Dr. Ray Peat, Brad Marshall on Reductive Stress, Solutions to PUFA Obesity (Part 2) [v12l5nx].vtt

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 I want to hone in on the topic like Brad suggested about reductive stress in our obesity panel,

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 which you both were a part of.

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 I saw, Brad, you were smiling, you know, very happily when you heard Dr. Pete reference

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 reductive stress.

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 So I want you guys to unleash, but try as best as you can to make this accessible for

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 people who are a little new, but don't

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 let it hold you back too much.

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 Go and try to find the balance there.

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 Explain what is this reductive stress and how is this connected to PUFA and how is this

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 causing obesity?

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 Dr. Peat? The PUFA role is, part of it is just a physical chemical effect, how the fat molecule affects

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 the ionic balance of the cytoplasm and so on. But the reductive stress link to the PUFA,

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 a lot of it is through thyroid function and estrogen

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 because PUFA in the bloodstream will activate estrogen

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 while blocking thyroid.

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 Thyroid promotes an oxidative state.

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 Estrogen promotes a reductive state.

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 And so reductive stress goes with a ratio

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 of estrogen to thyroid.

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 And the immediate triggers for the fat balance. A lot of people have assumed

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 that something interferes with the oxidation of fat causing obesity. But in fact, fat people during exercise

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 burn more fat than normal lean people.

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 Estrogen makes women burn a much higher proportion

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 of fat than men burn relative to sugar metabolism, creating

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 a reductive state. synthesis of fat is increased,

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 while the oxidation is also increased.

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 And so simply the fact that people get fatter

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 made a lot of people think it's failure to oxidize fat,

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 but actually the failure to,

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 the tendency or being pushed to oxidize fat,

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 it's called the Randle effect or the Randle cycle.

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 If you are forced to oxidize fat, which fat people do very well, women do better than

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 men, that turns off your ability to oxidize glucose. And so it slows your actual oxidative consumption

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 of oxygen and production of the oxidizing balance

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 and so reductive stress.

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 The Randle cycle is a way of seeing what is forcing you into that choice to use fat

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 for energy rather you're in a reductive condition

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 by failing to oxidize glucose.

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 And that reductive condition is part

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 of what activates fatty acid synthase.

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 So you increase your production of fat,

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 well, actually, but not to a degree that compensates

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 while you're also increasing fat oxidation.

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 And that is also characteristic of cancer.

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 Cancer consumes lots of fat,

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 ends up making people waste away with cachexia.

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 But at the same time,

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 cancer activates the fatty acid synthase system.

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 And then if you can stop the fatty acid synthase system. And if you can stop the fatty acid synthase,

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 you cure both cancer and obesity.

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 And that's under the control of the redox balance.

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 So Brad, how does that fit with what you think about

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 with reductive stress and obesity

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 and try to translate this as best as you can, Bert?

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 Yeah, I think that's about right.

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 And I just wanna, you know.

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 I don't mean that insultingly either.

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 I'm just trying, I'm not a specialist like you guys,

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 so I'm trying to process this.

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 Right, and I always,

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 and this is something that I always struggle

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 to sort of define succinctly.

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 You don't have to give us all the explanations,

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 but give us a little bit of intermediate., but give us a little bit of intermediate.

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 I'll give you a little bit of information.

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 So our food, our food is, when we eat our food,

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 it's in the reduced state.

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 So carbohydrate is mostly carbon connected to hydrogen,

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 and it's also connected to oxygen.

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 And then fat is just carbon connected to hydrogen. And in those electrons

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 that live between the carbon and the hydrogen, they would be happier, or at least the oxygen

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 would be happier, if they were connected to oxygen. And so when we eat our food, it's fat,

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 which is like just carbon and hydrogen, but when we exhale it,

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 it's CO2 and H2O.

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 All those hydrogens have recombined with oxygen, and all those carbons have recombined with

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 oxygen, and that's how they leave.

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 When carbon and hydrogen leave our body after we, quote, burn the fuel, it's very oxidized, but it comes into our

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 body very reduced. And so, basically, fuel calories are all in the reduced state. And

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 the whole point of our, you know, of our metabolism is we oxidize the reduced fuel that

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 we eat. And so what happens is reductive stress in a cell sort

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 of looks like a bit like the cell has overeaten what you find

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 you have you find too much things in the reduced state and

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 this is and this usually is stated in terms of

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 intermediates. So like, so the citric acid cycle or the TCA cycle or the Krebs cycle,

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 depending on what you want to call it is,

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 is really at the heart of our metabolism. And it's this cycle, you know,

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 it's usually drawn as a circle. Um, it doesn't really spin in a circle,

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 but that doesn't matter. Every time you go around the circle,

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 you need three molecules of NAD plus,

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 which is oxidized it's oxidized NAD and it all gets converted to NADH.

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 And so for each like, p, you know, for each glucose, you need

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 like six of these NAD plus, in order to oxidize the glucose for

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 a fat molecule, you need way more, I don't know, it's a, it's

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 a big number, it's like you need 40 or something of these NAD plus

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 to oxidize the fat.

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 And so it turns out that our metabolic rate

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 is really limited by how much of this NAD plus that we have.

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 And the main way that we reconvert the NADH

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 back to NAD plus is by burning calories.

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 So if you, you know, whatever,

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 when we get up and we walk

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 our muscle cells and our legs are burning calories, and what's happening is the NADH is

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 giving its electrons to the electron transport chain that's making ATP, we're burning that ATP,

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 and every time we're burning ATP, we're generating more NAD+. But at some point, if more fuel is coming into the cell

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 than is really required, if we're not exercising,

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 that's when you can have this buildup of things like NADH.

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 And when that happens, NAD plus drops.

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 And you can have more of something called

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 acetyl CoA comes in.

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 All of us.

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 Is this the same thing that Paul Saladino was explaining

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 when he said the cells are getting so fat,

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 they're bursting from-

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 Well, that's later.

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 That's once you've stored fat.

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 This is sort of before that.

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 This is like, what happened, this is like,

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 so all of our fuels,

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 whether it's glucose, whether it's fat,

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 whether it's alcohol, they all get converted to acetyl-CoA.

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 They really get converted to acetyl groups.

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 CoA just is sort of the chaperone,

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 but they all get converted in this CO, acetyl-CoA.

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 And the acetyl group has a bunch of these electrons

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 and the electrons need to go somewhere, right?

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 So it's really all about the flow of the electrons.

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 The acetyl group is just two carbons

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 and like four hydrogens attached to it.

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 And so what you've got is you have a bunch

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 of high energy electrons and they,

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 those electrons all need to somehow recombine

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 with oxygen to make CO2 and H2O.

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 That's how they're going to leave the

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 body. And so what you have, if you have a bunch of these acetyl groups, you have all of these

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 electrons and they need to somehow get out. Right. And so, so the body essentially has a choice.

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 How do we get rid of the electrons? We can do one of two things. We can either burn the electrons

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 as, you know, as energy, as calories, we can do some kind of thermogenesis,

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 or we can, just as Dr. P suggested,

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 we can start converting them into fat.

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 So we can build them back into fat and we can store them.

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 And so, our metabolic rate within each cell,

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 as calories come in, our metabolic rate within each cell,

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 as calories come in, our mitochondria literally have a decision to make,

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 and they can either burn that fuel

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 or they can store that fuel.

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 And what determines that is the rate of reductive stress

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 that the cell is in.

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 If the cell sees that there's a lot of NADH

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 and not much NAD+, and if there's a lot

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 of these, if there's a lot of this acetyl-CoA around, which is basically, it's all fuel,

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 right?

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 The cell sees, the mitochondria sees fuel burning up, both as NADH and as acetyl-CoA.

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 Now the cell is in reductive stress.

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 When that happens, the cell is going to make the decision,

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 we need to store this as fat because it's building up and we're not burning it fast enough. Right?

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 That's what this - so the cell is monitoring this kind of reductive stress. And so, okay, well,

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 what is the thing that has changed? Why did we not used to be in this reductive stress? And now we are because we ate these vegetable oils.

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 And what I believe it is, is there is a system in the

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 mitochondria, and it is, it's sort of a detoxification system,

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 if you want to call it that, although that's not really how I

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 think of it. What it is, is saturated fat, when we burn

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 them in the mitochondria, create a lot of reactive oxygen species.

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 And what that means is, the electrons, instead of making ATP, they're just, they're kicking out of the electron transport chain,

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 and they don't make it all the way through. And what happens is they recombine with oxygen to form this thing called superoxide. And superoxide is a

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 reactive oxygen species, it's a free radical, and everyone

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 thinks that it's bad. But the more that we learn about it, we

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 actually have this very efficient system in the

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 mitochondria, which gets rid of the kind of danger of it. And

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 this is done by something called glutathione, which a lot of

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 people probably heard about, it's called the

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 body's master antioxidant. The glutathione is our superoxide

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 dismutase comes in first, it makes hydrogen peroxide. The

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 hydrogen peroxide is very efficiently eliminated by

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 glutathione. And then glutathione reductase gives us

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 a molecule of NADP plus and this other enzyme called NNT

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 converts that to NAD plus.

