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Abstract Context We compared the incidence of hypoglycemia after Roux-en-Y gastric bypass (RYGB) vs sleeve gastrectomy (SG). Design, Setting, and Main Outcome Measures Randomized, open-label trial conducted at the outpatient obesity clinic in a university hospital in Rome, Italy. The primary aim was the incidence of reactive hypoglycemia (<3.1 mmol/L after 75-g oral glucose load) at 1 year after surgery. Secondary aims were hypoglycemia under everyday life conditions, insulin sensitivity, insulin secretion, and lipid profile. Results Of 175 eligible patients, 120 were randomized 1:1 to RYGB or SG; 117 (93%) completed the 12-month follow-up. Reactive hypoglycemia was detected in 14% and 29% of SG and RYGB patients (P = 0.079), respectively, with the effect of treatment in multivariate analysis significant at P = 0.018. Daily hypoglycemic episodes during continuous glucose monitoring did not differ between groups (P = 0.75). Four of 59 RYGB subjects (6.8%) had 1 to 3 hospitalizations for symptomatic hypoglycemia vs 0 in SG. The static β-cell glucose sensitivity index increased after both treatments (P < 0.001), but the dynamic β-cell glucose sensitivity index increased significantly in SG (P = 0.008) and decreased in RYGB (P = 0.004 for time × treatment interaction). Whole-body insulin sensitivity increased about 10-fold in both groups. Conclusions We show that reactive hypoglycemia is no less common after SG and is not a safer option than RYGB, but RYGB is associated with more severe hypoglycemic episodes. This is likely due to the lack of improvement of β-cell sensitivity to changes in circulating glucose after RYGB, which determines an inappropriately high insulin secretion. We found that reactive hypoglycemia is no less common after SG than after RYGB, but RYGB is associated with more severe hypoglycemic episodes.

Background/Objectives: Nutritional patterns influence the gut–brain axis and immune signaling with potential consequences for depression and anxiety. We conducted a review focused on clinically meaningful psychiatric outcomes (symptom severity/diagnosis) to synthesize recent evidence (2020–2025) on Mediterranean-style dietary interventions; ultra-processed food (UPF) exposure; and psychobiotic/prebiotic strategies, integrating mechanistic insights relevant to practice. Methods: Searches in PubMed/MEDLINE, Scopus, and Web of Science (January 2020–October 2025) combined terms for diet, Mediterranean diet (MD), UPF, microbiota, probiotics, psychobiotics, depression, and anxiety. Eligible designs were randomized/controlled trials (RCTs), prospective cohorts, and systematic reviews/meta-analyses reporting clinical psychiatric outcomes in adults. We prioritized high-quality quantitative syntheses and recent RCTs; data were extracted into a prespecified matrix and synthesized narratively. Results: Recent systematic reviews/meta-analyses support that MD interventions reduce depressive symptoms in adults with major or subthreshold depression, although large, long-term, multicenter RCTs remain a gap. Exposure to UPF is consistently associated with higher risk of common mental disorders and depressive outcomes in large prospective cohorts. Psychobiotics (specific probiotic strains and prebiotics) show small-to-moderate benefits on depressive symptoms across clinical and nonclinical samples, with heterogeneity in strains, dosing, and duration. Mechanistic reviews implicate microbiota-derived metabolites (short-chain fatty acids) and immune–inflammatory signaling (including tryptophan–kynurenine pathways) as plausible mediators. Conclusions: Clinically, emphasizing Mediterranean-style dietary patterns, reducing UPF intake, and considering targeted psychobiotics may complement standard psychiatric care for depression. Future work should prioritize adequately powered, longer RCTs with standardized dietary protocols and microbiome-informed stratification to clarify responders and mechanisms.

