Genetically proxied telomere length, epigenetic age acceleration and healthspan
In a two-sample Mendelian randomization study, genetically proxied longer leukocyte telomere length was associated with extended healthspan, while four genetically proxied epigenetic age acceleration biomarkers showed no consistent association. [1]
Automatic summary · not editorially reviewed
The key findings
Healthspan was defined as age at first diagnosis of any of eight major chronic conditions or death, based on 300,447 unrelated European-ancestry UK Biobank participants. [1]
Genetically proxied longer leukocyte telomere length was associated with extended healthspan in the main analysis (β = 0.106; 95% CI: 0.054–0.158). [1]
The four genetically proxied epigenetic age acceleration biomarkers did not show consistent evidence of an association with healthspan. [1]
The source at a glance
- Study type / format
- Two-sample Mendelian randomization study (abstract)
- Population / context
- 300,447 unrelated European-ancestry UK Biobank participants for healthspan; genetic instrument sources with up to 472,174 individuals for LTL and about 35,000 per EAA biomarker.
- Summary based on
- Study abstract
- Original publication
- September 10, 2026
Healthspan outcome in UK Biobank Europeans
The study asked whether two kinds of biological aging biomarkers, leukocyte telomere length (LTL) and epigenetic age acceleration (EAA), show evidence of potential effects on healthspan. Healthspan was defined as age at first diagnosis of any of eight major chronic conditions or death. Summary statistics came from 300,447 unrelated participants of European ancestry in the UK Biobank.
Supporting source [1]
Longer LTL linked to longer healthspan
Genetic instruments for LTL came from published genome-wide association studies with up to 472,174 individuals; instruments for four EAA biomarkers came from studies with about 35,000 individuals each. In the main inverse-variance-weighted analysis, genetically proxied longer LTL was associated with extended healthspan (β = 0.106; 95% CI: 0.054–0.158; p = 6.9 × 10). The association was robust across multiple sensitivity analyses.
Supporting source [1]
EAA biomarkers showed no consistent association
In contrast, the four genetically proxied EAA biomarkers did not show consistent evidence of an association with healthspan. The authors conclude that the findings provide genetic evidence consistent with a potential role of LTL in healthspan, but little support for comparable associations involving the genetically proxied components of the evaluated EAA biomarkers. They note that the findings do not exclude potential associations with environmentally or physiologically acquired EAA.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a two-sample Mendelian randomization study using genetic instruments, not a trial. The healthspan outcome came from UK Biobank participants of European ancestry, so generalization is limited. The authors state that the findings do not exclude associations with environmentally or physiologically acquired EAA.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Feng B, Yang R, Wang GR, Hu Q, Zhao C. · europepmc.org · September 10, 2026