David Sinclair· PhD
Rapamycin is one of the most effective known cancer-preventive agents in mice. Lifespan extension in mice may largely reflect a delay of multiple forms of cancer
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The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
Rapamycin is one of the most effective known cancer-preventive agents in mice. Lifespan extension in mice may largely reflect a delay of multiple forms of cancer
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
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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.
at least part of the story is that one of the steps in the progression to cancer is evolving to ignore that signal to break yeah turning down mTOR so rapamycin may not be effective there
So do we think that in as much as, say, taking these agents would allow you to live longer by not dying from cancer at the same period of time, does it delay the time it takes for cancer to become clinically detectable and or delay the demise of the animal once it has that cancer?
And the argument has been that rapamycin itself has cancer cell autonomous effect. Independent of the immune modulation problem.
But once that cell exists and now has to start growing and also escaping the immune system, I do think that's probably what you're going to affect.
we know that mtor which is the the the target of rapamycin right the protein that rapamycin inhibits plays this fundamental role in regulating cell division and cell cycle right so if you inhibit in a non-cancerous cell if you inhibit mtor enough you will stop the cell cycle the cell will stop dividing right but there are mutations that can happen that lead to cancer that cause the cell to no longer pay attention to the mtor break right and so once that's happened if that's the type of cancer you have that no longer responds to mtor inhibition rapamycin won't do anything to cell cycle and that in that case so that's a really i think specific example that you can point to
but after that mutation happens and the cell's not responding to rapamycin anymore because it doesn't sense the mtor break it's completely ineffective right so that that i think is a is a case where the mechanisms have changed right the the mechanisms that are important for preventing cancer before that mutation occurred are different from the mechanisms that might deal with that cancer after that mutation has occurred
there rapamycin will be quite effective at preventing cancer before that mutation happens but after that mutation happens and the cell's not responding to rapamycin anymore because it doesn't sense the mtor break it's completely ineffective
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.