A biopsychosocial perspective on obesity and eating disorders: A narrative overview and exploratory study of ghrelin, LEAP2, trait impulsivity, and eating psychopathology.

Dysregulated eating in obesity and eating disorders (ED) is associated with complex relationships between peripheral hormonal signals and neurobehavioral characteristics. Ghrelin and its endogenous antagonist liver-expressed antimicrobial peptide-2 (LEAP2) have been implicated in the regulation of energy homeostasis and food intake, while trait impulsivity has been proposed as a transdiagnostic characteristic associated with dysregulated eating. This study aimed to integrate narrative evidence with exploratory empirical data to examine associations between ghrelin, LEAP2, and trait impulsivity in women with obesity, with and without ED, and to explore their associations with food addiction (FA) and eating psychopathology. A total of 164 adult women (67 with obesity, 35 with obesity + ED, 62 healthy controls) completed anthropometric assessments, fasting ghrelin and LEAP2 determinations, and psychometric measures of trait impulsivity, FA, and eating psychopathology. Group comparisons and exploratory structural equation modeling (SEM) were used to explore associations between endocrine and behavioral variables. Women with obesity (with or without ED) showed significantly lower ghrelin levels than controls, while LEAP2 concentrations did not differ between groups. Trait impulsivity and FA scores were higher in the obesity + ED group. Within this subgroup, SEM analyses identified positive associations of trait impulsivity and FA with eating psychopathology, while LEAP2 was positively associated with trait impulsivity and FA scores. Previous research has pointed to potential associations of ghrelin and LEAP2 with obesity and ED, as well as with behavioral characteristics related to dysregulated eating, although the available evidence remains limited and heterogeneous. In our study, ghrelin was lower in women with obesity, whereas LEAP2 did not differ between groups. The observed associations involving LEAP2 emerged only in the exploratory SEM analysis and should therefore be interpreted cautiously. These findings are hypothesis-generating and do not provide evidence of mechanistic or causal relationships. Further research in larger and longitudinal samples is needed to replicate these findings and clarify the relationships among endocrine and behavioral factors.