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

描述（由申请人提供）：应激性饮食可能是青少年肥胖发展的关键风险因素。应激相关的下丘脑-垂体-肾上腺（HPA）轴的激活和随之而来的皮质醇升高在应激诱导进食中起着核心作用。青春期是研究压力饮食关联的关键发育时期，因为它的特点是更容易受到压力的影响，成年后持续肥胖的可能性也很高。低收入青少年在这方面是一个特别高风险的群体，鉴于他们生活的紧张环境（例如，邻里暴力）和易受饮食特定压力源（例如，食物供应不足）的影响，他们可能特别容易受到应激性饮食的影响。然而，关于青少年应激性饮食的现有研究较少，存在以下限制：1)未能检查皮质醇反应和情绪饮食模式如何相互作用，影响青少年应激后的饮食摄入；2)未能通过实验操纵暴露于压力源对瘦弱与肥胖青少年能量摄入的影响；3)关注中等收入家庭的经济同质样本。本研究通过验证的实验范式（Trier Social Stress Test for Children; TSST-C），扩展了对青少年应激性饮食的生物行为过程的理解，同时研究了肥胖和瘦弱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，该实验范式已知会导致青少年皮质醇升高。我们的初步数据表明，肥胖青少年对TSST-C的皮质醇反应比瘦弱青少年更强。建议的R03将比较肥胖（n = 40）和瘦弱（n = 40）低收入青少年（12-17岁）在压力诱导后与对照日的能量摄入。具体目的是：(1)确定低收入肥胖青少年在应激诱导下的皮质醇反应是否与低收入瘦弱青少年不同；(2)确定应激后的能量摄入是否与情绪性饮食得分较高的低收入青少年的皮质醇反应更密切相关；(3)探索皮质醇应激反应或感知应激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，本研究的发现将为旨在检查皮质醇反应和情绪性饮食在低收入青少年肥胖发展中的作用的程序化研究提供坚实的基础。这项研究对公众健康的潜在影响是巨大的，

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.