Background: Epigenetic clocks derived from DNA methylation estimate biological aging and have been associated with cardiometabolic death. We evaluated whether substituting epigenetic age for chronologic age within PREVENT altered associations with all-cause and cardiovascular mortality or improved discrimination. Methods: We analyzed National Health and Nutrition Examination Survey 1999-2002 data linked to National Death Index follow-up through December 31, 2019. Adults aged 50-79 years without baseline cardiovascular disease and with DNA methylation data were included. PREVENT is a primary-prevention framework incorporating demographic, cardiometabolic, renal, and treatment factors. Exposures were PREVENT estimates calculated using chronologic age or 8 epigenetic ages substituted for chronologic age, with other inputs unchanged. Survey weighted Cox models estimated associations with all-cause and cardiovascular mortality per 5-percentage-point higher predicted risk. Weighted Harrell C statistics assessed discrimination; 95% CIs were obtained by bootstrap resampling. Results: The cohort included 1,516 participants (weighted mean age, 60.3 years; SD, 8.0) with a mean follow-up of 17.35 years; 507 participants died, including 140 cardiovascular deaths. Each 5-percentage-point increase in chronologic PREVENT risk was associated with all-cause mortality (HR, 1.57; 95% CI, 1.45-1.70) and cardiovascular mortality (HR, 1.66; 95% CI, 1.501.84). Biologic variants showed similar associations for all-cause mortality (HR range, 1.391.57) and cardiovascular mortality (HR range, 1.47-1.67). Chronologic PREVENT showed higher discrimination for all-cause mortality (C, 0.74; 95% CI, 0.72-0.77) than biologic variants (C range, 0.66-0.73) and for cardiovascular mortality (C, 0.78; 95% CI, 0.73-0.84) than biologic variants (C range, 0.71-0.77). Conclusions: Biologic PREVENT variants were associated with mortality but did not improve discrimination compared with chronologic PREVENT, suggesting biological aging metrics may complement rather than replace chronological age in cardiovascular risk prediction.
Ramzi Ibrahim, B. Tamarappoo, Kwan S. Lee et al.· Circulation. Population heal...· 0 citations
Emerging evidence links air pollution exposure to metabolic dysfunction; however, few studies have examined diabetes-related mortality in relation to ambient air pollutants using high-resolution exposure data at the population level. In the United States, particularly in large and geographically diverse states such as California, exposure contrasts and population heterogeneity provide an important setting to evaluate these associations.
We conducted a matched case–control analysis using California Department of Public Health (CDPH) Vital Records (2010–2021). Diabetes-related mortality events (ICD-10 E11) were identified as primary or contributory causes. Decedents (cases) were geocoded to residential addresses, and one-year rolling averages of fine particulate matter (PM
2.5
) before death were assigned as individual exposures. Each death record was matched to its selected controls based on month and year of birth and race-ethnicity. Controls were identified from the same statewide CDPH mortality database and were eligible because they had not died by the corresponding case’s date of death. Because the number of eligible controls varied across matched strata, controls were randomly sampled within each matched stratum to achieve an overall control-to-case ratio of approximately 2:1 for the study population. The final dataset included 60,824 diabetes-related deaths and 119,053 controls. Exposures were standardized by their interquartile range (IQR) and conditional logistic regression models estimated associations between 1 year rolling average fine particulate matter (PM
2.5
) exposure and odds of diabetes-related mortality, adjusting for age, sex, race-ethnicity, marital status, and education. Nitrogen dioxide (NO
2
) was included as a co-pollutant for confounding control.
PM
2.5
exposure (per 2.65 μg/m
3
IQR increase) was associated with a 18% higher odds of diabetes-related mortality (OR = 1.18; 95% CI: 1.15–1.22) before traffic indicator NO
2
adjustment and showed a stronger association with 21% higher odds (OR = 1.21; 95% CI: 1.17–1.25) after NO
2
adjustment. Health economics analysis estimated that reducing PM
2.5
exposure by its IQR could avoid losses of $31.2 million per 100,000 people.
Higher ambient PM
2.5
exposure was associated with increased odds of diabetes-related mortality in California even after adjustment for NO
2
and other impact factors. These findings support the need for continued strengthening of ambient air quality regulations.
Richy Zheng, Jason G. Su, E. Shahriary et al.· Frontiers in Public Health· 0 citations
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