All the other epigenetic clocks have their issues (the 1st and 2nd generation clicks do not respond to calorie restriction, and even DunedinPACE increases after partial reprogramming). The meaningfulness of any of the CpG sites is unknown (and are not significant to the calculation of DamageAgea and AdaptAge). But the DamageAge and AdaptAge Ying CpG sites are different and the real ones
I got my data plugged in and there are VERY VERY sharp discrepancies that I don’t know what to make of yet…
DunedinPACE is 0.59. Of all the epigenetic clocks, PhenoAge is by far the lowest (the first-generation epigenetic clocks have little functional significance and I can cry less over them b/c I do way better on 2nd/3rd generation). The first-generation epigenetic clocks are MORE correlated with AdaptAge than DamageAge (meaning HorvathAge and especially HannumAge are more associated with “adaptive/protective” changes w/age than damaging changes w/age).
But DunedinPoAM (precursor and less accurate than DunedinPACE) is barely over 1.
DamageAge and AdaptAge… I don’t know what to make of yet… There’s a huge discrepancy I need to figure out better, because there’s a chance this massive discrepancy could be rare enough to be socially important…
HannumAge is MORE associated with adapt-age than damage-age, as is HorvathAge. DNAm that contribute to HorvathAge/HannumAge have little functional significance (in fact, slight acceleration of HannumAge may be protective - HannumAgeAA has the opposite effects of GrimAgeAA)
GrimAge outperforms phenoage…
Then there’s GrimAge2, which supposedly outperforms GrimAge (GrimAge2 is ONLY trained on people over 40 )
Talked to jesse pogalnik yesterday, who has some experience with it (and who recently published the DamageAge/AdaptAge papers). There’s thought that AdaptAge increases after recovery from stress [stress is when DamageAge may increase]. We still don’t know if DamageAge/AdaptAge are more dynamic/changeable/intervention-friendly than other clocks