Peter Attia

Yeah.

And the other thing I think that is missing from this discussion, this is where I think inflammation serves as a great analogy.

So I think most people on the surface understand that a constant on state of the inflammatory system would be bad.

But of course, if you had no inflammatory response, that would be also bad.

So the ideal state is inflammation when you need it, otherwise off.

Inflammation when you need it, otherwise off.

And I think that's probably the right way to think about this, which is we want mTOR on when it has a job to do, and we want it relatively silent when we don't.

And I think if rapamycin is geroprotective, and when I say if, I mean in humans, I think it's unambiguously protective across most species, but we still don't know if the species of interest is going to benefit from this drug.

And we may never, by the way.

But it's probably working by tamping down the chronic inflammatory component of what we see with mTOR activation, which, by the way, might actually involve inflammation as well as one of the many things.

So there's also this challenge of trying to get folks to understand the difference between chronic and acute things.

Cortisol, great example.

So cortisol, vital hormone.

The appropriate rhythm of cortisol is essential for life.

If you took that away, you would actually be dead.

That's called Addison's disease.

But cortisol constantly being on would also be a problem.

That would be Cushing's disease.

So both extremes, bad.

It's do you know when you need it and what it's supposed to do?