Peter Attia· MD
with rapamycin we don't have a great biochemical proxy we can't measure at otha g we can't count our senescence cells you know we can't look at inflammation within our muscles things that we believe would be improving
Loading…
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.
with rapamycin we don't have a great biochemical proxy we can't measure at otha g we can't count our senescence cells you know we can't look at inflammation within our muscles things that we believe would be improving
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
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.
where rapamy acts I don't know that we would see anything getting significantly better right because if we think that the main places that rapamy is is going to act would be on uh autophagy. Well there's no way you're going to measure autophagy. You're not going to feel autophagy. You're not going to see it or measure it. Um, does it tamp down on certain subsets of scinesscent cells? That that's certainly plausible. Again, I don't know how we're going to see or measure or necessarily even feel that.
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.