New study links faster biological aging to diabetes and social factors
For years, scientists have tried to understand and measure how people age. While birthdates tell us how long someone has lived, they don’t necessarily explain how their body has biologically progressed.
To bridge that gap, researchers must look beyond a person’s chronological age and examine the biological aging processes that account for biological factors and the interplay with environmental factors. One tool scientists use is the epigenetic clock, a method that analyzes changes in DNA methylation to estimate how quickly a person’s body may be aging. A new study from UCLA Joe C. Wen School of Nursing Associate Professor Su Yon Jung, PhD, MPH, explores the link between this aging measure, impact of social factors on aging, and the development of type 2 diabetes (T2DM).
Published in Aging & Disease (25 IF = 9.6, ranked #3 out of 123 journals in the Geriatrics and Gerontology category), the study examined data from > 1,500 diabetes-free women in the Women’s Health Initiative, a massive decades-long national health cohort study. By analyzing data from an average period of 19 years, Dr. Jung was able to find a correlational pathway between epigenetic aging and the development of T2DM and insulin resistance (IR).
That is, women who developed T2DM had greater accelerated epigenetic aging then women who did not. Faster biological aging was also seen among African American women and among those with insulin resistance.
But researchers wanted to look beyond biological aging itself. Dr. Jung examined social conditions, including social support, access to healthcare, and other social determinants of health (SDOH), to investigate the effect of social adversity on the racial differences in aging acceleration and metabolic diseases.She found that lower levels of SDOH contributed to greater accelerated aging, but a mediation effect of SDOH together with aging on T2DM and IR.
This result provides justification that existing epigenetic clocks don’t fully capture the racial disparity in rapid aging process and the effect of social adversity in biological pathways of T2DM/IR.
Of note, experiences related to SDOH can build over many years, and today's biological aging clocks cannot be designed to identify the full impact of those experiences.
This understand opens the door to a new generation of epigenetic clocks, ones designed to better account for the social and environmental conditions that shape health over a lifetime.