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 So what happens is for every molecule of superoxide

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 that is generated in the mitochondria

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 and goes through that pathway, we get an NAD plus back.

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 And so essentially the faster that we can drive,

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 because remember, reductive stress is just too many

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 electrons that haven't recombined with oxygen.

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 So every electron that comes out of the electron transport

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 chain and creates superoxide and then is efficiently, you know, detoxified

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 or whatever you want to call it by the body.

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 Well, that's another electron.

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 That's like, it's like a, it's like a pressure valve

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 that opens up and it's like, okay, well

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 if there's too much energy in this cell

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 we open the pressure valve, we just blow off some

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 of the extra pressure and now we're no longer

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 in reductive stress because those electrons can just flow straight back

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 to oxygen and it's all dealt with very efficiently.

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 And the problem is that the PUFA,

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 when they go through the mitochondria,

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 they don't create as much input at complex two of

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 the mitochondrial electron transport chain. And that's what

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 drives the the the RLS in the first place. So my argument is

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 that this thing that we've all been very scared of this idea of

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 creating reactive oxygen species in the mitochondria sounds very

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 scary. But when everything is working correctly,

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 when everything was the way that it used to be, that, and let me be very clear about

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 the pathway of this, it's reactive oxygen species, and then it's superoxide dismutase,

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 oxygen species and then it's superoxide dismutase and that makes it into hydrogen peroxide, glutathione turns the hydrogen

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 peroxide into water, and then glutathione peroxidase, or

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 sorry, glutathione reductase gives us an NADP plus back and

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 then NADP plus swaps the NADP plus into NAD plus.

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 And that NAD plus is what allows our metabolism

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 to just keep on cranking.

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 And so that system of getting rid

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 of the reactive oxygen species is actually,

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 that's the top gear of our metabolism.

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 And the PUFA eliminates it.

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 And everybody's like, well, PUFA are great

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 because they eliminate, you know,

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 when we oxidize PUFA in our mitochondria,

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 we're not making as many reactive oxygen species.

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 And that's true, we're not.

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 But the problem is that the reactive oxygen species

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 actually are the fifth gear of our metabolism.

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 You know, that's what I think.

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 And that's what I think is ultimately

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 the problem with the PUFA.

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 The alternative to all of that though

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 is to oxidize more glucose.

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 And the medical doctrine about diabetes

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 has totally deranged,

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 made it impossible for them to understand

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 what reductive stress is.

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 They say that eating too much sugar

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 can cause reductive stress.

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 And they say,

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 reductive stress and they say, see the people who are making lactic acid

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 showing excess reduction are doing it

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 because they have high glucose.

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 They put the blame on glucose rather than seeing

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 it's the oxidation of fats blocking through the Randle cycle effect,

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 blocking the ability to oxidize glucose to carbon dioxide. And if you think of the meaning of oxygen, where the concept came from, it means acid

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 source, oxy, acid, and gin.

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 And oxygen is recognized as the acidifier of the cytoplasm.

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 And the cytoplasm is alive when it's acidic.

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 The living state depends on oxygen

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 creating a constant acid tension,

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 in effect a deficiency of electrons. Basically, by the presence of carbon dioxide

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 attaching to the protein water system of the cell, oxygen making carbon dioxide acidifies the cell and sustains life.

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 The diabetes theory gets it exactly backwards seeing glucose as a reductant.

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 Glucose is the formation of fat. reduction condition produced by a deficiency of carbon dioxide from lower glucose consumption.

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 The deficiency of carbon dioxide is what turns on the fatty acid synthase and turns on the production of fat even when we should be using the energy

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 rather than storing it as fat. that is where the reductive imbalance becomes obvious with oxidation of glucose to carbon

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 dioxide, decreasing the oxidative state of the cytoplasm or favoring a reductive state

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 of the cytoplasm. And that's why breathing

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 carbon dioxide is therapeutic in so many ways. Anti-inflammatory, pro-respiratory.

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 Dr. Rhee, what was the thing that you said turns on the fatty acid synthase? A reductive state. Right. And one of

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 the functions, how the sick cell is seeing it, is like age pigment production. The process of making

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 The process of making fat is one way of disposing of the free electrons, keeping the cell acidified to the degree that lets becomes an electron sink.

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 So it's defensive, but with a lot of bad consequences.

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 Yeah, I mean, I think I agree

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 with most of what you're saying. I do have this question, I think, which is

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 what in your opinion would be the difference between me eating bread with

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 butter versus bread with soybean oil? How does the bread with soybean oil lead to reductive stress versus

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 the bread with butter?

0:22:10.760 --> 0:22:20.160
 Probably the major, both immediate and long-range effects are to block thyroid function and

0:22:20.160 --> 0:22:23.320
 activate estrogen function.

0:22:23.320 --> 0:22:25.520
 Right.

0:22:26.840 --> 0:22:28.680
 That happens right in the bloodstream

0:22:28.680 --> 0:22:31.440
 as you're absorbing the fat.

0:22:31.440 --> 0:22:36.440
 It turns several switches all in the wrong direction.

0:22:41.520 --> 0:22:43.000
 I know, yeah, I mean, I don't,

0:22:43.000 --> 0:22:46.820
 that's where I don't know that much about how estrogen works,

0:22:48.960 --> 0:22:50.680
 but it's very interesting.

0:22:50.680 --> 0:22:53.120
 So Brad, are you guys, can you help me understand?

0:22:53.120 --> 0:22:56.280
 It sounds like you guys are both saying high PUFA diet

0:22:57.360 --> 0:23:00.640
 causes this reductive stress problem in the cells,

0:23:00.640 --> 0:23:02.680
 which leads to obesity, but there's a little bit

0:23:02.680 --> 0:23:04.640
 of difference in how this works for both of you?

0:23:04.640 --> 0:23:05.460
 I don't understand it.

0:23:05.460 --> 0:23:11.620
 Yeah, I mean, I believe that we're both, I mean, we are both very much on the same page with the idea that

0:23:11.620 --> 0:23:19.420
 reductive stress is a buildup of molecules in the reduced state. The

0:23:19.420 --> 0:23:25.800
 example molecule that I mentioned was NADH, is the reduced version of NAD. And so when

0:23:25.800 --> 0:23:33.200
 you, when the cell is in the reduced state, as Dr. Pete said, that raises

0:23:33.200 --> 0:23:40.760
 the production of fatty acid synthase, which I'm 100% in agreement with,

0:23:40.760 --> 0:23:45.280
 absolute agreement. So I think what we are both in agreement with is when

0:23:46.560 --> 0:23:54.320
 when the state, when the cell becomes too reduced, that is when de novo lipogenesis happens. And that

0:23:54.320 --> 0:24:03.920
 is when we start making fat from our food, rather than burning fat. I think what we have

0:24:10.600 --> 0:24:18.360
 burning fat. I think what we have differences in is perhaps what causes the reductive stress in the first place when we eat, you know,

0:24:18.360 --> 0:24:23.280
 polyunsaturated fat, and there's a good chance that we're actually both correct.

0:24:23.280 --> 0:24:25.480
 We're talking about two different mechanisms,

0:24:25.480 --> 0:24:30.940
 but as far as I know, they might be reinforcing mechanisms. I don't think there's any reason

0:24:30.940 --> 0:24:33.600
 to think that one, you know...

0:24:33.600 --> 0:24:38.240
 So you're saying what? Because Dr. Pete's saying it's estrogen, right?

0:24:38.240 --> 0:24:48.000
 Dr. Pete is saying that it has effects on, yes, estrogen and... And thyroid. estrogen and, um, and thyroid, thyroid hormone.

0:24:48.480 --> 0:24:55.080
 And you're saying it's what I am suggesting that it actually has to do with, uh, this

0:24:55.100 --> 0:25:06.760
 mitochondrial system of, of ROS, this, uh, system of, of reactive oxygen species removal, which involves glutathione

0:25:06.760 --> 0:25:13.360
 reductase and the enzyme called NNT, both of which together,

0:25:13.400 --> 0:25:18.760
 while removing reactive oxygen species, they end up oxidizing

0:25:18.760 --> 0:25:24.440
 the NADH back to NAD+. So it's this kind of physical mechanism

0:25:24.480 --> 0:25:28.640
 of oxidizing NADH and giving us back NAD+,

0:25:28.640 --> 0:25:33.560
 with a net result that the reactive oxygen species are eliminated.

0:25:33.560 --> 0:25:49.640
 If you increase your thyroid function, which increases oxidation of glucose and production of CO2, the production of reactive oxygen species

0:25:49.640 --> 0:25:58.000
 declines sharply as oxygen consumption increases.

0:25:58.000 --> 0:26:08.680
 Uncoupling to survive, there's a good paper with that title. The faster you run the electron transport chain

0:26:09.800 --> 0:26:14.800
 oxidizing all the way to oxygen,

0:26:16.120 --> 0:26:21.120
 and the mechanism is that that increases your CO2 production

0:26:22.960 --> 0:26:30.640
 and it simultaneously suppresses reactive oxygen formation.

