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I want to hone in on the topic like Brad suggested about reductive stress in our obesity panel, which you both were a part of. I saw, Brad, you were smiling, you know, very happily when you heard Dr. Peat reference reductive stress. So I want you guys to unleash, but try as best as you can to make this accessible for people who are a little new, but don't let it hold you back too much. Go and try to find the balance there.
Explain what is this reductive stress and how is this connected to PUFA and how is this causing obesity? Dr. Peat? The PUFA role is, part of it is just a physical chemical effect, how the fat molecule affects the ionic balance of the cytoplasm and so on. But the reductive stress link to the PUFA, a lot of it is through thyroid function and estrogen because PUFA in the bloodstream will activate estrogen while blocking thyroid. Thyroid promotes an oxidative state. Estrogen promotes a reductive state. And so reductive stress goes with a ratio of estrogen to thyroid.
And the immediate triggers for the fat balance. A lot of people have assumed that something interferes with the oxidation of fat causing obesity. But in fact, fat people during exercise burn more fat than normal lean people. Estrogen makes women burn a much higher proportion of fat than men burn relative to sugar metabolism, creating a reductive state. synthesis of fat is increased, while the oxidation is also increased. And so simply the fact that people get fatter made a lot of people think it's failure to oxidize fat, but actually the failure to,
the tendency or being pushed to oxidize fat, it's called the Randle effect or the Randle cycle. If you are forced to oxidize fat, which fat people do very well, women do better than men, that turns off your ability to oxidize glucose. And so it slows your actual oxidative consumption of oxygen and production of the oxidizing balance and so reductive stress. The Randle cycle is a way of seeing what is forcing you into that choice to use fat for energy rather you're in a reductive condition by failing to oxidize glucose. And that reductive condition is part
of what activates fatty acid synthase. So you increase your production of fat, well, actually, but not to a degree that compensates while you're also increasing fat oxidation. And that is also characteristic of cancer. Cancer consumes lots of fat, ends up making people waste away with cachexia. But at the same time, cancer activates the fatty acid synthase system. And then if you can stop the fatty acid synthase system. And if you can stop the fatty acid synthase, you cure both cancer and obesity. And that's under the control of the redox balance.
So Brad, how does that fit with what you think about with reductive stress and obesity and try to translate this as best as you can, Bert? Yeah, I think that's about right. And I just wanna, you know. I don't mean that insultingly either. I'm just trying, I'm not a specialist like you guys, so I'm trying to process this. Right, and I always, and this is something that I always struggle to sort of define succinctly. You don't have to give us all the explanations,
but give us a little bit of intermediate., but give us a little bit of intermediate. I'll give you a little bit of information. So our food, our food is, when we eat our food, it's in the reduced state. So carbohydrate is mostly carbon connected to hydrogen, and it's also connected to oxygen. And then fat is just carbon connected to hydrogen. And in those electrons that live between the carbon and the hydrogen, they would be happier, or at least the oxygen
would be happier, if they were connected to oxygen. And so when we eat our food, it's fat, which is like just carbon and hydrogen, but when we exhale it, it's CO2 and H2O. All those hydrogens have recombined with oxygen, and all those carbons have recombined with oxygen, and that's how they leave. When carbon and hydrogen leave our body after we, quote, burn the fuel, it's very oxidized, but it comes into our body very reduced. And so, basically, fuel calories are all in the reduced state. And
the whole point of our, you know, of our metabolism is we oxidize the reduced fuel that we eat. And so what happens is reductive stress in a cell sort of looks like a bit like the cell has overeaten what you find you have you find too much things in the reduced state and this is and this usually is stated in terms of intermediates. So like, so the citric acid cycle or the TCA cycle or the Krebs cycle, depending on what you want to call it is,
is really at the heart of our metabolism. And it's this cycle, you know, it's usually drawn as a circle. Um, it doesn't really spin in a circle, but that doesn't matter. Every time you go around the circle, you need three molecules of NAD plus, which is oxidized it's oxidized NAD and it all gets converted to NADH. And so for each like, p, you know, for each glucose, you need like six of these NAD plus, in order to oxidize the glucose for a fat molecule, you need way more, I don't know, it's a, it's
a big number, it's like you need 40 or something of these NAD plus to oxidize the fat. And so it turns out that our metabolic rate is really limited by how much of this NAD plus that we have. And the main way that we reconvert the NADH back to NAD plus is by burning calories. So if you, you know, whatever, when we get up and we walk our muscle cells and our legs are burning calories, and what's happening is the NADH is
giving its electrons to the electron transport chain that's making ATP, we're burning that ATP, and every time we're burning ATP, we're generating more NAD+. But at some point, if more fuel is coming into the cell than is really required, if we're not exercising, that's when you can have this buildup of things like NADH. And when that happens, NAD plus drops. And you can have more of something called acetyl CoA comes in. All of us. Is this the same thing that Paul Saladino was explaining when he said the cells are getting so fat, they're bursting from-
Well, that's later. That's once you've stored fat. This is sort of before that. This is like, what happened, this is like, so all of our fuels, whether it's glucose, whether it's fat, whether it's alcohol, they all get converted to acetyl-CoA. They really get converted to acetyl groups. CoA just is sort of the chaperone, but they all get converted in this CO, acetyl-CoA. And the acetyl group has a bunch of these electrons and the electrons need to go somewhere, right? So it's really all about the flow of the electrons. The acetyl group is just two carbons
and like four hydrogens attached to it. And so what you've got is you have a bunch of high energy electrons and they, those electrons all need to somehow recombine with oxygen to make CO2 and H2O. That's how they're going to leave the body. And so what you have, if you have a bunch of these acetyl groups, you have all of these electrons and they need to somehow get out. Right. And so, so the body essentially has a choice.
