That is true for therapies which work on damage (SENS). But if we see aging as a process which creates the damages, than it is reasonable to stop it on early age.
Also, I’ve seen a recent article “Longevity‐related molecular pathways are subject to midlife “switch” in humans” which implies that many interventions should happen early in life.
Evidence in mice studies does indicate that earlier therapies (for example of senolytics) do facilitate greater life extension. However, with better anti-aging technologies the ‘switch’ (from the paper you refer to) could theoretically be reversed, as there’s no biological law that would prevent restoring a phenotypically older individual back to a more youthful state.
That is true for therapies which work on damage (SENS). But if we see aging as a process which creates the damages, than it is reasonable to stop it on early age.
Also, I’ve seen a recent article “Longevity‐related molecular pathways are subject to midlife “switch” in humans” which implies that many interventions should happen early in life.
Thanks for great post!
Evidence in mice studies does indicate that earlier therapies (for example of senolytics) do facilitate greater life extension. However, with better anti-aging technologies the ‘switch’ (from the paper you refer to) could theoretically be reversed, as there’s no biological law that would prevent restoring a phenotypically older individual back to a more youthful state.