0:26:30.640 --> 0:26:49.000
 So the relatively quiet mitochondrion can be producing very toxic reactive oxygen species. And if you can get it revved up with thyroid and glucose

0:26:49.000 --> 0:26:54.000
 and CO2, that suppresses the reactive oxygen.

0:26:54.760 --> 0:26:57.480
 Right, and I don't disagree with any of that.

0:26:57.480 --> 0:26:59.620
 And what I've seen is that,

0:27:01.520 --> 0:27:03.240
 you know, for instance,

0:27:04.680 --> 0:27:12.040
 in a lot of mouse models, for instance, in a lot of mouse models, for instance, there is a mouse model

0:27:12.040 --> 0:27:24.120
 that sort of stimulates intense reductive stress, which is they've made a knockout of

0:27:24.120 --> 0:27:29.400
 the gene S three. And so anyway, I don't want to go into the

0:27:29.400 --> 0:27:32.900
 whole story of that. But But those mice, as Dr. Pete

0:27:32.900 --> 0:27:37.200
 suggests, while they're on a high glucose or a high starch

0:27:37.200 --> 0:27:42.300
 diet, they burn tons of glucose, and they're just fine. But when

0:27:42.300 --> 0:27:45.560
 they start to oxidize too much

0:27:45.560 --> 0:27:48.360
 fat, that's when they get into problems. And that's when you

0:27:48.360 --> 0:27:54.280
 see fatty acid synthase spike. And so I think that this this

0:27:54.320 --> 0:27:58.360
 RLS system that I'm talking about, and this RLS removal

0:27:58.360 --> 0:28:02.760
 system is very specific to when the animal is on a high fat

0:28:02.760 --> 0:28:06.280
 diet, or when the animal is actually a high fat diet or when the animal is actually burning a lot of its

0:28:06.280 --> 0:28:09.720
 own fat, presumably.

0:28:09.720 --> 0:28:16.400
 I think that the ability to burn glucose is clearly good.

0:28:16.400 --> 0:28:18.720
 If you can burn glucose, that's great.

0:28:18.720 --> 0:28:21.760
 That's what healthy animals are supposed to be able to do.

0:28:21.760 --> 0:28:26.000
 I think that's very clear that that's true in humans. And it's more when we

0:28:26.640 --> 0:28:32.880
 burn a high fat diet, that's when we tend to see the reductive stress. And so I think that the

0:28:34.080 --> 0:28:40.960
 system that I'm talking about really is specific to the quality of the fat that you're burning

0:28:40.960 --> 0:28:45.580
 when you're burning fat, which I also agree with Dr. P that that happens.

0:28:46.480 --> 0:28:49.420
 Mostly, one, if you're eating a high-fat diet,

0:28:49.420 --> 0:28:51.720
 but also if you're obese,

0:28:53.020 --> 0:28:57.440
 you tend to rely a lot more on that leg of your metabolism,

0:28:57.440 --> 0:28:59.040
 which is burning fat.

0:28:59.040 --> 0:29:01.480
 And that is when you can get into more trouble

0:29:01.480 --> 0:29:03.680
 with reductive stress.

0:29:03.680 --> 0:29:05.040
 And so I'm in 95% agreement, I think trouble with reductive stress. Um, and so I, I, I,

0:29:05.200 --> 0:29:08.960
 you know, I'm in 95% agreement, I think with Dr. Pete.

0:29:13.000 --> 0:29:13.920
 Dr. Pete, what is,

0:29:14.480 --> 0:29:18.520
 what do you think of Brad's explanation of that specific mechanism that he's

0:29:18.520 --> 0:29:21.760
 describing for the, I think it's right.

0:29:23.520 --> 0:29:26.120
 It looks like you're in 100% agreement, Brad.

0:29:26.120 --> 0:29:29.840
 It sounds that way.

0:29:29.840 --> 0:29:35.240
 So Brad has a specific, you're doing some experimentation to try to solve this obesity

0:29:35.240 --> 0:29:40.520
 problem using your own experimentation, and I wanted to see if Dr. Pete can see if that's

0:29:40.520 --> 0:29:41.520
 on the right path.

0:29:41.520 --> 0:29:44.120
 Would you mind sharing, Brad, with the class a little bit?

0:29:44.120 --> 0:29:47.360
 Yeah. and see if that's on the right path. Would you mind sharing, Brad, with the class a little bit? Yeah, well, yeah, I mean, I actually,

0:29:47.360 --> 0:29:49.600
 there is one that I'm actually very curious

0:29:49.600 --> 0:29:52.120
 about Dr. Peat's specific supplement

0:29:55.480 --> 0:29:56.800
 that I've been thinking about,

0:29:56.800 --> 0:29:58.360
 and I suspect he's not gonna like it,

0:29:58.360 --> 0:29:59.800
 but I'll let him answer.

0:29:59.800 --> 0:30:04.160
 Dr. Peat, I've been looking at the supplement

0:30:04.160 --> 0:30:05.000
 of lipoic acid.

0:30:06.860 --> 0:30:11.460
 And the reason is that it seems to oxidize NADH

0:30:11.460 --> 0:30:13.320
 back to NAD plus.

0:30:13.320 --> 0:30:14.800
 And I was wondering if that's something

0:30:14.800 --> 0:30:17.200
 you're familiar with and or had any thoughts on.

0:30:19.340 --> 0:30:23.560
 No, I don't know for dispositive it's electrons.

0:30:24.660 --> 0:30:29.560
 What's that? How does it dispose of? It seems like it seems like

0:30:29.560 --> 0:30:38.080
 what happens it has a it has two cysteines that when you consume

0:30:38.080 --> 0:30:51.720
 it are oxidized. And within hours, the molecules are taken up into, well, it seems like it has two, it

0:30:51.720 --> 0:30:54.480
 has a, I believe, a right handed and left handed version.

0:30:54.480 --> 0:31:00.360
 And one of them go into the mitochondria and the other go into the cytoplasm and those

0:31:00.360 --> 0:31:03.640
 cysteines get reduced.

0:31:03.640 --> 0:31:08.560
 And then the body essentially eliminates the lipoic acid.

0:31:08.560 --> 0:31:14.260
 And so it's a naturally produced cofactor that is used in a bunch of human enzymes.

0:31:14.260 --> 0:31:22.140
 And so it's a human compound that seems like it behaves differently if used as a supplement

0:31:22.140 --> 0:31:29.320
 versus how the body creates it. But essentially, you eat it in the oxidized form.

0:31:29.320 --> 0:31:33.000
 It relatively rapidly is reduced and then broken down

0:31:33.000 --> 0:31:35.120
 and excreted, seems to be how it works.

0:31:38.200 --> 0:31:41.900
 It's a pretty long track record of having good evidence,

0:31:41.900 --> 0:31:43.860
 both in mouse and human studies.

0:31:43.860 --> 0:31:48.200
 And it's something that I've been experimenting with.

0:31:50.820 --> 0:31:54.920
 I've read a lot about it, but I'm not sure

0:31:54.920 --> 0:31:59.920
 how safe its disposal of the electrons is.

0:32:02.940 --> 0:32:11.840
 Right, yeah, I mean, it's like a lot of things, there are certainly lots of questions about

0:32:11.840 --> 0:32:13.000
 it.

0:32:13.000 --> 0:32:17.040
 But it does seem to be one of the few

0:32:17.040 --> 0:32:19.960
 Why is he worried about the electrons?

0:32:19.960 --> 0:32:21.480
 Is that going to cause obesity?

0:32:21.480 --> 0:32:39.040
 Is that what Dr. Peat, you're saying he might cause obesity too? No, no, just that anything that alters the cysteine and glutathione balance is likely

0:32:39.040 --> 0:32:54.320
 to be harmful more often than helpful. In this case, it seems like it is specifically, it is using the, well, yeah, it is oxidizing

0:32:54.320 --> 0:32:59.960
 NADH back to NAD+.

0:32:59.960 --> 0:33:09.800
 Seems to be its primary mode of action. And then that does sometimes have downstream effects on.

0:33:09.800 --> 0:33:12.840
 It actually tends to wind up with a more reduced glutathione

0:33:12.840 --> 0:33:17.400
 pool, but it seems like its primary mode of action

0:33:17.400 --> 0:33:21.720
 is to oxidize NADH back to NAD+.

0:33:25.160 --> 0:33:32.160
 NADH back to NAD+. That should be good.

0:33:32.160 --> 0:33:45.000
 A test would be, if you look at the resting lactate content of the blood with a supplement of lipoic acid lower that,

0:33:46.520 --> 0:33:49.900
 indicating that it is affecting the whole system

0:33:50.920 --> 0:33:54.080
 pretty much in a constructive way.

0:33:55.280 --> 0:33:58.720
 Right, yeah, in my case with a little lactate meter

0:33:58.720 --> 0:34:00.580
 that I had, it did seem to do that,

0:34:00.580 --> 0:34:03.520
 but then I ran out of the test strips

0:34:03.520 --> 0:34:09.360
 and I haven't been able to get more yet. So in one small experiment, it seemed like it did that, but I need to repeat that

0:34:09.880 --> 0:34:14.140
 But that's good, because that's exactly the test that I was planning on using.

