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Hello everyone. Welcome to the Dr. Paul Mason Show. I'm Allison and I'm with Dr. Paul Mason. Paul, you recently gave a lecture to a whole bunch of GPs. And on YouTube, you've got a few questions. Papa Carnivore 15, for example, says, "My brother and sister are both physicians. And despite both of them being obese, diabetic, high blood pressure, they feel that I'm being irresponsible for eating carnivore and crazy because of the way I'm eating." He's lost 120 lbs, reversed type 2 diabetics, diabetes among other things. What have you got to say about this kind of circumstance?
>> Well, it's a pretty common happening actually. I mean, it's just an example. Uh, we probably shouldn't say medical gaslighting, but it certainly exhibits a cognitive dissonance that a lot of doctors have. So, in medical school, we're taught to a certain curriculum. That curriculum tells us how good the food pyramid is and that saturated fat is bad and red meat is bad and so on and so forth. So the very concept of a carnivore diet being healthy is a complete anathema to what doctors know and I say no >> uh in quotations >> and the trouble is that even though we get taught that it doesn't make it true. And so Papa Carnivore's two siblings, so his brother and his sister, who are both medical doctors themselves, they've witnessed with their own eyes his health transformation. You don't lose 12 pounds, reverse type 2 diabetes, and a litany of other medical conditions that he lists, including hypertension, fatty liver disease, reflux, migraines, arthritis, even bipolar. Um, so it's absolutely amazing the reverse what he describes in his health.
>> And even though they're they've been witness to that with their own eyes, they still can't bring themselves to concede that perhaps what they got taught in medical school >> may not have been correct. It's a perfect example of that cognitive dissonance that a lot of doctors have. But fortunately, not every doctor has that. So there's numerous examples. So I would argue that most doctors practicing low carb medicine, ketogenic, you know, profering ketogenic diets and so on and so forth, most doctors around the world today who are practicing like that >> have been introduced to these concepts through their patients. >> So I've got no end of doctors who I speak to who tell me, look, I saw a patient do this. So Dr. David Unwin from the UK is a perfect example. He actually was taught about the low carb diet from a patient who was actually effectively managed her diabetes with that >> and she actually came to him and she was quite annoyed that he had never told her about it and >> the reason he hadn't told her about it was because it was new to him. So >> fortunately there are a lot of doctors who are actually open-minded enough to be able to learn with their eyes. >> But still there's a lot of doctors out there who uh that's a bridge too far. >> Okay. Okay. And so if we talk about the dietary guidelines then in general, there's another comment saying dietary guidelines are not rules and they're not based on science. Does that tie into what you're saying?
>> Well, I mean the point is that as doctors, we're we're sometimes afraid to go too far off the reservation. We feel that we might get in trouble from the the health regulators. But the simple fact is that we're not bound to abide by what's in the dietary guidelines. There's a very particular carve out in the dietary guidelines that said they only apply to the healthy population. So basically that means >> if as a doctor you have a patient with a condition that can be impacted by nutrition >> which is most all of them. >> Yeah. >> And so many people would fall in that category. >> Then the dietary guidelines officially do not apply to that patient. >> Okay. So this notion that as doctors we're bound to, you know, preach what was in the the food pyramid or on the the dietary guideline plate and so on and so forth. That doesn't apply to people who are not well. >> And if you're seeing your doctor, >> invariably you're not well. >> Yeah. Yeah. That makes perfect sense to me. Um, I've got another question for you actually or really a comment and uh it's about you may ask for CTCA to check if there's any soft plaque in the coronary arteries.
>> Well, this was actually a comment that somebody made to Papa Carnivore. Um, obviously talking about his metabolic health. Papa carnivores come from a position where his health was obviously not not very good. And uh this is just another mean. So what they're recommending is to do a CT scan of the heart to look for any calcium deposition, okay, >> in the blood vessels around the heart and that can actually be a good indicator of your risk of future heart attack basically. But this comment here, you may ask for a CTCA to check if there's any soft plaque in the coronary arteries. Now the the C CA bit talks about a coronary angiogram where you actually inject a dye into the blood vessels and that actually helps actually uh highlight if there's with via shadowing whether there's any indentations going on into the center of the vessel what we call the lumen. So the lumen is called the hollow part of the vessel. Now yes you can check for soft plaque in the coronary arteries but my personal opinion is that in most cases the presence or absence of calcification and the degree of calcification is more useful than the presence of soft plaque and certainly from a a modeling point of view when we try and predict future risk of future heart attack the calcification on its own is the most useful. Now why is that important? Because injecting something into your arteries can have side effects. I've had more than one patient who's actually had a heart attack >> on the table. >> Oh, really? >> While they've been having an angio done. Now, that doesn't mean now most people don't have that. >> Yes. >> But it is a known risk factor and it's a known side effect. And if you're not getting much more value out of it in terms of you know future predictions or if it's not going to modify your medical care then I would all you know the question has to be asked is it worth doing the angio in addition >> to the CT scan just to measure the calcium. Now just one other point when we're talking about the difference between soft plaque and hard plaque and this is a very vexed question in medicine and the notion is the standard orthodoxy thinks about it like once you've got soft plaque that soft plaque then turns into >> okay >> hard plaque but that that's not a natural evolution. In actual fact they're two distinct pathologies. Soft plaque lays the foundation for hard plaque, but it doesn't turn into hard plaque. Now, that sounds like a real esoteric nuance to try and emphasize, but let's get down to brass tech. So, first of all, soft plaque, we've got an abundance of evidence that soft plaque is basically maturing or evolving thrombosis, which is basically a blood clot that's adherent to the inside wall of the blood vessel. And as it matures and evolves over time, that becomes a soft plaque. And it looks like that. It's uh blood cells which form the basis of clots are very rich in cholesterol and so on and so forth in their membranes. And there's reasons why we can actually see a lot of these lipids within the wall. Then for the soft plaque then to form the basis of hard plaque. Hard plaque is actually basically calcification of microbial biofilm. So what does that even mean?
