Shocking NEW Cause of Heart Attacks (Not LDL Cholesterol) Dr Kendrick

You're going to die of a heart attack. You'll be dead tomorrow.

No, it's like no. LDL has no effect whatsoever on the risk of heart disease. It might be it's got an inverse risk. In other words, the lower your LDL level is, the more likely you are to die.

Dr. Malcolm Kendrick, cardiovascular expert, best-selling author. He spent decades inside the system. Now he's breaking the myths it was built on.

Carbohydrates aren't deadly substances that will kill you, but you will reach a point where they will be damaging and they will kill you. Fat in a diet has no impact on VLDL. And VLDL is the only source of LDL. And yet, when people say if you eat too much fat, your LDL level will go up. And I go, okay, talk me through the process. And he'll go, is it good for your heart? What about bacon ribeye? Saturated animal fat has never been damaging. I mean, the don't eat so many bloody carbohydrate diet is healthy for you. Science is there. The truth is there. It doesn't go away.

Do you think statins prevent someone from getting a heart attack? This is I've I've been sued for this. Um, your brain is 25% made of cholesterol. So, imagine blocking cholesterol production in your brain. What do you think that's going to do, gentlemen?

We've all heard this statement. If you care about your heart, stay away from saturated fat. Foods like butter, meat, and bacon have been blamed for heart attacks for decades. But what would actually happen if you were to eat high fat for just 30 days? What's going to happen to your cholesterol, especially your LDL cholesterol? What's going to happen to your blood pressure and your arteries? Well, that's exactly the question that we're answering today.

Today, my guest speaker is Dr. Malcolm Kendrick. He's a best-selling author and one of the most outspoken voices in cardiovascular health. And his research has reshaped how many people, including doctors, think about heart disease. And in this conversation, we're diving deep into the science, the controversy, and the real effects of eating fat on your heart and your health.

So, Dr. Kendrick, my first question, if someone is just eating eggs, bacon, and red meat every single day, is that going to destroy their heart? Well, no. What everyone thinks is bad for you with regard to your heart which is eggs have got lots of cholesterol, butter is got fat in it. I mean the thing the basic things that people say are bad for you like ribeye steaks and butter and cream and cheese and whatever. Um, I looked at this. I've been looking at this for many, many years and and it's just complete nonsense there. There is no evidence. There has never been any evidence whatsoever, not a molecule of evidence that eating a diet like that will be harmful to your heart.

Such evidence that I've found um, and when you're looking at diet evidence, it's always rather difficult to get any absolutes because as you can imagine, they ask people about their diet and everybody lies to start with and then everyone tells you things like, "Well, I eat nothing but a cabbage leaf and stuff like this." And you think, "Well, that's really just nonsense." But in so much as it's been done, the the evidence is that if you eat a higher fat, and by which I mean animal fat, not vegetable fat diet, that this has positive impacts on all the things that might affect your heart. I think the most important one of those is probably blood sugar levels because in general, if you're eating fat, you're not eating carbohydrates. And if you're not eating carbohydrates, your blood sugar level isn't going to start going out of control. You're not going to put pressure on your liver to deal with all that extra carbohydrate, etc., etc. So, yes, it's it's sort of ironic.

I did um um the man who's sort of most famous behind this is Ancel Keys who did his infamous six or seven country study depending on who you read where he sort of drew a graph showing that the more fat you ate, the more heart disease you had. And it was a sort of went up to infinity very rapidly. But he chose his countries. He he looked at 21 countries and then and then actually had you chosen had he put France in there for instance the graph would have gone upside down quite quickly for him. Um, but he chose not to because he had an idea he had a belief he had an absolute belief that if you ate fat and or cholesterol and or he never made it very clear what he was talking about that your blood cholesterol would go up and then you would have heart disease and then you would die of heart attacks. Now that evidence was was was poor to non-existent to complete nonsense.

In fact, he did a study in the 1960s and 1970s and he did it in uh in I think it was primarily in mental hospitals so you could really control the diet of these people where he swapped out um fats saturated fats for polyunsaturated fats and the the people's cholesterol level whatever he meant by that it's difficult to define went down which was theoretically good but actually for every one millimole fall in your cholesterol level, the rate of heart disease death went up 20%. Which the the there's two interesting things about that study. First is it completely contradicted everything everybody thinks. It completely contradicted everything he'd ever said and it wasn't published. It was just suppressed. But the data were found in 2016 and were published like 50 years after he did this study. The data came out showing everything he had said was contradicted by his study and you can find examples of this again and again and again and then you think well why didn't what happened you know the the original Framingham study which you may have heard of which was set up in the states just after the second world war and they ke this was also another place where this idea came about from and what they actually found with with regards to cholesterol and they never published this data It was found if you like in the same way by researchers who were sort of scraping around found that the people whose cholesterol levels fell over 25 years of the study were the people whose heart disease rates went up the most during that period which was again an exact contradiction.

