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.
My dissertation uses the Cebu Longitudinal Health and Nutrition Survey and Philippine DHS data to examine how political, environmental, and institutional exposures shape health and aging across the life course.
This study estimates long-run effects of third-trimester exposure to two sequential shocks on a 1983-84 Filipino birth cohort: an El Nino drought among the most severe in four centuries, and the assassination of Ninoy Aquino, which triggered a national political-economic crisis and regime change. Peak drought births were born larger yet showed more wasting at age 2, greater visceral fat and hypertension at 35, and faster epigenetic aging at ages 21 and 40. Direct effects persisted after accounting for maternal nutrition, infant feeding, and early diarrhea. Assassination exposure had no detectable birth outcome effects but predicted faster epigenetic aging and higher hypertension at 35, concentrated in urban areas where political mobilization was most intense. In a context defined more by climate and political uncertainty than overt nutritional deprivation, prenatal stress programmed development, leaving detectable long-run epigenetic signatures.
The long-run biological consequences of disaster-induced human capital losses are understudied. This study estimates the effects of childhood housing damage from Typhoon Ruping (1990) on epigenetic aging at age 40 in the CLHNS cohort. The pooled effect is near-null, but housing damage accelerated biological aging among urban and peri-urban participants while leaving rural participants unaffected, consistent with heterogeneous returns to education across labor market contexts. High school completion predicted slower aging in urban but not rural settings despite equivalent schooling losses in both strata.
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.