WEBVTT 0:00:00.000 --> 0:00:07.800 I want to hone in on the topic like Brad suggested about reductive stress in our obesity panel, 0:00:07.800 --> 0:00:09.000 which you both were a part of. 0:00:09.000 --> 0:00:16.020 I saw, Brad, you were smiling, you know, very happily when you heard Dr. Peat reference 0:00:16.020 --> 0:00:17.160 reductive stress. 0:00:17.160 --> 0:00:23.480 So I want you guys to unleash, but try as best as you can to make this accessible for 0:00:23.480 --> 0:00:25.260 people who are a little new, but don't 0:00:25.260 --> 0:00:26.460 let it hold you back too much. 0:00:26.460 --> 0:00:28.780 Go and try to find the balance there. 0:00:28.780 --> 0:00:34.000 Explain what is this reductive stress and how is this connected to PUFA and how is this 0:00:34.000 --> 0:00:35.340 causing obesity? 0:00:35.340 --> 0:00:54.840 Dr. Peat? The PUFA role is, part of it is just a physical chemical effect, how the fat molecule affects 0:00:54.840 --> 0:01:05.000 the ionic balance of the cytoplasm and so on. But the reductive stress link to the PUFA, 0:01:08.560 --> 0:01:13.560 a lot of it is through thyroid function and estrogen 0:01:13.720 --> 0:01:18.720 because PUFA in the bloodstream will activate estrogen 0:01:20.280 --> 0:01:23.000 while blocking thyroid. 0:01:23.000 --> 0:01:27.100 Thyroid promotes an oxidative state. 0:01:27.920 --> 0:01:31.680 Estrogen promotes a reductive state. 0:01:31.680 --> 0:01:36.680 And so reductive stress goes with a ratio 0:01:37.000 --> 0:01:41.080 of estrogen to thyroid. 0:01:42.080 --> 0:01:57.000 And the immediate triggers for the fat balance. A lot of people have assumed 0:01:57.000 --> 0:02:09.520 that something interferes with the oxidation of fat causing obesity. But in fact, fat people during exercise 0:02:12.040 --> 0:02:16.160 burn more fat than normal lean people. 0:02:18.040 --> 0:02:23.040 Estrogen makes women burn a much higher proportion 0:02:23.880 --> 0:02:32.560 of fat than men burn relative to sugar metabolism, creating 0:02:32.560 --> 0:02:45.000 a reductive state. synthesis of fat is increased, 0:02:45.680 --> 0:02:49.560 while the oxidation is also increased. 0:02:51.020 --> 0:02:56.020 And so simply the fact that people get fatter 0:02:56.040 --> 0:03:01.040 made a lot of people think it's failure to oxidize fat, 0:03:01.680 --> 0:03:05.000 but actually the failure to, 0:03:07.160 --> 0:03:12.160 the tendency or being pushed to oxidize fat, 0:03:16.640 --> 0:03:20.560 it's called the Randle effect or the Randle cycle. 0:03:21.760 --> 0:03:30.760 If you are forced to oxidize fat, which fat people do very well, women do better than 0:03:30.760 --> 0:03:45.000 men, that turns off your ability to oxidize glucose. And so it slows your actual oxidative consumption 0:03:49.040 --> 0:03:54.040 of oxygen and production of the oxidizing balance 0:03:57.880 --> 0:03:59.580 and so reductive stress. 0:04:01.120 --> 0:04:14.200 The Randle cycle is a way of seeing what is forcing you into that choice to use fat 0:04:14.200 --> 0:04:25.000 for energy rather you're in a reductive condition 0:04:29.200 --> 0:04:32.340 by failing to oxidize glucose. 0:04:33.420 --> 0:04:38.420 And that reductive condition is part 0:04:43.020 --> 0:04:45.000 of what activates fatty acid synthase. 0:04:47.240 --> 0:04:51.640 So you increase your production of fat, 0:04:51.640 --> 0:04:56.640 well, actually, but not to a degree that compensates 0:04:57.560 --> 0:05:01.780 while you're also increasing fat oxidation. 0:05:03.240 --> 0:05:08.280 And that is also characteristic of cancer. 0:05:08.560 --> 0:05:12.480 Cancer consumes lots of fat, 0:05:12.480 --> 0:05:16.880 ends up making people waste away with cachexia. 