Cortisol Stress Response & Intake in Obese Binge Eaters

描述（由申请人提供）：我们将研究皮质醇作为暴食症（BED）中暴食的中介物的作用，BED的特征是大约30%的肥胖个体接受治疗。鉴于BED的患病率和相关的发病率，确定这种疾病的病理生理机制至关重要。一些研究人员提出，皮质醇直接刺激食欲。皮质醇被认为是人类食物摄入增加的媒介，但这还没有被广泛研究。在临床实践中，肥胖患者经常报告压力是暴饮暴食的主要诱因，但这种关系背后的生物学机制知之甚少。我们的目的是实验测试的假设，外源性管理的皮质醇和内源性产生的皮质醇后，实验室压力与更大的食物摄入量在床上。具体来说，在不同的日子，我们将给予氢化可的松与安慰剂相比，并测量皮质醇水平和摄入量从一个多项目的膳食后，真实的生活人际排斥范式，耶鲁人际压力（YIPS），与无压力控制。1目的是证明皮质醇水平（通过曲线下面积评估）与两组的食物摄入量增加有关。我们还假设，与肥胖的非BED个体相比，BED受试者将显示出对YIPS的皮质醇反应性增加，这将与更大的饥饿感、更大的进食欲望和膳食摄入相关。48例肥胖（BMI，kg/m2 >30），绝经前妇女使用随机区组设计，将被分配接受以下每种条件：1）氢化可的松250（微克/千克）+多项目; 2）安慰剂药丸+多项目餐; 3）耶鲁人际压力源（YIPS）+多项目餐;（4）无应激对照+多项目膳食。皮质醇、饥饿感、饱腹感和进食欲望将在基线和每30分钟进行一次评估，持续135分钟。拟议的研究将作为确定皮质醇是床上暴饮暴食的关键介质的第一步。令人鼓舞的发现应该会导致一个人的RO 1雇用更多的参与者来研究更广泛的激素，更精细的糖皮质激素反馈模型，以及在标准治疗之前和之后在压力进食模型中发挥作用的其他心理因素，以及新的皮质醇减少药物和减压心理疗法。

DESCRIPTION (provided by applicant): 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.