Background The aim of the present study was to assess the cost-effectiveness of bariatric surgery, non-surgical weight loss and pharmacological non-surgical weight loss (BS-WL, NS-WL, PNS-WL) to avoid or delay total knee arthroplasty (TKA) in subjects with end-stage knee osteoarthritis and obesity. Methods The quality-adjusted life years (QALYs) and incremental cost-effectiveness ratio (ICER) were computed using a Markov State Model simulating outcomes and costs in 4000 potential subjects followed for 25 years. Model inputs were derived from the literature and internet sources. Deterministic and probabilistic sensitivity analyses were performed to assess the robustness of the model assumptions. Results BS-WL and PNS-WL increased QALYs from 7.70 (TKA-only group) to 8.96 and 8.41, respectively, while NS-WL marginally increased QALY to 7.86. The BS-WL and PNS-WL ICERs were $27,127 and $33,461, respectively, far below the willingness-to-pay threshold of $50,000. However, the NS-WL ICER was $57,843. The percentage of subjects needing first revision was greater after TKA-only (26.4%) and lower with the other strategies (12.9% with BS-WL, 23.5% with NS-WL and 20.1% with PNS-WL). The most sensitive parameter was BS-WL success in weight loss; 20% of the key input parameter variations produced BS-WL ICERs that were always below the threshold, as for the PNS-WL strategy. Conclusions Bariatric surgery is effective and cost-effective in delaying or preventing TKA in patients with severe obesity and reducing the need for primary and secondary surgical revision. Despite current limitations on the long-term effects of available antiobesity medications, semaglutide appears to also be cost-effective, while non-surgical weight loss is the least effective strategy. Clinicians and policy makers should consider the cost-effectiveness of losing weight prior to total knee replacement in patients with obesity.

Background: Artificial sweeteners, widely used as non-nutritive sugar substitutes, are increasingly prevalent in ultra-processed products. Although promoted for weight management due to their minimal caloric content, their impact on systemic inflammation remains uncertain. This systematic review of animal studies aims to evaluate the association between artificial sweetener consumption and inflammatory biomarkers. Methods: A systematic literature search was conducted up to May 2025 across PubMed, Web of Science, and Scopus, following PRISMA guidelines and registered in PROSPERO (CRD420251084004). Risk of bias was assessed using the ARRIVE guidelines and SCYRCLE’s risk of bias tool. Results: Thirty-seven animal studies were included: aspartame (n = 17), sucralose (n = 16), acesulfame potassium (n = 5), and saccharin (n = 4). Protocols varied in terms of dosage, exposure duration, animal models, and assessment of inflammatory outcomes, including C-reactive protein, interleukins (IL-6 and IL-1β), and tumor necrosis factor alpha. Aspartame and sucralose could elevate inflammatory markers, with sucralose also disrupting gut integrity and microbiota. Acesulfame K and saccharin showed variable, dose-dependent effects. Conclusions: This systematic review of animal studies suggests a possible mechanistic association between the consumption of certain artificial sweeteners and systemic inflammation. However, this relationship remains to be clarified and warrants exploration through well-designed, large-scale randomized controlled trials.

Bipolar disorder (BD) is a severe psychiatric illness characterized by recurrent mood episodes and significant psychosocial impairment. Emerging evidence supports a bidirectional link between diet and mental health, with growing interest in nutritional psychiatry. This narrative review examines the psychological and psychiatric impact of diet in BD, focusing on biological mechanisms (gut–brain axis, neuroinflammation, oxidative stress, neurotransmitter synthesis, and HPA axis dysregulation) and the role of specific dietary patterns, including Western, Mediterranean, ketogenic, and anti-inflammatory diets. Key micronutrients such as omega-3 fatty acids, B-vitamins, magnesium, and vitamin D are explored in relation to mood regulation. This review also addresses psychological factors, including emotional eating, disordered eating behaviors, and the symbolic meaning of food in BD. Furthermore, it highlights the integration of nutritional psychoeducation into psychotherapy, the impact of comorbidities (e.g., obesity, metabolic syndrome), and the role of lifestyle factors such as sleep and physical activity. Despite promising findings, current research is limited by methodological heterogeneity. Future perspectives should include interdisciplinary, personalized interventions that incorporate nutritional strategies into standard care for BD.

