Decelerated Biological Aging Mediates the Association Between Life’s Essential 8 and Mortality in Hypertension: Evidence from NHANES and the Klemera-Doubal Model

Background: Hypertension is a major modifiable risk factor for cardiovascular diseases (CVD) and premature mortality, yet clinical outcomes vary significantly even among individuals with similar blood pressure control. Life’s Essential 8 (LE8), a comprehensive cardiovascular health (CVH) metric, may influence outcomes through biological aging pathways, but evidence in hypertensive populations remains limited. Methods: This prospective cohort study analyzed data from 9,376 hypertensive adults in the National Health and Nutrition Examination Survey (NHANES, 2007–2018). LE8 scores were derived from eight modifiable components (diet, physical activity, nicotine exposure, sleep, BMI, non-HDL cholesterol, blood glucose, and blood pressure). Biological age was estimated using the Klemera-Doubal method (KDM-BA) based on six clinical biomarkers. Mortality outcomes were ascertained via linkage to the National Death Index. Survey-weighted Cox regression and mediation analyses assessed associations and mediating effects of KDM-BA. Results: Over a median follow-up of 6.34 years, higher LE8 scores were dose-dependently associated with lower all-cause mortality (High vs. Low CVH: HR 0.22, 95% CI 0.16–0.30) and CVD mortality (HR 0.31, 95% CI 0.20–0.50). Each 10-point LE8 increase reduced all-cause mortality risk by 27% (HR 0.73, 95% CI 0.68–0.78). KDM-BA mediated 13.5% (all-cause mortality) and 32.9% (CVD mortality) of these associations (both p < 0.001). High CVH participants exhibited slower biological aging (KDM-BA acceleration: −9.97 vs. +6.87 in Low CVH, p < 0.001). Conclusions: In hypertensive adults, better CVH measured by LE8 is associated with decelerated biological aging and reduced mortality, with biological aging mediating approximately one-third of the protective effect against CVD mortality. Optimizing LE8 metrics may offer dual benefits for blood pressure control and aging modulation.