Physiological Reactivity, Leptin and Loss of Control Eating in Youth

描述（由申请人提供）： 虽然在儿童期很少观察到完全综合征的暴食症（BED），但青少年经常报告饮食失控（暴食）发作。10，11暴食的特征是青少年报告在进食时缺乏控制的经历，无论报告的食物量如何。与没有报告暴食行为的儿童相比，那些暴食者更有可能患有更严重的肥胖症，报告抑郁和焦虑症状增加，饮食认知紊乱，自尊心降低。12此外，青少年暴食可能预测部分或全部综合征BED的发展，13过度体重增加，14-16和代谢综合征的组成部分，17使他们在晚年有可能患上更严重的心血管和内分泌系统并发症。在患有BED的成年人中，数据表明对压力的生理反应更大，包括实验室压力源后心率变异性（HRV）降低。然而，还没有研究调查过年轻人对实验室压力的生理反应。此外，不断发展的研究表明，心率变异性、慢性交感神经激活和食欲激素瘦素之间存在联系，尤其是在女性中。19 - 27然而，研究青年中这些关系的数据有限。28迄今为止，还没有研究探讨青年中暴食、实验室压力和生理反应之间的联系。本研究旨在探讨这些关系超重的女孩（8-17岁）与和没有暴饮暴食，使用有效的心理生理技术，特别是唾液皮质醇，心率变异性和血清瘦素。我们假设，与没有暴饮暴食的超重女孩相比，暴饮暴食的女孩对实验室诱导的压力的生理反应能力受损，如皮质醇和HRV降低所示。我们进一步预测，高瘦素水平将与不良的HRV反应，以实验室应激与青少年之间的饮食。本研究的具体目的如下：1.探讨肥胖女孩在实验室应激后，进食与不进食的皮质醇及心率变异性的变化。检测基线血浆瘦素水平与心率变异性的关系; 3.探讨进食与血浆瘦素、心率变异性的关系。参与者将是60名超重女孩（8- 17岁），其中一半将在评估前一个月报告发生过LOC饮食事件。将在给予实验室认知应激源之前收集空腹血浆瘦素。皮质醇和HRV的测量将在应激之前、期间和之后连续收集。还将在每个时间点收集感知压力的主观测量值。鉴于暴食可能预示着许多不良的心理和生理结果，研究结果将阐明青年暴食的性质及其生理相关性，这将有助于为肥胖人群的重要子集提供预防和干预措施，以减少饮食病理学的恶化和BED的发展。

DESCRIPTION (provided by applicant): While full-syndrome binge eating disorder (BED) is rarely observed in childhood, loss of control (LOC) eating episodes are often reported by youth.10,11 LOC eating is characterized by eating episodes wherein youth report an experience of lacking of control while eating, irrespective of the amount of food reportedly consumed. Compared with children who do not report LOC eating behaviors, those with LOC are more likely to have greater adiposity, to report increased symptoms of depression and anxiety, disturbed eating cognitions, and lower self-esteem.12 Further, LOC eating in youth may predict the development of partial or full-syndrome BED,13 excess weight gain,14-16 and components of the metabolic syndrome,17 placing them at risk for developing more severe health complications of the cardiovascular and endocrine systems in later life. Among adults with BED, data indicate greater physiological response to stress, including decreased heart rate variability (HRV)18 following laboratory stressors. However, no study has examined physiological responses to laboratory stressors among youth with LOC eating. Additionally, a developing body of research indicates links between HRV, chronic sympathetic activation, and the appetitive hormone leptin, especially among women.19- 27 However, there are limited data examining these relationships in youth.28 To date, no studies have explored the links between LOC eating, laboratory stress, and physiological reactivity in youth. The present study seeks to explore these relationships among overweight girls (8-17 y) with and without LOC eating, using well- validated psychophysiological techniques; specifically salivary cortisol, HRV and serum leptin. We hypothesize that compared to overweight girls without LOC eating, those with LOC eating will have an impaired ability to respond physiologically to laboratory-induced stress, as indicated by decreased cortisol and HRV. We further anticipate that higher leptin levels will be associated with poorer HRV reactivity to a laboratory stressor among youth with LOC eating. Specific aims of the current study are as follows: 1. To explore changes in cortisol and HRV among overweight girls with and without LOC eating following a laboratory stressor; 2. to examine the relationship between baseline plasma leptin and HRV; and 3. to examine the relationship between LOC eating, plasma leptin and HRV. Participants will be 60 overweight girls (8-17y), half of whom will report episodes of LOC eating in the month prior to assessment. Fasting plasma leptin will be collected prior to administration of a laboratory cognitive stressor. Measures of cortisol and HRV will be collected continuously prior to, during, and following the stressor. Subjective measures of perceived stress will be collected at each time point as well. Given that LOC eating may be predictive of a host of adverse psychological and physiological outcomes, the study results will elucidate the nature of LOC eating in youth and its physiological correlates, which will help to inform prevention and intervention efforts for a significant subset of the obese population in an effort t reduce the exacerbation of eating pathology and development of BED.