PROJECT SUMMARY
This study will examine the contributions of socioeconomic status (SES) over the lifecourse to epigenetic
age acceleration across adulthood. Numerous studies have established that age-related degenerative disease
and mortality follow SES gradients. Early life SES has been shown to be associated with many markers of
health across the lifecourse independent of SES in adulthood. This suggests that age-related decline is not
simply the result of individual lifestyle decisions in adulthood but that it is also influenced by the
socioeconomic conditions that individuals grow and develop within across the lifecourse. “Epigenetic
clocks,” which measure various dimensions of biological aging using DNA methylation, hold promise to help
describe healthy versus pathological aging. Epigenetic age acceleration, defined as having advanced
estimated epigenetic clock age relative to one’s chronological age, is highly predictive of future age-related
degenerative disease and mortality. Adding to well-documented socioeconomic gradients in biomarkers of
inflammation, immunological function, and cardiovascular disease risk, recent studies have found that
lower SES is associated with increased epigenetic age acceleration, particularly when using epigenetic clocks
trained on clinical or phenotypic markers of aging. However, much of this evidence comes from studies
using retrospective data on SES, which may be affected by recall and other biases. This study is innovative
because it uses rich longitudinal data on SES measured prospectively over two decades among the mother
and offspring participants in the Cebu Longitudinal Health and Nutrition Survey (CLHNS). The CLHNS is
an ongoing birth cohort study that has followed several thousand women and their children in Metropolitan
Cebu, Philippines since 1983. Recent improvements in life expectancy in Cebu have corresponded to an
increased public health burden of age-related disease and functional decline. DNA methylation data from
blood samples collected in 2005 among both generations were used to measure epigenetic age acceleration
from five epigenetic clocks shown to predict future health and aging in the CLHNS. This study addresses
the following aims: 1) Estimate the total and direct associations between lifecourse SES measures and
epigenetic age acceleration in young adulthood (for offspring) and middle adulthood (for mothers) and 2)
In offspring, estimate associations between intergenerational educational attainment trajectories and
epigenetic age acceleration. Training activities will focus on gaining skills in rigorous epidemiological
methods for longitudinal exposures and mediation, including semiparametric methods that incorporate
machine learning algorithms. Grounded in rigorous approaches from social epidemiology, this study will
generate evidence to clarify the contributions of lifecourse SES to epigenetic aging across adulthood, while
also identifying modifiable SES factors that may inform the design of interventions to reduce biological
aging and age-related degenerative disease.