0:34:14.140 --> 0:34:18.240
 So I'm glad that you think that's maybe on the right track.

0:34:18.240 --> 0:34:23.440
 Brad, what about your starchylic oil, your tropical nut oil, and your succulinate or

0:34:23.440 --> 0:34:25.640
 whatever that is. succinate, yeah.

0:34:25.640 --> 0:34:32.720
 Well, succinate is one that I've been.

0:34:32.720 --> 0:34:36.920
 So this is, I think, this is very specific to the idea

0:34:36.920 --> 0:34:54.000
 of when we see obesity, and when we see animals in torpor, they have down-regulated activity

0:34:54.000 --> 0:34:58.560
 of their mitochondrial complex II.

0:34:58.560 --> 0:35:03.120
 Especially in torpor, that is one of the first things that is lowered as the animal goes

0:35:03.120 --> 0:35:08.520
 into torpor. And so complex 2 is the

0:35:08.520 --> 0:35:15.320
 very thing that is driving the system that I was talking about with the ROS

0:35:15.320 --> 0:35:22.600
 production and the glutathione reductase and the NNT. And so to me when I see that

0:35:22.600 --> 0:35:27.600
 that in obesity and in torpid animals, they're both lowering this

0:35:27.600 --> 0:35:33.520
 complex two, I think, well, maybe we need to return that complex two activity.

0:35:33.520 --> 0:35:40.240
 And the first way that you do that is by getting out of reductive stress, because what happens

0:35:40.720 --> 0:35:45.640
 in reductive stress is that complex two becomes acetylated.

0:35:45.880 --> 0:35:48.680
 So when I was saying that one of the things that builds up in

0:35:48.680 --> 0:35:52.240
 reductive stress is this acetyl coenzyme a, well, those,

0:35:52.520 --> 0:35:56.120
 those acetyl groups, um, actually, uh,

0:35:56.160 --> 0:36:00.960
 will stop your, um, it seems to be a natural process.

0:36:00.960 --> 0:36:02.120
 This isn't done with an enzyme.

0:36:02.120 --> 0:36:06.060
 Those acetyl groups will literally stick on to your mitochondrial enzymes,

0:36:06.120 --> 0:36:09.600
 and they'll stop working. So complex one that transfers

0:36:09.600 --> 0:36:12.040
 electrons will just stop working, complex two will stop

0:36:12.040 --> 0:36:16.400
 working. And, and so pretty soon, all your mitochondrial

0:36:16.400 --> 0:36:19.920
 enzymes are not working anymore. And, and then you wonder, like,

0:36:19.920 --> 0:36:23.320
 why, why am I not able to burn energy? And it's like, Oh, well,

0:36:23.760 --> 0:36:26.240
 all my mitochondrial enzymes are turned off because I'm in

0:36:26.260 --> 0:36:29.600
 reductive stress, right. And so the first step is to get out of

0:36:29.600 --> 0:36:32.920
 reductive stress. And that is, and that's why, you know, I've

0:36:32.920 --> 0:36:36.320
 been thinking about things like lipoic acid as a help. And then

0:36:36.680 --> 0:36:41.960
 once you've done that, and you can do that, you can perhaps do

0:36:41.960 --> 0:36:46.000
 that with some intermittent fasting. But once you've

0:36:46.000 --> 0:36:56.000
 done that and gotten your mitochondrial enzymes working again, then the best way to stimulate

0:36:56.000 --> 0:37:01.200
 complex two, which is the first thing to get turned off in torpor, is to give it its preferred

0:37:01.200 --> 0:37:05.280
 fuel, which is the succinate. And so most what

0:37:05.280 --> 0:37:08.800
 you see is that the difference between PUFA and saturated fat

0:37:08.800 --> 0:37:15.160
 is PUFA has less input to complex two and monounsaturated

0:37:15.160 --> 0:37:19.200
 fat has less input to complex two. So the idea is that if you

0:37:19.200 --> 0:37:23.480
 were to eat some unsaturated fat with succinate, you're sort of

0:37:23.480 --> 0:37:29.080
 mimicking as if you had eaten the saturated fat in the first

0:37:29.080 --> 0:37:33.400
 place. Now that is not going to fix the effects that Dr. Pete

0:37:33.400 --> 0:37:49.100
 has suggested on estrogen. And yeah, and thyroid hormone, but at least biochemically,

0:37:51.920 --> 0:37:55.820
 it restores the balance of complex one and complex two inputs that saturated fat would have

0:37:55.820 --> 0:38:00.820
 at the mitochondrial entrance point, if that makes sense.

0:38:01.860 --> 0:38:03.960
 It was kind of a lot of jargon there, but.

0:38:03.960 --> 0:38:11.000
 Dr. Pete, does that succinate idea have any resonance with your research?

0:38:11.000 --> 0:38:14.000
 Is that I say the word right, succinate?

0:38:14.000 --> 0:38:16.000
 Succinate is what I say.

0:38:16.000 --> 0:38:20.000
 Yeah, it's a possibility.

0:38:20.000 --> 0:38:26.000
 Do you have another alternative, you know, recommendation for people trying to overcome

0:38:26.000 --> 0:38:31.000
 the obesity problem caused by this PUFA problem?

0:38:31.000 --> 0:38:56.120
 Starting with close attention to your thyroid and carbon dioxide levels. The fact that carbon dioxide in itself will turn off the production of lactate shows

0:38:56.120 --> 0:39:10.340
 that its action on the cytoplasm in many different ways is restorative of the oxidative state.

0:39:10.340 --> 0:39:25.000
 The gaseous CO2 is a powerful acid, a Lewis acid, that binds to the proteins above other things.

0:39:26.960 --> 0:39:30.040
 And in binding to the protein,

0:39:30.040 --> 0:39:34.120
 it acidifies the protein and the whole cytoplasm,

0:39:36.040 --> 0:39:39.880
 correcting in an instantaneous way

0:39:39.880 --> 0:39:42.640
 some of the reductive stress.

0:39:44.280 --> 0:39:52.120
 Simply retracting the electrons into the system, making it more

0:39:52.120 --> 0:39:53.120
 acidic.

0:39:53.120 --> 0:39:59.000
 Brad, what does that mean to you?

0:39:59.000 --> 0:40:00.000
 Can you explain?

0:40:00.000 --> 0:40:06.680
 You know, even I'm going to have to think about that one for a bit.

0:40:06.680 --> 0:40:09.200
 What does that mean in terms of a dietary intervention though?

0:40:09.200 --> 0:40:11.640
 Like what is that, Dr. Peat?

0:40:11.640 --> 0:40:17.520
 Are you saying increase your carbohydrates to burn, to get rid of the obesity problem?

0:40:17.520 --> 0:40:19.920
 Yeah, yeah.

0:40:19.920 --> 0:40:29.280
 You don't want to overload either on fat or protein because that can interfere with your

0:40:29.280 --> 0:40:37.880
 ability to oxidize enough glucose, carbohydrate.

0:40:37.880 --> 0:40:42.920
 I think...

0:40:42.920 --> 0:40:44.720
 So you want to keep your protein moderate?

0:40:44.720 --> 0:40:47.000
 Is that what you're saying?

0:40:47.000 --> 0:40:48.000
 Yeah.

0:40:48.000 --> 0:41:12.520
 The ketogenic diet often is high protein, among other things, but the ketogenic diet is powerfully stressfull, reductively by interfering with thyroid function and the consumption of electrons

0:41:12.520 --> 0:41:30.520
the concept of oxidation, if you start with Szent-Gyorgi and Gilbert Ling, the meaning of oxidation looks very

0:41:31.520 --> 0:42:14.360
 different from the standard medical thinking in terms on the Lewis acid approach. The Lewis acid of electrons and CO2 is a powerful acceptor of a set of electrons. And in doing that,

0:42:14.360 --> 0:42:31.360
 it through an inductive effect, the affinity for electrons is transmitted from the carbon dioxide through the adjoining parts

0:42:31.360 --> 0:42:51.120
 of a protein chain. And that's at the root of what reductive stress is doing wrong. The CO2 acidifies the system, retracts electrons, makes them less

0:42:51.120 --> 0:43:07.640
 reactive, less harmful. And that goes back to the very beginning of the century with Moses Gomberg and his understanding. He was

0:43:07.640 --> 0:43:32.000
 one that first produced a stable free radical. And one of his students was, powerful electron acceptors, as therapeutic agents. And that

0:43:32.000 --> 0:43:52.240
 combination of thinking of Moses Gomberg and W.F. Koch was a powerful influence on St. Georgie and working more or less at the same time, Gilbert Ling was playing the

0:43:52.240 --> 0:44:20.840
 same ideas of the long-range inducting effects of protein, of electron affinity agent, especially carbon dioxide.

0:44:20.840 --> 0:44:28.380
 You know, Dr. Gabrielle Lyon, I was listening to her, she's a natural, holistic doctor.

