We will investigate the role of cortisol as a mediator for binge eating in binge eating disorder (BED), which characterizes roughly 30% of obese individuals presenting for treatment. Given the prevalence of BED and the associated morbidities, it is essential to identify pathophysiological mechanisms for this disorder. Several researchers have proposed that cortisol directly stimulates appetite. Cortisol has been proposed to be a mediator for increased food intake in humans, but this has not been widely studied. In clinical practice, obese patients often report stress as a primary trigger for binge eating, but the biological mechanism underlying this relationship is poorly understood.
We aim to experimentally test the hypotheses that both exogenously administered cortisol and endogenously produced cortisol following a laboratory stress are related to greater food intake in BED. Specifically, on separate days, we will administer hydrocortisone compared to a placebo and measure cortisol levels and intake from a multiple-item meal following a real life interpersonal rejection paradigm, The Yale Interpersonal Stressor (YIPS), compared to a no-stress control. 1 objective is to demonstrate that cortisol levels, assessed by area under the curve, are related to increased food intake across both groups. We also hypothesize that the BED subjects will show increased cortisol responsivity to the YIPS, which will be associated with greater hunger, greater desire to eat, and meal intake, compared to obese non-BED individuals. 48 obese (BMI, in kg/m2 >30), pre-menopausal women (24 BED vs. 24 non-BED), using a randomized block design, will be assigned to receive each of the following conditions: 1) hydrocortisone 250 (microgram/kg) + multiple-item; 2) placebo pill + multiple-item meal; 3) Yale Interpersonal Stressor (YIPS) + multiple-item meal and; 4) no-stress control + multiple-item meal. Cortisol, hunger, fullness, and desire to eat will be assessed at baseline and every 30-min. for a period of 135 min. The proposed study will serve as a first step towards identifying cortisol as a key mediator of binge eating in BED. Encouraging findings should lead to an individual RO1 employing a larger number of participants to investigate a broader array of hormones, more elaborate glucocorticoid feedback models, and other psychological factors that play a role in the stress-eating model, before and after standard treatment, as well as new cortisol reduction medications and stress reduction psychotherapies.