>> So you know when you uh if you don't brush your teeth for a day or two when you're a child but you know like if you >> if you get soft furry feelings remembering a kid you know had fruit leaves for breakfast. you used to have this often feeling of soft fluffy stuff on your your teeth. >> That's what we call dental plaque. And what it is, it's actually made by bacteria. >> Okay? >> And the bacteria make a almost like a protective shield. It's got a lot of chemicals called proteoglycans and so on and so forth in it. >> And that is called a biofilm. Now that biofilm can then become mineralized and it gets mineralized by the minerals from your saliva. So things like calcium and phosphate they form things called hydroxy appatite >> and that passively mineralizes and then it becomes calculus really hard something your dentist basically has to chisel off your teeth. So the calcification there is actually a product of microbes the biofilm that then gets passively mineralized by the the minerals in your saliva and that is also why the calculus dental calculus usually forms on the lower teeth because that's where saliva pulls. So on your top teeth it's not bathed in saliva. It can't actually take in all of those minerals. So the heart arteries is that the same the soft plaque actually serves as a nidis or a focus at where you can get microbes lodging in and we know that the blood is not sterile. lots of microbes in the blood. >> And so if you have the soft plaque and you have circulating microbes, they can lodge in the soft plaque and over time that will form a biofilm. >> And then on the understanding that the the concentration of calcium in your blood is actually higher, okay, >> than in your saliva, you'll understand that then we've set the stage where you can get calcification >> of that bofilm. So with a soft plaque, is there any risk in terms of that narrowing the lumen like the whole of the artery itself, or is it risk only that microbes can settle there and be calcified?
>> Well, there's absolutely risk that it will narrow it. Um, but the the thing is the degree of narrowing has to be fairly significant. You need more than a 70% blockage before you start getting any restriction of blood flow. And just a gradual blockage of the artery usually doesn't kill people cuz what actually happens we have a something called angiogenesis which is where the body will create new blood vessels and basically that's to create detours. So if we've got a main blood vessel >> and it's got a blockage here then you'll actually have these small blood vessels we call them collateral supply that will branch off and go around it. It's exactly like a bypass would if you had road works. >> So gradually forming a progressive blockage in a blood vessel usually doesn't have catastrophic consequences. What does is if it gets blocked quickly, >> okay? >> And then you don't have time for that collateral circulation to develop. So what will typically block a blood vessel quickly? >> Well, that's actually a blood clot. So, so when we talked about the soft >> uh plaque as being a maturing blood clot, >> well, that's usually that's what we call a non-lusive blood clot. So, it's a blood clot in the vessel, but it hasn't blocked the complete lumen and it hasn't gone the whole way across. If it happens to go the whole way across, >> then that's bad news bear. If it's in the wrong artery, for example, the left anterior descending artery of the heart, the one we call the widow maker, >> well then you lose a, you know, blood supply to the major pumping chamber of the heart, the left ventricle, >> and that's, you know, often fatal. >> So yeah, there is a um thrombosis can be bad and thrombosis, if you have a sudden heart attack, thro, it's usually thrombosis that will actually kill you. But one of the biggest predictors of having an olusive thrombus is actually having the presence of that calcification to begin with. >> Okay. And so you were talking about the tests that people have that you do or don't order. And you were saying the angiogram which is testing the soft plaque is therefore you considering the risk of whether or not someone does that and whether it would make a meaningful change to the therapy afterwards. But what would you use to test for the hard plaque or what do you think are the best tests to do?
>> Just doing the CT scan. Okay, >> just doing a CT. So a CT scan is a three-dimensional X-ray. And the beautiful thing is that the X-rays see calcific tissue very well. It's, you know, the X-rays will show your bone if you've got calcium lining the blood vessels. A CT scan or a threedimensional X-ray will show that superbly. So the gold standard for assessing coronary artery calcification is the CT scan. Okay. >> Um, so the question is whether or not you also do the angio to have a look at the soft plug. And we've actually got lots of research that shows that once your calcium score goes over 100 that there's really no predictive value that you that you add by actually injecting the dye. >> Okay. To do the to test with the soft plaque. Um, I've got a great one for you here, Paul. Um, it is carnivores tend to drop dead with no warning. the saturated fat is found in their arteries afterwards.
>> Right? So, this is uh this comment is from what is going on peeps. Um, it's a little bit hard to know how to respond to this. This is a completely vacuous comment with no substantiation at all. There's no um research that's been cited. It's just a blanket comment. Carnivals drop dead with no warning. Um, I'd simply have to say that that there is no substantive evidence of that at all. And when we actually look at the science of we'll look at Papa Carnivore's example, do we really think it's likely to lose 120 lbs, reverse type 2 diabetes, reverse fatty liver, reverse hypertension, you know, improve bipolar, so on and so forth. Do we really think it's plausible that with all of those changes that Papa Carnivore is now less healthy >> than he was to begin with? >> I mean that that's clearly nonsense. Um unfortunately some people do believe that saturated fat is a problem. So they've also um what is going on peeps also says tests can show the type of fat in the arteries as in beef fat or pork or chicken fat. Well that's just patent nonsense. Now there is a common misconception from saturated fat and this belief that saturated fat is harmful comes from one finding >> and it's the fact that people who are metabolically unwell tend to have higher levels of saturated fat in their circulation. >> Um, it's what one in particular we call palmitic acid. >> Okay. >> Now this is a saturated fat that we can also consume. But here's the thing that most people don't get that eating carbohydrates will actually give you higher palmetic acid levels, higher saturated fat levels in your blood >> than eating saturated fat itself. >> Now, how is that even possible? >> I don't know. I need help with this one. Paul, tell us. >> Dooo lipogenesis. >> Okay. >> So, not a little. It sounds complicated, but it's quite easy. Basically, when your body has excess carbohydrates, >> it can't deal with it. So, the the the pressure relief valve is to turn that carbohydrate into fat. >> Mhm. >> And a lot of that fat that it's turned into is palmetic acid, this saturated fat. And we actually have randomized control trial research that demonstrates eating higher a higher carbohydrate diet leads to higher levels of saturated fat in the blood than people eating an isocaloric amount of saturated fat. >> Okay. >> So, so okay, it's turning um then fat into palmic acid. >> Palmitic acid. >> Palmitic acid. So, can people eat as much as they want as long as it's not carbohydrate?
