ArticleiScience2026
Association between biological aging and coronary heart disease: A secondary analysis of two observational studies.
Article in iScience, 2026. 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
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
1 citing paper in PubMed.
- [Application of biological age for cardiovascular risk prediction in a community-based Chinese cohort].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While aging is a well-established contributor to cardiovascular disease, the specific relation between biological aging-as assessed by PhenoAge and PhenoAge acceleration-and the risk of coronary heart disease (CHD) requires further evidence to elucidate. This study conducted a cross-sectional analysis using data from the National Health and Nutrition Examination Survey (NHANES), alongside both cross-sectional and prospective analyses using data from the UK Biobank, to investigate the association between biological aging and CHD risk across two large cohorts. The results indicated that each unit increase in PhenoAge and PhenoAge acceleration was significantly associated with a higher risk of CHD. Compared to individuals without accelerated aging, those experiencing accelerated aging face a significantly higher risk. These findings suggest that PhenoAge and its acceleration are significant risk factors for CHD development. Moreover, surrogate markers of biological aging may serve as valuable tools for both the primary and secondary prevention of CHD.
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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 Socratic graph.