Background: Investigations on the relationship between obesity, binge eating and the function of hypothalamic–pituitary–adrenal (HPA) axis have led to inconsistent results. General psychopathology affects HPA axis function. The present study aims to examine correlations between binge eating, general psychopathology and HPA axis function in obese binge eaters. Methods: Twenty-four hour urinary free cortisol (UFC/24 h) was measured in 71 obese binge eating women. The patients were administered psychometric tests investigating binge eating, psychopathology and clinical variables. The relationship between binge eating, psychopathology and urinary cortisol was investigated, controlling for age and BMI. Results: We found an inverse correlation between UFC/24 h and binge eating, depression, obsessive-compusive symptoms, somatization and sensitivity. In a regression model a significant inverse correlation between urinary cortisol and psychopathology was confirmed. Conclusions: Urinary cortisol levels in obese patients with binge eating disorder show an inverse correlation with several dimensions of psychopathology which are considered to be typical of a cluster of psychiatric disorders characterized by low HPA axis function, and are very common in obese binge eating patients. If these results are confirmed, UFC/24 h might be considered a biomarker of psychopathology in obese binge eaters.
Binge eating disorder (BED) is characterized by recurrent episodes of binge eating in the absence of purging or other compensatory behaviors (American Psychiatric Association, 2000); it is thought to be a frequent condition in individuals seeking treatment for obesity (Spitzer et al., 1993). The role of HPA (hypothalamic–pituitary–adrenal) axis in obesity and its comorbidities is currently debated (Abraham, Rubino, Sinaii, Ramsey, & Nieman, 2013). Dysfunctions in the HPA axis are thought to play a role in eating disorder psychopathology (Lo Sauro, Ravaldi, Cabras, Faravelli, & Ricca, 2008); in particular binge eating episodes are often preceded by stress and negative affect (Laessle, Schulz, 2009 and Levine, Marcus, 1997) and a growing body of research shows that cortisol released during stress might promote hunger and feeding behavior (Tataranni et al., 1996). Indeed, some studies found an augmented cortisol secretion as a result of laboratory stress in obese BED subjects compared to non-BED obese subjects (Gluck, 2006, Gluck et al, 2004 and Gluck et al, 2004); in another study patients who developed weight gain after a stressful event have been found to show higher twenty-four hour urinary free cortisol (UFC/24 h) than patients who did not identify a stressful event before the onset of weight gain (Vicennati, Pasqui, Cavazza, Pagotto, & Pasquali, 2009). These data might suggest the presence of higher baseline cortisol levels in some obese BED patients. However, one study examining the HPA in BED found normal cortisol suppression after dexamethasone suppression test (Yanovski, Yanovski, & Gwirtsman, 1993). Some studies that relied on single measurements of evening (Coutinho, Moreira, Spagnol, & Appolinario, 2007) and morning (Monteleone et al, 2000 and Monteleone et al, 2003) cortisol levels in women with BED reported normal levels.