>> No. I mean, you can if you forcefeed yourself too much fat, of course you can gain weight. >> Th this is another question entirely. This is a question of satiety. >> Now, have you ever stopped eating a a tub of Pringles because you are full? >> I don't know the answer to that. I don't eat Pringles or or a bag of chips or something. >> Sometimes I stop cuz I'm full. Yes. The point is you generally you can keep going. They don't trigger your satiety signals the way. But >> what about if you were eating some fatty steak? >> There reaches a point where you're saying this is really tasteful. >> I enjoy it, but I'm going to stop. >> I've had enough. The difference is healthy foods like fatty red meat will trigger your satiety signals much sooner than carbohydrates will. So the con the concept of these foods actually causing so we're talking about something different now. We're not talking about circulating saturated fat. We're talking about stored fat within the body. Um, but the simple fact is that healthy food will trigger your satiety signal a lot earlier >> and you'll end up eating less. >> So, if you were to forcefeed the same amount, well, sure, >> yeah, then you can gain weight on a highfat diet, >> but in general, people find it much easier to valitionally control their intake. This question comes from uh John Hogue and he's talking about Apo and LDL um and whether this actually causes heart disease and he's made the comment and there's a little bit of a spelling error but we know what he means. It's meant to be Mandelian randomization also does not establish causation. It's still just a correlation. And that is absolutely correct. And this is just something I think it's worth touching on. Uh there's been a lot of noise in the literature recently about this type of research called Mandelian randomization that is held up as proving that LDL is harmful. The notion is that amongst the the breadth of the human population, we all have a slightly different genome. we have slightly different genes and some people have genes that are associated with higher LDL levels. >> Okay. >> And then the the notion is that if we then look at people with those genes and see if they are prone to having other adverse health effects then that will prove that the LDL is causing the other health effects. >> Now simplistically speaking there that seems to make sense. the gene causes high LDL. If we see what uh what pro other health problems you've got, then that proves that you've got a problem. >> But here's the problem. It's called genetic pleotropy. >> Okay. >> Now, one gene has multiple influences. >> Yes. >> One gene. Uh and the gene that helps regulate LDL also affects your blood clotting risk. >> Okay. It also affects your diabetes risk and so on and so forth. And we know that if we've talked about atherosclerosis um being strongly related to blood clotting and thrombus in the blood vessels and if you know we can see how that's a problem for heart disease. We know that diabetes is a massive risk factor. So people are having you know in the order of four or five times increased risk depending on how poorly controlled related to their their diabetes is well risk of heart disease. So if you've got a gene that affects LDL and affects diabetes risk and affects clotting risk, >> how can you attribute any adverse health outcome solely to the LDL? >> I mean, it's just hopelessly confounded. The very premise of Mandelian randomized trials is fundamentally flawed, >> impossible really. >> They cannot ever prove causation. They can only show correlation. So what we mean is just because two things occur side by side doesn't mean that one causes the other. >> So what do you do with that information as a doctor then if you can't >> Well, when I read that research >> and if I see it's making claims about LDL that are unfounded, >> I ignore it. >> Okay. that that I mean the whole research on mandelian randomization being purported to show the harms of LDL is just an academic nonsense. >> Someone else here, I cannot pronounce their name, says, "Make sure you eat vegetables and take dietary fiber supplements."
>> Okay, so I got this one. It's Wuzzy. >> Oh, great. Yes, >> wle Y. >> Got to the end of the alphabet. That was their thing. I think Wuzzy is going for taking out the crown of troll of the week with this kind of comment. I I don't think it's serious. Um the reality, well, they may be serious. Um I mean, there's a lot of people that I hear talking about um fiber and its correlation to all cause mortality. >> Well, let's talk about the veggies first. So, why do we need to eat vegetables? So when I was brought up, we were told that vegetables were nutritious. >> Yes. Eat your veggies. >> And one of the most common things we got told was that it was good for your eyes. >> Carrots. Yes. >> Now, do you know where that myth came from? >> No. >> It's actually from World War II. >> Okay. So the UK um buffins scientists they developed a new radar and so where they were able to hopefully um detect all the night fighters and so on and so forth. So it it was designed to work at night and they could detect the the German fighters as they were coming in >> and they this was shrouded in secrecy. >> So they didn't want the Germans to realize that they had this new technology. So they spread a myth that the betaarotene, the vitamin A, which is by the way very poorly bioavailable because it's a plant form of a nutrient, not the not the animal version, animal vitamin A is at least 12 times more bioavailable than the plant version. Okay, >> so so you know that that myth just falls down at the very first turtle. But anyway, they spread the myth that they were feeding all their pilots lots of carrots and improving their night vision. That is that that's the truth. So that's where this whole concept that eating carrots is good for your vision came from. It was it was a ploy designed to deceive the Germans >> in World War II. >> Okay. Well, it was a great marketing success cuz we still talk about it now. >> But the point is that so I referred to the bioavailability of nutrients in plants. So generally the bio the nutrients in plants are less available and less effective than the equivalent nutrient from an animal source. Furthermore, there's not a single nutrient in vegetables >> that is essential for survival >> that you cannot get from animal food. >> Okay. But what about like I think they taste pretty good, Paul. I quite enjoy eating zucchinis for example. >> Yeah. So >> I still want to eat them. >> And to be fair, so nobody's saying that you shouldn't eat vegetables, >> but what I'm saying is if you think if you're eating vegetables thinking that they're going to make you healthy, that they're going to provide you with unique nutrition that you can't get from animal foods. Well, that's not true. But if you're having it out of social reasons, >> um you don't want to be a social prior when you go out to eat, that that that's a legitimate reason to eat >> or enjoying the flavor >> or or if you enjoy it, you know, you like the mouth feel, you want the variety, you know, you're getting a bit of pallet fatigue. There's lots of reasons why you would it would be very reasonable for you to consume vegetables. And it's not necessarily that they're unhealthy for the most part. I mean there's, you know, there's lots of vegetables that have low levels of chemicals that would cause this irritation and that, you know, most people, a lot of people can come >> from pesticides or you mean in the vegetable itself? >> Well, both. So, I mean that, you know, there's a >> we've got a real problem in Australia with pesticides. um and farming has become reliant on pesticides and these pesticides often are present in residues in the food um even after they've been washed and cooked and so on and so forth. And I think this there's going to be a lot more to this story in the future. But it's also true that plants because they lack the ability to run away, they have their own internal defense chemicals to try and deter predators from eating them. And a predator for a plant could be a cow or a goat or something like that. say herb of all predators, but um a lot of foods. I mean, you know, we're sort of laughing about this little weed that we plucked from the garden before. If we were to eat that, >> we can probably assume that would get sick because there's some chemicals in there that are deterring caterpillars and goats and so on and so forth from eating it. Cuz the simple fact is if it was nutritious and easy to eat and digest and not dangerous for it then the caterpillars would demolish it and the plant would go extinct. >> So these you know plants often have these chemicals. So things like um >> uh you know if you have mustard for example you know it's very strong and pungent. You can imagine if you had too much of that it might not be good for you. But did you know that the brassica class of vegetables, the cauliflower and the broccoli, >> they're actually derived, they're mutant forms of mustards? That's where they come from. >> So vegetables can contain some chemicals that are irritating. But >> having said that, we've got an omnivorous gastrointestinal tract that does have some capacity >> to u to deal with some of those chemicals. Not all of them, but there are some things that we can digest. So, not all vegetables are bad for everybody. Um, but I think it would also be equally true to say that nobody needs vegetables. >> Okay. Yeah. And for some people have more of a reaction to some vegetables than others. Uh, fiber, dietary fiber, is it helping us to live longer?
