Role of energy balance behaviors in modifying biobehavioral risk factors for childhood obesity

能量平衡行为在改变儿童肥胖生物行为危险因素中的作用

• 批准号: 10561378
• 负责人: Tanja V.E. Kral
• 金额: $ 67.16万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 2023
• 资助国家: 美国
• 起止时间: 2023-03-01 至 2027-12-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10561378
• 关键词: Address; Adult; Age; Appetitive Behavior; Area; Behavior; Behavioral; Biology; Body fat; Body mass index; Calories; Child; Child Rearing; Childhood; Chronic Disease; Circadian Rhythms; Complex; Consumption; DNA; Desire for food; Diet; Dietary intake; Disease; Eating; Eating Behavior; Energy Intake; Energy Metabolism; Environment; Family; Family Characteristics; Family Research; Food; Genes; Genetic; Genetic Predisposition to Disease; Genetic Risk; Genotype; Glean; Goals; Heritability; Household; Hunger; Individual; Intervention; Knowledge; Learning; Literature; Measures; Nutritional Study; Obesity; Outcome; Parents; Pattern; Phenotype; Physical activity; Prevention; Prospective Studies; Research; Resources; Rest; Risk; Risk Factors; Role; Sampling; Single Nucleotide Polymorphism; Sleep; Socioeconomic Status; Strategic Planning; Stress; System; Testing; Time; Translating; United States; United States National Institutes of Health; Variant; Weight; Youth; behavioral phenotyping; biobehavior; early childhood; eating in absence of hunger; energy balance; family influence; feeding; fighting; genetic risk factor; health disparity; high risk; minority children; obesity development; obesity in children; obesity prevention; obesity risk; precision nutrition; primary outcome; prospective; protective factors; public health relevance; racial diversity; risk mitigation; trait; waist circumference

Obesity is a multifactorial disease which results from complex interactions among multiple genes, behaviors, and environmental factors. A heightened genetic risk does not always translate to the development of obesity among children, which points to the presence of risk-modifying factors that likely relate to energy balance behaviors as key behavioral drivers. This study will build on our prior research to comprehensively examine the interplay between genotype and phenotype and, for the first time, systematically assess if energy balance behaviors in the context of the family environment, alone or in combination, can modify behavioral and genetic predispositions to childhood obesity. Specifically, this research aims to prospectively evaluate the extent to which associations of a heightened drive to eat (HDE) on 1-year changes in weight and adiposity outcomes are independent or additive to those of a genetic risk for obesity among children, ages 5 to 7, from families with low resource backgrounds. HED will be conceptualized as a broader behavioral phenotype which combines hyperphagic appetitive traits (i.e., the relative reinforcing value of food, a rapid eating rate, and eating in the absence of hunger). Children’s genotype will be assessed using a genetic risk score (GRS), which serves as an aggregate measure from multiple obesity risk single nucleotide polymorphisms (SNPs). In addition, the study aims to prospectively examine risk-modifying energy balance behaviors in areas of diet, physical activity, and sleep that may mitigate the detrimental impact of a HDE or high genetic risk on weight and adiposity outcomes and test whether these factors differ for HDE versus a high genetic risk of obesity on those outcomes. Lastly, the research aims to examine the impact of family-level influences in areas of family functioning and parent feeding on risk-modifying energy balance behaviors in children. Primary outcomes will include 1-year changes in children’s body mass index (BMI) z-score, percent body fat, and waist circumference. Identifying behavioral and family factors that may mitigate the impact of obesity risk on weight and adiposity outcomes is critical for moving the prevention of childhood obesity into a new direction. If successful, the knowledge gleaned from this research will offer new and powerful targets for addressing health disparities in obesity and formulating tailored family-based interventions in the fight against childhood obesity.

肥胖是一种多因素疾病，是多种基因、行为和环境因素之间复杂相互作用的结果。呼吸遗传风险并不总是转化为儿童肥胖的发生，这表明存在可能与肥胖相关的风险调节因素。本研究将建立在我们之前的研究基础上，全面检查基因型和表型之间的相互作用，并首次系统地评估家庭环境中的能量平衡行为是否单独或组合。 ，可以改变行为和遗传倾向具体来说，本研究旨在前瞻性评估胃肠道进食驱动力 (HDE) 与体重和肥胖结果的一年变化的关联程度与儿童肥胖遗传风险的关联程度。来自资源背景较低的家庭的 5 至 7 岁儿童，HED 将被概念化为一种更广泛的行为表型，其中结合了贪食性食欲特征（即食物的相对强化价值、快速进食速度以及在没有食物的情况下进食）。儿童的基因型将使用遗传风险评分（GRS）进行评估，该评分是多种肥胖风险单核苷酸多态性（SNP）的综合衡量标准。此外，该研究旨在前瞻性地研究儿童的风险调节能量平衡行为。饮食、体力活动和睡眠等领域可能会减轻 HDE 或高遗传风险对体重和肥胖结果的不健康影响，并测试这些因素对于 HDE 与肥胖的高遗传风险对这些结果是否有所不同。旨在检查家庭功能和父母喂养方面的家庭层面影响对儿童风险调节能量平衡行为的影响主要结果将包括儿童体重指数 (BMI) z 分数、身体脂肪百分比和的 1 年变化。确定可能减轻肥胖风险对体重和肥胖结果影响的行为和家庭因素对于将儿童肥胖的预防转向新的方向至关重要。如果成功，从这项研究中收集到的知识将提供新的、强有力的目标。解决健康差距问题肥胖问题并制定针对儿童肥胖的量身定制的家庭干预措施。