Psychobiology of Eating Disorders

Background: Various mental health and eating behavior variables have been independently associated with predicting weight loss in individuals with obesity. This study aims to investigate a mediation model that assesses the distinct contributions of these variables in predicting weight changes in patients with obesity following an outpatient behavioral weight loss intervention (BWLI). Methods: General mental health (depression, anxiety, stress, impulsivity), eating behavior (cognitive restraint, disinhibition, hunger), eating disorder pathology, and body mass index (BMI) were assessed in a group of 297 patients with obesity at the admission of a BWLI program. BMI was re-evaluated during the final treatment session. A mediation model was employed to examine whether mental health and eating behavior variables predicted BMI changes, with eating disorder pathology serving as a mediator. The model was tested both overall and within two patient subgroups: those with regular binge eating (≥four episodes/month) and those without. Results: In the overall sample (n = 238), the relationships between depression, impulsivity, and cognitive restraint with BMI change were mediated by eating disorder pathology. In the subgroup with regular binge eating (n = 99, 41.6%), the associations between stress and disinhibition with BMI change were additionally mediated by eating disorder pathology. In the subgroup without regular binge eating, eating disorder pathology showed no mediating effect. Discussion: Multiple mental health and eating behavior variables assessed at admission predicted BMI changes, particularly when mediated by eating disorder pathology in patients with regular binge eating. A comprehensive psychopathological assessment prior to starting BWLI may help identify multiple factors affecting prognosis and treatment outcomes. Long-term follow-up studies in this field are required. Full article

Human genetic studies have associated Neuronatin gene variants with anorexia nervosa (AN) and obesity. Studies on the expression of the Neuronatin gene product, a proteolipid, are lacking. We investigated the relationship between circulating Neuronatin, body mass index (BMI), body composition (BC), physical activity (PA), and psychometric outcomes in patients with AN, normal weight, and obesity. Plasma Neuronatin was measured by ELISA in (1) 79 subjects of five BMI categories (AN/BMI < 17.5 kg/m²; normal weight/BMI 18.5–25 kg/m²; obesity/BMI 30–40 kg/m²; obesity/BMI 40–50 kg/m²; obesity/BMI > 50 kg/m²) with assessment of BC (bioimpedance analysis; BIA); (2) 49 women with AN (BMI 14.5 ± 1.8 kg/m²) with measurements of BC (BIA) and PA (accelerometry); (3) 79 women with obesity (BMI 48.8 ± 7.8 kg/m²) with measurements of anxiety (GAD-7), stress (PSQ-20), depression (PHQ-9) and eating behavior (EDI-2). Overall, a positive correlation was found between Neuronatin and BMI (p = 0.006) as well as total fat mass (FM; p = 0.036). In AN, Neuronatin did not correlate with BMI, FM, or PA (p > 0.05); no correlations were found between Neuronatin and psychometric outcomes in obesity (p > 0.05). The findings suggest an FM-dependent peripheral Neuronatin expression. The decreased Neuronatin expression in AN provides evidence that Neuronatin is implicated in the pathogenesis of eating disorders. Full article

Binge eating disorder (BED) is a complex and heritable mental health disorder, with genetic, neurobiological, neuroendocrinological, environmental and developmental factors all demonstrated to contribute to the aetiology of this illness. Although psychotherapy is the gold standard for treating BED, a significant subgroup of those treated do not recover. Neurobiological research highlights aberrances in neural regions associated with reward processing, emotion processing, self-regulation and executive function processes, which are clear therapeutic targets for future treatment frameworks. Evidence is emerging of the microbiota-gut-brain axis, which may mediate energy balance, high-lighting a possible underlying pathogenesis factor of BED, and provides a potential therapeutic strategy. Full article