Aims/hypothesisThe small intestine plays an important role in hepatic and whole-body insulin sensitivity, as shown by bariatric surgery. Our goal was to study whether routes and dose of glucose administration have an acute impact on insulin sensitivity. The primary endpoint of this proof-of-concept study was the difference in insulin-mediated metabolic clearance rate (MCR/I) of glucose between the oral and intravenous routes of glucose administration. Secondary endpoints were differences in insulin effect on proteolysis, ketogenesis, lipolysis and glucagon levels.MethodsIn this parallel cohort study, we administered multiple oral glucose loads to 23 participants (aged between 18 and 65 years) with morbid obesity and with normal or impaired glucose tolerance or type 2 diabetes. In a different session, we administered isoglycaemic intravenous glucose infusions (IGIVI) to match the plasma glucose levels observed during the oral challenges. Glucose rate of appearance (Ra) and disappearance (Rd) and endogenous glucose production (EGP) were calculated by infusing [6,6-2H2]glucose with or without oral [U-13C6]glucose. Plasma small polar metabolites were measured by gas chromatography and time-of-flight mass spectrometry. Lipids were measured by ultra-HPLC and quadrupole mass spectrometry. Glucagon-like peptide-1, insulin, C-peptide and glucagon were also measured. Participants, caregivers, people doing measurements or examinations, and people assessing the outcomes were unblinded to group assignment.ResultsGlucose MCR/I was significantly higher during IGIVI than during oral glucose administration, independently of glycaemic status (12 ± 6 for IGIVI vs 7.4 ± 3 ml min−1 kg−1 per nmol/l for oral, p< 0.001 from paired t test). Insulin secretion was higher during oral administration than during IGIVI (p< 0.001). The disposition index was significantly lower during the oral procedure: 4260 ± 1820 vs 5000 ± 2360 (ml min−1 kg−1 (nmol/l)−1 pmol/min; p = 0.005). Insulin clearance was significantly higher when glucose was infused rather than ingested (2.53 ± 0.82 vs 2.16 ± 0.49 l/min in intravenous and oral procedure, respectively, p = 0.006). The efficacy of insulin in inhibiting lipolysis and proteolysis was decreased after oral glucose loads. A heat map diagram showed a different pattern for the metabolites between the two routes of glucose administration.Conclusions/interpretationOur study shows that insulin sensitivity depends on the route of glucose administration, the oral route leading to increased insulin secretion and compensatory insulin resistance compared with the intravenous route. The efficacy of insulin in blocking lipolysis and protein breakdown is lower after oral glucose loads vs the intravenous route. Our findings suggest that, while the glucose-mediated incretin release is followed by an increase in insulin release, the effect of the released insulin is limited by an increase in insulin resistance.Trial registrationClinicalTrials.gov NCT03223129.

Background: Bipolar disorder (BD) is a chronic psychiatric condition characterized by recurrent mood episodes and substantial functional impairment. Emerging evidence highlights the role of nutrition in modulating neurobiological pathways and influencing the course of BD. However, systematic recommendations for dietetic prescriptions remain limited. Methods: This narrative review was conducted by searching PubMed, Scopus, and Web of Science up to October 2025. Keywords included “bipolar disorder,” “nutrition,” “dietary interventions,” and “nutritional psychiatry.” Studies focusing on nutritional patterns, dietary components, and dietetic recommendations relevant to BD were included. Evidence was synthesized narratively to identify potential dietary strategies and gaps in current knowledge. Results: The available literature suggests that nutritional interventions may influence mood stabilization, metabolic comorbidities, and treatment response in BD. Key findings highlight the potential benefits of Mediterranean-style diets, omega-3 fatty acids, micronutrients (including magnesium, zinc, and vitamins D and B-complex), and dietary approaches targeting inflammation and oxidative stress. Conversely, Western-style diets, rich in saturated fats and refined sugars, appear to exacerbate mood instability and metabolic burden. Despite promising findings, heterogeneity across studies and the scarcity of randomized controlled trials limit firm conclusions. Conclusions: Nutrition represents a promising adjunctive strategy in the management of BD. Dietetic prescriptions may contribute to improved outcomes by addressing both psychiatric symptoms and physical health comorbidities. Future research should prioritize well-designed clinical trials to establish evidence-based guidelines for integrating nutrition into BD management.

