课题基金 / 基金详情

Biobehavioral Mechanisms Linking Stress and Obesity in Low-Income Children

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:
8401054
负责人:
Julie C Lumeng
金额:
$44.49万
依托单位国家:
美国
项目类别:
财政年份:
2012
资助国家:
美国
项目状态:
已结题
起止时间:
2012-09-25 至 2015-06-30

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项目成果

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中文摘要
翻译
描述(由申请人提供):高度压力和贫困人群更容易肥胖,最终更容易发生肥胖相关的合并症。预防这些不利的健康结果依赖于在生命早期预防肥胖的发展,因为肥胖一旦建立,往往会持续存在,预防比治疗更有效。对于低收入儿童来说,预防肥胖是非常紧迫的,因为肥胖在这一人口中很常见,并可能导致以后生活中的重大健康差异。目前的预防方案效果有限,需要新的干预目标。压力和饮食行为之间的联系是一个潜在的新目标。我们的研究项目集中在低收入家庭儿童的压力,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,降低饱腹感反应,以及对食物发脾气;这些饮食行为反过来可能导致肥胖。然而,这项早期的工作已经清楚地表明,通过饮食行为将压力与肥胖联系起来的途径是复杂和多因素的,涉及生物和行为途径。到目前为止,我们只研究了一部分饮食行为,这些行为可能会在压力和肥胖之间产生联系。其他可能受压力影响的机制,如对食物作为奖励的高度敏感性或延迟食物满足的能力差,尚未在该模型中进行研究。这种饮食行为如何随着时间的推移而聚集和发展,压力的不同方面(即,慢性与直接压力源)与这些行为有关,基因型如何调节这种关联仍然是未知的。我们建议研究这些过程可能是由压力驱动的,并最终导致儿童肥胖。本申请是为了响应RFA- HL-12-037:“联系心理社会压力和行为的机制途径”而提交的,目的是提供对心理和生物行为过程的更深入理解,这些过程将心理社会压力与饮食行为和最终肥胖联系起来。其目标是:目标1:研究低收入家庭儿童7岁时心理社会压力(慢性和即时压力)与促肥胖饮食行为(包括饱腹感反应、食物强化价值和延迟食物满足的能力)和体重指数(BMI)z评分的横截面关系。目的2:在我们的低收入儿童队列中测试压力饮食行为联系的遗传调节因子。目标3:研究生命早期(3岁)慢性应激和应激反应与3至7岁之间促肥胖饮食行为变化的纵向关联。对早期生活中心理社会压力与特定的,良好的表型饮食行为和从童年开始的过度体重增加之间关系的发展的进一步理解可能为低收入儿童(高风险的人口统计学群体)的新型肥胖预防工作带来希望。 公共卫生相关性:心理社会压力与暴饮暴食和肥胖的发展有关,但这些联系的机制还不清楚,特别是在儿童中。对社会背景和人际压力与饮食行为和儿童时期体重过度增加之间关系的发展有了更好的理解,这可能为肥胖预防的新目标带来希望。鉴于心理压力和肥胖在低收入儿童中更为常见,这项工作也可能为解决肥胖流行的社会经济差异带来特别的希望。
英文摘要
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. PUBLIC HEALTH RELEVANCE: Psychosocial stress is linked with overeating and the development of obesity, but the mechanisms underlying these associations are not well-understood, particularly in children. Improved understanding of the development of associations of social-contextual and interpersonal stress with eating behavior and excessive weight gain beginning in childhood may hold promise for novel targets for obesity prevention. Given that psychosocial stress and obesity are both more common among low-income children, the work may also hold particular promise for addressing socioeconomic disparities in obesity prevalence.
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Michigan Institute for Clinical and Health Research (MICHR)
Fundamental Biobehavioral Mechanisms Underlying the Integrated Development of Emotion, Attachment, and Nutritive Intake in the Mother-Infant Dyad
Michigan Institute for Clinical and Health Research (MICHR)
Michigan Institute for Clinical and Health Research (MICHR)
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