>> I don't believe it is. Now all the research that and you'll see headlines saying you know scientists sign fiber is linked to a longer diet or associated with these are all weasel words. So we talked earlier with mandelian randomization how it was confusing correlation things occurring together with causation with one of those things actually affecting the other and resulting the other. For example, if I walk outside and I see my shadow and my shadow always occurs at the same time as the sun is shining, does that mean that my shadow brings up the sun? >> They're occurring together. >> No, >> clearly not. My shadow does not make the sunrise every day. >> But it seems to because whenever I can see the sun, my shadows there. So that that's that's what correlation is. Correlation just means two things associate together. So when we look at the a lot of research where they're purporting to extol the benefits of fiber, they're invariably using what we call epidemiological research which is all about association. To demonstrate causation, we need to actually give somebody fiber >> and we need to have a control group where they don't get given fiber and we usually need large enough numbers of people in both groups. what we call statistical power and then we can actually assess the difference between the two groups after a period of time. Now if we do that then we can make the claim of causation but the research on fiber claiming benefit has never been done to that level. It's always been epidemiological. It's always been association. I have another question here from Vain. How many studies are sitting in basements waiting to be published someday? And this is a comment really that reflects the fact that I can't remember the research of the other one that it refers to. So you'll have to help me.
>> This refers to two studies. the Sydney Diet Heart Study and the Minnesota Coronary Experiment and both the data from both of these studies, so mortality data which actually confirmed that replacing saturated fat with polyunsaturated seed oil was actually delterious to health. That information wasn't published until about 40 years after those original studies. >> Crazy, isn't it? >> Were finished and only after the original study documents were discovered in two different basements, two different studies. So this raises the problem of what we call publication bias. >> So historically speaking, uh it's only research with positive findings that have been published. And in this vein, we're not just talking about findings of okay, we had a significant finding, but a positive finding in this sense talks about a finding that confirmed the preconceived biases of the researchers. So Dr. Ivan France, one of the lead investigators of the coroner uh Minnesota coronary experiment, he was actually asked by Gary Tabs in an interview about why there was a long delay in publishing and because I think they took 15 years or something to publish a redacted sense of their findings initially. They said, "Well, why the long delay?" And quote unquote, he said, "We were just disappointed in the way it turned out." So the findings of the study weren't what they expected, weren't what they wanted, >> so they didn't publish. >> And this is a huge problem. So I just came across this recently. I was looking uh at some research on a peptide called BPC body protection compound 157. >> Okay. >> And there was only there was two studies that have been performed to what I can understand on human subjects and they would be very revealing to know if it actually worked. >> And neither of those the results of the studies have been published. now whether the studies were abandoned because they weren't getting the right results or just not published because they didn't get the right results or what happened. But the problem is this publication bias where we tend not to publish um what we don't like or you know a finding that might contradict our own practice. This is a real problem in science and supposedly now we've actually got registers where when you uh when you start to do research you're meant to register it in advance and that's meant to make sure that everything does end up being published. But I'm not sure that that register system is working particularly well even now. >> So how do you get a like how do you then when you're researching a topic consider that there might be information out there that you don't have? What is kind of some of the sources where you really look to to double check what information is out there?
>> I mean one of the problems if it's not being published and sometimes we just don't know. We just can't find we just can't find it. So I think in the absence or of data my next step is to go to something called biological plausibility. >> So biological plausibility just says look with our understanding of biochemistry and medicine and pathophysiology and all the all the medical sciences does this make sense? Is it plausible that this could cause this? And if there's a often there's a very clear reason why something might lack clear biological plausibility in which case happy to disregard it. And if there is a clear biological you know theory as to how something could work well that just tells us we need to dig a little bit harder go a little bit longer. And the simple fact is that there's a lot of things that have even just come out in the last few years that are quite unique and have shed a lot of light on things that I'm thinking about that you know 5 10 years ago we just had no idea about. So sometime hopefully those uh those holes get filled in the future, but they they don't always get filled. And I'm sure there's some very important scientific findings that have been discovered that have never been made public knowledge. >> Well, and it also leads you to think that someone might have discovered it and that because it's not known, then no one else has been able to build on it either. I mean, I think it would be fantastic scientific process. So this whole notion of the lipid heart hypothesis has set science back more than 50 years >> um because people have been clinging to this notion that trying to believe that saturated fat in the diet increases LDL levels which it doesn't and somehow that LDL is then inherently dangerous and it's not inherently dangerous. It it can be problematic if it oxizes but it's not inherently dangerous. So if we understand that, you know, that's a consequence of the lipid heart hypothesis that's really set medical science back decades, >> generation, two generations. >> Paul Carn Goth would like to know if you're going to publish a book >> in your spare time.
