Andrew Huberman· PhD
can we use exogenous molecules to Target those specifically you gave one example which I I would argue is the single best example which is rapy so rapy targets a very specific Hallmark of aging and we can talk
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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.
can we use exogenous molecules to Target those specifically you gave one example which I I would argue is the single best example which is rapy so rapy targets a very specific Hallmark of aging and we can talk
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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 we talk about all of these things that occur in an aging phenotype where we see more inflammation we see a greater abundance of senescent cells we see reduced uh nutrient sensing capacity of mtor which you described as the probably the most important nutrient sensing system in our body um so so we have you know these somewhere between 9 and 14 the number just keeps changing arbitrarily but it doesn't really matter we have these Central things that everybody would agree Define what an aging phenotype is and can we use exogenous molecules to Target those specifically you gave one example which I I would argue is the single best example which is rapy
and the idea there is that you're limiting mtor you're causing your cells to grow less mature slower and and in that sense slowing down aging is that the idea yeah I mean you know and this will be an important theme today right it's like we can talk all day long about mechanisms and theoretical Arguments for why it would work and I think my conviction around taking Ramy is less about um sort of looking at the molecular explanation for why Rapa Works although I find that to be quite convincing and why does the inhibition of mtor stimulate a top Agy why would that suppress ccent cells
How does Rapamy work rapamyson's potential in longevity centers around its ability to inhibit something called mTorc1 This is a growth pathway whose overactivation plays a role in many age related diseases
Rapamy's potential in longevity centers around its ability to inhibit something called mtorc1. This is a growth pathway whose overactivation plays a role in many age related diseases.
and so so really it's these sasps getting whacked that is how it would act through via the senescent pathway as opposed to targeting a senescent cell directly but that's by the way that's been my reading of the literature
i don't think it's analytic in the sense that it that it at least the classical way people have thought about analytics where it kills the senescent cell right i absolutely think it turns down the chronic inflammatory signaling that is driven by p16 p21 nf kappa b yes we see that in mice multiple tissues no question about it
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.