2 replies to this topic

[poonja]

I assume that many of you have become aware that recent research (just google rapamycin telemeres) demonstrates that people with short telemeters who use rapamycin may be/are shortening rather than lengthening their lifespan.  I am 73 years old and will be suspending my use pending further information.

[QuestforLife]

What the study showed (https://doi.org/10.1...467-020-14962-1), was that cells with short telomeres use elevated mTOR as a survival mechanism, and that interfering with that shortened life in telomerase-deficient mice strains (bred for several generations to give them short telomeres). TERT-deficit mice are quite a nice model for human aging, but I would be a little cautious applying this straight to humans. Note the study itself only sought to apply the findings to humans with telomere diseases. 

 

Also of note is that normal mice also get progressively shorter telomeres with age (doi/10.1073/pnas.1902452116), but they still benefit substantially from rapamycin. Perhaps there is a maximum age beyond which rapamycin shortens, not lengthens life in mice (and potentially humans), but further lifespan studies will be needed to prove this. 

[Engadin]

What the study showed (https://doi.org/10.1...467-020-14962-1), was that cells with short telomeres use elevated mTOR as a survival mechanism, and that interfering with that shortened life in telomerase-deficient mice strains (bred for several generations to give them short telomeres). TERT-deficit mice are quite a nice model for human aging, but I would be a little cautious applying this straight to humans. Note the study itself only sought to apply the findings to humans with telomere diseases. 

 

Also of note is that normal mice also get progressively shorter telomeres with age (doi/10.1073/pnas.1902452116), but they still benefit substantially from rapamycin. Perhaps there is a maximum age beyond which rapamycin shortens, not lengthens life in mice (and potentially humans), but further lifespan studies will be needed to prove this. 

 

 

Given the almost non-existent side effects for rapamycin anti-aging very low doses, the point would be to find the threshold in human telomeres length behind which rapamycin becomes a harming strategy more than a beneficial one. And just in case that limit would be found out soon, are present telomere-length tests precise and wide enough to take a valid decision on anti-aging rapamycin use?. By wide I mean that given different organs age at a different rate in humans, it could be the case that anti-aging rapa can be OK for some organs but not for others. IMHO it'll keep being a difficult decision to take for a while yet.