Journal September 27, 2026 4 min read

What markers track GrimAge?

GrimAge is a second-generation epigenetic clock trained on plasma protein surrogates and smoking history. This page summarises what the research literature reports about the markers it tracks and the models in which thos

peptides-pro Editorial

GrimAge is a second-generation DNA methylation clock, sometimes written as the GrimAge epigenetic clock and grouped with the DNA methylation age (DNAm) clocks. It is not a single analyte but a composite score: it is built from DNA methylation surrogates for a set of plasma proteins together with a DNAm-based estimate of smoking pack-years, and it is read out as an age acceleration residual — the difference between the GrimAge estimate and chronological age. The evidence block for this page does not supply a sequence, formula or molecular weight for GrimAge, because GrimAge is a statistical model rather than a molecule; the identifiers that apply are those of the methylation array used to generate the input data, which the evidence here does not specify.

The work in this area centres on epigenetic clocks as a class of ageing biomarker, and on the DNA methylation marks that serve as their inputs.

Research Studies

GrimAge and epigenetic age acceleration in the Korean population

A genome-wide association study examined epigenetic age acceleration across multiple epigenetic clocks in a Korean cohort, with the stated aim of exploring ethnic differences and individual variability in Asian populations [3]. The study is reported as identifying Asian-specific genetic susceptibility for epigenetic age acceleration. It is a reference point for the general claim that genetic contributions to clock-based age acceleration can differ between populations; it is not a GrimAge-specific marker list.

GrimAge and seasonality in adult biological age

A registered study set out to evaluate how seasonal variation influences biological age in adults, and to use that information to improve the design and analysis of long-term lifestyle interventions targeting biological clocks [1]. The rationale given is that biological age clocks measured from blood or saliva are useful for assessing the pace of ageing and for calculating age acceleration [1]. The study is framed around clocks as a class rather than around GrimAge alone.

GrimAge and epigenetic outcomes after autologous bone marrow procedures

A pilot study in adults with Parkinson's disease or Parkinson-plus syndromes evaluated safety, tolerability and exploratory epigenetic outcomes after a single same-day autologous bone marrow procedure [2]. Ten participants underwent posterior superior iliac spine bone marrow aspiration under local anaesthesia; the unprocessed aspirate was filtered and given intravenously in normal saline, and a centrifuged concentrate was atomised intranasally. Cells were not expanded in culture or genetically modified [2]. The epigenetic outcomes were exploratory, and the study population was adults with PD or PPS.

GrimAge and the choice of clock in age-acceleration studies

Across the studies above, age acceleration is treated as a derived quantity rather than a direct measurement: it is the gap between a clock estimate and chronological age [1]. Because different clocks are trained on different inputs, a genetic or environmental association found for one clock need not transfer to another — the Korean GWAS deliberately used multiple epigenetic clocks for this reason [3].

GrimAge and sample type

The evidence describes biological age clocks as measurable from blood or saliva [1]. No study in this evidence block reports a head-to-head comparison of GrimAge values between those two matrices, so no such comparison is made here.

GrimAge and intervention design

One stated purpose of clock research in this evidence is trial design: seasonality is treated as a source of variation that long-term lifestyle interventions targeting biological clocks would need to account for [1]. This is a methodological point about study conduct, not a claim about any compound.

GrimAge and model systems

None of the evidence supplied here reports GrimAge findings in animals or in vitro. The studies described are human: a Korean population cohort [3], an adult seasonality study [1], and a ten-participant pilot in adults with PD or PPS [2]. Where a reader encounters animal-only or cell-culture claims about GrimAge markers, those claims are not supported by this evidence block.

GrimAge and what the evidence does not establish

The evidence does not provide a list of the individual protein surrogates or the smoking variable that constitute GrimAge, does not give effect sizes for any marker, and does not report that any intervention changed GrimAge. Claims of that kind should be left out until supported.

If you are reading this for personal health reasons

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