The Relation of Genetic Factors, Food Cues, and Self-Regulation with Excess Consumption and Adiposity in Children

项目摘要 儿童肥胖症是一个严重的公共卫生问题，影响着大约1250万儿童和青少年 在美国在我们目前的肥胖环境中，儿童经常可以获得高度 可口的食品，如含有高水平糖、盐和脂肪的包装食品。重要的是，大多数儿童 即使他们已经吃得很饱，也会继续食用美味的食物。该过量 在没有饥饿的情况下进食（EAH）与儿童体重增加有关。的 本研究的总体假设是，一些儿童在遗传上易患EAH， 对环境食物线索的反应，并进一步认为自我调节能力可以保护儿童免受这种影响。 奖励驱动的暴饮暴食拟议的目标是我们初步研究的一个重大扩展 （1R21HD 076097），提供了初步证据，表明脂肪中的肥胖风险等位基因 质量和肥胖相关（FTO）基因与更大的EAH和脑奖励区活动有关， 食物线索我们最初的探索性奖励导致了有趣的发现，提出了一些新的令人兴奋的问题 和研究方向。在我们目前的扩展研究中，我们将直接评估食物提示相关的神经系统是否会发生变化。 活动与提示EAH和肥胖增加有关，这是一个具有重要公共卫生意义的结果。我们将 还纳入了自我调节能力的强大措施，以研究这种可改变的特征如何影响 EAH的神经奖赏活动与随后的肥胖增加之间的关联。我们扩大的研究 这也将促进我们对肥胖受其他因素影响的生物机制的理解。 已知的遗传性肥胖风险因素，如黑皮质素4受体（MC4R）基因。这项扩展研究使用了 全面的，多学科的方法，以增加我们对遗传因素如何相互作用的理解， 环境食物线索影响儿童肥胖饮食行为。大多数孩子每天都有很高的 暴露于外部食物线索。除了整天闻到和看到实际的食物外，许多 儿童还通过电视和互联网食品广告的形式体验到许多食品提示， 快速的渴望和EAH。事实上，食品制造商每年花费大约18亿美元， 通过电视广告、互联网等方式向12岁以下儿童推销可口食品 横幅和弹出式广告，以及互联网广告游戏。因此，提示EAH可能是孩子的重要驱动力 肥胖症的流行研究结果将对个性化的儿童肥胖症有重要意义 干预和预防计划，也将影响电视和互联网上的公共政策话语 向儿童做不健康食品的广告。在一个超过三分之一的儿童超重或 肥胖，必须了解和系统地改变环境因素，导致过度 消费

Project Summary Childhood obesity is a critical public health problem that affects approximately 12.5 million children and teens in the United States. In our current obesogenic environment, children frequently have access to highly palatable foods such as packaged foods containing high levels of sugar, salt and fat. Importantly, most children will continue to consume highly palatable foods, even after they have eaten to satiety. This excess consumption, termed eating in the absence of hunger (EAH), is associated with child weight gain. The overarching hypothesis of the present study is that some children are genetically predisposed to EAH in response to environmental food cues, and further that self-regulatory capacity can protect children from this reward-driven overeating. The proposed aims are a major expansion of our preliminary study (1R21HD076097) in 9-10 year olds (n=172) that provides initial evidence that obesity risk alleles in the fat mass and obesity-associated (FTO) gene relate to greater EAH and brain reward-region activity in response to food cues. Our initial exploratory award led to intriguing findings that raise a number of new exciting questions and research directions. In our current expanded study, we will directly assess whether food-cue-related neural activity relates to cued EAH and adiposity gain—an outcome with critical public health significance. We will also incorporate a robust measure of self-regulatory capacity to study how this modifiable trait influences the association between neural reward activity with EAH and subsequent adiposity gain. Our expanded research will also advance our understanding of the biological mechanisms by which adiposity is affected by other known genetic obesity risk factors like melanocortin 4 receptor (MC4R) gene. This expanded study uses a comprehensive, multidisciplinary approach to increase our understanding of how genetic factors interact with environmental food cues to affect obesogenic eating behaviors in children. Most children have a very high daily exposure to external food cues. In addition to smelling and seeing actual food throughout the day, many children also experience numerous food cues in the form of TV and Internet food advertisements (ads) that can prompt cravings and EAH. Indeed, food manufacturers spend approximately 1.8 billion dollars a year marketing highly palatable foods to children under 12 years old through methods such as TV ads, Internet banner and pop-up ads, and Internet advergames. Thus, cued EAH could be an important driver of the child obesity epidemic. The study findings will have important implications for individualized child obesity intervention and prevention programs, and will also impact the public policy discourse on TV and Internet advertising of unhealthy foods to children. In a country where over one third of children are overweight or obese, it is essential to understand and systematically change environmental factors that lead to excess consumption.