Key result
Biological age acceleration linked to ~29% higher risk of aortic valve stenosis.
Why the study?
Biological age acceleration is thought to be a major risk factor for age-related diseases, but its role in aortic valve stenosis remained uncertain.
Is biological age acceleration associated with an increased risk of aortic valve stenosis in adult cohort populations?
Cohort (n=9,640)
Yes
Is biological age acceleration associated with an increased risk of aortic valve stenosis in adult cohort populations?
Biological age acceleration derived from clinical biomarkers is independently and potentially causally associated with an increased risk of aortic valve stenosis, offering a tool to help identify high-risk populations for early preventive intervention.
Answers are grounded in this paper and cite their sources.
Biological age acceleration was associated with higher aortic valve stenosis risk; leaves open whether targeting aging prevents disease.
Introduction Biological age acceleration (BAA) is thought to be a major risk factor for age-related diseases, but its role in aortic valve stenosis (AVS) remains uncertain. We aimed to assess the associations between biological aging and the risk of AVS. Methods This study involved 4526 participants from the Real-world Data of Cardiometabolic Protection (RED-CARPET) study and 5114 participants from the Atherosclerosis Risk in Communities (ARIC) study. BAA was assessed using clinical biomarkers through the Klemera-Doubal method (KDM) and the PhenoAge algorithm. We employed multivariable logistic regression and restricted cubic spline (RCS) regression to examine the association between BAA and AVS risk. Additionally, Mendelian randomization (MR) analysis was conducted to assess causality. Results In the RED-CARPET cohort of 4526 participants (mean age 60.93 years, 33.5% female), 113 AVS events were recorded. In the ARIC cohort of 5114 participants (mean age 51.94 years, 56.4% female, 82.3% White), there were 266 AVS events. After fully adjusting for confounding variables, each standard deviation increase in BAA was significantly associated with elevated AVS risk (RED-CARPET: KDM-BA acceleration: OR 1.29, 95% CI 1.07−1.55; PhenoAge acceleration: OR 1.48, 95% CI 1.24−1.77; ARIC: KDM-BA acceleration: OR 1.42, 95% CI 1.24−1.63; PhenoAge acceleration: OR 1.30, 95% CI 1.11−1.51). The RCS regression model revealed significant linear relationships between BAA and the risk of AVS in both cohorts. MR analysis suggested a potential causal relationship between KDM-BA acceleration and AVS risk (OR 1.38, 95% CI 1.21–1.57). Conclusion BAA, as derived from clinical biomarkers, is independently associated with an increased risk of AVS. This finding suggests that BAA, as a composite indicator of systemic biological aging, may complement traditional risk factors in the early identification of high-risk populations for AVS, and offer the possibility of early intervention for prevention.
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Zheng et al. (2026) conducted a cohort in Aortic valve stenosis (n=9,640). Biological age acceleration (Klemera-Doubal method and PhenoAge algorithm) vs. Per standard deviation increase in biological age acceleration was evaluated on Aortic valve stenosis (AVS) (OR 1.29, 95% CI 1.07-1.55). Biological age acceleration was independently and causally associated with increased risk of aortic valve stenosis (MR OR 1.38; 95% CI 1.21-1.57).
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