has hit on our lives since early 2020. During different contagion waves, both malnutrition and overweight significantly correlated with patient mortality. Immune-nutrition (IN) has shown promising results in the clinical course of pediatric inflammatory bowel disease (IBD) and in both the rate of extubation and mortality of patients admitted to an intensive care unit (ICU). Thus, we wanted to assess the effects of IN on a clinical course of patients admitted to a semi-intensive COVID-19 Unit during the fourth wave of contagion that occurred at the end of 2021. Methods: we prospectively enrolled patients admitted to the semi-intensive COVID-19 Unit of San Benedetto General hospital. All patients had a biochemical, anthropometric, high-resolution tomography chest scan (HRCT) and complete nutritional assessments at the time of admission, after oral administration of immune-nutrition (IN) formula, and at 15 days interval follow-up. Results: we enrolled 34 consecutive patients (age 70.3 ± 5.4 years, 6 F, BMI 27.0 ± 0.5 kg/m²). Main comorbidities were diabetes (20%, type 2 90 %), hyperuricemia (15%), hypertension (38%), chronic ischemic heart disease (8 %), COPD (8%), anxiety syndrome (5%), and depression (5%). 58% of patients were affected as moderately-to-severely overweight; mini nutritional assessment (MNA) score (4.8 ± 0.7) and phase angle (PA) values (3.8 ± 0.5) suggestive of malnutrition were present in 15% of patients, mainly with a history of cancer. After 15 days upon admission, we recorded 3 deaths (mean age 75.7 ± 5.1 years, BMI 26.3 ± 0.7 kg/m²) and 4 patients were admitted to the ICU. Following IN formula administration, inflammatory markers significantly decreased (p < 0.05) while BMI and PA did not worsen. These latter findings were not observed in a historical control group that did not receive IN. Only one patient needed protein-rich formula administration. Conclusions: in this overweight COVID-19 population immune-nutrition prevented malnutrition development with a significant decrease of inflammatory markers.

Functional dyspepsia (FD) is a disorder of gut–brain interaction affecting approximately 7% of the global population under Rome IV criteria, characterised by postprandial fullness, early satiation, epigastric pain, and/or epigastric burning in the absence of identifiable organic disease. Meal ingestion is the dominant symptom trigger in the majority of patients, yet the relationship between diet and FD is bidirectional: dietary exposures drive symptoms through established pathophysiological mechanisms, while FD itself can promote maladaptive eating behaviours and progressive dietary restriction with nutritional and psychological consequences. The pathophysiological substrate linking diet to symptom generation encompasses impaired gastric accommodation and emptying, visceral hypersensitivity to mechanical and chemical stimuli, low-grade duodenal mucosal immune activation and epithelial barrier impairment, alterations of the small intestinal microbiota, and gut–brain axis dysregulation. Dietary fat is the macronutrient most consistently implicated, acting through cholecystokinin-mediated chemosensory and mechanosensory pathways. Cross-sectional population data suggest that a high protein intake may also be associated with epigastric pain, although this association did not persist after multivariable adjustment, while the evidence linking total carbohydrate intake to symptoms remains sparse and inconsistent, so that no recommendation on total carbohydrate intake can currently be made. Cognitive factors, including learned food beliefs, expectancy, and nocebo effects, further modulate symptom perception independently of actual nutrient content. Among dietary patterns, Mediterranean-style eating offers the most coherent mechanistic rationale and the strongest observational support, while a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) shows selective benefit in patients with postprandial distress syndrome features or prominent bloating. Common triggers including spicy foods, coffee, and alcohol show heterogeneous evidence driven by individual sensitivity rather than dose-related effects. Nutritional concerns are substantial: clinically significant weight loss affects approximately 35% of tertiary-care patients, and nearly 40% screen positive for avoidant/restrictive food intake behaviour using validated screening tools. Dietary management should therefore be individualised, nutritionally adequate, and integrated within a broader biopsychosocial framework, with screening for disordered eating before any elimination strategy is initiated.

Ultra-processed foods (UPFs) provide more than half of daily energy intake in several high-income countries, and their consumption is increasing worldwide. Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) are chronic gastrointestinal conditions whose burden has grown alongside industrialized dietary patterns. Here, we summarize the epidemiological, mechanistic and clinical evidence linking UPF consumption to both conditions. Most prospective cohorts and meta-analyses associate higher UPF intake with incident Crohn’s disease, whereas associations with ulcerative colitis are weaker and inconsistent. In IBS, observational studies, including a large prospective cohort, suggest a modest, dose-dependent association with risk, although data are limited and the diagnostic criteria have recently changed with Rome V. Mechanistically, both disorders may converge on the intestinal microenvironment: in experimental models, emulsifiers alter microbial composition and metabolism, the mucus layer, epithelial barrier integrity and mucosal immune activation, and non-nutritive sweeteners alter microbial composition and epithelial barrier function, although human data are limited and causality has not been established. We also discuss IBS-like symptoms in quiescent IBD, dietary management in both conditions, and the main knowledge gaps, including exposure assessment, residual confounding and the need for adequately powered intervention trials.