>> So I have actually started writing a book. >> Okay. What's it about? >> Well, it's hard to know what to make it about. I was hoping to make it about everything health and talking about general health concepts and and things that are that are not accepted mainstream yet. >> Yeah. >> But should be. So the very premise that the food we eat has a massive impact on our health. A root cause mechanistic understanding of how diet actually impacts us. So there's several new concepts on things like lipid rafts and so on and so forth. And the role of infection is something that I'm digging into deeply. But uh at the moment I'm a little bit distracted. I'm writing a a you could call it a quasi thesis at the moment on something I'm over 100,000 words in. And unfortunately until I get that knocked off, which is still probably going to be another few months. Um I'm probably not going to have a chance to come back to the book. >> Well, that might be your first book, although it's not it's technically a book. You mentioned about infection that you've been looking into a lot. um earlier when we talked about um calcification in the blood vessels coming from an infection coming into the softs plaque. I mean is that common knowledge? No. Look, no it it's really not common knowledge. Um the medical profession that actually understands this more than anybody else I suspect is dentists. uh dentists understand dental plaque obviously very well and they've also understood for decades the connection between poor dental health and poor cardiovascular health because the very same microbes that can cause dental plaque can also cause coronary plaque. So we've got poramonus gingervus which is a very common bacterium in the mouth and it's been well established that if you've got gum disease and you brush your teeth then within you know within a minute bacteria from your mouth will enter your circulation. >> Okay. Um we also know that and it's not just that infection we know that when we do um biopsies so when people have open heart surgery so basically what that means is you you cut down the sternum you separate the sternum to expose the heart and you cut out diseased sections of arteries and you put in replacement sections usually vein or arterial graft. Now so what you've got you've got this diseased artery and you can look at that in the lab and when scientists inspect those diseased arteries for infection more often than not they find evidence of infection. So take helico back to pylori for example. It's something that we consider you know not benign but okay it's very common. 30% of the world's population probably has it maybe more. >> So the research will show that between I think it's between about 30% and 48% of diseased arteries actually contain helicoacttoid DNA. >> Right. Oh my goodness. It sounds like a big deal. Well, look, again, that's correlation, not causation. But if you understand this whole notion that bacteria um can they can create an oxidation state that increases your risk of thrombosis. So the risk of occlusive thrombus would theoretically be higher. That's what I'm talking about biological plausibility. We know that coronary artery plaque uh you know if we understand that helicoacttor pylori is a bacterium that can secrete a bofilm and so on and so forth. All of these things uh they do, you know, they feed together. Hugely important. I think >> it it's poorly understood um by most people, but certain, you know, dentists, they've got very good visibility, they'll say if you've got >> gum disease, you're a sitting duck in terms of heart disease. And it makes sense. >> Dr. Paul, I've got a comment for you that was from YouTube. It's a diet most people can't afford. And this is a comment really about carnivore, eating a lot of meat. What would you say to people who feel they can't afford that or think it's unaffordable for other people as well?
>> Well, I think the fitness ripoffs makes a a point that concerns a lot of people. So, we know that generic carbohydrates like uh rice and flour and so on and so forth is relatively affordable and relatively cheap and that is absolutely true. >> So, I think I'd have two points. So this is I think this is more true for developing countries than western countries. In western countries um being on a vegan diet is also expensive with all the fancy foods that most people are having. They're going to farmers markets. They're paying um premium prices so on and so forth. Um and people on omnivorous diets are often having a lot of snack foods. So the industrial snack foods that you snack on when you're watching TV or you know so on and so forth or >> Yeah. things like this, >> they're they're all expensive. They got wonderful profit margins and I think that, you know, they're expensive enough >> that uh if you were to stop having those kind of foods, then the food bill would come down. So, the beautiful thing is um we're 1:30 in the afternoon at the moment. I've had one thing to eat today. Uh I'm absolutely not hungry. I could easily go through to 5:00 without eating again. When you're on a healthy diet and you're in ketosis, >> you don't feel the need to snack. So, a lot of that discretionary food intake when you're eating healthily just reduces. >> Furthermore, um yes, it I I believe that the healthiest, most nutrient-dense food is probably something like a grass-fed steak, which is very expensive. But the reality is grain-fed meat is still far superior than most other alternatives. So I guess the idea is don't let perfect be the enemy of good. >> So if you can't afford grass-fed beef, then there's no problem with having some grainfed ground mints. And the fatty mints, the 18% fat mints you get from the supermarket, which is still quite affordable, is actually the mints that I personally buy. I prefer we actually chasing the fat. So most people are paying a premium for the the lean mints. You can get the fatty mints. Um would it be better to have freerange organic eggs? Yes. But is eggs still a nutrient powerhouse? And if you just get the cheaper eggs, is that still better than other alternatives? Absolutely. So if you focus on, you know, the affordable meats, you know, go and get some canned fish, go and get some So it is still possible to buy nutrientdense food um that while it might not be perfect, it's still a whole lot better than the regular omnivorous diet. >> Well, and there's a cost of being unwell also, isn't there? So, you know, if you have to take time off work because you're sick or, you know, going to doctors is expensive. Or you pay the butcher or you pay the doctor. >> Yeah, >> that's right. We're going to talk about GLP1s now. Paul, there's a question from Epsio Alexis. You're better with these names than me. Um, and >> Spino Alexis. >> Yeah, that'll do. Um, and they ask about um muscle and bone loss coming from insufficient diet amount and formulation when someone's taking GLP ones. And might need a bit of context about this. I think the idea is that so we know that people taking ampic and wobbi they lose a lot of weight. So the question is why? So normally the GLP1 glucagon like peptide 1 is a natural hormone that's released by the stomach and it's got a halflife of 2 minutes. >> Is that right? >> So it ends up being cleaved. I've got this uh DPP uh 4 enzyme I think it is um that cleaves it. >> And so so you eat something, you get a transient signal and it says you're done, you're full, you stop eating, the signal is gone. Now what we do with semaglutide is we modify it so that that signal becomes a week-l long signal. Not two minutes, >> okay, >> whole week, >> okay, >> completely changes >> your physiology and it ends up rather than that two minutes saying stop eating now wait until your next meal you just stop eating and they've shown that ad libertum intake which basically means your voluntary intake how much you know you can eat as much as you want will reduce by about 30%. Okay. >> Now, most people when they are on a Zenic and they reduce their diet by 30%. They're not changing the types of foods they eat. They don't say, "I'm now having 30% less opportunity to give my body nutrients. >> I'm going to make sure that I'm going to focus on nutrient-dense foods. >> I'm not going to have the empty carbohydrates. I'm not going