The Impact of Obesity, Cardiovascular Diseases and Diabetes on Labor Market Participation and Productivity

自1975年以来，全世界的肥胖人数几乎增加了两倍。尽管估计表明肥胖的遗传率超过60%，但进化的人类表型不能用基因型的变化来解释，因为它发生得太快了。因此，对肥胖流行的普遍解释是基因与环境的相互作用。虽然基因型在中期是由外源决定和固定的，但个体对不断变化的致肥环境（节省劳动力的技术、价格、可获得性和食物的能量含量）的反应在很大程度上是遗传的。这些观察结果是我们研究的灵感来源。拟议的研究项目包括三个工作包。第一个工作包侧重于实证估计肥胖、糖尿病、心血管疾病和高血压对就业、工资和其他劳动力市场结果的因果影响。我们使用遗传标记作为疾病的工具，并通过控制暴露于日益肥胖的环境的持续时间来考虑基因与环境的相互作用。我们使用了从健康与退休研究（HRS）中获得的1900年至1958年间出生的美国成年人的大样本的基因型数据和劳动力市场结果，并将其与从全基因组关联研究中获得的遗传信息结合起来。在工作包2中，我们研究了肥胖与人类衰老过程中其他健康缺陷的发展之间的关系。我们通过构建一个脆弱指数来衡量个人的健康状况，该指数将生物衰老过程定义为内在的、累积的、渐进的和有害的功能丧失。我们使用与WP 1相同的数据源和工具变量策略来确定肥胖对生理性衰老的影响。然后，我们测试肥胖对劳动力市场结果的影响是否以及在多大程度上是通过不断增加的虚弱来调节的。在工作包3中，我们利用实证研究结果发展了一种新的肥胖经济学理论，该理论解释了体重的演变及其对健康、老龄化、生产力和劳动力供给的影响。具体而言，我们进一步发展了健康赤字模型，该模型使用脆弱指数作为衡量人类健康和衰老的指标。我们还研究了有限理性行为在不完全自我控制和时间不一致决策中的作用。我们使用HRS数据和WP 1和WP 2的结果校准了模型的数值版本，并使用这些模型来推断食品价格变化、医疗进步和遏制肥胖流行的政策干预所引发的行为变化。

Worldwide obesity has nearly tripled since 1975. Although estimates suggest heritability of obesity of more than 60 percent, the evolving human phenotype cannot be explained by a changing genotype because it occurred too rapidly. The prevailing explanation for the obesity epidemic is thus gene-environment interaction. While genotypes are exogenously determined and fixed in the medium run, the individual response to a changing obesogenic environment (labor saving technology, price, availability, and energy content of food) is largely genetic. These observations are the inspiration for our study.The proposed research project consists of three work packages. The first work package focuses on empirically estimating the causal effect of obesity, diabetes, CVDs, and hypertension on employment, wages, and other labor market outcomes. We use genetic markers as instruments for the diseases and take gene-environment interaction into account by controlling for the duration of exposure to an increasingly obesogenic environment. We use genotyped data and labor market outcomes from a large panel of US American adults born between 1900 and 1958 obtained from the Health and Retirement Study (HRS) and combine it with genetic information obtained from genome-wide association studies.In work package 2, we investigate the association between obesity and the development of other health deficits in the course of human aging. We measure individual health by constructing a frailty index, which captures in one number the biological aging process defined as the intrinsic, cumulative, progressive, and deleterious loss of function. We use the same data sources and instrumental variable strategy as WP 1 to determine the impact of obesity on physiological aging. We then test whether and to which extent the impact of obesity on labor market outcomes is mediated through increasing frailty. In work package 3 we use the empirical findings to develop a new economic theory of obesity, which explains the evolution of body weight and its impact on health, aging, productivity, and labor supply. Specifically, we further develop the health deficit model, which uses the frailty index as measure of human health and aging. We also investigate the role of bounded rational behavior in form of imperfect self-control and time inconsistent decision making. We calibrate numerical versions of the model with the HRS data and the results from WP 1 and 2 and use these models for inferences on the behavioral changes that are elicited by changing food prices, medical progress, and policy interventions to curb the obesity epidemic.