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。高遗传风险并不总是转化为儿童肥胖的发展，这表明存在风险修正因素，这些因素可能与能量平衡行为有关，是关键的行为驱动因素。这项研究将建立在我们以前的研究，全面研究基因型和表型之间的相互作用，并首次系统地评估在家庭环境中的能量平衡行为，单独或组合，是否可以改变儿童肥胖的行为和遗传倾向。具体而言，本研究旨在前瞻性地评估增强的进食欲望（HDE）对体重和肥胖结果的1年变化的关联在多大程度上独立于或添加到来自低资源背景家庭的5至7岁儿童的肥胖遗传风险。HED将被概念化为一种更广泛的行为表型，其结合了贪食食欲特征（即，食物的相对强化价值，快速进食速度，以及在没有饥饿的情况下进食）。儿童的基因型将使用遗传风险评分（GRS）进行评估，该评分作为多个肥胖风险单核苷酸多态性（SNP）的综合指标。此外，该研究旨在前瞻性地检查饮食，体力活动和睡眠领域的风险修正能量平衡行为，这些行为可能减轻HDE或高遗传风险对体重和肥胖结果的不利影响，并测试这些因素是否不同HDE与肥胖的高遗传风险对这些结果的影响。最后，本研究旨在探讨家庭功能和父母喂养对儿童风险修正能量平衡行为的影响。主要结果将包括儿童体重指数（BMI）z评分、体脂百分比和腰围的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预防推向新的方向至关重要。如果成功的话，从这项研究中收集到的知识将为解决肥胖症的健康差异和制定针对儿童肥胖症的家庭干预措施提供新的和强有力的目标。