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

肥胖是一种多因素疾病，是多种基因、行为和环境因素复杂相互作用的结果。遗传风险的增加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之前的研究基础上，全面检查基因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，无论是单独还是联合使用，是否可以改变儿童肥胖的行为和遗传倾向。具体地说，这项研究旨在前瞻性地评估高进食动力(HDE)与体重和肥胖结果一年变化的相关性与来自低资源背景家庭的5至7岁儿童肥胖的遗传风险的相关性是独立的或相加的。HED将被概念化为一种更广泛的行为表型，它结合了过度吞噬的食欲特征(即食物的相对强化价值、快速进食速度和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，GRS是多个肥胖风险单核苷酸多态(SNPs)的综合衡量标准。此外，这项研究旨在前瞻性地检查饮食、体力活动和睡眠领域中可能减轻HDE或高遗传风险对体重和肥胖结果的有害影响的风险修改能量平衡行为，并测试这些因素对HDE的影响是否不同于肥胖对这些结果的高遗传风险。最后，本研究旨在考察家庭功能和父母喂养方面的家庭层面影响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分数、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的影响的行为和家庭因素，对于将儿童肥胖的预防推向新的方向至关重要。如果成功，从这项研究中收集的知识将为解决肥胖症的健康差距和制定针对儿童肥胖症的量身定做的以家庭为基础的干预措施提供新的和强大的目标。

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.