How do we get rid of the electrons? We can do one of two things. We can either burn the electrons as, you know, as energy, as calories, we can do some kind of thermogenesis, or we can, just as Dr. P suggested, we can start converting them into fat. So we can build them back into fat and we can store them. And so, our metabolic rate within each cell, as calories come in, our metabolic rate within each cell, as calories come in, our mitochondria literally have a decision to make, and they can either burn that fuel
or they can store that fuel. And what determines that is the rate of reductive stress that the cell is in. If the cell sees that there's a lot of NADH and not much NAD+, and if there's a lot of these, if there's a lot of this acetyl-CoA around, which is basically, it's all fuel, right? The cell sees, the mitochondria sees fuel burning up, both as NADH and as acetyl-CoA. Now the cell is in reductive stress. When that happens, the cell is going to make the decision,
we need to store this as fat because it's building up and we're not burning it fast enough. Right? That's what this - so the cell is monitoring this kind of reductive stress. And so, okay, well, 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. And what I believe it is, is there is a system in the mitochondria, and it is, it's sort of a detoxification system,
if you want to call it that, although that's not really how I think of it. What it is, is saturated fat, when we burn them in the mitochondria, create a lot of reactive oxygen species. And what that means is, the electrons, instead of making ATP, they're just, they're kicking out of the electron transport chain, 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 reactive oxygen species, it's a free radical, and everyone
thinks that it's bad. But the more that we learn about it, we actually have this very efficient system in the mitochondria, which gets rid of the kind of danger of it. And this is done by something called glutathione, which a lot of people probably heard about, it's called the body's master antioxidant. The glutathione is our superoxide dismutase comes in first, it makes hydrogen peroxide. The hydrogen peroxide is very efficiently eliminated by glutathione. And then glutathione reductase gives us a molecule of NADP plus and this other enzyme called NNT converts that to NAD plus.
So what happens is for every molecule of superoxide that is generated in the mitochondria and goes through that pathway, we get an NAD plus back. And so essentially the faster that we can drive, because remember, reductive stress is just too many electrons that haven't recombined with oxygen. So every electron that comes out of the electron transport chain and creates superoxide and then is efficiently, you know, detoxified or whatever you want to call it by the body. Well, that's another electron. That's like, it's like a, it's like a pressure valve
that opens up and it's like, okay, well if there's too much energy in this cell we open the pressure valve, we just blow off some of the extra pressure and now we're no longer in reductive stress because those electrons can just flow straight back to oxygen and it's all dealt with very efficiently. And the problem is that the PUFA, when they go through the mitochondria, they don't create as much input at complex two of the mitochondrial electron transport chain. And that's what drives the the the RLS in the first place. So my argument is
that this thing that we've all been very scared of this idea of creating reactive oxygen species in the mitochondria sounds very scary. But when everything is working correctly, when everything was the way that it used to be, that, and let me be very clear about the pathway of this, it's reactive oxygen species, and then it's superoxide dismutase, oxygen species and then it's superoxide dismutase and that makes it into hydrogen peroxide, glutathione turns the hydrogen peroxide into water, and then glutathione peroxidase, or sorry, glutathione reductase gives us an NADP plus back and
then NADP plus swaps the NADP plus into NAD plus. And that NAD plus is what allows our metabolism to just keep on cranking. And so that system of getting rid of the reactive oxygen species is actually, that's the top gear of our metabolism. And the PUFA eliminates it. And everybody's like, well, PUFA are great because they eliminate, you know, when we oxidize PUFA in our mitochondria, we're not making as many reactive oxygen species. And that's true, we're not. But the problem is that the reactive oxygen species actually are the fifth gear of our metabolism.