0:44:28.380 --> 0:44:34.460
 She has a concept called muscle-centric medicine that she believes you've got to really get

0:44:34.460 --> 0:44:42.780
 a lot of protein, especially animal protein, to improve your metabolism and ward off problems

0:44:42.780 --> 0:44:43.780
 like obesity.

0:44:43.780 --> 0:44:45.160
 It's all about gaining muscle.

0:44:45.160 --> 0:44:47.200
 She's very pro lots of protein,

0:44:47.200 --> 0:44:50.800
 but you're saying protein is in the way here

0:44:50.800 --> 0:44:52.920
 of solving obesity?

0:44:54.080 --> 0:44:56.800
 Especially some of the amino acids

0:44:58.440 --> 0:45:01.960
 that are anti-thyroid, anti-metabolic,

0:45:01.960 --> 0:45:11.480
 and cytotoxic amino acids, especially methionine, cysteine, and tryptophan.

0:45:11.480 --> 0:45:29.500
 But some of the other cytotoxins like glutamate and aspartate contribute to the problem. Once your growth slows down, then you should reduce the ratio

0:45:29.500 --> 0:45:36.940
 of protein to carbohydrates. So in your 20s and 30s, there should be a drastic cutback

0:45:36.940 --> 0:45:41.940
 in the proportion of protein to carbohydrates.

0:45:41.940 --> 0:45:47.720
 And that won't cause deterioration of muscle organs or whatever?

0:45:47.720 --> 0:45:55.440
 No, actually it helps.

0:45:55.440 --> 0:46:12.080
 If you look at restriction of just single amino acids, animal experiments found that putting methionine intake right down to the

0:46:12.080 --> 0:46:28.360
 bare limit that you need for exchanging, for renewing cells that are turning over. There's a certain amount that is required,

0:46:28.360 --> 0:46:32.640
 but anything beyond that begins to have

0:46:32.640 --> 0:46:34.320
 anti-metabolic effects.

0:46:34.320 --> 0:46:39.320
 And just by restricting mesianin to that bare minimum,

0:46:40.520 --> 0:46:45.000
 they got a 40% lifespan extension in animals

0:46:47.420 --> 0:46:50.640
 and restricting other amino acids,

0:46:51.660 --> 0:46:56.660
 you get great benefits, not necessarily as high as 40%.

0:47:01.460 --> 0:47:03.660
 Dr. Pete, I know that there is,

0:47:03.660 --> 0:47:08.160
 well, I've read a few papers recently suggesting that

0:47:08.160 --> 0:47:12.680
 branched chain amino acids, at least high circulating levels of branched chain amino

0:47:12.680 --> 0:47:22.040
 acids, were very preferred for beginning new fat chains in de novo lipogenesis.

0:47:22.040 --> 0:47:26.980
 I believe this was specific to white adipose tissue,

0:47:26.980 --> 0:47:28.960
 white fat.

0:47:28.960 --> 0:47:30.900
 Is that something you're familiar with

0:47:30.900 --> 0:47:34.240
 or do you think it's a similar

0:47:34.240 --> 0:47:36.380
 to what you were talking about?

0:47:36.380 --> 0:47:39.320
 Yeah, too much of several of the amino acids

0:47:40.400 --> 0:47:45.000
 can derange things and turn your metabolism upside down.

0:47:47.240 --> 0:47:48.080
 Yeah.

0:47:49.360 --> 0:47:51.720
 So you're suggesting that someone who's dealing

0:47:51.720 --> 0:47:53.820
 with serious obesity should increase

0:47:53.820 --> 0:47:56.120
 their carbohydrate consumption,

0:47:56.120 --> 0:47:59.400
 of course, avoid high PUFA foods

0:47:59.400 --> 0:48:03.640
 and moderate their protein consumption, is that correct?

0:48:03.640 --> 0:48:04.480
 Yes.

0:48:07.440 --> 0:48:15.000
 And does your prescription for obesity include lots of exercise of any type? No, not especially.

0:48:15.000 --> 0:48:26.320
 And there's no fasting or anything? No, normal activity.

0:48:26.320 --> 0:48:31.040
 So is that, is there specific carbohydrates you're suggesting for obesity that people

0:48:31.040 --> 0:48:33.800
 eat to lose weight that way?

0:48:33.800 --> 0:48:35.320
 No, no.

0:48:35.320 --> 0:48:51.360
 Anything that the digestive system works with, if it's indigestible, you don't want things that cause gas and discomfort.

0:48:51.360 --> 0:48:52.920
 I'm interested in exploring this.

0:48:52.920 --> 0:48:56.440
 I did carnivore for several months, nose to tail carnivore, Dr. Peat.

0:48:56.440 --> 0:49:05.000
 I was eating kidneys and liver and, you know, muscle meat, ribeyes, and that was it.

0:49:05.440 --> 0:49:07.500
 And I did it for months doing that,

0:49:07.500 --> 0:49:08.540
 testicle, everything.

0:49:08.540 --> 0:49:11.120
 I mean, I've tried everything, pancreas.

0:49:12.340 --> 0:49:16.620
 And I lost a lot of weight and I noticed

0:49:16.620 --> 0:49:18.860
 how I'd wake up and it was like when I woke up,

0:49:18.860 --> 0:49:20.580
 it was like, bam, the lights came on,

0:49:20.580 --> 0:49:21.820
 there was no grogginess.

0:49:21.820 --> 0:49:24.500
 Like when I eat a high carb diet,

0:49:24.500 --> 0:49:26.080
 and when I'm struggling with

0:49:26.080 --> 0:49:31.840
 weight, and I'm trying to eat a high-carb diet, I get groggy, I get brain fog. So what you're

0:49:31.840 --> 0:49:36.800
 saying is so, I mean, and I know you're saying the PUFAs are what's causing that, but when

0:49:36.800 --> 0:49:42.560
 someone's not eating PUFA, you're saying to increase the carbohydrates. But what was I

0:49:42.560 --> 0:49:46.720
 experiencing? I don't mean, I'm not asking you to get into my particular situation, but how come

0:49:46.720 --> 0:49:53.480
 I was finding energy and waking up fully alert when I was on a nose-to-tail carnivore diet?

0:49:53.480 --> 0:50:05.000
 The good thing about an all animal food diet is that it doesn't contain the lectins and botanical toxins.

0:50:08.760 --> 0:50:13.760
 Plants being sedentary need chemical defenses.

0:50:16.360 --> 0:50:21.360
 And so even most of the plant materials

0:50:22.760 --> 0:50:25.000
 that are good foods

0:50:25.480 --> 0:50:30.480
 do contain anti-metabolic and even toxic materials.

0:50:32.600 --> 0:50:37.400
 The PUFA function in seeds,

0:50:38.520 --> 0:50:42.360
 a lot of it looks like it's specifically

0:50:43.320 --> 0:50:50.320
 aimed at blocking animal digestion to defend the plant

0:50:50.320 --> 0:50:59.720
 making the seeds especially toxic but leaves are also among the most toxic

0:50:59.720 --> 0:51:08.560
 parts of the plant. They're essential for the plant's energy production and growth, but the fruits

0:51:08.560 --> 0:51:37.920
 are the lowest in defensive toxins. Often the fruit vegetables often have useful antibiotics and lack the mammalian

0:51:37.920 --> 0:51:46.640
 toxins that above ground parts of the plant need. So the root vegetables don't have to worry about

0:51:46.640 --> 0:51:57.520
 grazers, but they are defensive against fungus, bacteria, and worms. And so they

0:51:57.520 --> 0:52:05.000
 can improve our intestinal conditions by some antibiotic effects.

0:52:06.300 --> 0:52:09.740
 So would you be okay then, or would you recommend

0:52:09.740 --> 0:52:12.800
 or be friendly with a nose-to-tail carnivore diet

0:52:12.800 --> 0:52:15.520
 that wasn't so heavy on muscle meats,

0:52:15.520 --> 0:52:18.680
 but maybe you incorporate shellfish and liver

0:52:18.680 --> 0:52:19.880
 and other things we're gonna get

0:52:19.880 --> 0:52:21.340
 some of the carbohydrates from,

0:52:21.340 --> 0:52:24.200
 or you think that's not enough carbohydrates

0:52:24.200 --> 0:52:25.960
 for a healthy long-term

0:52:25.960 --> 0:52:26.960
 diet?

0:52:26.960 --> 0:52:45.000
 Yeah, I think for a relatively methionine and tryptophan-deficient diet is better than The things you gain from a basically meat diet

0:52:46.400 --> 0:52:51.400
 are digestibility and freedom from plant toxins,

0:52:53.280 --> 0:52:58.280
 but still you have the metabolic suppressive effect

0:52:58.600 --> 0:53:00.520
 of the tryptophan.