0:05:16.880 --> 0:05:18.640 But at the same time, 0:05:18.640 --> 0:05:23.640 cancer activates the fatty acid synthase system. 0:05:24.000 --> 0:05:26.940 And then if you can stop the fatty acid synthase system. And if you can stop the fatty acid synthase, 0:05:27.780 --> 0:05:30.920 you cure both cancer and obesity. 0:05:32.540 --> 0:05:37.460 And that's under the control of the redox balance. 0:05:39.620 --> 0:05:41.820 So Brad, how does that fit with what you think about 0:05:41.820 --> 0:05:43.360 with reductive stress and obesity 0:05:43.360 --> 0:05:46.260 and try to translate this as best as you can, Bert? 0:05:46.260 --> 0:05:48.160 Yeah, I think that's about right. 0:05:48.160 --> 0:05:52.080 And I just wanna, you know. 0:05:52.080 --> 0:05:53.520 I don't mean that insultingly either. 0:05:53.520 --> 0:05:55.440 I'm just trying, I'm not a specialist like you guys, 0:05:55.440 --> 0:05:57.120 so I'm trying to process this. 0:05:57.120 --> 0:05:57.960 Right, and I always, 0:05:57.960 --> 0:05:59.480 and this is something that I always struggle 0:05:59.480 --> 0:06:02.640 to sort of define succinctly. 0:06:02.640 --> 0:06:04.300 You don't have to give us all the explanations, 0:06:04.300 --> 0:06:05.480 but give us a little bit of intermediate., but give us a little bit of intermediate. 0:06:05.480 --> 0:06:07.120 I'll give you a little bit of information. 0:06:07.120 --> 0:06:11.360 So our food, our food is, when we eat our food, 0:06:11.360 --> 0:06:12.920 it's in the reduced state. 0:06:12.920 --> 0:06:17.920 So carbohydrate is mostly carbon connected to hydrogen, 0:06:19.600 --> 0:06:21.280 and it's also connected to oxygen. 0:06:21.280 --> 0:06:28.880 And then fat is just carbon connected to hydrogen. And in those electrons 0:06:28.880 --> 0:06:34.720 that live between the carbon and the hydrogen, they would be happier, or at least the oxygen 0:06:34.720 --> 0:06:42.240 would be happier, if they were connected to oxygen. And so when we eat our food, it's fat, 0:06:42.240 --> 0:06:45.180 which is like just carbon and hydrogen, but when we exhale it, 0:06:45.180 --> 0:06:48.400 it's CO2 and H2O. 0:06:48.400 --> 0:06:52.200 All those hydrogens have recombined with oxygen, and all those carbons have recombined with 0:06:52.200 --> 0:06:57.420 oxygen, and that's how they leave. 0:06:57.420 --> 0:07:08.120 When carbon and hydrogen leave our body after we, quote, burn the fuel, it's very oxidized, but it comes into our 0:07:08.120 --> 0:07:17.240 body very reduced. And so, basically, fuel calories are all in the reduced state. And 0:07:17.240 --> 0:07:25.040 the whole point of our, you know, of our metabolism is we oxidize the reduced fuel that 0:07:25.040 --> 0:07:29.640 we eat. And so what happens is reductive stress in a cell sort 0:07:29.640 --> 0:07:33.640 of looks like a bit like the cell has overeaten what you find 0:07:33.640 --> 0:07:37.600 you have you find too much things in the reduced state and 0:07:37.600 --> 0:07:40.800 this is and this usually is stated in terms of 0:07:40.800 --> 0:07:47.960 intermediates. So like, so the citric acid cycle or the TCA cycle or the Krebs cycle, 0:07:47.960 --> 0:07:49.960 depending on what you want to call it is, 0:07:50.000 --> 0:07:53.960 is really at the heart of our metabolism. And it's this cycle, you know, 0:07:53.960 --> 0:07:57.760 it's usually drawn as a circle. Um, it doesn't really spin in a circle, 0:07:57.760 --> 0:08:00.480 but that doesn't matter. Every time you go around the circle, 0:08:00.480 --> 0:08:03.960 you need three molecules of NAD plus, 0:08:04.360 --> 0:08:08.840 which is oxidized it's oxidized NAD and it all gets converted to NADH. 0:08:09.160 --> 0:08:13.960 And so for each like, p, you know, for each glucose, you need 0:08:13.960 --> 0:08:20.160 like six of these NAD plus, in order to oxidize the glucose for 0:08:20.160 --> 0:08:23.440 a fat molecule, you need way more, I don't know, it's a, it's 0:08:23.440 --> 0:08:27.540 a big number, it's like you need 40 or something of these NAD plus 0:08:27.540 --> 0:08:28.700 to oxidize the fat. 0:08:28.700 --> 0:08:31.660 And so it turns out that our metabolic rate 0:08:31.660 --> 0:08:35.280 is really limited by how much of this NAD plus that we have. 0:08:35.280 --> 0:08:39.800 And the main way that we reconvert the NADH 0:08:39.800 --> 0:08:42.680 back to NAD plus is by burning calories. 0:08:42.680 --> 0:08:44.280 So if you, you know, whatever, 0:08:44.280 --> 0:08:45.920 when we get up and we walk 0:08:47.680 --> 0:08:52.720 our muscle cells and our legs are burning calories, and what's happening is the NADH is 0:08:53.360 --> 0:08:59.680 giving its electrons to the electron transport chain that's making ATP, we're burning that ATP, 0:08:59.680 --> 0:09:09.800 and every time we're burning ATP, we're generating more NAD+. But at some point, if more fuel is coming into the cell 0:09:10.160 --> 0:09:14.240 than is really required, if we're not exercising, 0:09:14.240 --> 0:09:19.240 that's when you can have this buildup of things like NADH. 0:09:20.780 --> 0:09:23.920 And when that happens, NAD plus drops. 0:09:25.740 --> 0:09:28.480 And you can have more of something called 0:09:28.480 --> 0:09:31.620 acetyl CoA comes in. 0:09:31.620 --> 0:09:32.460 All of us. 0:09:32.460 --> 0:09:34.240 Is this the same thing that Paul Saladino was explaining 0:09:34.240 --> 0:09:36.100 when he said the cells are getting so fat, 0:09:36.100 --> 0:09:37.420 they're bursting from- 0:09:37.420 --> 0:09:38.260 Well, that's later. 0:09:38.260 --> 0:09:39.780 That's once you've stored fat. 0:09:39.780 --> 0:09:41.180 This is sort of before that. 0:09:41.180 --> 0:09:43.800 This is like, what happened, this is like, 0:09:43.800 --> 0:09:46.720 so all of our fuels, 0:09:46.720 --> 0:09:48.960 whether it's glucose, whether it's fat, 0:09:48.960 --> 0:09:53.960 whether it's alcohol, they all get converted to acetyl-CoA. 0:09:54.280 --> 0:09:56.440 They really get converted to acetyl groups. 0:09:56.440 --> 0:09:58.520 CoA just is sort of the chaperone, 0:09:58.520 --> 0:10:02.920 but they all get converted in this CO, acetyl-CoA. 0:10:02.920 --> 0:10:05.460 And the acetyl group has a bunch of these electrons 0:10:05.460 --> 0:10:08.320 and the electrons need to go somewhere, right? 0:10:08.320 --> 0:10:10.440 So it's really all about the flow of the electrons. 0:10:10.440 --> 0:10:12.200 The acetyl group is just two carbons 0:10:12.200 --> 0:10:14.820 and like four hydrogens attached to it. 0:10:15.840 --> 0:10:17.560 And so what you've got is you have a bunch 0:10:17.560 --> 0:10:19.400 of high energy electrons and they, 0:10:19.400 --> 0:10:21.760 those electrons all need to somehow recombine 0:10:21.760 --> 0:10:24.720 with oxygen to make CO2 and H2O. 0:10:24.720 --> 0:10:25.520 That's how they're going to leave the 0:10:25.520 --> 0:10:30.640 body. And so what you have, if you have a bunch of these acetyl groups, you have all of these 0:10:30.640 --> 0:10:36.160 electrons and they need to somehow get out. Right. And so, so the body essentially has a choice. 