to have bread. I'm gonna choose an egg. I'm I'm not going to have, you know, what have you. They're not making choices to increase the nutrient density. And the reality is that on our current modern diets, people are very close to their nutrient thresholds for or or you know, just barely getting their the nutrients they need. And if you drop that up by 30%, they become malnourished. And one of the consequences of that is that then your body loses the building blocks, the substrates it needs to make lean tissue, including muscle. And that's why so when we see about 40% of the weight that's lost on these drugs is actually lean tissue, muscle and bone. Um that's one of the reasons why. And so the weight loss effectively the weight loss on these drugs mimics that that occurs with starvation. It's very similar to say what would happen in somebody with anorexia. >> So, so it's a starvation weight loss. So, when uh Espino Alexis has asked is the muscle and loss bone coming from insufficient diet amount um or is it coming from a signal of the GLP1? Well, both. It's coming from a signal of the GLP1, but it's been amplified from 2 minutes to a week. And that signal then causes insufficient intake. And because people aren't having nutrient-dense foods, they're just having the regular diet. They're becoming malnourished. So, you may have heard of something called a zmpic face. >> I have. Yeah. >> So, >> and you can see it in some people. >> What you said and a lot of there's a whole cosmetic industry about this now where surgeons are going around injecting fat trying to get the normal facial contours back cuz people look unhealthy. We have a thing called cancer cohexia where people with cancer when they're quite unwell they they just waste away. um or there's a lipodistrophe we see with in AIDS patients with on certain medications where their their face would just waste and what actually happens is it's actually muscle loss. People think it's fat loss, but in your face, uh, if you have a look at an anatomy book underneath the skin, you've got these huge muscles. We've got massa and temporalis. These muscles, they're what we call the muscles of mastication, the muscles of eating, chewing food. And the those muscles under the skin are what gives our face the contours, that healthy looking contour. And if you're losing a bunch of muscle, you don't just lose it here, you lose it on your face as well. So that's the very premise of a zmpic face. Just as an aside. >> Yeah. Okay. I mean, also as an aside, if someone becomes a carnivore and they have to chew a lot and build up the size of the mass muscle, would that like also help them look healthier?
>> Well, I mean, presumably yes, but I think you probably just need to get a slow cooker if your meat's that tough. >> Oh, okay. Um, uh, also Subash G342 got a GLP ad, um, while he was watching your video, Paul, which is got some great irony to it.
>> Well, I mean, the the point is I mean, these things are heavily promoted the these these drugs. I mean, you know, we're feeding people this algorithm. We're we're relying on their their self-consciousness. So many people are so desperate to lose weight. This is just they're just targets for pharmaceutical company advertising. And do you think the GLP1 ad tells people that 40% of the weight they're going to lose is going to be muscle and bone? Do they get told that their bone is going to continue to degrade that the longer they're on it? And if they stop it >> because of the side effects that within 12 months they're going to have regained 60% of the weight that they've lost, probably just regaining the fat. We don't know if they regain the muscle and bone. I mean, the answer is pretty clear that those that information is probably not in the ads. >> Probably not. And perfect timing for this comment from In Macen. Uh, is this the next tobacco or asbestos disaster?
>> Well, they've actually made the comment. So, uh, wow. This is the next tobacco or asbestos disaster. So, I think in is probably missing something here. And I I feel the pesticide disaster is probably one that that could be added to this and that's one that I sincerely believe we're going to have a lot more visibility of in future about the catastrophic harms that it's doing. And I think it's almost criminal that
In Australia, a farmer can spray a wheat crop with Roundup with glyphosate 7 days before harvest. Is that right? I I think honestly, I I think I think we've moved so far from what is natural in the drive to optimize production, and I think the, you know, the consequences are going to be felt in future.
So Paul, we have another comment, um, from May Bing, which is really about weight loss, I think, and the discipline that it can take to eat differently. She says, or he says, "I'm sure most of the information is good, but ignoring that, the reality is that very few people have that kind of discipline. That is a fact that leads them to become obese, and it is not that helpful to anyone to say that people just have to change their diet. So your lecture should include something on how difficult it is for people to follow, um, eating nutrient-dense food and keeping up with those instructions."
Well, I think maybe 4912 actually makes a legitimate point here. So, let's consider, for example, alcohol and heroin. Which one's harder to give up?
I I don't have any personal comments on that, Paul.
So, so we would often see that people can give up the hard drugs easier, like heroin or something like that. So, the question is why? Because it legitimately is probably more addictive, okay, than alcohol or smoking or something like that.
I have heard sugar is more addictive.
Well, the the reason is, if we're having a look at that, is that in everyday life, you have access to alcohol, you're exposed to alcohol. So that constant exposure to it, that constant temptation does genuinely make it harder. So it it it amplifies the addictive potential, if you will. And sugar is no different. You every time you watch TV, if you watch TV, you're going to get ads selling junk food. Every time you go to the supermarket, you've got the junk food staring at you. Even if you're trying to stay on the outside of the supermarket, you've still got to go through the checkout where all the chocolate bars are. Um, you fill your car up with petrol. You're going to...
There's a concept of treating yourself as well. "I deserve a treat because I had a difficult day." And this type of food is a treat food. That's the concept.
They've completely given us this notion that we deserve it. Exactly. I mean, it's very effective marketing. But the point is, I guess, it is difficult, and we are surrounded by this. And these foods are crafted by scientists to be as addictive as possible. There's something called the bliss point, um, which is the point, the optimum ratio of sugars and salts and fats, and then we get the right mouthfeel. Maybe just a little bit of crunch, maybe a little bit of sticky goo, or or what have you. But scientists spend a lot of time and energy, very expensive scientists, very well-paid scientists, to actually craft food to hijack our our normal physiology. Humans, we're not designed to eat these kind of foods. We we don't come across these foods in nature. They they hijack our senses, and so they absolutely are addictive. So, and I think that's what maybe 4912 is saying. But the point is that we shouldn't have to white-knuckle it. So yes, there is an addictive element to it that that we are constantly exposed to. That is a societal failure. That is society setting us up for an obesogenic society. And the only way that you can get away from that is by eating natural food. So most of my patients, when they go onto a natural food diet, so they're only eating food that their grandparents, their grandmother would recognize, they're only eating food that they can construct in the kitchen themselves. They're not industrially crafted foods to, you know, why do you think they have salt in Coca-Cola? We think of Coke as being sweet. Well, the salt makes you a bit a little bit thirsty. You want to drink a little bit more, uh, but we don't want it salted because you might not like it, so we just throw in a little bit more sugar. I mean, this is all scientifically performed.