0:53:00.520 --> 0:53:03.960
 Dr. P, what do you think of the idea

0:53:03.960 --> 0:53:09.840
 that in a healthy person - and we see this all

0:53:09.840 --> 0:53:14.020
 over the world - that we should be burning a lot of carbohydrate and it's really good

0:53:14.020 --> 0:53:27.360
 for you, but in an obese person who has stored up a lifetime of polyunsaturated and monounsaturated fat, if that person then immediately tries to switch

0:53:27.360 --> 0:53:30.620
 to a high carbohydrate diet, it doesn't work

0:53:30.620 --> 0:53:34.600
 because you're still gonna have the reductive stress

0:53:34.600 --> 0:53:37.580
 because anytime between meals, you're switching back

0:53:37.580 --> 0:53:40.300
 to burning your own body fat, which is full

0:53:40.300 --> 0:53:44.460
 of polyunsaturated and monounsaturated fats.

0:53:44.440 --> 0:53:45.560
 of polyunsaturated and monounsaturated fats.

0:53:50.560 --> 0:53:52.280
 Yeah, and keeping adequate glycogen stores is essential

0:53:57.280 --> 0:53:57.320
 so that you don't have these surges of PUFA

0:53:59.840 --> 0:54:01.200
 coming out of your tissues.

0:54:04.620 --> 0:54:05.000
 And to store adequate glycogen,

0:54:05.000 --> 0:54:09.240
 it not only requires a carbohydrate in the diet,

0:54:09.240 --> 0:54:12.400
 but a good thyroid function.

0:54:12.400 --> 0:54:16.860
 And so to unload the PUFA safely,

0:54:16.860 --> 0:54:20.840
 you need thyroid and glycogen

0:54:20.840 --> 0:54:25.000
 to activate the liver's detoxifying system.

0:54:26.100 --> 0:54:31.100
 When the liver is supported with its carbohydrate

0:54:31.420 --> 0:54:36.420
 and thyroid, it can produce the detoxifying

0:54:38.740 --> 0:54:43.400
 glucuronidation and sulfation systems

0:54:43.400 --> 0:54:45.000
 that will treat circulating PUFA

0:54:46.840 --> 0:54:51.840
 as toxins and during the night instead of circulating

0:54:52.520 --> 0:54:55.020
 and poisoning your brain progressively

0:54:56.360 --> 0:54:59.520
 because your glucose drops during the night,

0:55:00.440 --> 0:55:05.000
 creates lipolysis, bad fatty acids equilibrate

0:55:05.160 --> 0:55:08.800
 into your brain, cause brain damage every night.

0:55:10.000 --> 0:55:15.000
 If you keep your carbohydrate and thyroid up

0:55:16.880 --> 0:55:21.080
 in a good range, then your liver recognizes

0:55:21.080 --> 0:55:29.960
 those circulating PUFA molecules as toxins to be sulfated and glucuronidated

0:55:29.960 --> 0:55:36.200
 for excretion through the kidneys, so you don't have to oxidize them.

0:55:36.200 --> 0:55:38.120
 Interesting.

0:55:38.120 --> 0:55:45.200
 So, you know, I want you to be right, Dr. Pete,

0:55:45.200 --> 0:55:46.880
 because I want to eat ice cream and stuff,

0:55:46.880 --> 0:55:48.760
 but it hasn't worked out for me when I've done it,

0:55:48.760 --> 0:55:51.360
 so I gotta figure out how to do that right, you know?

0:55:51.360 --> 0:55:52.200
 You know?

0:55:57.240 --> 0:56:01.760
 Some of the safest carbohydrates are orange juice

0:56:01.760 --> 0:56:17.280
 and grape juice, because those are high in the flavonoids, which have the - inside

0:56:17.280 --> 0:56:32.740
 the cell, they work as pro-oxidants. What about, would you still recommend people avoid common wheat products when they're in

0:56:32.740 --> 0:56:35.020
 an obese state or overweight state like that?

0:56:35.020 --> 0:56:36.820
 At the poop?

0:56:36.820 --> 0:56:54.840
 If they have digestive reactions to them, yeah, bread, industrial bread is a big problem because of the way it's made.

0:56:54.840 --> 0:57:13.360
 Instead of traditional leavening, which broke down a lot of the toxins, the quick production methods leave a lot of the seed toxins in it.

0:57:13.360 --> 0:57:26.080
 Like you mentioned, white rice is a detoxified grain carbohydrate that is relatively safe.

0:57:28.000 --> 0:57:30.240
 So you would recommend that people just up their carbohydrate intake,

0:57:30.240 --> 0:57:31.840
 they don't have to add extra diet,

0:57:31.840 --> 0:57:35.680
 I mean exercise regimen into your prescription for obesity,

0:57:35.680 --> 0:57:37.720
 they just need to up their carbohydrate intake

0:57:37.720 --> 0:57:39.560
 to how many carbs a day,

0:57:39.560 --> 0:57:42.300
 how many grams of carb are we talking about here?

0:57:42.300 --> 0:57:50.980
 Oh, there are lots of animal and human experiments showing that you can add hundreds of calories

0:57:50.980 --> 0:58:05.000
 of carbohydrate to a standard diet without increasing any fat storage, because that moderate amount of increased carbohydrate

0:58:06.100 --> 0:58:10.340
 increases the metabolic rate by,

0:58:10.340 --> 0:58:14.300
 usually the experiments show a 20% increase

0:58:14.300 --> 0:58:18.260
 in metabolic rate when you add a few hundred calories

0:58:18.260 --> 0:58:20.820
 of carbohydrate to a standard diet.

0:58:22.140 --> 0:58:25.440
 Dr. Peat, is there a study like that

0:58:25.440 --> 0:58:27.240
 that you can remember off the top of your head

0:58:27.240 --> 0:58:28.840
 that would be a good one to read?

0:58:29.840 --> 0:58:30.680
 No.

0:58:33.640 --> 0:58:35.440
 Yeah, sorry, I don't mean to put you on the spot.

0:58:35.440 --> 0:58:37.540
 I know it's hard to remember these things.

0:58:37.540 --> 0:58:38.940
 I can rarely remember either.

0:58:41.760 --> 0:58:44.520
 So you're saying, are we talking like 500 carbs a day

0:58:44.520 --> 0:58:45.600
 or what are we talking about

0:58:45.600 --> 0:58:46.600
 here?

0:58:46.600 --> 0:58:49.600
 Three or four hundred has been used in…

0:58:49.600 --> 0:58:50.600
 What did you say?

0:58:50.600 --> 0:58:51.600
 I'm sorry, I didn't hear you.

0:58:51.600 --> 0:58:57.680
 Three or four hundred calories extra.

0:58:57.680 --> 0:58:59.800
 What does that translate into grams of carbs?

0:58:59.800 --> 0:59:01.560
 I'm thinking about like packaging and stuff.

0:59:01.560 --> 0:59:02.560
 It's about a hundred grams.

0:59:02.560 --> 0:59:03.560
 Four hundred would be a hundred grams.

0:59:03.560 --> 0:59:04.560
 Yeah.

0:59:04.560 --> 0:59:05.280
 So he's saying eat a hundred grams. 400 would be a hundred grams.

0:59:05.280 --> 0:59:06.280
 Yeah.

0:59:06.280 --> 0:59:08.120
 So he's saying eat a hundred carbs a day?

0:59:08.120 --> 0:59:11.040
 Is that what you're saying, Dr. Pete?

0:59:11.040 --> 0:59:14.720
 Oh, at least that.

0:59:14.720 --> 0:59:17.800
 That's still considered low carb by a lot of American standards though.

0:59:17.800 --> 0:59:19.240
 I'm trying to understand.

0:59:19.240 --> 0:59:22.600
 Yeah, I think several hundred.

0:59:22.600 --> 0:59:25.760
 That's extra added to a standard diet.

0:59:25.760 --> 0:59:26.600
 I'll tell you that.

0:59:26.600 --> 0:59:29.240
 He's saying that they've showed that if you take someone

0:59:29.240 --> 0:59:32.600
 that's at weight balance at say 2,500 calories a day

0:59:32.600 --> 0:59:35.680
 on their normal diet, you can give them an additional

0:59:35.680 --> 0:59:40.000
 300 calories of pure carbs on top of that 2,500

0:59:40.000 --> 0:59:41.720
 without weight gain.

0:59:41.720 --> 0:59:44.400
 Yeah, that's been done in several different

0:59:44.400 --> 0:59:48.680
 animal experiments as well as a few human experiments.

0:59:48.680 --> 0:59:52.000
 So how do you burn all that toxic PUFA fat

0:59:52.000 --> 0:59:53.800
 that you've stored if you're obese?

0:59:55.380 --> 0:59:57.240
 You don't really want to burn it.

0:59:57.240 --> 1:00:00.760
 You want to support your liver so it can excrete it.

1:00:16.200 --> 1:00:28.000
 excreted. When you wake up with foamy urine in the morning, a lot of that is the PUFA that has been detoxified and turned into a sulfate or a glucuronide with a soapy function, so it goes into the urine.

1:00:28.000 --> 1:00:32.000
 So you secrete the PUFA, you do not burn the PUFA.

1:00:32.000 --> 1:00:34.000
 That's the safe way to get rid of it.

