An epigenetic biomarker of aging for lifespan and healthspan.
Level 3 - non-randomized controlled study
Non-randomized observational biomarker development and cohort validation study
PubMed 29676998 · doi:10.18632/aging.101414
What was done
Authors developed a second-generation epigenetic aging biomarker, termed DNAm PhenoAge, using a two-step process incorporating composite clinical measures of phenotypic age reflecting lifespan and healthspan. The biomarker was developed using whole blood data and assessed across diverse tissues, cell types, and aging-related clinical outcomes, accompanied by transcriptional pathway analysis in sorted cells.
What was found
The abstract reports no numerical values, correlation coefficients, or hazard ratios. Qualitatively, DNAm PhenoAge was reported to outperform previous chronological age-trained measures in predicting all-cause mortality, cancers, healthspan, physical functioning, and Alzheimer's disease. Epigenetic age acceleration was associated with increased activation of pro-inflammatory and interferon pathways, alongside decreased activation of transcriptional and translational machinery, DNA damage response, and mitochondrial signatures.
Why it matters
This work shifted epigenetic clock development toward multi-system phenotypic and functional outcomes, creating a tool to quantify biological aging and morbidity risk.
Limits
The abstract reports no sample sizes, demographic characteristics, or quantitative effect estimates. As an observational biomarker study, these associations do not demonstrate that the identified DNA methylation patterns causally drive phenotypic aging.
Cited by
- supports The PhenoAge epigenetic clock, published in 2018, was trained on clinical lab test markers combined into a mortality-predictive measure rather than directly on chronological age.