I study how social and environmental conditions become biologically embedded across the life course, using epigenetic clocks, causal inference methods, and ecosocial theory. I also work on translating and integrating causal inference frameworks across epidemiology, biostatistics, and econometrics.
I am a sixth-year PhD candidate in Anthropology and MPH student in Epidemiology at Northwestern University, supported by an NIH F31 Predoctoral Fellowship from the National Institute on Aging and a prior NSF Graduate Research Fellowship. I complete both degrees in 2026.
Does prenatal exposure to acute political-economic crisis accelerate biological aging decades later? The August 21, 1983 assassination of Benigno Aquino triggered capital flight, rapid inflation, and political revolution in the Philippines, a country already made economically vulnerable by a decade of martial law borrowing. The Cebu Longitudinal Health and Nutrition Survey enrolled pregnant women across 33 metropolitan Cebu barangays from May 1983 to April 1984, bracketing the shock. A difference-in-differences design crosses gestational timing relative to the assassination with location, exploiting that central Cebu City bore the brunt of post-assassination political mobilization and urban economic disruption while peripheral barangays had lower intensity immediate political-economic disruption, allowing us to identify the incremental effect of intensified crisis exposure while partialing out shared prior stressors, such as an El Niño drought affecting all individuals early in gestation. We find no effects on birth outcomes, infant growth, or cardiometabolic health at age 35, and no effects on epigenetic aging at age 21. By age 40, however, prenatal exposure predicts significant acceleration of biological aging across five of six epigenetic clocks, providing a window into clinical disparities that may emerge as the cohort continues to age.
Socioeconomic disparities in biological aging are well documented, but how their sources shift across the life course remains unclear. Using four decades of prospective CLHNS data and nonparametric causal decomposition methods, I find that large childhood wealth disparities in epigenetic aging are already present by age 21 but partially converge by midlife. At age 21, disparities reflect strong early-life biological embedding. By 40, they are shaped less by persistent early-life differences than by unequal biological returns to education, with schooling protecting health most among those who were already advantaged in childhood.
Volunteer-based seroprevalence surveys oversample white, educated, and higher-income participants, producing estimates that can not only attenuate true disparities but reverse them entirely. This study uses a 2020 Chicago community antibody survey to estimate neighborhood-level SARS-CoV-2 infection risk before vaccine rollout, applying Bayesian multilevel regression with poststratification to correct for non-representative sampling and propagate uncertainty in test accuracy. Adjusted estimates revealed a stark gradient: seroprevalence in the most deprived neighborhoods was more than twice that of the most privileged, measured using an index of racialized economic segregation. The unadjusted data showed the opposite pattern. The findings illustrate how standard surveillance methods can obscure the structural inequities they are meant to document.
To learn more about my research and publications, see my CV or my Google Scholar.