What question did this study set out to answer?

The research aims to explore the neurocognitive mechanisms and hormone associations in obesity with and without eating disorders.

March 29, 2026Open Access

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

Key Points

The research aims to explore the neurocognitive mechanisms and hormone associations in obesity with and without eating disorders.
Cross-sectional analysis of 171 women categorized into obesity with eating disorders, obesity without, and healthy controls.
Neurocognitive assessments included attention/inhibition and decision-making tasks.
Measured impulsivity and fasting levels of hormones like ghrelin, insulin, leptin, and LEAP2.
Applied structural equation modeling to analyze relationships between neurocognition and hormonal levels.
Obesity with eating disorders showed greater attentional lapses and higher impulsivity compared to healthy controls.
LEAP2 levels were higher, and ghrelin levels were lower in both obesity groups versus healthy controls.
Leptin was found to uniquely predict attentional lapses, slower reaction times, and impulsivity traits.

Abstract

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.

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