Biobehavioral Influences on Stress-Induced Eating In Low-Income Adolescents

描述(由申请人提供)：压力诱导的饮食可能是青少年肥胖发展的一个关键风险因素。应激相关的下丘脑-垂体-肾上腺(HPA)轴的激活和随后皮质醇的升高在应激诱导的进食中起着核心作用。青春期是研究压力-进食联系的关键发育期，因为它的特点是对压力的脆弱性增加，成年后持续肥胖的可能性很高。在这方面，低收入青少年是一个特别高风险的群体，考虑到他们所处的紧张环境(如邻里暴力)和易受特定进食压力(如食物供应不足)的影响，他们可能特别容易受到压力引起的进食的影响。然而，关于青少年压力诱导进食的现有研究很少，原因是：1)未能研究皮质醇反应和情绪化饮食模式如何相互作用，以影响青少年在压力后的饮食摄入量；2)未能通过实验控制暴露在压力源下对苗条青少年和肥胖青少年能量摄入量的影响；3)关注中等收入家庭的经济同质性样本。这项拟议的研究通过同时检查肥胖和瘦低收入青少年皮质醇反应性、情绪性饮食和客观能量摄入之间的关系，扩展了对青少年应激诱导饮食背后的生物行为过程的理解，使用了一种经过验证的实验范式(Trier Social Stress Test for Children；TSST-C)，该范式已知会导致青少年皮质醇水平上升。我们的初步数据表明，与瘦青少年相比，肥胖青少年对TSST-C表现出更高的皮质醇反应性。建议的R03将比较肥胖(n=40)和瘦(n=40)低收入青少年(12-17岁)在压力诱导后与对照组的能量摄入量。具体目的是：(1)确定低收入肥胖青少年与低收入肥胖青少年对压力诱导的皮质醇反应性是否不同；(2)确定在情绪化进食得分较高的低收入青少年中，压力后的能量摄入与皮质醇反应性是否有更强的相关性；以及(3)探索皮质醇应激反应或感知压力是否更能预测青少年的能量摄入。与NICHD肥胖研究战略核心的使命一致，这项研究的结果将为旨在研究皮质醇反应和情绪化进食在低收入青少年肥胖发展中的作用的一系列方案研究提供坚实的基础。这项研究对公众健康的潜在影响是显著的， 鉴于这一发现将有助于确定低收入青少年中肥胖风险较高的一部分。或许同样重要的是，这些数据将为针对暴露在高压力环境中的低收入青少年量身定做的新的或强化的干预措施的开发提供信息，通过识别将这些年轻人置于肥胖风险中的特定生理路径(HPA轴激活)和行为模式(情绪化进食)，并可以针对这些青少年加强行为体重控制干预。

DESCRIPTION (provided by applicant): Stress-induced eating may be a critical risk factor for the development of obesity in youth. Stress- related activation of the hypothalamic-pituitary-adrenal (HPA) axis and consequent elevations in cortisol play a central role in stress-induced eating. Adolescence is a key developmental period to examine the stress-eating association as it is marked by increased vulnerability to stress and high probability of sustained obesity into adulthood. Low-income adolescents are a particularly high-risk group in this regard and may be especially susceptible to stress-induced eating given the stressful environments in which they live (e.g., neighborhood violence) and vulnerability to eating-specific stressors (e.g., insufficiet food availability). However, the small body of available research on stress-induced eating in youth is limited by 1) failure to examine how cortisol response and patterns of emotional eating interact to impact dietary intake following stress in youth, 2) failure to experimentally manipulat the effects of exposure to a stressor on energy intake in lean versus obese adolescents, and 3) the focus on economically homogenous samples of middle-income families. The proposed study extends the understanding of biobehavioral processes underlying stress-induced eating in youth by concurrently examining associations between cortisol reactivity, emotional eating and objective energy intake in obese and lean low-income adolescents, using a validated experimental paradigm (Trier Social Stress Test for Children; TSST-C) known to produce elevations in cortisol in adolescents. Our preliminary data suggest that obese adolescents show greater cortisol reactivity to the TSST-C compared to lean adolescents. The proposed R03 will compare energy intake in obese (n = 40) and lean (n = 40) low- income adolescents (12-17 years) following stress induction versus a control day. Specific Aims are to: (1) determine if low-income obese adolescents differ from low-income lean adolescents in cortisol reactivity to stress-induction, (2) determine if energy intake following stress is more strongly related to cortisol reactivity among low-income adolescents who score higher on emotional eating, and (3) explore whether cortisol stress reactivity or perceived stress is more predictive of energy intake in adolescents. Consistent with the mission of the NICHD Obesity Research Strategic Core, findings from this study will provide a strong foundation for a programmatic line of research designed to examine the role of cortisol reactivity and emotional eating in the development of obesity in low-income adolescents. The potential public health impact of this study is significant, given that findings will help to identify a subgroup of low-income adolescents at heightened risk for obesity. Perhaps equally important, these data will inform the development of new or augmented interventions tailored for low-income adolescents who are exposed to high-stress environments, by identifying specific physiologic pathways (HPA axis activation) and behavioral patterns (emotional eating) that put these youth at risk for obesity and can be targeted to enhance behavioral weight control intervention.