Physiological Reactivity, Leptin and Loss of Control Eating in Youth

描述(由申请人提供)： 虽然儿童暴饮暴食障碍(BED)在儿童时期很少观察到，但青少年经常报告失控(LOC)进食发作。10，11 LOC进食的特点是进食发作，年轻人报告在进食时失去控制的经历，无论报告的食物量是多少。与没有报告进食LOC行为的儿童相比，LOC患者更容易肥胖，报告抑郁和焦虑症状增加，饮食认知障碍，以及自尊降低。12此外，青少年进食LOC可能会预测部分或全部综合征的发展，13超重增加，14-16和代谢综合征的组成部分，17使他们面临在以后的生活中发展为更严重的心血管和内分泌系统健康并发症的风险。在有床的成年人中，数据表明对压力有更大的生理反应，包括在实验室应激源后心率变异性(HRV)降低18。然而，还没有研究考察摄入低碳水化合物的年轻人对实验室应激源的生理反应。此外，越来越多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的联系，特别是在妇女中。19-27然而，在年轻人中检验这些关系的数据有限。28到目前为止，还没有研究探索摄入低碳水化合物、实验室压力和青年生理反应之间的联系。本研究试图使用经过充分验证的心理生理学技术，特别是唾液皮质醇、心率变异性和血清瘦素，来探索超重女孩(8-17岁)在进食和不进食LOC的情况下的这些关系。我们假设，与不吃低碳水化合物的超重女孩相比，吃低碳水化合物的女孩对实验室诱导的压力的生理反应能力将受到损害，皮质醇和心率变异性下降。我们进一步预计，在摄入低脂食物的年轻人中，较高的瘦素水平将与较差的HRV对实验室应激源的反应性相关。本研究的具体目的如下：1.探讨超重女孩在实验室应激源作用下进食LOC前后皮质醇和心率变异性的变化；2.检测基线血浆瘦素与HRV的关系；3.研究进食LOC与血浆Leptin和HRV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进食LOC的情况。空腹血浆瘦素将在给予实验室认知应激源之前收集。皮质醇和心率变异性的测量将在应激源之前、期间和之后持续收集。感知压力的主观测量也将在每个时间点收集。鉴于进食LOC可能预示着一系列不良的心理和生理后果，研究结果将阐明青少年进食LOC的性质及其生理相关性，这将有助于为相当一部分肥胖人口提供预防和干预措施，以努力减少进食病理的恶化和床上的发育。

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.