Biological age acceleration and incident liver cancer in UK Biobank
In a UK Biobank cohort of 274,966 people followed a median 14.67 years, each 1-SD higher biological age acceleration was associated with higher liver cancer incidence; this is an association, not proof of cause. [1]
Automatic summary · not editorially reviewed
The key findings
The prospective UK Biobank cohort included 274,966 participants with a mean age of 55.75 years, 53.8% female, and 325 incident liver cancer cases over a median 14.67 years. [1]
Each 1-SD increase in biological age acceleration was associated with higher liver cancer risk (KDM-BA HR 1.28, 95% CI 1.16–1.41; PhenoAge HR 1.32, 95% CI 1.22–1.43). [1]
Mediation analyses suggested KDM-BA acceleration is partially mediated by liver enzymes, while PhenoAge acceleration appears to act largely through direct mechanisms. [1]
The source at a glance
- Study type / format
- Prospective cohort study (abstract)
- Population / context
- 274,966 UK Biobank participants, mean age 55.75 years, 53.8% female.
- Summary based on
- Study abstract
- Original publication
- July 20, 2026
UK Biobank cohort of 274,966 adults
This prospective cohort used UK Biobank data. Biological age was assessed with two algorithms, the Klemera-Doubal method (KDM-BA) and PhenoAge. The 274,966 participants had a mean age of 55.75 years (SD 8.10) and 53.8% were female. Over a median follow-up of 14.67 years, 325 incident liver cancer cases were documented. The authors note that conventional liver cancer risk factors are well established, but the role of biological aging was poorly understood.
Supporting source [1]
Higher acceleration linked to more liver cancer
After multivariable adjustment, each 1-standard-deviation increase in biological age acceleration was associated with elevated liver cancer risk: hazard ratio 1.28 (95% confidence interval 1.16–1.41) for KDM-BA acceleration and 1.32 (1.22–1.43) for PhenoAge acceleration. A nonlinear dose-response relationship was reported for KDM-BA acceleration. Mediation analyses examined whether the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) mediate the relationship. The authors conclude that KDM-BA acceleration is partially mediated by liver enzymes, while PhenoAge acceleration appears to act largely through direct mechanisms.
Supporting source [1]
Abstract-only scope and association limits
The available text is an abstract; the full text was not reviewed. The design is a prospective cohort, so the reported links are associations and do not establish that accelerated biological aging causes liver cancer. The abstract reports 325 incident cases and a median follow-up of 14.67 years, but does not detail how biological age was measured beyond naming the two algorithms, nor how confounders were chosen. Subgroup and sensitivity analyses are mentioned without their results.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Prospective cohort design, so associations are not causal. Details of measurement, confounder selection and subgroup/sensitivity results are not reported in the abstract.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Liu X, Yang S, Zhang C, Chen P, Li J. · europepmc.org · July 20, 2026