This is not true. Aging doesn’t develop, rather, it is an ongoing process of damage accumulation (i.e. hallmarks of aging) that occurs as a by-product of metabolism, explained in the original post. Aging occurs in both young and old people, although the rate of aging accelerates as diseases of aging develop.
Reversing the damage associated with the hallmarks of aging at any chronological/biological age is likely to improve their phenotype and expected longevity. The more advanced the anti-aging technologies become, the better equipped we will be to reverse large amounts of damage associated with advanced age. That said, there is no reason to think that there is a cliff after which aging cannot be reversed.
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.
I see. in that case perhaps we would need emergency authorization for anyone who needs it to stay within escape velocity timeline. though that definition is too complex for me to see a scenario where FDA approves it (at least not without massive pressure).
Another option is to advocate for emergency authorization for old people.
Unfortunately, it seems that most intervention works before aging actually developed, so we need to give them to younger people, at least before 50.
This is not true. Aging doesn’t develop, rather, it is an ongoing process of damage accumulation (i.e. hallmarks of aging) that occurs as a by-product of metabolism, explained in the original post. Aging occurs in both young and old people, although the rate of aging accelerates as diseases of aging develop.
Reversing the damage associated with the hallmarks of aging at any chronological/biological age is likely to improve their phenotype and expected longevity. The more advanced the anti-aging technologies become, the better equipped we will be to reverse large amounts of damage associated with advanced age. That said, there is no reason to think that there is a cliff after which aging cannot be reversed.
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.
I see. in that case perhaps we would need emergency authorization for anyone who needs it to stay within escape velocity timeline. though that definition is too complex for me to see a scenario where FDA approves it (at least not without massive pressure).
Yes, I hope regulators will give older individuals who are soon to die of aging the option to have access to more radical life-extension therapies.