You know, that's what I think. And that's what I think is ultimately the problem with the PUFA. The alternative to all of that though is to oxidize more glucose. And the medical doctrine about diabetes has totally deranged, made it impossible for them to understand what reductive stress is. They say that eating too much sugar can cause reductive stress. And they say, reductive stress and they say, see the people who are making lactic acid showing excess reduction are doing it because they have high glucose. They put the blame on glucose rather than seeing
it's the oxidation of fats blocking through the Randle cycle effect, 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 source, oxy, acid, and gin. And oxygen is recognized as the acidifier of the cytoplasm. And the cytoplasm is alive when it's acidic. The living state depends on oxygen creating a constant acid tension, in effect a deficiency of electrons. Basically, by the presence of carbon dioxide
attaching to the protein water system of the cell, oxygen making carbon dioxide acidifies the cell and sustains life. The diabetes theory gets it exactly backwards seeing glucose as a reductant. Glucose is the formation of fat. reduction condition produced by a deficiency of carbon dioxide from lower glucose consumption. 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 rather than storing it as fat. that is where the reductive imbalance becomes obvious with oxidation of glucose to carbon
dioxide, decreasing the oxidative state of the cytoplasm or favoring a reductive state of the cytoplasm. And that's why breathing carbon dioxide is therapeutic in so many ways. Anti-inflammatory, pro-respiratory. Dr. Rhee, what was the thing that you said turns on the fatty acid synthase? A reductive state. Right. And one of the functions, how the sick cell is seeing it, is like age pigment production. The process of making 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.
So it's defensive, but with a lot of bad consequences. Yeah, I mean, I think I agree with most of what you're saying. I do have this question, I think, which is what in your opinion would be the difference between me eating bread with butter versus bread with soybean oil? How does the bread with soybean oil lead to reductive stress versus the bread with butter? Probably the major, both immediate and long-range effects are to block thyroid function and activate estrogen function. Right. That happens right in the bloodstream as you're absorbing the fat.
It turns several switches all in the wrong direction. I know, yeah, I mean, I don't, that's where I don't know that much about how estrogen works, but it's very interesting. So Brad, are you guys, can you help me understand? It sounds like you guys are both saying high PUFA diet causes this reductive stress problem in the cells, which leads to obesity, but there's a little bit of difference in how this works for both of you? I don't understand it.
Yeah, I mean, I believe that we're both, I mean, we are both very much on the same page with the idea that reductive stress is a buildup of molecules in the reduced state. The example molecule that I mentioned was NADH, is the reduced version of NAD. And so when you, when the cell is in the reduced state, as Dr. Peat said, that raises the production of fatty acid synthase, which I'm 100% in agreement with, absolute agreement. So I think what we are both in agreement with is when
when the state, when the cell becomes too reduced, that is when de novo lipogenesis happens. And that is when we start making fat from our food, rather than burning fat. I think what we have 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, polyunsaturated fat, and there's a good chance that we're actually both correct. We're talking about two different mechanisms, but as far as I know, they might be reinforcing mechanisms. I don't think there's any reason
to think that one, you know... So you're saying what? Because Dr. Peat's saying it's estrogen, right? Dr. Peat is saying that it has effects on, yes, estrogen and... And thyroid. estrogen and, um, and thyroid, thyroid hormone. And you're saying it's what I am suggesting that it actually has to do with, uh, this mitochondrial system of, of ROS, this, uh, system of, of reactive oxygen species removal, which involves glutathione reductase and the enzyme called NNT, both of which together, while removing reactive oxygen species, they end up oxidizing
the NADH back to NAD+. So it's this kind of physical mechanism of oxidizing NADH and giving us back NAD+, with a net result that the reactive oxygen species are eliminated. If you increase your thyroid function, which increases oxidation of glucose and production of CO2, the production of reactive oxygen species declines sharply as oxygen consumption increases. Uncoupling to survive, there's a good paper with that title. The faster you run the electron transport chain oxidizing all the way to oxygen, and the mechanism is that that increases your CO2 production and it simultaneously suppresses reactive oxygen formation.
