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

• 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
• 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

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）：高度压力和贫困的人口更有可能肥胖，最终更有可能发展与肥胖相关的合并症。防止这些不良健康结果依赖于防止生命范围内肥胖的发展，因为一旦建立，肥胖就倾向于持久，预防比治疗更有效。对于低收入儿童来说，预防肥胖是高度紧急的，因为肥胖症在这种人群的早期很普遍，并且可能在以后的生活中会导致重大健康差异。当前的预防计划的有效性有限，需要进行干预的新目标。压力与饮食行为之间的关联是一个潜在的新目标。我们的研究计划着重于低收入儿童的压力，饮食行为和肥胖之间的联系。我们的初步发现表明，在幼儿期，反映慢性压力的皮质醇分泌模式可能会在没有饥饿感，饱腹感反应性降低以及对食物上发脾气的情况下促进饮食。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，并且涉及生物学和行为途径。迄今为止，我们只检查了一部分饮食行为，这些行为可以调节压力与肥胖之间的联系。在此模型中尚未检查其他可能受压力影响的机制，例如对食物的高度敏感或延迟对食物满足的能力的不良能力。这种饮食行为可能会随着时间的流逝而聚集并发展，压力的不同方面（即慢性和直接压力源）与这些行为如何相关，以及基因型如何调节此类关联仍然未知。我们建议研究如何通过压力驱动这些过程，并最终导致儿童肥胖。该应用是针对RFA-HL-12-037提交的：“将社会心理压力和行为联系起来的机械途径”，目的是对将心理心理压力与饮食行为与饮食行为和最终肥胖联系起来的心理和生物行为过程有更深入的了解。目的是：目标1：检查社会心理压力（慢性和直接压力）与促进肥胖的饮食行为的横断面关系（包括饱腹感反应，增强食物的价值以及延迟食物的满足能力）和体重指数（BMI）在7岁时的Z分数（BMI）。目标2：测试我们低收入儿童队列中应激行为联系的遗传主持人。目标3：检查生命早期（3岁）的慢性压力和对压力的反应性的纵向关联，促进肥胖的饮食行为的变化3至7岁。对早期生活中的社会心理压力的发展发展与特定，良好的饮食行为和体重增加的过度增长的发展有望有望有望在低收入儿童中有希望，这是一个高风险的人群群体。