The fetal-origins hypothesis has recently achieved “textbook” status in medicine (see Co- lin D. Rudolph and Abraham M. Rudolph, 2003; David A. Warrell et al., 2003) and is drawing increasing attention from social scien- tists (e.g., Anne Case et al., 2005; Janet Currie and Enrico Moretti, 2005). The hypothesis holds that disruptions to fetal nutrition can exert persistent effects on subsequent health.1 From the perspective of a health production function, determinants of health may be divided into (i) post-birth health investments (e.g., Medicare) 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 un- derstood. Experimental evidence from animal studies has established that maternal nutrition has a causal effect on subsequent health. Still, re- searchers have questioned the causality of statis- tical associations drawn from human population- based studies of size at birth and subsequent health (e.g., Kathleen M. Rasmussen, 2001).Aparticular concern is whether omitted factors might bias or even account for the positive correlations between measures of early-life and adult health. Recent research has used the 1918 Influenza Pandemic as a natural experiment for studying the effects of fetal health (Almond, 2003). In contrast to typical influenza strains, the 1918 * Almond: Department of Economics, Columbia Univer- sity, 420 W. 118th Street, New York, NY 10027; Mazum- der: Federal Reserve Bank of Chicago. Views expressed here do not necessarily reflect those of the Federal Reserve System. Almond gratefully acknowledges financial support from the National Institute on Aging, grant no. R03 AG0239-01. 1 Also known as the “Barker Hypothesis,” for research by epidemiologist David Barker at the University of Southampton. 258 virus disproportionately affected young adults: approximately one-third of pregnant women contracted the debilitating virus. The Pandemic arrived without warning and was highly con- centrated between October 1918 and January 1919. As a result, the long-term damage pre- dicted by the fetal-origins hypothesis is simi- larly concentrated. Approximately two-thirds of those in utero during the height of the Pandemic would have been born in the first six months of 1919. In order to bias estimates of long-term fetal effects, post-birth health investments would have to behave in the same abrupt man- ner as the Pandemic. Using Decennial Census data for 1960–1980, Almond (2003) found that cohorts in utero dur- ing the height of the Pandemic displayed re- duced educational attainment, increased rates of disability, lower income, and lower socioeco- nomic status. However, the absence of specific health outcomes in the Census precludes iden- tification of physiologic pathways and therefore limits the relevance of the findings for physi- cians and epidemiologists. Using data from the Survey of Income and Program Participation (SIPP), this study finds that cohorts in utero during the Pandemic ex- hibit impaired health outcomes relative to co- horts born a few months earlier or later. That these patterns are manifest 65–80 years after the Pandemic suggests that changes to fetal health can have life-long effects.
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