ArticleCommunications medicine2026
Associations of biological ageing and genetic risk with incident abdominal aortic aneurysm.
Article in Communications medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundAbdominal aortic aneurysm (AAA) is a degenerative cardiovascular disorder prevalent with ageing. While accelerated biological ageing contributes to age-related diseases, its specific role in AAA risk remains unclear. This study investigates the relationships between biological ageing and risk of incident AAA and genetic predisposition to the disease.
methodsThis retrospective study used UK Biobank data from 350,483 participants without AAA at baseline. Biological age was assessed using Klemera-Doubal Method (KDMAge) and phenotypic age (PhenoAge) algorithms. Accelerated biological ageing was determined through residual analysis against chronological age, with values above 0 indicating accelerated ageing. Cox proportional hazards models evaluated the associations of biological age accelerations with AAA risk. Polygenic risk scores were calculated to evaluate genetic predisposition to AAA. We also examined the interactions between biological age accelerations and genetic predisposition on the risk of AAA.
resultsHere we show that participants with accelerated biological ageing have an elevated risk of AAA onset compared to those without, with hazard ratios (HRs) of 1.29 (95% CI 1.17-1.42) for KDMAge and 1.63 (95% CI 1.47-1.81) for PhenoAge. For joint associations, participants with accelerated biological ageing and high genetic risk have the highest risk of incident AAA (KDMAge: HR 2.15, 95% CI 1.81-2.54; PhenoAge: HR 2.72, 95% CI 2.26-3.28). There is a significant additive interaction between high genetic risk and accelerated biological ageing of PhenoAge.
conclusionsAccelerated biological ageing is significantly associated with an increased risk of AAA incidence, suggesting its potential as a focal point for risk assessment and targeted intervention development.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.