DNA clock

Horvath clock

Chain of Methyl groups on DNA has been found very correlated with number of years before death accurate in plants, animals and people after AI models on populations. They are different in epigenomes and DNA. The epigenetic version is, said by Digilog believers as me, to be caused by aging, more accurate and a very good predictor of any claims by anyone! Amazon India used to do tests before Covid but has paused. Will someone find who does now?
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DNA Methylation-Based Biomarkers and the Epigenetic Clock Theory of Ageing

Abstract

Identifying and validating molecular targets of interventions that extend the human health span and lifespan has been difficult, as most clinical biomarkers are not sufficiently representative of the fundamental mechanisms of ageing to serve as their indicators. In a recent breakthrough, biomarkers of ageing based on DNA methylation data have enabled accurate age estimates for any tissue across the entire life course. These 'epigenetic clocks' link developmental and maintenance processes to biological ageing, giving rise to a unified theory of life course. Epigenetic biomarkers may help to address long-standing questions in many fields, including the central question: why do we age?
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It is possible to scientifically measure effects on life. Mobile radiation has NO effect, proponents can be reliably called subhuman.

Premature aging induced by radiation exhibits pro-atherosclerotic effects mediated by epigenetic activation of CD44 expression.

Lowe D, Raj K. Aging Cell. 2014 Oct;13(5):900-10. doi: 10.1111/acel.12253. Epub 2014 Jul 25. PMID: 25059316 Free PMC article.
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Rapamycin is a toxic anti aging drug. One cannot hower use it to cheat because it is toxic and is an anti-aging chemical.

Rapamycin Retards Epigenetic Age in
g of Keratinocytes Independently of Its Effects on Replicative ,Senescence Proliferation and Differentiation

 Abstract

The advent of epigenetic clocks has prompted questions about the place of epigenetic ageing within the current understanding of ageing biology. It was hitherto unclear whether epigenetic ageing represents a distinct mode of ageing or a manifestation of a known characteristic of ageing. We report here that epigenetic ageing is not affected by replicative senescence, telomere length, somatic cell differentiation, cellular proliferation rate or frequency. It is instead retarded by rapamycin, the potent inhibitor of the mTOR complex which governs many pathways relating to cellular metabolism. Rapamycin, however, is also an effective inhibitor of cellular senescence. Hence cellular metabolism underlies two independent arms of ageing - cellular senescence and epigenetic ageing. The demonstration that a compound that targets metabolism can slow epigenetic ageing provides a long-awaited point-of-entry into elucidating the molecular pathways that underpin the latter. Lastly, we report here an in vitro assay, validated in humans, that recapitulates human epigenetic ageing that can be used to investigate and identify potential interventions that can inhibit or retard it.