0:10:36.880 --> 0:10:41.520 How do we get rid of the electrons? We can do one of two things. We can either burn the electrons 0:10:42.080 --> 0:10:46.800 as, you know, as energy, as calories, we can do some kind of thermogenesis, 0:10:46.800 --> 0:10:51.060 or we can, just as Dr. P suggested, 0:10:51.060 --> 0:10:53.100 we can start converting them into fat. 0:10:53.100 --> 0:10:56.120 So we can build them back into fat and we can store them. 0:10:57.160 --> 0:11:02.160 And so, our metabolic rate within each cell, 0:11:05.000 --> 0:11:05.820 as calories come in, our metabolic rate within each cell, 0:11:09.260 --> 0:11:10.960 as calories come in, our mitochondria literally have a decision to make, 0:11:10.960 --> 0:11:13.220 and they can either burn that fuel 0:11:13.220 --> 0:11:15.000 or they can store that fuel. 0:11:15.000 --> 0:11:18.980 And what determines that is the rate of reductive stress 0:11:18.980 --> 0:11:20.120 that the cell is in. 0:11:20.120 --> 0:11:24.260 If the cell sees that there's a lot of NADH 0:11:24.260 --> 0:11:26.960 and not much NAD+, and if there's a lot 0:11:26.960 --> 0:11:32.560 of these, if there's a lot of this acetyl-CoA around, which is basically, it's all fuel, 0:11:32.560 --> 0:11:33.560 right? 0:11:33.560 --> 0:11:40.280 The cell sees, the mitochondria sees fuel burning up, both as NADH and as acetyl-CoA. 0:11:40.280 --> 0:11:42.320 Now the cell is in reductive stress. 0:11:42.320 --> 0:11:45.280 When that happens, the cell is going to make the decision, 0:11:45.280 --> 0:11:51.920 we need to store this as fat because it's building up and we're not burning it fast enough. Right? 0:11:51.920 --> 0:11:58.080 That's what this - so the cell is monitoring this kind of reductive stress. And so, okay, well, 0:11:58.080 --> 0:12:05.680 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. 0:12:07.440 --> 0:12:11.960 And what I believe it is, is there is a system in the 0:12:11.960 --> 0:12:16.240 mitochondria, and it is, it's sort of a detoxification system, 0:12:16.240 --> 0:12:18.520 if you want to call it that, although that's not really how I 0:12:18.520 --> 0:12:22.640 think of it. What it is, is saturated fat, when we burn 0:12:22.640 --> 0:12:26.660 them in the mitochondria, create a lot of reactive oxygen species. 0:12:26.660 --> 0:12:39.040 And what that means is, the electrons, instead of making ATP, they're just, they're kicking out of the electron transport chain, 0:12:39.040 --> 0:12:46.440 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 0:12:46.440 --> 0:12:49.120 reactive oxygen species, it's a free radical, and everyone 0:12:49.120 --> 0:12:54.040 thinks that it's bad. But the more that we learn about it, we 0:12:54.040 --> 0:12:56.280 actually have this very efficient system in the 0:12:56.280 --> 0:13:01.380 mitochondria, which gets rid of the kind of danger of it. And 0:13:01.380 --> 0:13:04.760 this is done by something called glutathione, which a lot of 0:13:04.760 --> 0:13:06.600 people probably heard about, it's called the 0:13:06.600 --> 0:13:11.760 body's master antioxidant. The glutathione is our superoxide 0:13:11.760 --> 0:13:16.120 dismutase comes in first, it makes hydrogen peroxide. The 0:13:16.120 --> 0:13:18.360 hydrogen peroxide is very efficiently eliminated by 0:13:18.360 --> 0:13:24.120 glutathione. And then glutathione reductase gives us 0:13:24.120 --> 0:13:27.800 a molecule of NADP plus and this other enzyme called NNT 0:13:29.200 --> 0:13:31.800 converts that to NAD plus. 0:13:31.800 --> 0:13:36.800 So what happens is for every molecule of superoxide 0:13:37.720 --> 0:13:39.640 that is generated in the mitochondria 0:13:39.640 --> 0:13:43.400 and goes through that pathway, we get an NAD plus back. 0:13:43.400 --> 0:13:48.400 And so essentially the faster that we can drive, 0:13:49.200 --> 0:13:53.840 because remember, reductive stress is just too many 0:13:53.840 --> 0:13:57.580 electrons that haven't recombined with oxygen. 0:13:57.580 --> 0:14:01.280 So every electron that comes out of the electron transport 0:14:01.280 --> 0:14:06.660 chain and creates superoxide and then is efficiently, you know, detoxified 0:14:06.660 --> 0:14:08.580 or whatever you want to call it by the body. 0:14:08.580 --> 0:14:10.140 Well, that's another electron. 