Peter Attia

So if you're consuming three of those a day, that would be three grams of additional electrolytes, which based on what you're also getting in your food, a lot of people would say, gosh, that's too many electrolytes.

But you're not seeing the effect because of the lack of chloride.

Yeah.

And I think a lot of them are recommending, in my mind, erroneously, like two to three.

Okay, I want to talk about two particular applications with ketogenic diets, one of which you've spoken about a little bit, the other one we've sort of talked about kind of indirectly.

But let's say a word about what you think the future is for ketogenic diets and the treatment of cancer, and then separately for the treatment of dementia, specifically potentially Alzheimer's disease, but any form of dementia.

You're at the entry of that zone.

Let me ask a point-blank question, Dom.

Glioblastoma carries with it a mortality rate of 100%.

So it's been said that any patient who survives a glioblastoma has been misdiagnosed.

They didn't have glioblastoma.

It's one of the cancers that really gives cancer a bad name.

Is there any evidence that any form of ketogenic diet, even at a one-to-one ratio of glucose to ketone, is going to produce a durable remission in a patient with the GBM?

In an RCT, when you place full standard of care versus full standard of care plus ketogenic therapy, what is the difference in median survival?

But it's hard to imagine you're ever going to get glucose to less than 40% of the brain's fuel, which would be a big achievement.

If you did all of those tricks, you ramped up ketones, you took glucose down peripherally to 2.5, even 3 millimole.

So if you have a glucose to ketone index of 1.1 and they're both sitting at 3 millimole, then you're doing all those therapies.

The neurons are still getting 40 to 50% of their energy from glucose.

None of this has been demonstrated clinically.

This is all kind of anecdotal, meaning we don't have evidence in a clinical trial that this works.