1:00:34.000 --> 1:00:35.000
 Yeah.

1:00:35.000 --> 1:00:39.000
 And that takes several years once you stop eating high PUFA foods, right?

1:00:39.000 --> 1:00:48.320
 Or no? Typically, both animal and human experiments suggest four years for a complete turnover.

1:00:48.320 --> 1:00:49.320
 Wow.

1:00:49.320 --> 1:00:56.440
 So you just got to urinate it all away.

1:00:56.440 --> 1:00:58.840
 Is there another way to get out of it, to get rid of it?

1:00:58.840 --> 1:01:01.360
 That's what I've come across.

1:01:01.360 --> 1:01:03.280
 Oh my goodness.

1:01:03.280 --> 1:01:04.280
 Wow.

1:01:04.280 --> 1:01:05.360
 Wow. That's what I've come across. Oh my goodness, wow.

1:01:08.800 --> 1:01:11.900
 Wow, does that mean that if you're burning, so you're upping your carbohydrate intake

1:01:11.900 --> 1:01:16.900
 and then you don't have to add extra exercise or anything

1:01:17.840 --> 1:01:22.000
 and then that will burn the fat, the health weight,

1:01:22.000 --> 1:01:24.820
 you're burning, but how do you get rid of the fat

1:01:24.820 --> 1:01:25.640
 if you're not burning it, you're exc, but how do you get rid of the fat if you're not burning it?

1:01:25.640 --> 1:01:27.760
 I mean, you're excreting it, okay, okay.

1:01:27.760 --> 1:01:28.600
 Yeah.

1:01:30.640 --> 1:01:31.480
 Wow.

1:01:31.480 --> 1:01:34.440
 And the thyroid is essential

1:01:34.440 --> 1:01:37.960
 for liver detoxifying systems.

1:01:37.960 --> 1:01:39.880
 So just eating lots of carbohydrates,

1:01:39.880 --> 1:01:43.000
 including table sugar, can help you lose weight.

1:01:43.000 --> 1:01:49.480
 Right, it's been done experimentally.

1:01:49.480 --> 1:01:53.420
 But so everybody who's overeating carbs and gaining weight are doing it because they've

1:01:53.420 --> 1:01:57.400
 got, they're eating high PUFA too, right?

1:01:57.400 --> 1:01:58.400
 Yeah.

1:01:58.400 --> 1:01:59.400
 Okay.

1:01:59.400 --> 1:02:03.040
 And Brad, you're saying, I don't agree, or at least not necessarily, I'm not saying you're

1:02:03.040 --> 1:02:07.580
 saying disagree, but you're saying that's not enough because if you're dysfunctional

1:02:07.580 --> 1:02:11.800
 from the high PUFA accumulation you can't go straight to high carb because

1:02:11.800 --> 1:02:19.020
 that's why you're doing all your experiments. Well yeah I mean this is

1:02:19.020 --> 1:02:29.960
 this is the first time that I've heard the idea that we can eliminate the PUFA through urine. And I'm, like I say, I'm not highly

1:02:30.400 --> 1:02:33.440
 familiar with all of Dr. Pete's work. So I'm, that's

1:02:33.440 --> 1:02:37.960
 interesting to me. It certainly had not been on my radar.

1:02:38.240 --> 1:02:41.160
 Brad, I'd rather drink orange juice than sterculic oil, if

1:02:41.160 --> 1:02:41.680
 this is true.

1:02:41.680 --> 1:02:45.960
 Well, yeah. And so I'm like, well, I mean, I don't know. You know, that's interesting.

1:02:45.960 --> 1:02:50.960
 And so, but I do, I do, here's what I do agree with,

1:02:51.080 --> 1:02:56.080
 that clearly, metabolically healthy people

1:02:56.500 --> 1:02:59.000
 can consume an awful lot of carbohydrate

1:02:59.000 --> 1:03:02.560
 without it being a long-term problem.

1:03:02.560 --> 1:03:04.840
 I think that's, I think that's clear.

1:03:04.840 --> 1:03:10.320
 And I, and I agree with Dr. Pete on that.

1:03:10.320 --> 1:03:18.720
 And I also think that when I said the average West Coast adult male, according to the USDA,

1:03:18.720 --> 1:03:29.000
 was eating 5,000 calories a day in the 1930s, and Dr. Pete said, well, in the 1950s, in the Forest Service,

1:03:29.000 --> 1:03:37.040
 I was eating 9,000 calories a day. I think that was fairly normal, and when I say things

1:03:37.040 --> 1:03:42.080
 like that, everybody's like, no, that can't be possible, that can't be possible. I think

1:03:42.080 --> 1:03:46.040
 it's true. All of the evidence that we have suggested

1:03:46.040 --> 1:03:50.840
 It was true, but people don't want there's a sort of a vociferous

1:03:53.120 --> 1:03:58.280
 Somehow that really like hits at people's core beliefs, and they don't like hearing that

1:03:59.120 --> 1:04:03.360
 And then when we say well, it's not really because of exercise and dr.

1:04:03.360 --> 1:04:06.060
 P just said well when I was eating 9,000 calories a day,

1:04:06.060 --> 1:04:08.040
 I was just walking through the woods

1:04:08.040 --> 1:04:09.560
 and like placing small trees.

1:04:09.560 --> 1:04:11.680
 It wasn't particularly arduous work.

1:04:11.680 --> 1:04:13.440
 Sure, I mean, I was walking around.

1:04:15.520 --> 1:04:17.080
 And I think that that-

1:04:17.080 --> 1:04:19.640
 Is that important, Dr. Pete, that you walk around a lot,

1:04:19.640 --> 1:04:22.680
 even if it's brisk or not brisk or whatever?

1:04:23.520 --> 1:04:28.480
 Yeah, just not feeling trapped in an office cubicle

1:04:29.120 --> 1:04:34.120
 is a very de-stressing experience.

1:04:35.580 --> 1:04:39.420
 Just free movement is the important thing.

1:04:41.200 --> 1:04:43.000
 For how long a day?

1:04:44.200 --> 1:04:58.080
 Oh, well, people are sedentary mostly because they're trapped by circumstances.

1:04:58.080 --> 1:05:10.720
 If you have an opportunity to shoot baskets or play tennis or something. The fun of an activity is what's important.

1:05:10.720 --> 1:05:16.600
 Is sunlight very important for this metabolic rate increase that you're talking about?

1:05:16.600 --> 1:05:35.280
 Oh, definitely sunlight and vitamin D support the metabolic rate to the extent that you can correct obesity mostly by increasing

1:05:35.280 --> 1:05:45.960
 a person's vitamin D and calcium intake as a very anti-obesity action.

1:05:45.960 --> 1:05:50.160
 So Dr. Peat, you're suggesting that Brad doesn't, or he's talking about this experimentation

1:05:50.160 --> 1:05:55.720
 of trying to stop this reductive stress problem caused by the high PUFA.

1:05:55.720 --> 1:06:02.960
 You're saying you don't need to have an intermediary stage where you introduce these other, you

1:06:02.960 --> 1:06:07.080
 know, these lipoic acid and the succinate and all that, you

1:06:07.080 --> 1:06:10.440
 don't need to do that. You can go straight to high carb and up your

1:06:10.440 --> 1:06:19.680
 carbohydrates and you can burn, you can lose weight that way. Yeah. And you're

1:06:19.680 --> 1:06:25.980
 saying that even table sugar for massively obese people or just go wild on the table sugar can still

1:06:25.980 --> 1:06:26.980
 help or no?

1:06:26.980 --> 1:06:36.360
 Well, it isn't nutritional in other ways, but a couple of my articles I write about

1:06:36.360 --> 1:06:45.000
 a French and an English doctor who found that they could cure diabetes very quickly

1:06:46.360 --> 1:06:50.600
 by letting people eat all of the sugar

1:06:50.600 --> 1:06:54.880
 in addition to their beef and potato diet

1:06:54.880 --> 1:06:56.320
 or whatever they were eating.

1:06:57.480 --> 1:07:02.480
 And they often craved so much sugar

1:07:02.800 --> 1:07:08.720
 that they would eat approaching a pound of sugar per day,

1:07:09.680 --> 1:07:15.200
 as well as their other foods. And after just a couple of weeks of doing that,

1:07:15.920 --> 1:07:29.560
 they stopped wasting away. People who were obviously going to die quickly from the wasting of diabetes.

1:07:29.560 --> 1:07:37.200
 The wasting stopped in a couple of weeks and they recovered the ability to oxidize glucose

1:07:37.200 --> 1:07:41.080
 and could go back to a standard diet and go to work.

1:07:41.080 --> 1:07:46.520
 Well, how come people find benefit on diabetes doing ketosis though?

1:07:46.520 --> 1:07:50.280
 You know I've heard so many different stories of people you know doing

1:07:50.280 --> 1:07:55.760
 carnivore or ketogenic diets and having huge rebounding in health with diabetes

1:07:55.760 --> 1:08:01.800
 they report. Is that two ways to skin a cat or what's going on there?