0:14:10.140 --> 0:14:14.420 That's like, it's like a, it's like a pressure valve 0:14:14.420 --> 0:14:16.220 that opens up and it's like, okay, well 0:14:16.220 --> 0:14:18.420 if there's too much energy in this cell 0:14:18.420 --> 0:14:20.980 we open the pressure valve, we just blow off some 0:14:20.980 --> 0:14:23.140 of the extra pressure and now we're no longer 0:14:23.140 --> 0:14:26.740 in reductive stress because those electrons can just flow straight back 0:14:26.740 --> 0:14:30.040 to oxygen and it's all dealt with very efficiently. 0:14:31.860 --> 0:14:34.860 And the problem is that the PUFA, 0:14:38.980 --> 0:14:41.260 when they go through the mitochondria, 0:14:41.260 --> 0:14:45.360 they don't create as much input at complex two of 0:14:45.360 --> 0:14:48.000 the mitochondrial electron transport chain. And that's what 0:14:48.000 --> 0:14:52.560 drives the the the RLS in the first place. So my argument is 0:14:53.080 --> 0:14:56.960 that this thing that we've all been very scared of this idea of 0:14:56.960 --> 0:15:03.000 creating reactive oxygen species in the mitochondria sounds very 0:15:03.000 --> 0:15:07.120 scary. But when everything is working correctly, 0:15:07.120 --> 0:15:14.000 when everything was the way that it used to be, that, and let me be very clear about 0:15:15.440 --> 0:15:24.640 the pathway of this, it's reactive oxygen species, and then it's superoxide dismutase, 0:15:27.360 --> 0:15:31.120 oxygen species and then it's superoxide dismutase and that makes it into hydrogen peroxide, glutathione turns the hydrogen 0:15:31.120 --> 0:15:35.400 peroxide into water, and then glutathione peroxidase, or 0:15:35.400 --> 0:15:40.120 sorry, glutathione reductase gives us an NADP plus back and 0:15:40.120 --> 0:15:45.000 then NADP plus swaps the NADP plus into NAD plus. 0:15:45.200 --> 0:15:48.340 And that NAD plus is what allows our metabolism 0:15:48.340 --> 0:15:50.300 to just keep on cranking. 0:15:50.300 --> 0:15:53.680 And so that system of getting rid 0:15:53.680 --> 0:15:56.720 of the reactive oxygen species is actually, 0:15:56.720 --> 0:15:59.480 that's the top gear of our metabolism. 0:15:59.480 --> 0:16:02.360 And the PUFA eliminates it. 0:16:02.360 --> 0:16:04.480 And everybody's like, well, PUFA are great 0:16:04.480 --> 0:16:07.160 because they eliminate, you know, 0:16:07.160 --> 0:16:10.000 when we oxidize PUFA in our mitochondria, 0:16:10.000 --> 0:16:12.280 we're not making as many reactive oxygen species. 0:16:12.280 --> 0:16:14.440 And that's true, we're not. 0:16:14.440 --> 0:16:18.200 But the problem is that the reactive oxygen species 0:16:18.200 --> 0:16:22.420 actually are the fifth gear of our metabolism. 0:16:23.340 --> 0:16:25.520 You know, that's what I think. 0:16:25.520 --> 0:16:27.540 And that's what I think is ultimately 0:16:27.540 --> 0:16:30.380 the problem with the PUFA. 0:16:32.680 --> 0:16:35.560 The alternative to all of that though 0:16:35.560 --> 0:16:39.240 is to oxidize more glucose. 0:16:39.240 --> 0:16:44.240 And the medical doctrine about diabetes 0:16:44.920 --> 0:16:45.000 has totally deranged, 0:16:48.520 --> 0:16:51.600 made it impossible for them to understand 0:16:51.600 --> 0:16:54.520 what reductive stress is. 0:16:54.520 --> 0:16:58.920 They say that eating too much sugar 0:16:58.920 --> 0:17:01.420 can cause reductive stress. 0:17:02.560 --> 0:17:04.080 And they say, 0:17:04.000 --> 0:17:08.400 reductive stress and they say, see the people who are making lactic acid 0:17:08.400 --> 0:17:13.400 showing excess reduction are doing it 0:17:13.960 --> 0:17:17.780 because they have high glucose. 