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 and CO2, that suppresses the reactive oxygen. Right, and I don't disagree with any of that. And what I've seen is that, you know, for instance, in a lot of mouse models, for instance, in a lot of mouse models, for instance, there is a mouse model that sort of stimulates intense reductive stress, which is they've made a knockout of the gene S three. And so anyway, I don't want to go into the
whole story of that. But But those mice, as Dr. Peat suggests, while they're on a high glucose or a high starch diet, they burn tons of glucose, and they're just fine. But when they start to oxidize too much fat, that's when they get into problems. And that's when you see fatty acid synthase spike. And so I think that this this RLS system that I'm talking about, and this RLS removal system is very specific to when the animal is on a high fat
diet, or when the animal is actually a high fat diet or when the animal is actually burning a lot of its own fat, presumably. I think that the ability to burn glucose is clearly good. If you can burn glucose, that's great. That's what healthy animals are supposed to be able to do. I think that's very clear that that's true in humans. And it's more when we burn a high fat diet, that's when we tend to see the reductive stress. And so I think that the
system that I'm talking about really is specific to the quality of the fat that you're burning when you're burning fat, which I also agree with Dr. P that that happens. Mostly, one, if you're eating a high-fat diet, but also if you're obese, you tend to rely a lot more on that leg of your metabolism, which is burning fat. And that is when you can get into more trouble with reductive stress. And so I'm in 95% agreement, I think trouble with reductive stress. Um, and so I, I, I,
you know, I'm in 95% agreement, I think with Dr. Peat. Dr. Peat, what is, what do you think of Brad's explanation of that specific mechanism that he's describing for the, I think it's right. It looks like you're in 100% agreement, Brad. It sounds that way. So Brad has a specific, you're doing some experimentation to try to solve this obesity problem using your own experimentation, and I wanted to see if Dr. Peat can see if that's on the right path. Would you mind sharing, Brad, with the class a little bit?
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, there is one that I'm actually very curious about Dr. Peat's specific supplement that I've been thinking about, and I suspect he's not gonna like it, but I'll let him answer. Dr. Peat, I've been looking at the supplement of lipoic acid. And the reason is that it seems to oxidize NADH back to NAD plus. And I was wondering if that's something you're familiar with and or had any thoughts on.
No, I don't know for dispositive it's electrons. What's that? How does it dispose of? It seems like it seems like what happens it has a it has two cysteines that when you consume it are oxidized. And within hours, the molecules are taken up into, well, it seems like it has two, it has a, I believe, a right handed and left handed version. And one of them go into the mitochondria and the other go into the cytoplasm and those cysteines get reduced. And then the body essentially eliminates the lipoic acid.
And so it's a naturally produced cofactor that is used in a bunch of human enzymes. And so it's a human compound that seems like it behaves differently if used as a supplement versus how the body creates it. But essentially, you eat it in the oxidized form. It relatively rapidly is reduced and then broken down and excreted, seems to be how it works. It's a pretty long track record of having good evidence, both in mouse and human studies. And it's something that I've been experimenting with. I've read a lot about it, but I'm not sure
how safe its disposal of the electrons is. Right, yeah, I mean, it's like a lot of things, there are certainly lots of questions about it. But it does seem to be one of the few Why is he worried about the electrons? Is that going to cause obesity? 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 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
NADH back to NAD+. Seems to be its primary mode of action. And then that does sometimes have downstream effects on. It actually tends to wind up with a more reduced glutathione pool, but it seems like its primary mode of action is to oxidize NADH back to NAD+. NADH back to NAD+. That should be good. A test would be, if you look at the resting lactate content of the blood with a supplement of lipoic acid lower that, indicating that it is affecting the whole system pretty much in a constructive way.
Right, yeah, in my case with a little lactate meter that I had, it did seem to do that, but then I ran out of the test strips 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 But that's good, because that's exactly the test that I was planning on using. So I'm glad that you think that's maybe on the right track. Brad, what about your starchylic oil, your tropical nut oil, and your succulinate or whatever that is. succinate, yeah.
Well, succinate is one that I've been. So this is, I think, this is very specific to the idea of when we see obesity, and when we see animals in torpor, they have down-regulated activity of their mitochondrial complex II. Especially in torpor, that is one of the first things that is lowered as the animal goes into torpor. And so complex 2 is the very thing that is driving the system that I was talking about with the ROS production and the glutathione reductase and the NNT. And so to me when I see that
that in obesity and in torpid animals, they're both lowering this complex two, I think, well, maybe we need to return that complex two activity. And the first way that you do that is by getting out of reductive stress, because what happens in reductive stress is that complex two becomes acetylated. So when I was saying that one of the things that builds up in reductive stress is this acetyl coenzyme a, well, those, those acetyl groups, um, actually, uh, will stop your, um, it seems to be a natural process. This isn't done with an enzyme.
