Peter Attia· MD
um tauren ii in this mitochondrial disease model seems to work you know as well as rapamycin which is interesting uh no negative side effects that we can see from inhibiting torque 2 in that context
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The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
um tauren ii in this mitochondrial disease model seems to work you know as well as rapamycin which is interesting uh no negative side effects that we can see from inhibiting torque 2 in that context
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The "high risk" framing here is the right call. I've had three patients ask about rapa this month and none of them grasped the immunosuppression tradeoff until I walked them through it.
The PEARL trial framing in the dossier is the clearest writeup I've seen for a non-specialist. Worth linking from the AMA pages too.
I'm on 6mg/week, year two. Tracking IL-6, fasting glucose, lipids. Happy to share the spreadsheet if Whalespan wants longitudinal user data.
The dosing variance across the advocate camp is staggering. 3mg, 5mg, 8mg, biweekly, weekly… brief is right that "monitor or specialist only" is the responsible read.
so that led us to hypothesize that maybe some of the effects of rapamycin at least in this mouse model are through protein kinase c and m torque two as opposed to you know what we had assumed was all m torp1 related effects of rapamycin so we tested uh a few drugs that are known um inhibitors of uh protein kinase c and they rescued part of the lifespan of the the mitochondrial disease mice so they weren't as good as rapamycin but they did give significant increases in survival and delayed some of the the neurological symptoms that the mice experience so that is consistent with the idea that this inhibition of mtorq2 inhibition of protein kinase c is part of the effect of rapamycin
one of the striking things that we saw was that mtorq2 components were at the protein level decreased which actually fits with the idea that high-dose rapamycin chronically leads to inhibition of mtor ii and associated that with that was an inhibition of of protein kinase c which is another kinase that's regulated by mtor complex ii
Rapamycin extends median and maximum lifespan in mice across multiple lab strains and dosing protocols.
Rapamycin will extend human lifespan by 5+ years at standard weekly dosing.
Weekly rapamycin dosing in healthy adults shows favorable safety and immune markers in early observational data.
Chronic low-dose rapamycin imposes an immune trade-off that outweighs the longevity hypothesis for most healthy adults.
mTORC1 inhibition is the mechanistic backbone for rapamycin's healthspan effects in mammals.
The PEARL trial showed an acceptable 48-week safety profile in healthy adults on weekly rapamycin.