0:17:17.780 --> 0:17:22.080 They put the blame on glucose rather than seeing 0:17:23.440 --> 0:17:33.040 it's the oxidation of fats blocking through the Randle cycle effect, 0:17:33.040 --> 0:17:50.900 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 0:17:50.900 --> 0:17:56.720 source, oxy, acid, and gin. 0:17:56.720 --> 0:18:05.000 And oxygen is recognized as the acidifier of the cytoplasm. 0:18:05.240 --> 0:18:10.240 And the cytoplasm is alive when it's acidic. 0:18:13.200 --> 0:18:17.140 The living state depends on oxygen 0:18:17.140 --> 0:18:21.460 creating a constant acid tension, 0:18:23.040 --> 0:18:33.000 in effect a deficiency of electrons. Basically, by the presence of carbon dioxide 0:18:33.000 --> 0:18:47.000 attaching to the protein water system of the cell, oxygen making carbon dioxide acidifies the cell and sustains life. 0:18:47.000 --> 0:18:55.920 The diabetes theory gets it exactly backwards seeing glucose as a reductant. 0:18:55.920 --> 0:19:36.160 Glucose is the formation of fat. reduction condition produced by a deficiency of carbon dioxide from lower glucose consumption. 0:19:36.160 --> 0:19:55.720 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 0:19:55.720 --> 0:20:12.200 rather than storing it as fat. that is where the reductive imbalance becomes obvious with oxidation of glucose to carbon 0:20:12.200 --> 0:20:22.600 dioxide, decreasing the oxidative state of the cytoplasm or favoring a reductive state 0:20:22.600 --> 0:20:27.440 of the cytoplasm. And that's why breathing 0:20:27.440 --> 0:20:38.000 carbon dioxide is therapeutic in so many ways. Anti-inflammatory, pro-respiratory. 0:20:38.120 --> 0:20:50.400 Dr. Rhee, what was the thing that you said turns on the fatty acid synthase? A reductive state. Right. And one of 0:20:50.400 --> 0:21:01.440 the functions, how the sick cell is seeing it, is like age pigment production. The process of making 0:21:15.520 --> 0:21:25.240 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. 0:21:30.240 --> 0:21:36.000 So it's defensive, but with a lot of bad consequences. 0:21:38.560 --> 0:21:42.760 Yeah, I mean, I think I agree 0:21:44.660 --> 0:21:49.200 with most of what you're saying. I do have this question, I think, which is 0:21:49.200 --> 0:21:58.520 what in your opinion would be the difference between me eating bread with 0:21:58.520 --> 0:22:09.160 butter versus bread with soybean oil? How does the bread with soybean oil lead to reductive stress versus 0:22:09.160 --> 0:22:10.760 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. Peat 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. Peat's saying it's estrogen, right? 0:24:38.240 --> 0:24:48.000 Dr. Peat 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. Peat 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. Peat. 0:29:13.000 --> 0:29:13.920 Dr. Peat, 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. Peat 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. Peat 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. Peat, 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 Szent-Györgyi 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. Peat, 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. Peat, 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. Peat? 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. Peat'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. Peat 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. Peat 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. Peat, 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 Szent-Györgyi'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 Szent-Györgyi 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.