Heterogeneity in disease resistance and the impact of antibiotics in the US.

We hypothesize that the impact of antibiotics is moderated by a population's inherent (genetic) resistance to infectious disease. Using the introduction of sulfa drugs in 1937, we show that US states that are more genetically susceptible to infectious disease saw larger declines in their bacterial mortality rates following the introduction of sulfa drugs in 1937. This suggests area-level genetic endowments of disease resistance and the discovery of medical technologies have acted as substitutes in determining levels of health across the US. We also document immediate effects of sulfa drug exposure to the age of the workforce and cumulative effects on educational attainment for cohorts exposed to sulfa drugs in early life.

Multigenerational Effects of Early-Life Health Shocks.

A large literature has documented links between harmful early-life exposures and later-life health and socioeconomic deficits. These studies, however, have typically been unable to examine the possibility that these shocks are transmitted to the next generation. Our study uses representative survey data from the United States to trace the impacts of in utero exposure to the 1918 influenza pandemic on the outcomes of the children and grandchildren of those affected. We find evidence of multigenerational effects on educational, economic, and health outcomes.

Can education rescue genetic liability for cognitive decline?

Although there is a vast literature linking education and later health outcomes, the mechanisms underlying these associations are relatively unknown. In the spirit of some medical literature that leverages developmental abnormalities to understand mechanisms of normative functioning, we explore the ability of higher educational attainments to "rescue" biological/genetic liabilities in brain function through inheritance of a variant of the APOE gene shown to lead to cognitive decline, dementia, and Alzheimer's disease in old age. Deploying a between-sibling design that allows quasi-experimental variation in genotype and educational attainment within a standard gene-environment interaction framework, we show evidence that the genetic effects of the "risky" APOE variant on old-age cognitive decline are absent in individuals who complete college (vs. high school graduates). Auxiliary analyses suggest that the likely mechanisms of education are most consistent through changing brain processes (i.e., "how we think") and potentially building cognitive reserves, rather than alleviating old age cognitive decline through the channels of higher socioeconomic status and resources over the life course.

Interactive effects of in utero nutrition and genetic inheritance on cognition: new evidence using sibling comparisons.

A large literature links early environments and later outcomes, such as cognition; however, little is known about the mechanisms. One potential mechanism is sensitivity to early environments that is moderated or amplified by the genotype. With this mechanism in mind, a complementary literature outside economics examines the interaction between genes and environments, but often problems of endogeneity and bias in estimation are uncorrected. A key issue in the literature is exploring environmental variation that is not exogenous, which is potentially problematic if there are gene-environment correlation or gene-gene interactions. Using sibling pairs with genetic data in the Wisconsin Longitudinal Study we extend a previous, and widely cited, gene-environment study that explores an interaction between the FADS2 gene, which is associated with the processing of essential fatty acids related to cognitive development, and early life nutrition in explaining later-life IQ. Our base OLS findings suggest that individuals with specific FADS2 variants gain roughly 0.15 standard deviations in IQ for each standard deviation increase in birth weight, our measure of the early nutrition environment; while, individuals with other variants of FADS2 do not have a statistically significant association with early nutrition, implying the genotype is influencing the effects of environmental exposure. When including family-level fixed effects, however, the magnitude of the gene-environment interaction is reduced by half and statistical significance dissipates, implying the interaction between FADS2 and early nutrition in explaining later life IQ may in part be due to unobserved, family-level factors. The example has wider implications for the practice of investigating gene-environment interactions when the environmental exposure is not exogenous and robustness to unobserved variation in the genome is not controlled for in the analysis.