Growing evidence indicates that the gut microbiota is not a static ecosystem but a rhythmic metabolic organ whose oscillatory activity is tightly coordinated with host circadian biology. Disruption of this temporal alignment, through irregular diet, sleep disturbance, shift work, or social jet lag, may profoundly alter microbial composition and the production of neuroactive metabolites. These alterations have emerged as potential contributors to the pathophysiology of mood disorders. This review introduces the concept of chrono-metabolic psychiatry, a framework integrating circadian rhythms, gut microbiota dynamics, and host metabolic signaling in the development and course of depressive and bipolar disorders. In this framework, the term \"chrono-metabolic\" refers to the integration of biological timing, host metabolic regulation, and microbiota-derived metabolic signaling. Chrono-metabolic psychiatry therefore shifts the focus from static dysbiosis or neurotransmitter imbalance alone to the time-dependent interactions among circadian misalignment, microbial rhythmicity, immune regulation, metabolite production, and affective instability. Diurnal fluctuations in short-chain fatty acids, tryptophan-kynurenine metabolites, bile acids, and microbial-derived neurotransmitters interact with clock gene regulation, hypothalamic-pituitary-adrenal axis activity, neuroinflammation, and synaptic plasticity. Chrono-disruption may represent a transdiagnostic vulnerability factor and may confirm the bidirectional relationship between mood instability and microbiota rhythmicity. Emerging therapeutic implications, including chrono-nutrition, time-restricted feeding, targeted probiotic administration (\"chronobiotics\"), and the microbiota-modulating effects of psychotropic medications are discussed. By shifting from a compositional to a temporal-metabolic perspective, this model highlights the importance of microbial oscillations rather than static dysbiosis alone. Integrating circadian biology into microbiota research may enable metabolomic stratification and pave the way for precision psychiatry approaches grounded in host-microbe metabolic crosstalk. Future longitudinal and time-resolved multi-omics studies are needed to validate this framework and to translate it into clinically actionable interventions.

Background: The gut microbiota plays a crucial role in brain development and function, especially in early life. Disruptions in the pediatric microbiota–gut–brain axis have been linked to neurodevelopmental and psychiatric disorders. We hypothesize that early-life dysbiosis can perturb neurodevelopment via the pediatric microbiota–gut–brain axis, increasing risk and/or severity of neuropsychiatric outcomes, and that microbiota-targeted strategies may mitigate this risk. Methods: We conducted a narrative review by searching PubMed, Scopus, and Web of Science up to January 2025 for studies addressing pediatric microbiota, neuropsychiatric development, and interventions. Human and animal studies were included if they provided mechanistic or clinical insights. Results: Key determinants of microbiota development in childhood include mode of delivery, feeding practices, antibiotic exposure, diet, and environment. Altered microbial composition has been associated with autism spectrum disorder, attention-deficit/hyperactivity disorder, mood disorders, anxiety, and anorexia nervosa. Mechanistic pathways involve immune modulation, neural signaling (including the vagus nerve and enteric nervous system), and microbial metabolites such as short-chain fatty acids. Interventions targeting the microbiota—ranging from dietary strategies and probiotics to psychobiotics and fecal microbiota transplantation—show promise but require further pediatric-focused trials. Conclusions: The pediatric microbiota–gut–brain axis represents a critical window for neuropsychiatric vulnerability and intervention. Early-life strategies to support a healthy microbiota may help reduce the risk or severity of psychiatric disorders. Future research should prioritize longitudinal pediatric cohorts and clinical trials to translate mechanistic insights into precision interventions.

Oropharyngeal dysphagia is prevalent in hospitalized geriatric and neurological populations and constitutes a major driver of disease-related malnutrition. Conventional texture-modified diets frequently rely on diluting solid foods with liquid agents to achieve safe swallowing consistency, a process that reduces caloric and protein density per gram and creates a so-called volume paradox, whereby large meal volumes deliver inadequate nutrients. This retrospective observational study, conducted at the Fondazione Policlinico Gemelli IRCCS in Rome, compared nutritional intake in 208 hospitalized dysphagic adults receiving either a traditional homogenized standard diet (THSD; n = 58) or a density-enriched dysphagia-prepared diet (DPD; n = 150). Following propensity-score matching, total daily energy intake was significantly higher with the DPD compared to the THSD (1024 ± 307 kcal vs. 523 ± 161 kcal; < 0.0001), as was total protein intake (37.3 ± 12.9 g vs. 26.2 ± 12.7 g; < 0.0001). Clinically meaningful differences were observed across all meal components, including a more than twofold advantage in breakfast protein content (6.6 ± 1.7 g vs. 3.0 ± 1.5 g). Despite these improvements, total energy and protein intake remained below estimated daily requirements in both groups, highlighting the need for systematic nutritional monitoring alongside catering optimization. These findings support density-enrichment as a practical and safe strategy for improving nutritional adequacy in dysphagic inpatients, with implications for reducing reliance on oral nutritional supplements and mitigating disease-related malnutrition in clinical settings.