Those acetyl groups will literally stick on to your mitochondrial enzymes, and they'll stop working. So complex one that transfers electrons will just stop working, complex two will stop working. And, and so pretty soon, all your mitochondrial enzymes are not working anymore. And, and then you wonder, like, why, why am I not able to burn energy? And it's like, Oh, well, all my mitochondrial enzymes are turned off because I'm in reductive stress, right. And so the first step is to get out of reductive stress. And that is, and that's why, you know, I've
been thinking about things like lipoic acid as a help. And then once you've done that, and you can do that, you can perhaps do that with some intermittent fasting. But once you've done that and gotten your mitochondrial enzymes working again, then the best way to stimulate complex two, which is the first thing to get turned off in torpor, is to give it its preferred fuel, which is the succinate. And so most what you see is that the difference between PUFA and saturated fat is PUFA has less input to complex two and monounsaturated
fat has less input to complex two. So the idea is that if you were to eat some unsaturated fat with succinate, you're sort of mimicking as if you had eaten the saturated fat in the first place. Now that is not going to fix the effects that Dr. Peat has suggested on estrogen. And yeah, and thyroid hormone, but at least biochemically, it restores the balance of complex one and complex two inputs that saturated fat would have at the mitochondrial entrance point, if that makes sense. It was kind of a lot of jargon there, but.
Dr. Peat, does that succinate idea have any resonance with your research? Is that I say the word right, succinate? Succinate is what I say. Yeah, it's a possibility. Do you have another alternative, you know, recommendation for people trying to overcome the obesity problem caused by this PUFA problem? 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 that its action on the cytoplasm in many different ways is restorative of the oxidative state.
The gaseous CO2 is a powerful acid, a Lewis acid, that binds to the proteins above other things. And in binding to the protein, it acidifies the protein and the whole cytoplasm, correcting in an instantaneous way some of the reductive stress. Simply retracting the electrons into the system, making it more acidic. Brad, what does that mean to you? Can you explain? You know, even I'm going to have to think about that one for a bit. What does that mean in terms of a dietary intervention though? Like what is that, Dr. Peat?
Are you saying increase your carbohydrates to burn, to get rid of the obesity problem? Yeah, yeah. You don't want to overload either on fat or protein because that can interfere with your ability to oxidize enough glucose, carbohydrate. I think... So you want to keep your protein moderate? Is that what you're saying? Yeah. 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
the concept of oxidation, if you start with Szent-Gyorgi and Gilbert Ling, the meaning of oxidation looks very 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, it through an inductive effect, the affinity for electrons is transmitted from the carbon dioxide through the adjoining parts 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
reactive, less harmful. And that goes back to the very beginning of the century with Moses Gomberg and his understanding. He was one that first produced a stable free radical. And one of his students was, powerful electron acceptors, as therapeutic agents. And that combination of thinking of Moses Gomberg and W.F. Koch was a powerful influence on Szent-Györgyi and working more or less at the same time, Gilbert Ling was playing the same ideas of the long-range inducting effects of protein, of electron affinity agent, especially carbon dioxide.
You know, Dr. Gabrielle Lyon, I was listening to her, she's a natural, holistic doctor. She has a concept called muscle-centric medicine that she believes you've got to really get a lot of protein, especially animal protein, to improve your metabolism and ward off problems like obesity. It's all about gaining muscle. She's very pro lots of protein, but you're saying protein is in the way here of solving obesity? Especially some of the amino acids that are anti-thyroid, anti-metabolic, and cytotoxic amino acids, especially methionine, cysteine, and tryptophan.
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 of protein to carbohydrates. So in your 20s and 30s, there should be a drastic cutback in the proportion of protein to carbohydrates. And that won't cause deterioration of muscle organs or whatever? No, actually it helps. If you look at restriction of just single amino acids, animal experiments found that putting methionine intake right down to the
bare limit that you need for exchanging, for renewing cells that are turning over. There's a certain amount that is required, but anything beyond that begins to have anti-metabolic effects. And just by restricting mesianin to that bare minimum, they got a 40% lifespan extension in animals and restricting other amino acids, you get great benefits, not necessarily as high as 40%. Dr. Peat, I know that there is, well, I've read a few papers recently suggesting that branched chain amino acids, at least high circulating levels of branched chain amino
acids, were very preferred for beginning new fat chains in de novo lipogenesis. I believe this was specific to white adipose tissue, white fat. Is that something you're familiar with or do you think it's a similar to what you were talking about? Yeah, too much of several of the amino acids can derange things and turn your metabolism upside down. Yeah. So you're suggesting that someone who's dealing with serious obesity should increase their carbohydrate consumption, of course, avoid high PUFA foods and moderate their protein consumption, is that correct? Yes.
