Neurocognitive performance and appetite-regulating hormones in obesity with and without eating disorders: A comprehensive review and empirical analysis

Obesity and eating disorders (ED) share neurocognitive vulnerabilities involving executive control and reward processing, yet the neuroendocrine–cognitive links underlying their comorbidity remain underexplored. This study synthesizes current evidence on neurocognitive mechanisms in obesity and ED and examines associations between neurocognition and appetite-regulating hormones in clinical groups. A cross-sectional analysis was conducted in 171 women: obesity with ED (OB + ED; n = 43), obesity without ED (OB–ED; n = 70), and healthy controls (HC; n = 58). Neurocognition was assessed using the Conners’ Continuous Performance Test-II (attention/inhibition) and Iowa Gambling Task (decision-making); impulsivity with UPPS-P; fasting ghrelin, insulin, leptin, and LEAP2 were measured. OB + ED showed higher omission errors than HC (p<0.001, d = 0.40) and higher commission errors than OB–ED (p=0.035, d = 0.46), indicating greater attentional lapses and impulsive responding. Iowa Gambling performance did not differ overall, but OB + ED outperformed OB–ED in mid-learning phases, suggesting enhanced feedback sensitivity. Impulsivity profiles diverged, with OB + ED showing higher Lack of Premeditation. Endocrine profiles revealed higher LEAP2 and lower ghrelin in both obesity groups versus HC, with insulin elevated in OB–ED. Structural equation modeling indicated leptin uniquely predicted attentional lapses, slower reaction times, and impulsivity traits, with downstream links to BMI and decision-making. These findings support integrated models in which leptin-linked neuroendocrine dysregulation intersects with attention, decision-making, and impulsivity in obesity and ED comorbidity, highlighting targets for mechanistically informed, combined metabolic–cognitive interventions.