Speaking to a colleague; he thinks measuring the original horvath epigenetic clock is useless given that it is not correlated with smoking status; and that at the very least one should use the newer epiclocks such as AccelGrimAge, and ideally one based on whole epimethylome sequencing rather than illumina EPIC 850k site arrays.
Also as levine's multi-biomarker phenotypical clock, such as CRP etc, predicts age and clinical outcome risk with similar accuracy at 4x lower the cost and its components have a lot more evidence for being causative of aging pathology... I'm still failing to see the point in measuring epiclocks every year for patients
So does zymo still use the original horvath epiclock?
https://www.zymoresearch.com/pages/human-dnage - they don't make it clear so you'd have to ask if they upgraded to grimaccelage etc.
Levine sums it up well in the discussion in this paper discussing newer epi clocks - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5940111/
"While DNAm PhenoAge greatly outperformed all previous DNAm biomarkers of aging (Supplement 1: Table S5), the utility of DNAm PhenoAge for estimating risk does not imply that it should replace clinical biomarkers when it comes to informing medical and health-related decisions."
and goes on to say how it is best stuck to research use
"That being said, when the aim is to study the mechanisms of the aging process, DNAm measures have advantages over clinical measures. First, they may better capture “pre-clinical aging” and thus may be more suited for differentiating aging in children, young adults, or extremely healthy individuals, for whom measures like CRP, albumin, creatinine, glucose, etc. are still fairly homogenous. Second, as demonstrated, these molecular measures can capture cell and/or tissue specific aging rates and therefore may also lend themselves to in vitro studies of aging, studies for which blood is not available, studies using postmortem samples, and/or studies comparing aging rates between tissues/cells"
Note that you can also adjust reference ranges of such clinical biomarkers to be stricter, as optimal clinical outcome ranges, e.g. setting CRP to under 0.2 rather than 0.7 for men (which may somewhat remove this (potentially still unactionable) clinical advantage of detecting pre-clinical pathology)
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