Practice English Speaking&Listening with: Inflammation and its role in Alzheimer's and Parkinson's | Tim Ferriss

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[Rhonda]: So you mentioned that you have Alzheimer's and Parkinson's on both sides of your family.

So I'm curious.

Has this changed your diet, your lifestyle?

[Tim]: Oh, definitely.

[Rhonda]: How so?

[Tim]: Well, the Parkinson's maybe a bit less so.

But on the Alzheimer's side, I have just looked at it like some scientists look at it, which

is as brain diabetes.

I think that's a helpful, simplified way of looking at it.

You I'm sure know much more about this than I do.

But there's the prevalent theory of why I say Alzheimer's has the effects it has on

cognitive performance or, in this case, degradation or otherwise.

For a long time, I was like, "It's the plaques, kind of like, plaques, it's this, it's that."

And it turns out to be more complicated than that because you have people who have massive

tangles of plaques but they seem asymptomatic.

They're 100 and x years old but they still play the piano every day or whatever it may

be.

Great movie called "The Lady and Number Six" as a side note, 109 year old piano player.

It doesn't get into Alzheimer's.

But where it has led me is just to be more cognizant of insulin, things that are related

to and/or affect insulin.

To look at not only ketosis but fasting, to look at cyclical ketogenic diets and so on,

targeted ketogenic diets where you're timing carbohydrate intake near workouts, which a

lot of endurance athletes do so they can consume like 300 or 400 grams of carbohydrates in

a day and still say in ketosis, pretty wild stuff.

[Rhonda]: Wow.

[Tim]: But what I start wondering, for instance in the case . . . because if I take supplemental

MCTs or even beta-hydroxybutyrate, and there are tasty ways to do it now.

I think it's Patrick Arnold and Prototype Nutrition.

They have a . . . well, people say KetoCaNa, C-A-N-A, but it tastes like Gatorade, basically

and it's beta-hydroxybutyrate.

If I take that when I'm not, say, above 0.6 millimolars ketones, I don't feel much.

But when my body has shifted into that fat-adapted state, I do feel it.

Off hand, I don't know what my status is from the genetic standpoint.

But what's been very interesting say for me when I'm thinking about it from the standpoint

of brain diabetes is it's not just enough . . . and this comes back to how people, if

they focus solely on the millimolar concentration, they can fool themselves because you can be

in non-nutritional ketosis but consuming a lot of supplemental beta-hydroxybutyrate and

be like, "Oh, I'm killing it.

I'm at two millimolars concentration."

Whereas I'm also taking my glucometer readings precisely because I don't want to be running

at 120 glucose and dismiss that.

If I wake up and I'm fasting 120 glucose each morning, something funny is going on that

I need to pay attention to.

Whereas if I drop into nutritional ketosis and let's just say I'm at 74, 80, even lower

and I have high millimolar, my response to at that point supplemental beta-hydroxybutyrate

is totally different.

[Rhonda]: That's interesting.

[Tim]: Anyway, I'm still kind of a novice in this space, but it's interesting stuff.

[Rhonda]: So the cyclical ketogenic diet is something that you do now practicing.

And that's, you think, as a consequence of thinking of Alzheimer's like type 2 diabetes.

It's really interesting, that connection between insulin resistance and type 2 diabetes.

I don't know if you measure any blood biomarkers or if you're aware of this, but there is a

biomarker that is present in blood that's called insulin-like receptor 1, IRS1 and it's

recently, very, very recently been shown to be a diagnostic for Alzheimer's 10 years in

advance with 100% accuracy.

[Tim]: [inaudible 00:19:13] [Rhonda]: So I don't think it's like something

that . . . well, you can modulate.

So 10 years in advance is a long to change.

[Tim]: Just by the way, you are fucked.

[Rhonda]: You're screwed.

[Tim]: Good luck with that.

Yeah.

[Rhonda]: It's inactive.

[Tim]: IRS1 using [inaudible 00:19:32] [Rhonda]: Yes.

What's interesting to me is I typically think of the connection between type 2 diabetes

and insulin resistance and Alzheimer's as the connection between inflammation and a

nerve degenerative disease because inflammation, we've now recently found that the lymphatic

system connects directly to the brain.

The lymphatic system is what carries blood cells, cytokines, inflammatory molecules and

inflammation is a major, major downstream consequence of being insulin resistance.

Inflammation causes reactive oxygen species, things that damage all sorts of cells.

But the inflammatory molecules get into the brain and they do start causing all sorts

of immune type reactions and aggregation of more amyloid beta plaques and all that stuff

starts to happen more quickly.

So I think that the inflammation . . . because if you look at people, type 2 diabetics, being

type 2 diabetic, you have a two-fold roughly increased chance of getting Alzheimer's.

But if you look at people with Alzheimer's, a small percentage of them have type 2 diabetes.

So I think that it's not just the insulin resistance.

I think there are the consequences, the byproducts, the indirect things that are associated with

. . . [Tim]: 100%

[Rhonda]: . . . type 2 diabetes that lead to Alzheimer's.

[Tim]: Yeah.

It's rarely, if ever, just one thing.

I think humans strive for simplicity and in sort of a sea of noise, especially if you're

not a trained scientist, it's like, "God, thank goodness somebody gave me a definitive

answer.

Now I know A causes B." It's like, okay, maybe as a temporary holding bay, we can use that

answer.

But it's probably not right.

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