Nutrients

Background: The concept of emotional eating (EE) originates in the early psychosomatic accounts of overeating, but its nosological status remains contested more than four decades after it was first scientifically explored. Although neither the DSM-5-TR nor the ICD-11 recognizes EE as a discrete entity, clinically significant presentations of EE are described in the literature and can currently be captured under residual diagnostic categories in the absence of specific criteria. Objective: To examine whether EE is best conceptualized as an independent disorder or a dimensional, transdiagnostic, nutritional-behavioral phenotype, and to identify requirements for its clinical validation. Methods: A conceptual analysis supported by a critical synthesis of the literature focused on phenotypic heterogeneity, nutritional correlates, measurement approaches, diagnostic boundaries, and clinical implications of EE. Results: Negative-affect EE (N-EE) has been linked to changes in food choice, diet quality, processing degree, eating patterns, and potential abdominal adiposity, but these associations do not resolve the contentious question of whether EE is a distinct clinical entity. Eating in response to emotional states has also been linked to depression, emotion dysregulation, dietary restraint, binge eating, body-image concerns, sleep disturbance, and obesity-related outcomes. However, these associations are heterogeneous and do not define a unique disorder. One important asymmetry further complicates classification: N-EE is more consistently associated with psychopathology, while positive EE (P-EE) often occurs in normative social contexts. The proposed framework positions EE as a dimensional, transdiagnostic phenotype and identifies convergent multimethod validity, clinically meaningful thresholds, and discriminant, longitudinal, nutritional, prognostic, and treatment validity beyond established eating and mood disorders as requirements for potential categorical recognition. Conclusions: The literature considered suggests that EE may be usefully approached as a dimensional, transdiagnostic nutritional-behavioral phenotype. This remains a provisional conceptual position rather than an empirically validated classification. Further multimethod and longitudinal research is needed to clarify clinical significance, diagnostic boundaries, and utility before considering independent diagnostic recognition.

Background/Objectives: Bariatric–metabolic surgery (BMS) improves obesity through neuroendocrine mechanisms involving bile acids (BAs) and nutrient-stimulated gastrointestinal hormones. However, the underlying pathophysiology involved remains poorly understood. BAs are essential for the digestion and absorption of dietary fat and fat-soluble vitamins and act as nutrient-responsive signaling molecules, so their handling after malabsorptive procedures is relevant both to metabolic outcomes and to nutritional status. Methods: We prospectively compared Roux-en-Y gastric bypass (RYGB) and single-anastomosis duodeno-ileal bypass with sleeve gastrectomy (SADI-S) in a single-center case-control study including 37 RYGB and 31 SADI-S patients with severe obesity and 19 non-obese controls. Before and one year after surgery, participants underwent a standardized mixed-meal test (nutrient challenge) with measurement of 14 individual BA fractions, insulin, GLP-1, ghrelin, FGF19, leptin, and adiponectin; bile acid malabsorption was assessed one year after surgery with the ⁷⁵Se-SeHCAT test, and weight was followed for up to 5 years. Results: Fasting total BAs increased after both techniques, with no significant between-technique difference in total BA exposure (primary outcome). The techniques were associated with distinct BA profiles: fasting concentrations of conjugated BAs (GCA, GCDCA, and TDCA) were higher after SADI-S than after RYGB (FDR-adjusted q < 0.05), with a similar but more variable pattern in postprandial AUCs, whereas RYGB was characterized by a greater postprandial rise in the unconjugated secondary BA DCA. After surgery, FGF19 increased progressively during the mixed-meal test, peaking at 90 min, and its increase correlated with the rise in conjugated BAs, particularly in SADI-S. The postprandial insulin peak shifted earlier in both techniques, with a lower insulin AUC in SADI-S; GLP-1 responses were supraphysiological, and ghrelin increased post RYGB but was suppressed after SADI-S. Leptin decreased markedly, and in an exploratory analysis, its decrease was associated with weight-loss success at 3 years. Weight loss was greater with SADI-S at 1 year, but not significantly different at 3 and 5 years; in an exploratory analysis, the increase in conjugated BAs correlated negatively with recurrence weight gain from nadir at 5 years. The SeHCAT test showed no bile acid malabsorption in SADI-S and normal retention in 90.6% of RYGB patients. Despite routine supplementation, total protein, zinc, copper, and the vitamin A/RBP and vitamin E/cholesterol ratios decreased after both techniques. Conclusions: In conclusion, RYGB and SADI-S are associated with differentiated BA and hormonal profiles. The predominance of conjugated BAs after SADI-S, which we hypothesize may be related to its longer biliopancreatic limb, emerges as a potential candidate mechanism for weight maintenance that requires confirmation and was not accompanied by clinically relevant bile acid malabsorption; however, the decreases observed in several micronutrients support careful nutritional follow-up after both techniques. Clinical trial registration: ISRCTN81954082.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide. Its prevalence is constantly increasing, particularly among obese individuals. Lifestyle modifications remain the first-line intervention for the management and treatment of MASLD. The most widely recommended dietary regime for MASLD is the Mediterranean Diet (MedDiet). Despite its countless benefits, this dietary regimen is difficult to follow in some cases. This study aimed to assess the effects of an 8-week Very Low-Calorie Ketogenic Diet (VLCKD) in obese patients with MASLD. Methods: The study included 55 obese adults aged 18–64 years, recruited from the Center of Nutrition for Obesity and Metabolic Diseases, National Institute of Gastroenterology “Saverio de Bellis” Research Hospital (Castellana Grotte, Bari, Italy). Anthropometry, body composition (BIA), liver status (FibroScan^®), serum biochemistry and circulating biomarkers of adipose dysfunction were assessed at baseline (T0) and post-intervention (T1). Results: Significant improvements in liver steatosis (CAP p < 0.0001), liver stiffness (p = 0.0005), anthropometric parameters (waist p < 0.0001), and body composition (FM p <0.0001) were observed. A significant reduction in leptin levels and an increase in sex hormone-binding globulin (SHBG p < 0.0001) were also observed. Conclusions: In this uncontrolled pre-post analysis, the 8-week VLCKD intervention was associated with improvements in hepatic steatosis, body weight, and fat mass, and selected circulating biomarkers of adipose tissue dysfunction in adults with obesity and MASLD.