Unlike chronological age (the number of years a person has lived), biological age accounts for environmental, genetic and lifestyle factors that influence the pace of age-related changes. Diet is thought to be one such factor; however, the relationship between diet and biological aging is not well understood, and efforts to characterize this relationship have struggled to disentangle the effects of diet from other variables. This doctoral dissertation project will examine the effect of diet on the rate of biological aging using a newly developed epigenetic clock, a biomarker of biological age. This fundamental research will advance knowledge about human biology, life history, and senescence. The project may also inform public health and aging research by quantifying how lifestyle factors like diet "get under the skin" to influence the aging process and age-related disease. In addition, this project will contribute to the education, training and professional development of a female graduate student in a STEM field, and will include science outreach and education activities to engage with K-12 and public audiences.
The mechanisms that regulate the rate of biological aging are unknown but may have origins in the epigenome, a collection of chemical modifications to DNA that influence how genes are turned on or off. The epigenome is able to connect environment to genetics, and therefore plays a key role in explaining how environment and lifestyle factors can shape the pace of biological aging at the molecular level. Recently, age predictor models called epigenetic clocks have been developed that use age-associated changes in the epigenome to generate estimates of biological age. These clocks can be used to study the phenomenon of accelerated aging, where biological age exceeds chronological age. This project will construct a multi-tissue epigenetic clock and use this clock to test the effect of diet on biological age in a non-human primate model. The central hypothesis of this research is that an obesogenic diet accelerates biological aging and caloric restriction slows biological aging. The researchers will collect and analyze genome-wide methylation data from banked liver samples using reduced representation bisulfite sequencing (RRBS) and combine these data with previously collected RRBS data from blood samples. A comparative non-human primate model with similar life history and disease risk can provide important insights into human aging.
This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.
