Genes, Education, and Gene-Education Interactions in Obesity and Mental Health

项目摘要 解决肥胖和抑郁症对人口健康至关重要，尤其是因为它们与 糖尿病，心脏病，中风和自杀，这反过来又导致了2015年美国预期寿命的下降。 《健康人2020》倡导的一项减少肥胖和抑郁症的政策是增加教育 这是一个很大的问题，因为它被视为健康差距的根本原因。就像肥胖和抑郁症 强有力的遗传基础，教育有可能通过调节 通过基因-环境（GxE）相互作用导致肥胖/抑郁的潜在遗传风险。GXE 当遗传风险的影响因环境而异时，就会发生相互作用。基因的影响 肥胖的可能性的倾向可能因教育程度而异。一个大学毕业生 肥胖的高遗传风险的人可能永远不会肥胖，因为教育与高收入有关 让个人吃得更健康，并有同龄人谁是意识到领导健康的生活方式。在 相比之下，具有高遗传风险的高中辍学者更有可能肥胖，因为他/她有低遗传风险。 收入，更有可能消费快餐，并与肥胖的同龄人互动。拟议项目将 应用计量经济学方法，工具变量和同胞内比较，使用准实验 教育程度的变化，以增加我们对教育，基因和 GxE对肥胖和抑郁症的相互作用。在一定条件下，准实验变量的使用 假设，产生的估计不受（i）未观察到的因素的影响， 与教育和健康相关，（ii）反向因果关系，（iii）基因-环境相关性，（iv）人口 分层，因此，这些估计可以给出一个因果解释的条件下，这些 假设。具体的目的是估计教育，遗传风险和GxE相互作用的主要影响， 肥胖和抑郁症使用（i）复活节学校离开规则作为自然实验在英国和数据 来自英国生物库，（ii）个人居住县接近中学毕业的当地因素 年龄（大学入学率、教育支出、失业率）作为教育工具， 全国健康与营养调查和全国青少年健康纵向研究（增补 健康）数据集，以及（iii）添加健康数据集中的兄弟固定效应方法。总体而言，该项目将 提供了一系列全面的结果和新的见解，因为我们比较了不同方法的结果， 数据集，不同教育水平和性别。该应用程序是对NIH PAR的直接响应- 16-080“教育和健康：新的前沿。

PROJECT SUMMARY Tackling obesity and depression is vital for population health, not least because they are associated with diabetes, heart disease, strokes, and suicide, which in turn led to the decrease in US life expectancy in 2015. One policy advocated by Healthy People 2020 to reduce obesity and depression is increasing educational attainment, as it is viewed as a fundamental cause of health disparities. As obesity and depression also have strong genetic bases, it is possible that education additionally improves population health by moderating the underlying genetic risk of being obese/depressed through gene-environment (GxE) interactions. GxE interactions occur when the effect of genetic risk varies across the environment. The influence of genetic predisposition towards the likelihood of being obese may differ by educational attainment. A college graduate with a high genetic risk of being obese may never be obese because education is associated with higher income affording the individual to eat healthier and having peers who are conscious about leading a healthy lifestyle. In contrast, a high school dropout with a high genetic risk is more likely to be obese because he/she has a low income, is more likely to consume fast food, and interacts with peers who are obese. The proposed project will apply econometric methods, instrumental variables and within-sibling comparisons, that use quasi-experimental variation in educational attainment to increase our understanding of causal relations of education, genes, and GxE interactions on obesity and depression. The use of quasi-experimental variation will, under certain assumptions, produce estimates that are not confounded by (i) the influence of unobserved factors that are correlated with education and health, (ii) reverse causality, (iii) gene-environment correlations, and (iv) population stratification, and these estimates can therefore be given a causal interpretation conditional on these assumptions. The specific aims are to estimate main effects of education, genetic risk, and GxE interactions on obesity and depression using (i) the Easter School Leaving Rule as a natural experiment in the UK and data from the UK Biobank, (ii) local factors in the individual’s county of residence near secondary school completion age (college availability, education expenditures, unemployment rate) as instruments for education in the National Health and Nutrition Examination Survey and the National Longitudinal Study of Adolescent Health (Add Health) datasets, and (iii) the sibling fixed-effects approach in the Add Health dataset. Overall, the project will provide a comprehensive array of results and new insights as we compare results from different methods, datasets, across different educational levels, and by gender. This application is in direct response to NIH PAR- 16-080 “Education and Health: New Frontiers.”