Biological age acceleration and bradyarrhythmia risk in UK Biobank
In a UK Biobank cohort of 298,214 people, faster biological aging on two measures was associated with higher bradyarrhythmia risk; epigenetic analyses prioritized aging-related DNA methylation sites. [1]
Automatic summary · not editorially reviewed
The key findings
Biological age acceleration was defined as the residual from regressing each biological aging measure on chronological age. [1]
Per 1-SD increase, PhenoAge and KDM biological age acceleration were each associated with a 13% higher bradyarrhythmia risk (HR 1.13, 95% CI 1.11-1.15). [1]
Epigenetic Mendelian randomization and colocalization analyses were used to prioritize aging-related DNA methylation CpG sites for bradyarrhythmias. [1]
The source at a glance
- Study type / format
- Observational cohort study with epigenetic Mendelian randomization and colocalization analyses (abstract)
- Population / context
- 298,214 UK Biobank cohort participants
- Summary based on
- Study abstract
- Original publication
- July 16, 2026
Biological age measures in 298,214 UK Biobank participants
The researchers calculated two established biological aging measures, the Klemera-Doubal Method (KDM) and Phenotypic Age (PhenoAge). Biological age acceleration was defined as the residual from regressing each measure on chronological age, meaning how much older a person's biological age appears than expected for their calendar age. They then used Cox proportional hazards models to assess associations between this acceleration and bradyarrhythmia risk in the UK Biobank cohort of 298,214 individuals.
Supporting source [1]
Higher acceleration linked to 13% higher risk per SD
Per 1-standard-deviation increase, PhenoAge acceleration and KDM biological age acceleration were each significantly associated with a 13% higher bradyarrhythmia risk (hazard ratio 1.13, 95% confidence interval 1.11-1.15). These are associations from an observational cohort, not evidence that accelerated aging causes bradyarrhythmia. The abstract does not report follow-up duration or how bradyarrhythmia was ascertained.
Supporting source [1]
Epigenetic analyses prioritized methylation sites, not proven mechanisms
The authors also performed epigenetic Mendelian randomization and colocalization analyses to prioritize aging-related DNA methylation CpG sites for bradyarrhythmias. The abstract does not report which sites were prioritized or their effect sizes. The conclusion describes a role of accelerated biological aging and underlying epigenetic modifications, but the abstract presents associations and prioritized sites, not demonstrated causal mechanisms or prevention strategies.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The abstract does not report follow-up duration, how bradyarrhythmia was ascertained, or which CpG sites were prioritized. Findings are observational associations, not proof of causation or of prevention strategies.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Song ZQ, Huang LJ, Liu K, Wu SK, Chen JR, Pei YZ, Chen YH. · europepmc.org · July 16, 2026