Douglas Almond

Human Capital Development Before Age Five

This chapter seeks to set out what economists have learned about the effects of early childhood influences on later life outcomes, and about ameliorating the effects of negative influences. We begin with a brief overview of the theory which illustrates that evidence of a causal relationship between a shock in early childhood and a future outcome says little about whether the relationship in question is biological or immutable. We then survey recent work which shows that events before five years old can have large long term impacts on adult outcomes. Child and family characteristics measured at school entry do as much to explain future outcomes as factors that labor economists have more traditionally focused on, such as years of education. Yet while children can be permanently damaged at this age, an important message is that the damage can often be remediated. We provide a brief overview of evidence regarding the effectiveness of different types of policies to provide remediation. We conclude with a list of some of the many outstanding questions for future research.

Is the 1918 Influenza Pandemic Over? Long‐Term Effects of In Utero Influenza Exposure in the Post‐1940 U.S. Population

This paper uses the 1918 influenza pandemic as a natural experiment for testing the fetal origins hypothesis. The pandemic arrived unexpectedly in the fall of 1918 and had largely subsided by January 1919, generating sharp predictions for long‐term effects. Data from the 1960–80 decennial U.S. Census indicate that cohorts in utero during the pandemic displayed reduced educational attainment, increased rates of physical disability, lower income, lower socioeconomic status, and higher transfer payments compared with other birth cohorts. These results indicate that investments in fetal health can increase human capital.

Inside the War on Poverty: The Impact of Food Stamps on Birth Outcomes

This paper evaluates the health impacts of a signature initiative of the War on Poverty: the introduction of the modern Food Stamp Program (FSP). Using variation in the month FSP began operating in each U.S. county, we find that pregnancies exposed to FSP three months prior to birth yielded deliveries with increased birth weight, with the largest gains at the lowest birth weights. We also find small but statistically insignificant improvements in neonatal mortality. We conclude that the sizable increase in income from FSP improved birth outcomes for both whites and African Americans, with larger impacts for African American mothers.

The Costs of Low Birth Weight

Low birth weight (LBW) infants experience severe health and developmental difficulties that can impose large costs on society. However, estimates of the return to LBW-prevention from cross-sectional associations may be biased by omitted variables, such as genetic factors. To address this, we compare the hospital costs, health at birth, and infant mortality rates between heavier and lighter infants from all twin pairs born in the United States. We also examine the effect of maternal smoking during pregnancy—the leading risk factor for LBW in the United States—on health among singleton births after controlling for detailed background characteristics. Both analyses imply substantially smaller effects of LBW per se than previously thought, suggesting two possibilities: 1) existing estimates overstate the true costs and consequences of LBW by at least a factor of four and by as much as a factor of twenty; or 2) different LBW-preventing interventions have different health and cost consequences, implying that policy efforts that presume a single return to reducing LBW will be suboptimal.

Trivers–Willard at birth and one year: evidence from US natality data 1983–2001

Trivers & Willard (TW) hypothesized that evolution would favour deviations from the population sex ratio in response to parental condition: parents in good condition would have more sons and parents in poor condition would have more daughters. We analyse the universe of US linked births and infant deaths to white mothers 1983–2001, covering 48 million births and 310 000 deaths. We find that (i) married, better educated and younger mothers bore more sons and (ii) infant deaths were more male if the mother was unmarried and young. Our findings highlight the potential role of offspring sex ratio as an indicator of maternal status, and the role of infant mortality in shaping a TW pattern in the breeding population.

The 1918 influenza pandemic and subsequent health outcomes : An analysis of SIPP data

The fetal-origins hypothesis has recently achieved “textbook” status in medicine (see Colin D. Rudolph and Abraham M. Rudolph, 2003; David A. Warrell et al., 2003) and is drawing increasing attention from social scientists (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. 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 fetalorigins 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 populationbased 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. 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 virus disproportionately affected young adults: approximately one-third of pregnant women contracted the debilitating virus. The Pandemic arrived without warning and was highly concentrated between October 1918 and January 1919. As a result, the long-term damage predicted by the fetal-origins hypothesis is similarly 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 manner as the Pandemic. Using Decennial Census data for 1960–1980, Almond (2003) found that cohorts in utero during the height of the Pandemic displayed reduced educational attainment, increased rates of disability, lower income, and lower socioeconomic status. However, the absence of specific health outcomes in the Census precludes identification of physiologic pathways and therefore limits the relevance of the findings for physicians and epidemiologists. Using data from the Survey of Income and Program Participation (SIPP), this study finds that cohorts in utero during the Pandemic exhibit impaired health outcomes relative to cohorts 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.

Lingering prenatal effects of the 1918 influenza pandemic on cardiovascular disease

Prenatal exposure to the 1918 influenza pandemic (Influenza A, H1N1 subtype) is associated with ⩾20% excess cardiovascular disease at 60 to 82 years of age, relative to cohorts born without exposure to the influenza epidemic, either prenatally or postnatally (defined by the quarter of birth), in the 1982-1996 National Health Interview Surveys of the USA. Males showed stronger effects of influenza on increased later heart disease than females. Adult height at World War II enlistment was lower for the 1919 birth cohort than for those born in adjacent years, suggesting growth retardation. Calculations on the prevalence of maternal infections indicate that prenatal exposure to even uncomplicated maternal influenza may have lasting consequences later in life. These findings suggest novel roles for maternal infections in the fetal programming of cardiovascular risk factors that are independent of maternal malnutrition.

Civil Rights, the War on Poverty, and Black-White Convergence in Infant Mortality in the Rural South and Mississippi

For the last sixty years, African-Americans have been 75% more likely to die during infancy as whites. From the mid-1960s to the early 1970s, however, this racial gap narrowed substantially. We argue that the elimination of widespread racial segregation in Southern hospitals during this period played a causal role in this improvement. Our analysis indicates that Title VI of the 1964 Civil Rights Act, which mandated desegregation in institutions receiving federal funds, enabled 5,000 to 7,000 additional black infants to survive infancy from 1965-1975 and at least 25,000 infants from 1965-2002. We estimate that by themselves these infant mortality benefits generated a welfare gain of more than

Health Capital and the Prenatal Environment: The Effect of Maternal Fasting During Pregnancy

7 billion (2005

Impacts of classifying New York City students as overweight

) for 1965-1975 and more than