The Association Between Accelerated Biological Aging and the Physical, Psychological, and Cognitive Multimorbidity and Life Expectancy: Cohort Study

IF 7.1 1区 医学 Q1 Biochemistry, Genetics and Molecular Biology
Aging Cell Pub Date : 2025-07-13 DOI:10.1111/acel.70142
Zuliyaer Talifu, Ziyang Ren, Chen Chen, Shuai Guo, Yu Wu, Yuling Li, Binbin Su, Xiaoying Zheng
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Abstract

As the global population ages, multimorbidity has become a critical public health issue. We analyzed 332,012 adults from the UK Biobank (2006–2022) to investigate the association between biological age—measured by the Klemera–Doubal method (KDM-BA) and phenotypic age (PhenoAge)—and a new comorbidity model encompassing physical, psychological, and cognitive disorders, with overall mortality outcomes over a median follow-up of 13.6 years. Logistic regression models examined the association between baseline health status and accelerated aging, while Cox proportional hazards models assessed mortality risk and disorder development. Cross-sectional analysis showed that accelerated aging was linked to higher comorbidity prevalence. Longitudinal follow-up revealed that individuals in the highest quartile (Q4) of aging speed (residual difference between estimated biological age and chronological age) had a 16%–17% higher risk of developing a single disorder, a 41%–44% higher risk of multimorbidity, and a 54% higher overall mortality risk compared with the lowest quartile (Q1). Among those with baseline single disorder, dual comorbidity, and triple morbidity, Q4 mortality risk increased by 89%–116%, 118%–166%, and 119%–156%, respectively. Multistate Markov models confirmed that accelerated aging (residual > 0) increased the risk of transitioning to disorder, comorbidity, and death by 12%–37%. Individuals aged 45 with triple comorbidity lost an average of 5.3 years in life expectancy (LE), further reduced by 5.8 to 7.0 years due to accelerated aging. This study highlights that KDM-BA and PhenoAge robustly predict multimorbidity trajectories, mortality, and shortened LE, supporting their integration into risk stratification frameworks to optimize interventions for high-risk populations.

Abstract Image

生物加速老化与身体、心理和认知多病和预期寿命之间的关系:队列研究。
随着全球人口老龄化,多病已成为一个重要的公共卫生问题。我们分析了来自英国生物银行(UK Biobank)(2006-2022)的332,012名成年人,以调查用klemera - double方法(KDM-BA)测量的生物年龄与表型年龄(PhenoAge)之间的关系,并研究了一种新的共病模型,包括身体、心理和认知障碍,在中位随访13.6年的总死亡率结果。Logistic回归模型检验了基线健康状况与加速衰老之间的关系,而Cox比例风险模型评估了死亡风险和疾病发展。横断面分析显示,加速衰老与较高的合并症患病率有关。纵向随访显示,与最低四分位数(Q1)相比,衰老速度(估计生物年龄与实足年龄之间的剩余差异)最高四分位数(Q4)的个体患单一疾病的风险高出16%-17%,多病风险高出41%-44%,总死亡风险高出54%。在基线单一疾病、双重合并症和三重发病的患者中,Q4死亡风险分别增加89%-116%、118%-166%和119%-156%。多状态马尔可夫模型证实,加速衰老(残余>)使过渡到疾病、合并症和死亡的风险增加了12%-37%。45岁伴有三重合并症的个体平均预期寿命减少5.3年,由于加速衰老,预期寿命进一步减少5.8 - 7.0年。该研究强调,KDM-BA和PhenoAge强有力地预测了多病轨迹、死亡率和缩短的寿命,支持将它们整合到风险分层框架中,以优化高危人群的干预措施。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Aging Cell
Aging Cell 生物-老年医学
CiteScore
14.40
自引率
2.60%
发文量
212
审稿时长
8 weeks
期刊介绍: Aging Cell, an Open Access journal, delves into fundamental aspects of aging biology. It comprehensively explores geroscience, emphasizing research on the mechanisms underlying the aging process and the connections between aging and age-related diseases.
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