And does your prescription for obesity include lots of exercise of any type? No, not especially. And there's no fasting or anything? No, normal activity. So is that, is there specific carbohydrates you're suggesting for obesity that people eat to lose weight that way? No, no. Anything that the digestive system works with, if it's indigestible, you don't want things that cause gas and discomfort. I'm interested in exploring this. I did carnivore for several months, nose to tail carnivore, Dr. Peat. I was eating kidneys and liver and, you know, muscle meat, ribeyes, and that was it.
And I did it for months doing that, testicle, everything. I mean, I've tried everything, pancreas. And I lost a lot of weight and I noticed how I'd wake up and it was like when I woke up, it was like, bam, the lights came on, there was no grogginess. Like when I eat a high carb diet, and when I'm struggling with weight, and I'm trying to eat a high-carb diet, I get groggy, I get brain fog. So what you're saying is so, I mean, and I know you're saying the PUFAs are what's causing that, but when
someone's not eating PUFA, you're saying to increase the carbohydrates. But what was I experiencing? I don't mean, I'm not asking you to get into my particular situation, but how come I was finding energy and waking up fully alert when I was on a nose-to-tail carnivore diet? The good thing about an all animal food diet is that it doesn't contain the lectins and botanical toxins. Plants being sedentary need chemical defenses. And so even most of the plant materials that are good foods do contain anti-metabolic and even toxic materials. The PUFA function in seeds,
a lot of it looks like it's specifically aimed at blocking animal digestion to defend the plant making the seeds especially toxic but leaves are also among the most toxic parts of the plant. They're essential for the plant's energy production and growth, but the fruits are the lowest in defensive toxins. Often the fruit vegetables often have useful antibiotics and lack the mammalian toxins that above ground parts of the plant need. So the root vegetables don't have to worry about grazers, but they are defensive against fungus, bacteria, and worms. And so they
can improve our intestinal conditions by some antibiotic effects. So would you be okay then, or would you recommend or be friendly with a nose-to-tail carnivore diet that wasn't so heavy on muscle meats, but maybe you incorporate shellfish and liver and other things we're gonna get some of the carbohydrates from, or you think that's not enough carbohydrates for a healthy long-term diet? Yeah, I think for a relatively methionine and tryptophan-deficient diet is better than The things you gain from a basically meat diet are digestibility and freedom from plant toxins,
but still you have the metabolic suppressive effect of the tryptophan. Dr. P, what do you think of the idea that in a healthy person - and we see this all over the world - that we should be burning a lot of carbohydrate and it's really good 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 to a high carbohydrate diet, it doesn't work because you're still gonna have the reductive stress because anytime between meals, you're switching back
to burning your own body fat, which is full of polyunsaturated and monounsaturated fats. of polyunsaturated and monounsaturated fats. Yeah, and keeping adequate glycogen stores is essential so that you don't have these surges of PUFA coming out of your tissues. And to store adequate glycogen, it not only requires a carbohydrate in the diet, but a good thyroid function. And so to unload the PUFA safely, you need thyroid and glycogen to activate the liver's detoxifying system. When the liver is supported with its carbohydrate and thyroid, it can produce the detoxifying glucuronidation and sulfation systems
that will treat circulating PUFA as toxins and during the night instead of circulating and poisoning your brain progressively because your glucose drops during the night, creates lipolysis, bad fatty acids equilibrate into your brain, cause brain damage every night. If you keep your carbohydrate and thyroid up in a good range, then your liver recognizes those circulating PUFA molecules as toxins to be sulfated and glucuronidated for excretion through the kidneys, so you don't have to oxidize them. Interesting. So, you know, I want you to be right, Dr. Peat, because I want to eat ice cream and stuff,
but it hasn't worked out for me when I've done it, so I gotta figure out how to do that right, you know? You know? Some of the safest carbohydrates are orange juice and grape juice, because those are high in the flavonoids, which have the - inside the cell, they work as pro-oxidants. What about, would you still recommend people avoid common wheat products when they're in an obese state or overweight state like that? At the poop? If they have digestive reactions to them, yeah, bread, industrial bread is a big problem because of the way it's made.
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. Like you mentioned, white rice is a detoxified grain carbohydrate that is relatively safe. So you would recommend that people just up their carbohydrate intake, they don't have to add extra diet, I mean exercise regimen into your prescription for obesity, they just need to up their carbohydrate intake to how many carbs a day, how many grams of carb are we talking about here?
Oh, there are lots of animal and human experiments showing that you can add hundreds of calories of carbohydrate to a standard diet without increasing any fat storage, because that moderate amount of increased carbohydrate increases the metabolic rate by, usually the experiments show a 20% increase in metabolic rate when you add a few hundred calories of carbohydrate to a standard diet. Dr. Peat, is there a study like that that you can remember off the top of your head that would be a good one to read? No.