So once we eat natural foods, this comes back to what we were saying earlier about satiety. You eat natural foods, um, your hunger signals work more normally, uh, and your cravings eventually will reduce. We've also got other pathologies. For example, um, human behavior is predicated on dopamine. This is the chemical in the mesolimbic pathway of the the brain that gives reward. And there's two human behaviors that human survival is predicated on. So eating and procreation. Both of those behaviors are essential. Without either of those behaviors, we wouldn't exist as a species. And they those behaviors exist because they're driven by dopamine. That that's that's what gives the human drive for both of those behaviors.
I was going to say sleeping as well.
Well, that's essential for living. Well, that's true. Your body will tell you when you need to sleep.
Can't help that one.
So, the problem is that food, by being crafted to be so addictive, that too releases dopamine into the mesolimbic pathway. And if we're in a state of poor health, that actually impacts our baseline levels of dopamine rather than being at normally here, they'll be down here. For example, and I'll give you, there's several reasons why poor health can contribute to low baseline levels of dopamine. So dopamine's one of what we call the catecholaminergic neurotransmitters. Um, and if we go to a biochemistry textbook and have a look at the the chemicals that's needed for the synthesis of it, we know you need B12, we know you need iron, we know you need zinc, so on and so forth. So, if you were to have a nutrient deficiency of any one of those, you would then have suboptimal levels of dopamine. We know chronic inflammation leads to lower levels, so on and so forth. So basically, we've got a lot of the population is running around with deficient levels, suboptimal levels of dopamine, and they've got access to scientifically crafted foods that will squirt a whole shot of dopamine into the mesolimbic pathway in the brain. So when people are finding they describe what we call comfort eating or something like that, what they're doing is they're self-medicating for a dopamine deficiency. They're getting a warm hug from the food, and it doesn't make them feel good. It makes them feel normal. They're living in a gray cloud, and it just gives them a transient respite from that cloud that they're living in. But that's the whole premise of addictive eating. And me being 4912 is absolutely correct. It it is it is addictive food, and it is hard. But the problem is we shouldn't have to white-knuckle it. We shouldn't be struggling with this every day. If we correct the underlying health issues and we restore a normal basal level of dopamine, and then we train our bodies, we break our addiction to these addictive foods. And the only way to do that is to stop eating that food. But once you break the cycle, it gets much easier.
So with your patients in your clinic, how long are you finding it takes people to break the cycle?
Really? Probably two to four weeks.
Okay.
And and it's pro it's not easy in that two to four weeks. I mean, for me personally, I remember I used to have a horribly high-carb diet, and I I remember just contemplating once, you know, I was just looking at some junk food, and it's like I can look at a chocolate cake from 10 paces and not feel any urges, and it's it's absolutely fabulous.
I mean, you know, with my my kids, it it's wonderful. So Fiona and I will we'll take them shopping, and we'll, you know, you know, they won't hassle us at the checkout. So we recently went on a holiday, and we saw there were in a street market, and they had some raw honeycomb. I thought, "Oh, let's just give the kids a little bit of honeycomb. That'll be lovely." Though, they absolutely tiny portions. And I gave it to my children, and uh, one of them said, "Oh, wow, this is nice." And the other one said, "Oh, this is too sweet."
I've asked them before if they wanted a donut, and they said no.
Well, what are you doing?
Just to test them out.
It's just but but genuinely, you know, that's a diet that they eat, and it was interesting to see that they had no interest actually in that.
No.
You weren't there. So, there was no reason why they couldn't have said yes.
But this is the interesting thing. So you can actually you can actually break these addictions. I personally think the easiest thing is to not form the addiction in the first place. But uh, you know...
Uh, Gary Jackson's got an interesting comment here about Northern Ireland who've recently set up localized obesity clinics, uh, and then they learn that it's sponsored by a pharmaceutical company selling GLP1s. I think this really shows the reach of big pharma and how pervasive it is. I'm sure I mean, that had to go through a whole series of approvals through, you know, layers of politicians and public servants and bureaucrats, I'm sure. And the fact that they were able to sell such an expensive intervention when we know that we've got healthy diets and proven things that we can do with diet that people are just simply not being effectively educated on. This is really quite sad. um, that pharmaceutical companies that are driven by profit can have so much influence over society when there's a much better alternative that would be much cheaper.
Well, and from what you were just saying, there are ways that people can help themselves transition to a more nutrient-dense diet so they don't even get the cravings for some of those foods that, um, do lead to a lack of sati...
Satiety.
Once you break it. Exactly. Once you break that, um, that addiction, it it just gets much easier.
Earthflute 2248 says, "I have a friend on Ozempic who said losing weight was more important to her than muscle and bone loss, hip fracture risk, and looking gaunt. Her doctor did explain the risks of taking a GLP1." I think that really shows how far society has failed these people. How far how much damage the medical profession has done, how much the promotion of the food pyramid, this notion that carbohydrates need to be the basis of the diet. So, simple fact is, we live in a society where image is valued. We're and then we also live in a society that tells people to eat a high-carbohydrate, low-fat diet. Now, the upshot of that is that if you want to have this image that the magazines and so on and so forth are telling you, the body shape that is desirable, then the only way to achieve that while eating the recommended diet is through basically self-mutilation to extreme restriction, um, going without, um, you know, starving yourself, white-knuckling it, uh, and that's that's really sad. So we create this sense where people desire to look healthy and slim and so on and so forth, and we give them the exact wrong information that makes it nigh on impossible for them to do that without starving themselves or half exercising themselves to death.
