ArticleGeroScience2026
Association of accelerated phenotypic aging, lifestyle and genetic risk with progression of cardiometabolic multimorbidity: a multi-state model analysis.
Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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.
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.
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Who cites it
2 citing papers in PubMed.
- Biological age acceleration and extrahepatic multimorbidity in U.S. adults with metabolic dysfunction-associated steatotic liver disease: a national cross-sectional study.Clinical and experimental hepatology · 2026Article
- Multi-target synergistic anti-aging: QG extends Caenorhabditis elegans lifespan through DAF-16/FOXO pathways, mitochondrial homeostasis and metabolic reprogramming.Biogerontology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
We aimed to use multi-state models to assess joint impacts of lifestyle and genetic risk with phenotypic age acceleration on cardiometabolic multimorbidity (CMM) trajectory, and to further explore whether phenotypic age acceleration mediates association between lifestyle and each transitions. We conducted a prospective cohort study included 365,573 adults free of cardiometabolic diseases (CMDs) at baseline in UK Biobank. Multi-state model was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of joint impacts of lifestyle and genetic risk with PhenoAgeAccel on CMM progression. Mediation analyses were conducted to explore indirect effect of PhenoAgeAccel on association between lifestyle and all transitions. During a median follow-up of 13.68 years, 54,483 participants developed first cardiometabolic diseases (FCMD), 7,397 developed CMM, and 27,288 died from any causes. Participants with accelerated phenotypic aging and unfavorable lifestyles had higher risks of all transitions, with HRs ranging from 1.53 (95% CI 1.37, 1.71) to 2.80 (2.62, 3.00). Additionally, those with accelerated phenotypic aging and high genetic risk showed a higher risk of FCMD incidence (HR 1.46; 95% CI 1.32, 1.61) and transition from FCMD to CMM (2.09; 2.02, 2.17). Furthermore, phenotypic age acceleration partially mediated the impact of lifestyle on all transitions, with mediation proportion varying from 6.28% (3.46, 9.10%) to 9.92% (6.37, 13.46%). Participants with phenotypic age acceleration have increased risk of CMM progression, especially among those with unfavorable lifestyles and high genetic risk. Phenotypic age acceleration partially mediated the relationship between lifestyle and CMM progression.
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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 OpenQuestion graph.