Yeah, sorry, I don't mean to put you on the spot. I know it's hard to remember these things. I can rarely remember either. So you're saying, are we talking like 500 carbs a day or what are we talking about here? Three or four hundred has been used in… What did you say? I'm sorry, I didn't hear you. Three or four hundred calories extra. What does that translate into grams of carbs? I'm thinking about like packaging and stuff. It's about a hundred grams. Four hundred would be a hundred grams. Yeah.
So he's saying eat a hundred grams. 400 would be a hundred grams. Yeah. So he's saying eat a hundred carbs a day? Is that what you're saying, Dr. Peat? Oh, at least that. That's still considered low carb by a lot of American standards though. I'm trying to understand. Yeah, I think several hundred. That's extra added to a standard diet. I'll tell you that. He's saying that they've showed that if you take someone that's at weight balance at say 2,500 calories a day on their normal diet, you can give them an additional
300 calories of pure carbs on top of that 2,500 without weight gain. Yeah, that's been done in several different animal experiments as well as a few human experiments. So how do you burn all that toxic PUFA fat that you've stored if you're obese? You don't really want to burn it. You want to support your liver so it can excrete it.
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. So you secrete the PUFA, you do not burn the PUFA. That's the safe way to get rid of it. Yeah. And that takes several years once you stop eating high PUFA foods, right? Or no? Typically, both animal and human experiments suggest four years for a complete turnover. Wow. So you just got to urinate it all away.
Is there another way to get out of it, to get rid of it? That's what I've come across. Oh my goodness. Wow. Wow. That's what I've come across. Oh my goodness, wow. Wow, does that mean that if you're burning, so you're upping your carbohydrate intake and then you don't have to add extra exercise or anything and then that will burn the fat, the health weight, you're burning, but how do you get rid of the fat if you're not burning it, you're exc, but how do you get rid of the fat if you're not burning it?
I mean, you're excreting it, okay, okay. Yeah. Wow. And the thyroid is essential for liver detoxifying systems. So just eating lots of carbohydrates, including table sugar, can help you lose weight. Right, it's been done experimentally. But so everybody who's overeating carbs and gaining weight are doing it because they've got, they're eating high PUFA too, right? Yeah. Okay. And Brad, you're saying, I don't agree, or at least not necessarily, I'm not saying you're saying disagree, but you're saying that's not enough because if you're dysfunctional
from the high PUFA accumulation you can't go straight to high carb because that's why you're doing all your experiments. Well yeah I mean this is 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 familiar with all of Dr. Peat's work. So I'm, that's interesting to me. It certainly had not been on my radar. Brad, I'd rather drink orange juice than sterculic oil, if this is true.
Well, yeah. And so I'm like, well, I mean, I don't know. You know, that's interesting. And so, but I do, I do, here's what I do agree with, that clearly, metabolically healthy people can consume an awful lot of carbohydrate without it being a long-term problem. I think that's, I think that's clear. And I, and I agree with Dr. Peat on that. And I also think that when I said the average West Coast adult male, according to the USDA,
was eating 5,000 calories a day in the 1930s, and Dr. Peat said, well, in the 1950s, in the Forest Service, I was eating 9,000 calories a day. I think that was fairly normal, and when I say things like that, everybody's like, no, that can't be possible, that can't be possible. I think it's true. All of the evidence that we have suggested It was true, but people don't want there's a sort of a vociferous Somehow that really like hits at people's core beliefs, and they don't like hearing that
And then when we say well, it's not really because of exercise and dr. P just said well when I was eating 9,000 calories a day, I was just walking through the woods and like placing small trees. It wasn't particularly arduous work. Sure, I mean, I was walking around. And I think that that- Is that important, Dr. Peat, that you walk around a lot, even if it's brisk or not brisk or whatever? Yeah, just not feeling trapped in an office cubicle is a very de-stressing experience. Just free movement is the important thing.
For how long a day? Oh, well, people are sedentary mostly because they're trapped by circumstances. If you have an opportunity to shoot baskets or play tennis or something. The fun of an activity is what's important. Is sunlight very important for this metabolic rate increase that you're talking about? Oh, definitely sunlight and vitamin D support the metabolic rate to the extent that you can correct obesity mostly by increasing a person's vitamin D and calcium intake as a very anti-obesity action. So Dr. Peat, you're suggesting that Brad doesn't, or he's talking about this experimentation
of trying to stop this reductive stress problem caused by the high PUFA. You're saying you don't need to have an intermediary stage where you introduce these other, you know, these lipoic acid and the succinate and all that, you don't need to do that. You can go straight to high carb and up your carbohydrates and you can burn, you can lose weight that way. Yeah. And you're saying that even table sugar for massively obese people or just go wild on the table sugar can still help or no?