Well, there's also an element of giving the like control to the external factors, isn't there? Because then, um, you know, as someone isn't well, then they need more external input, support, beauty interventions, whatever they may choose for some of this. Um, whereas sometimes if feeding your body nutrients helps actually have your own control over your body. But the problem is, so for for Earthflute's friend, who says, "Look, I I accept the risk of osteoporosis and gastroparesis and pancreatitis or what have you, or all these risks, they're prepared to accept that just to lose weight." Earth's friend is absolutely desperate for this, and I feel if they had been given the accurate information about how low-carbohydrate nutrient-dense diets could do that, then they would have done this decades ago.
Uh, and I've got lots of patients who we look at them, and we they're basically have an eating disorder. The only way a lot of people can maintain a so-called healthy weight on the recommended diet with behavior that is characteristic of an eating disorder.
Oh, Paul, I don't know if this guy's a fan of yours or not. Borisov says, "Is this the most talented data cherry-picker in the whole world?"
I don't know, Alison. To me, that sounds like high praise. Um,
You do have some fans online.
Cherry-picker. I mean, here's the thing, and I think this relates to the lecture where you're talking about weight loss, um, with a systematic reviews.
Well, basically, all the research that I presented in the talk that Boris Uravorov has responded to was the highest level evidence that we could find, that was always large-scale randomized control trials. Now, whether or not they were hidden or not is irrelevant. They were large-scale. They were randomized control trials, and randomized control trials will beat epidemiology every day of the week. When we look at the literature on weight loss, I think you know, we reviewed, you know, between 2003 and 200, you know, now, wherever there was, you know, over 70 randomized control trials. Basically, within that period, every randomized control trial that had been published comparing low-fat and low-carb diets in terms of weight loss, we included. Uh, so the accusation of cherry-picking, I think, is a little bit far-fetched when you look at the totality of the data, which I actually presented. And then when we're talking about specifics on Ozempic, and we're saying, well, it demonstrated, um, you know, 40% of the weight loss was muscle and bone. Well, that was the STEP 1 trial, which was actually funded by a drug company, and that was used as well to approve, uh, its use in in America, if I'm not wrong.
Well, yes, it was. And then when we talked about the data that demonstrated that females using, uh, semaglutide, this study showed that they had a five times increased risk of hip fracture. Well, that was from the SELECT trial, which was funded by a drug company. Uh, the drug company employees helped determine the methodology. They ran the trial, and they did the data interpretation on the trial, and then there was something like seven of the authors were also employees of the drug company who actually wrote the final paper, which was published. So, I mean...
That would suggest it's the best result they could find there.
Well, I mean, the point is, if I'm cherry-picking data from a study that's run by Big Pharma that's critical of Big Pharma, I I really don't see how an accusation of, you know, fudging the data can stand up.
So, here's a question from Intermittently Happy. Uh, what do you mean that calories in and calories out doesn't work?
Well, I mean, in one sense, calories in, the whole theory of calories in, calories out, which basically says if you if you burn more than you consume, you will lose weight, and if you consume more than you burn, you will gain weight. So that makes sense ostensibly. But what calories in, calories out doesn't tell us, it doesn't tell us why. It doesn't tell us why somebody, it it's a descriptive framework, but not an explanatory framework. It it simply says you got fat, therefore you were storing more than you were losing. Yeah, obviously. But why were you storing more? Where it lacks utility is it doesn't explain the hormonal influence in terms of driving eating behavior or driving energy expenditure. Now, just as an aside, I know there are, you know, some people out there who object to the use of the term calories in terms of talking about a a means of weight gain. And they're basically saying, well, you know, when you get fat, it's not actually a unit of energy that makes you fat. You're actually storing mass. You're storing molecules. And yeah, that's correct. But that's not the scientific lexicon, um, which is in standard use and which which I'm trying to use in debates and to convince other clinicians and so on and so forth about the merits of low-carbohydrate diets and so on and so forth. But I mean, just the principle that we gain and lose weight via gain and loss of mass is very obvious. For example, a lot of people are probably not realizing that when you actually lose weight, a lot of the weight you actually lose is, so we ask the question, where does the weight go? Well, a lot of it is carbon molecules that you lose via respiration, that you breathe them out as carbon dioxide. So, um, there were some comments here talking about whether we should be talking about, um, ingesting mass versus ingesting calories. And while, you know, it is absolutely correct that we do ingest mass, I guess it's a deliberate decision not to engage by talking about using a framework that would be meaningless to the people who we're trying to convince.
Paul, for people who are doing a ketogenic diet and maybe in a state of ketosis, there's a question from Chipoka who says, "I'm getting a bit of acetone breath during my ketosis. What does that mean? Is it ketoacidosis?"
Right? So, the the whole difference is, so ketosis and ketoacidosis share something in common. That's the presence of ketones within your body. Now, the difference between them is ketosis means that the pH, the acid, the acidity of your body is basically unchanged. Ketoacidosis means that your pH has lowered. It's now moved into an acidic state. So, it's possible to be breathing out ketones and be in ketosis. And it's possible to be breathing out ketones and be in ketoacidosis. So, Chapoka, it's not possible to know whether you're in ketosis or ketoacidosis simply by the presence of acetone on your breath. The only way to distinguish between the two would be to actually measure your pH. But let's just make the point very, very clear. Ketoacidosis is very, very unlikely unless you actually have deficient insulin levels, and that's how people with type 1 diabetes typically present. They usually present for the first time in acidosis, very, very sick individuals, and type 1 diabetes is defined as having a deficiency of insulin. So the insulin level is just simply far too low to control your blood glucose level. So they are very different. Nutritional ketosis, which is extremely uncommon, um, in so nutritional ketosis, uh, which is quite common, but is very distinct from ketoacidosis. Now, ketoacidosis simply on a low-carbohydrate diet is very uncommon, and it really only occurs in an insulin-deficient state.
So, Paul, that was the last comment on this lecture. Anything else you'd like to add on the topic of weight loss and use of GLP1s?
Not really. The only question I've really got is a burning question. I want to know, is that not a noxious weed, and is that going to kill us?
Stay tuned to find out. I mean, I didn't know you were such a good gardener of weeds. It is quite an impressive specimen.
That's a pretty strong ending for our first podcast.
That's a wrap. Dr. Paul Mason Show, episode...