Biobehavioral Mechanisms Linking Stress and Obesity in Low-Income Children

低收入儿童压力与肥胖之间的生物行为机制

基本信息

批准号：
8549242
负责人：
Julie C Lumeng
金额：
$ 47.84万
依托单位：
UNIVERSITY OF MICHIGAN AT ANN ARBOR
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-09-25 至 2015-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8549242
关键词：
3 year old 7 year old Accounting Address Affect Age Alleles Area Arthritis Asthma Attention Behavior Behavioral Behavioral Mechanisms Body mass index Cardiovascular Diseases Child Childhood Chronic Chronic stress Comorbidity Complex Data Development Dopamine D2 Receptor Early Intervention Eating Behavior Effectiveness Food Genes Genetic Genetic screening method Genotype Goals Health Hydrocortisone Hyperphagia Individual Differences Intervention Lead Life Life Cycle Stages Life Stress Link Literature Longevity Low income Mediating Modeling Nursery Schools Obesity Outcome Parents Pathway interactions Pattern Phenotype Population Prevalence Prevention Prevention program Process Psychosocial Stress Regulation Reporting Research Rewards Satiation Stimulus Stress Time Weight Gain Work aged biobehavior child well being cohort early childhood eating in absence of hunger effective therapy experience health disparity high risk improved novel obesity in children obesity prevention prevent programs psychologic public health relevance response social socioeconomics stressor

项目摘要

DESCRIPTION (provided by applicant): Highly stressed and impoverished populations are more likely to be obese, and ultimately more likely to develop obesity-associated comorbidities. Preventing these adverse health outcomes relies on preventing the development of obesity early in the life span, since obesity, once established, tends to persist and prevention is more effective than treatment. Preventing obesity is highly urgent for low-income children, since obesity is common early on in this demographic and may contribute to substantial health disparities later in life. Current prevention programs have limited effectiveness, and novel targets for intervention are needed. The association between stress and eating behavior is one potential novel target. Our research program focuses on links between stress, eating behavior, and obesity in low-income children. Our preliminary findings suggest that, in early childhood, patterns of cortisol secretion reflecting chronic stress may promote eating in the absence of hunger, reduced satiety responsiveness, and tantrums over food; these eating behaviors, in turn, may lead to obesity. This early work has made clear, however, that the pathways linking stress to obesity via eating behavior are complex and multifactorial, and involve biologic and behavioral pathways. To date we have examined only a subset of eating behaviors that could mediate links between stress and obesity. Other mechanisms that may be affected by stress, such as high sensitivity to food as a reward or poor ability to delay gratification for food, have not been examined in this model. How such eating behaviors may cluster and develop over time, how different aspects of stress (i.e., chronic vs. immediate stressors) relate to these behaviors, and how genotypes may moderate such associations remains unknown. We propose to examine how these processes may be driven by stress, and ultimately lead to obesity in children. This application is submitted in response to RFA- HL-12-037: "Mechanistic Pathways Linking Psychosocial Stress and Behavior" with the goal of providing a deeper understanding of the psychological and bio-behavioral processes that connect psychosocial stress with eating behaviors and ultimately obesity. The aims are: Aim 1: To examine the cross-sectional relationship of psychosocial stress (chronic and immediate stress) with obesity-promoting eating behaviors (including satiety responsiveness, reinforcing value of food, and the ability to delay gratification for food) and body mass index (BMI) z-score at age 7 years among low-income children. Aim 2: To test genetic moderators of stress-eating behavior links in our cohort of low-income children. Aim 3: To examine longitudinal associations of chronic stress and reactivity to stress early in life (age 3 years) with changes in obesity-promoting eating behaviors between ages 3 and 7 years. Improved understanding of the development of associations of psychosocial stress during early life with specific, well-phenotyped eating behaviors and excessive weight gain beginning in childhood may hold promise for novel obesity prevention efforts among low-income children, a demographic group at high risk.

描述（由申请人提供）：压力大和贫困的人群更有可能肥胖，并最终更有可能出现与肥胖相关的合并症。预防这些不良健康结果依赖于在生命早期预防肥胖的发生，因为肥胖一旦形成，往往会持续存在，而预防比治疗更有效。对于低收入儿童来说，预防肥胖非常紧迫，因为肥胖在这一人群的早期很常见，并且可能会导致以后生活中巨大的健康差异。目前的预防计划效果有限，需要新的干预目标。压力和饮食行为之间的关联是一个潜在的新目标。我们的研究项目重点关注低收入儿童的压力、饮食行为和肥胖之间的联系。我们的初步研究结果表明，在儿童早期，反映慢性压力的皮质醇分泌模式可能会促进在没有饥饿的情况下进食、降低饱腹感和对食物发脾气；这些饮食行为反过来可能导致肥胖。然而，这项早期工作已经明确表明，通过饮食行为将压力与肥胖联系起来的途径是复杂且多因素的，并且涉及生物和行为途径。迄今为止，我们只研究了一部分可能介导压力和肥胖之间联系的饮食行为。该模型尚未研究可能受压力影响的其他机制，例如对食物作为奖励的高度敏感性或延迟食物满足的能力较差。这些饮食行为如何随着时间的推移聚集和发展，压力的不同方面（即慢性压力源与直接压力源）如何与这些行为相关，以及基因型如何调节这种关联仍然未知。我们建议研究这些过程是如何由压力驱动的，并最终导致儿童肥胖。本申请是为了响应 RFA-HL-12-037：“连接心理社会压力和行为的机制途径”而提交，目的是更深入地了解将心理社会压力与饮食行为以及最终肥胖联系起来的心理和生物行为过程。。目标是：目标 1：研究心理社会压力（慢性和即时压力）与肥胖促进饮食行为（包括饱腹感反应、增强食物价值以及延迟对食物满足的能力）和身体的横断面关系低收入儿童 7 岁时的体重指数 (BMI) z 得分。目标 2：测试低收入儿童群体中压力饮食行为关联的遗传调节因素。目标 3：研究生命早期（3 岁）慢性压力和对压力的反应与 3 至 7 岁之间促进肥胖的饮食行为变化之间的纵向关联。更好地了解生命早期心理社会压力与特定的、表型良好的饮食行为以及童年开始的体重过度增加之间的关系，可能为低收入儿童（高风险人口群体）的新肥胖预防工作带来希望。