Well, it isn't nutritional in other ways, but a couple of my articles I write about a French and an English doctor who found that they could cure diabetes very quickly by letting people eat all of the sugar in addition to their beef and potato diet or whatever they were eating. And they often craved so much sugar that they would eat approaching a pound of sugar per day, as well as their other foods. And after just a couple of weeks of doing that,
they stopped wasting away. People who were obviously going to die quickly from the wasting of diabetes. The wasting stopped in a couple of weeks and they recovered the ability to oxidize glucose and could go back to a standard diet and go to work. Well, how come people find benefit on diabetes doing ketosis though? You know I've heard so many different stories of people you know doing carnivore or ketogenic diets and having huge rebounding in health with diabetes they report. Is that two ways to skin a cat or what's going on there?
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 diabetes. And obesity has been called diabetes only because it involves high blood sugar. It's a very different thing. Okay, I see what you're saying. I see Do you what about the argument that people in tradition and you know We were fat hunters. We evolved to eat. We were eating these massive fatty animals and then later on
Even in more indigenous, you know indigenous communities natives tribes and so forth they're always eating the organ meats and they're eating these fatty animals and megafauna. Does that not have any support for you? I think that's bragging by hunters who exaggerated their hunting abilities. I think the hunting gathering cultures really were basically living on the women's gathering of roots and fruits, and the men occasionally would have success hunting, but I don't think that there's any anthropological reality to the hunter-meat-eater origin of people. I think we're descended from fruit-eating monkeys.
So you don't buy the whole mammoths went extinct because they were being driven into extinction by all these archaic hunters going out? No. Okay. Interesting. But so very fascinating stuff. Brad, anything, any final thoughts or anything or questions? Yeah, I mean, sorry, just getting over the flu. Yeah, I mean, we went a lot of places there. I think it's a good discussion. I'm trying to think if there's anything in particular. I mean, you know, I think that Dr. Peat and I are in broad agreement that the process of this kind of
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 things in our cells is at the root cause that is driving both de novo lipogenesis and also our inability to efficiently use carbohydrates very broadly. And I think that, you know, the reasons why...how these polyunsaturated fats are driving this process, and then also, what are the most efficient ways to get back out of it once we're in it, you know, I think this is going to be topics of much interest
going forward. And obviously, you know, I think Dr. Peat and I agree very broadly on the basics of that core idea. And we have some disagreements on the edges, but that's okay, obviously. And I just think that really is where a lot of interest should be happening. And hopefully people are interested in this. And I'll certainly be writing a lot about it at fireinabottle.net. And I think that's really on the cutting edge of where things are going. And there's a lot of research right now. Brad, I would love to.
I want Dr. Peat to be right. Because I would rather, you know, I mean, that's what I want to, is there any way we could do an experiment? I mean, you're always doing these self experiments. Is there any experimentation you could do to try what he's saying and then see versus what you're doing and see what the markers are Yeah, perhaps. I'm gonna have to think about it after this for a little while, so, see how we can do this. I don't know. Like I said,
this is the first time you're hearing it, first time I'm hearing it, so I need to puzzle through it a bit before I can say that for sure. Dr. Peat, any thoughts you'd like to close with? Nope. Maybe reading some of Szent-Györgyi's work and Gilbert Ling's for a different perspective on the meaning of... I'm sorry, there's some kind of noise interference. Is that your thing, Brad? I'm sorry. For a different perspective on oxidation in the living system. Szent-Györgyi and Gilbert Ling, I think are always good sources. Wow. Well, very good.
I really appreciate your time, both of you. And Dr. Peat, how can people join your newsletter? Because I'm sure a lot of people would like to join your newsletter after this very interesting discussion. It's at RayPeat's newsletter at gmail.com. Okay, very good. And Brad, yours is fireinabottle.net, right? Yep. Your blog. And I'm FireBottle on Twitter, but yep, FireInABottle.net. Okay, and FireInABottle on Twitter. Thank you for, and Dr. Peat, thank you again for what you've done, because regardless of whatever lingering debates there may be, you certainly seem to be a voice in the wilderness
about the high-PUFA seed-oil problem for many decades. 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, just to clarify? Oh no, I started right away in the 70s after finishing my PhD. Thank you for doing that because, you know, I think there's going to be a huge cascade of people coming online to these ideas. So it's an idea whose time has come, as we say.
Yeah. Very good. Thank you, guys. All right, thank you.