1:08:15.520 --> 1:08:30.880
 What they call diabetes, many different things are called diabetes. This was a classical insulin deficient type 1 diabetes where cachexia and death from wasting are the very quick outcomes of classical

1:08:30.880 --> 1:08:32.680
 diabetes.

1:08:32.680 --> 1:08:41.680
 And obesity has been called diabetes only because it involves high blood sugar.

1:08:41.680 --> 1:08:44.960
 It's a very different thing.

1:08:44.960 --> 1:08:47.100
 Okay, I see what you're saying. I see

1:08:48.760 --> 1:08:53.040
 Do you what about the argument that people in tradition and you know

1:08:53.560 --> 1:08:58.740
 We were fat hunters. We evolved to eat. We were eating these massive fatty animals and then later on

1:08:59.400 --> 1:09:03.800
 Even in more indigenous, you know indigenous communities natives tribes and so forth

1:09:03.800 --> 1:09:05.420
 they're always eating the organ

1:09:05.420 --> 1:09:09.300
 meats and they're eating these fatty animals and megafauna.

1:09:09.300 --> 1:09:13.900
 Does that not have any support for you?

1:09:13.900 --> 1:09:28.180
 I think that's bragging by hunters who exaggerated their hunting abilities. I think the hunting gathering cultures

1:09:29.060 --> 1:09:34.060
 really were basically living on the women's gathering

1:09:34.940 --> 1:09:37.820
 of roots and fruits,

1:09:37.820 --> 1:09:42.820
 and the men occasionally would have success hunting,

1:09:44.020 --> 1:09:47.460
 but I don't think that there's any

1:09:48.980 --> 1:09:51.260
 anthropological reality to the

1:09:51.940 --> 1:09:53.900
 hunter-meat-eater

1:09:53.900 --> 1:09:57.180
 origin of people. I think we're descended from

1:09:58.180 --> 1:10:00.180
 fruit-eating monkeys.

1:10:00.940 --> 1:10:05.800
 So you don't buy the whole mammoths went extinct because they were being driven into extinction

1:10:05.800 --> 1:10:09.800
 by all these archaic hunters going out?

1:10:09.800 --> 1:10:10.800
 No.

1:10:10.800 --> 1:10:11.800
 Okay.

1:10:11.800 --> 1:10:12.800
 Interesting.

1:10:12.800 --> 1:10:15.840
 But so very fascinating stuff.

1:10:15.840 --> 1:10:21.600
 Brad, anything, any final thoughts or anything or questions?

1:10:21.600 --> 1:10:30.880
 Yeah, I mean, sorry, just getting over the flu.

1:10:30.880 --> 1:10:35.760
 Yeah, I mean, we went a lot of places there. I think it's a

1:10:35.760 --> 1:10:38.640
 good discussion. I'm trying to think if there's anything in

1:10:38.640 --> 1:10:52.840
 particular. I mean, you know, I think that Dr. Peat and I are in broad agreement that the process of this kind of

1:10:52.840 --> 1:11:08.240
 reductive stress and this over...I don't want to say overgrowth, but too much reduction, too much NADH and acetyl-CoA and all of these other reduced

1:11:08.240 --> 1:11:16.400
 things in our cells is at the root cause that is driving both de novo lipogenesis and also

1:11:16.400 --> 1:11:30.200
 our inability to efficiently use carbohydrates very broadly. And I think that, you know, the reasons why...how these polyunsaturated

1:11:30.200 --> 1:11:36.440
 fats are driving this process, and then also, what are the most efficient ways to get back

1:11:36.440 --> 1:11:43.280
 out of it once we're in it, you know, I think this is going to be topics of much interest

1:11:43.280 --> 1:11:49.120
 going forward. And obviously, you know, I think Dr. Peat and I agree very broadly

1:11:49.120 --> 1:11:52.320
 on the basics of that core idea.

1:11:52.320 --> 1:11:54.660
 And we have some disagreements on the edges,

1:11:54.660 --> 1:11:57.780
 but that's okay, obviously.

1:11:57.780 --> 1:12:00.680
 And I just think that really is where

1:12:04.280 --> 1:12:07.080
 a lot of interest should be happening.

1:12:07.080 --> 1:12:09.560
 And hopefully people are interested in this.

1:12:09.560 --> 1:12:11.720
 And I'll certainly be writing a lot about it

1:12:11.720 --> 1:12:13.440
 at fireinabottle.net.

1:12:13.440 --> 1:12:17.600
 And I think that's really on the cutting edge of where

1:12:17.600 --> 1:12:18.600
 things are going.

1:12:18.600 --> 1:12:20.280
 And there's a lot of research right now.

1:12:20.280 --> 1:12:21.520
 Brad, I would love to.

1:12:21.520 --> 1:12:23.160
 I want Dr. Peat to be right.

1:12:23.160 --> 1:12:24.840
 Because I would rather, you know, I mean,

1:12:24.840 --> 1:12:25.680
 that's what I want to,

1:12:25.680 --> 1:12:27.460
 is there any way we could do an experiment?

1:12:27.460 --> 1:12:29.600
 I mean, you're always doing these self experiments.

1:12:29.600 --> 1:12:32.120
 Is there any experimentation you could do

1:12:32.120 --> 1:12:35.200
 to try what he's saying and then see versus what you're doing

1:12:35.200 --> 1:12:36.480
 and see what the markers are

1:12:36.480 --> 1:12:37.320
 Yeah, perhaps.

1:12:37.320 --> 1:12:39.660
 I'm gonna have to think about it after this

1:12:39.660 --> 1:12:40.920
 for a little while, so,

1:12:42.360 --> 1:12:44.560
 see how we can do this.

1:12:44.560 --> 1:12:45.520
 I don't know. Like I said,

1:12:45.520 --> 1:12:47.440
 this is the first time you're hearing it, first time I'm

1:12:47.440 --> 1:12:51.360
 hearing it, so I need to puzzle through it a bit before I can

1:12:51.360 --> 1:12:55.120
 say that for sure. Dr. Peat, any thoughts you'd like to

1:12:55.120 --> 1:13:11.480
 close with? Nope. Maybe reading some of St. George's work and Gilbert Ling's for a different perspective on the

1:13:11.480 --> 1:13:12.480
 meaning of...

1:13:12.480 --> 1:13:15.200
 I'm sorry, there's some kind of noise interference.

1:13:15.200 --> 1:13:17.200
 Is that your thing, Brad?

1:13:17.200 --> 1:13:19.800
 I'm sorry.

1:13:19.800 --> 1:13:25.000
 For a different perspective on oxidation in the living system.

1:13:26.740 --> 1:13:28.820
 St. George and Gilbert Ling,

1:13:28.820 --> 1:13:32.060
 I think are always good sources.

1:13:34.760 --> 1:13:35.600
 Wow.

1:13:37.140 --> 1:13:37.980
 Well, very good.

1:13:37.980 --> 1:13:40.980
 I really appreciate your time, both of you.

1:13:40.980 --> 1:13:43.660
 And Dr. Peat, how can people join your newsletter?

1:13:43.660 --> 1:13:44.980
 Because I'm sure a lot of people would like

1:13:44.980 --> 1:13:50.280
 to join your newsletter after this very interesting discussion.

1:13:50.280 --> 1:13:55.760
 It's at RayPeat's newsletter at gmail.com.

1:13:55.760 --> 1:14:01.960
 Okay, very good. And Brad, yours is fireinabottle.net, right?

1:14:01.960 --> 1:14:02.960
 Yep.

1:14:02.960 --> 1:14:03.960
 Your blog.

1:14:03.960 --> 1:14:07.000
 And I'm FireBottle on Twitter, but yep, FireInABottle.net.

1:14:07.000 --> 1:14:09.000
 Okay, and FireInABottle on Twitter.

1:14:09.000 --> 1:14:15.800
 Thank you for, and Dr. Peat, thank you again for what you've done, because regardless of

1:14:15.800 --> 1:14:20.800
 whatever lingering debates there may be, you certainly seem to be a voice in the wilderness

1:14:20.800 --> 1:14:24.400
 about the high-PUFA seed-oil problem for many decades.

1:14:24.400 --> 1:14:29.640
 And you're like, were you lecturing before the 80s, or did you start in the 80 about the high-PUFA seed-oil problem for many decades. And you know, were you lecturing before the 80s or did you start in the 80s lecturing,

1:14:29.640 --> 1:14:30.640
 just to clarify?

1:14:30.640 --> 1:14:39.160
 Oh no, I started right away in the 70s after finishing my PhD.

1:14:39.160 --> 1:14:43.860
 Thank you for doing that because, you know, I think there's going to be a huge cascade

1:14:43.860 --> 1:14:45.960
 of people coming online to these ideas.

1:14:45.960 --> 1:14:50.520
 So it's an idea whose time has come, as we say.

1:14:50.520 --> 1:14:52.200
 Yeah.

1:14:52.200 --> 1:14:52.720
 Very good.

1:14:52.720 --> 1:14:54.320
 Thank you, guys.

1:14:54.320 --> 1:14:55.200
 All right, thank you.