The 1918 Influenza Pandemic and Subsequent Health Outcomes: An Analysis of SIPP Data

摘要

The fetal-origins hypothesis has recently achieved "textbook" status in medicine (e.g., Rudolph, 2003 and Warrell, 2003) and is drawing increasing attention from social scientists (e.g., Case, Fertig and Paxton, 2005; Currie and Moretti, 2005). The hypothesis holds that disruptions to fetal nutrition can exert persistent effects on subsequent health. From the perspective of a health production function, determinants of health may be divided into (ⅰ) post-birth health investments (e.g., vaccinations, diet, Medicare, etc.) and (ⅱ) the initial health endowment. The fetal-origins hypothesis emphasizes the importance of the initial health endowment, often proxied with birth weight, in determining adult health. Despite growing acceptance of the fetal-origins hypothesis by physicians and epidemiologists, the physiologic mechanisms by which fetal damage exerts long-term effects are relatively poorly understood. Experimental evidence from animal studies has established that maternal nutrition has a causal effect on subsequent health. Still, researchers have questioned the causality of statistical associations drawn from human population-based studies of size at birth and subsequent health (e.g., Kathleen M. Rasmussen, 2001). A particular concern is whether omitted factors might bias or even account for the positive correlations between measures of early-life and adult health.