Lactate and beta-hydroxybutyrate in the treatment of traumatic brain injury | Peter Attia

Lactate and beta-hydroxybutyrate in the treatment of traumatic brain injury | Peter Attia

[Rhonda]: Yeah. So back to the lactate thing, very interesting. Yeah, so read up on this, you know. George Brooks, a friend of mine, he’s working
now with some other physicians at UCLA looking at the effects of actually exogenous lactate
on helping treat TBI. Because TBI… [Peter]: Why not just exogenous BHB? [Rhonda]: Or, yeah, or that, exactly. [Peter]: I mean have you see what Dom D’Agostino
has done? [Rhonda]: I think I’ve read one of his studies
on cancer. I think it was cancer. [Peter]: Yeah. You should see Dom’s work in TBI. [Rhonda]: So this…oh, in TBI? [Peter]: Yeah. That’s how he got started. [Rhonda]: That they’re the same? [Peter]: He’s a neurobiologist. [Rhonda]: Oh, okay. [Peter]: The only reason he’s in cancer now
is because…he started out working a neurobiology… [Rhonda]: Interesting. [Peter]: …and using TBI models. [Rhonda]: I didn’t know that. Yeah, but it’s the same thing, lactate, beta-hydroxybutyrate,
it doesn’t matter. They’re going through the MCT… [Peter]: Yeah, they’re completely overcoming
head trauma. [Rhonda]: Yeah, they’re both doing similar
things. They’re both thermodynamically favorable,
they allow glucose sparing, they allow glucose to then be used to make glutathione, which
is important in the brain when you have damage. But what’s interesting is that TBI also disrupts
astrocytes’ ability to make lactate. And what I’m wondering when you were talking
about… [Peter]: But those two might just synergize. [Rhonda]: They might. [Peter]: Because I also think the trauma causes
an oxidative stress, so I think what’s happening is pyruvate dehydrogenase is getting interrupted
and all of a sudden you’re having a transient but violent interruption of energy to the
brain. And this is obviously of high interest to
the military because of blast injuries, and Dom would know this, so it’s absolutely worth
talking about this with him. I’m sure the DoD is all over this. I hope the DoD is all over this because the
interesting question is, do you have to have the BHB or the lactate in your system at the
time of injury to prevent it, or can administration be done immediately following the trauma? [Rhonda]: Or is there a kinetics? Is there a certain time? I think because of the fact that it allows
glucose sparing which if you have a trauma is…and this has been shown on animal models
for TBI, but this was done by putting glutathione transcranially which obviously is not going
to happen. But anyways, they could prevent, like, over
50% of the damage because they were able to sequester the reactive oxygen species that
start to cause all the damage in the inflammatory pathways that start to get out of control. So I think that if you allow that glucose
to be used for the pentose phosphate pathway within a certain time frame…I don’t know
what that time frame is. It was something within a couple of hours. Then, independent of allowing you neurons
to get this easier source of energy…if the neurons are using glucose because they need
energy but the glucose can’t be used to repair that damage to the pentose phosphate pathway,
I think that’s one component of it in terms of the temporal effects, like how soon after
the damage.

2 comments on “Lactate and beta-hydroxybutyrate in the treatment of traumatic brain injury | Peter Attia

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