ArticleHuman genomics2025
Biological aging and lifespan in men and women using a Mendelian randomization study.
Article in Human genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- A generator-matrix model quantifies the limited contribution of measured biomarkers to human mortality acceleration.medRxiv : the preprint server for health sciences · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIdentification of targets of intervention to promote lifespan is crucial given lifespan is an important measure of public health. Telomere length and epigenetic clocks are key biological markers of aging, whether they are targets of intervention in men or women is unclear. We examined their associations with sex-specific lifespan in a Mendelian randomization study.
methodsWe used genetic summary statistics of telomere length and lifespan (parental attained age and survival to recruitment) from the UK Biobank (n = ~ 0.5 million, mean age = ~ 57 years) and of epigenetic clocks (GrimAge, PhenoAge, HannumAge and Intrinsic epigenetic age acceleration) from a meta-analysis of 28 cohorts (n = 34,710). Using this data, we employed two-sample MR to estimate the causal effect of each aging biomarker on lifespan in men and women. Estimates were obtained using inverse variance weighting with sensitivity analysis.
resultsThere was no evidence that telomere length was associated with lifespan in men (0.17 years per standard deviation of log telomere length, 95% confidence interval (CI) -0.54 to 0.88, survival - 0.17 years, 95% CI -0.39 to 0.05) or in women (0.04, 95% CI -0.88 to 0.96), although telomere length was associated with poorer survival to recruitment in women (survival - 0.24 years, 95% CI -0.44 to -0.03). Associations of epigenetic clocks with lifespan and survival were null in both men and women. Sensitivity analysis gave similar estimates.
conclusionsTelomere length and commonly used epigenetic clocks may not be an appropriate target for promoting lifespan. Instead, efforts to develop interventions for aging should target causal drivers of lifespan.
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