Peter Attia

The amount of protein they require is totally different from us.

So I'm always really wary when I see these studies that are using the mouse model of atherosclerosis.

I understand why we do it, because it's much easier and cheaper than looking at primates.

And obviously, we can't do these studies in humans.

You can find a lot of things in mice when it comes to atherosclerosis that don't seem to matter whatsoever in human biology.

I would chalk this up to one of those examples.

People also don't appreciate how short the half-life of IGF-1 is.

It's a staggeringly short half-life molecule.

Oh, really?

Oh, yeah, yeah.

It's insanely short half-life.

What's the half-life?

When administered systemically, it's on the order of minutes.

Yeah.

And by the way, administering IGF systemically is a lousy way to get it to the muscle.

You want to think of it almost as a paracrine thing where it has to be delivered into the muscle.

So look, all roads for me still point back to this idea that, and I know you would agree with me, so it's not going to be that controversial, but exercise is the most important drug.

I'm just not aware of a drug

in quotes, that is better than exercise.

And I know there's this enormous effort to figure out a way to put exercise into a pill.