So every time you look at the evidence and you don't just listen to what people have said you find actually fat saturated fat and cholesterol are all very healthy things. I mean Ancel Keys himself started by saying if you eat cholesterol your cholesterol level will go up. He did experiments on humans and fed them eggs like 10 eggs a day or something. And what he found was it had absolutely no impact on their blood cholesterol level. None. Now he knew this. So he just changed his mind. He said, "Oh, it's not cholesterol. It's it's saturated fat that raises your cholesterol." And well um isn't that a completely different thing? These are not the same things. These are completely different molecules. They are completely different things. So you said it was one that was wrong. Now you're saying the other. You have no evidence for it and now the world believes this idea. I just I do find myself looking and thinking well evidence has no impact on you whatsoever. So what does you know? Absolutely.

I want to ask you more about LDL cholesterol because that's the main thing that people will say, "But I followed a higher fat diet." And by higher fat, we're talking about animal fats, butter, tallow, ghee, red meat, and eggs, and then my LDL has skyrocketed. Very first question for you. Is there any evidence between high LDL and heart attacks?

Yeah. Well, you're asking a simple question. It opens the doors to a million rooms which open doors to another million rooms and you find yourself in the 10 millionth room and you think how did I get here and what am I talking about? It's quite complicated. All right. I mean when I give talks on this I say to people first of all you have to understand what LDL is. You have to understand what cholesterol is because otherwise you're just talking gibberish essentially. I mean cholesterol is a molecule. It has a chemical formula. It's found in in human beings. 25% of our brain is made up of cholesterol for example. Most of our hormones like estrogen, progesterone, testosterone, blah blah blah. Vitamin D that is cholesterol. They very slightly adapt it. So it's hugely important substance all right in our bodies. But it can't float around in the bloodstream because it's not uh soluble in water and neither is fat. So in order to transport these things around the body, you have to wrap them up in a little molecule called a lipoprotein, which is if you like a taxi. So the LDL is is a taxi that carries cholesterol and a certain amount of fat and other things around the body. And so when you talk about LDL cholesterol, it's a sort of meaningless term because it's not cholesterol, it's LDL. It'd be like calling anyway the terminology is complete nonsense. All right, but it adds to the conf. It took me about a year to understand what are they talking about. All right. When someone says cholesterol, what do they mean? You know, and they mean anything by it actually. So, you have to be careful. And everyone says, "Oh, my cholesterol levels gone up." And I go, "I wonder what you are actually talking about. What did they tell you? What did they say?" You know, it's like it's it's just a catch-all meaningless term. But LDL is the one form of lipoprotein that is supposed to cause heart disease. Now there are many different lipoproteins. There's about last time I looked there was 47. All right. And you think well this area just becomes complicated. So but LDL is the fraction of lipoprotein that if it's raised is supposed to cause heart disease. How it's supposed to cause it? Now you want to go into that. We are in the 7,000th room of nonsense. All right.

However, so what happens um is your your liver makes lipoproteins, right? That's where they're made. The liver does all sorts of amazing stuff. Um, but it doesn't make LDL. It makes VLDL, which is very low-density lipoprotein. And it packs fats and cholesterol into this within the liver and then it sends it out into the bloodstream. And then as it travels around the body it loses its fat content mainly till it becomes more highly concentrated with cholesterol and then about 98% of that is reabsorbed back into the liver. So there's a certain reserve that floats around in your blood all the time. Now what makes your VLDL go up would be the interesting first question right and the answer to that is carbohydrates make your VLDL go up. Uh, why is that? Because if you have too many carbohydrates in your diet, your body can only store so many and then it has to convert the carbohydrates into fats and it does that in the liver. So the liver converts carbohydrates into glucose into fats. That makes the LDL molecule well it packs it into the VLDL molecule and it sends it out. Fat in a diet has no impact on VLDL because it isn't remotely the same system. It's just this is another part. If you eat fat, it doesn't actually go into your liver. If you eat fat, it's directly absorbed from your gut and then it goes directly from your gut through a little channel called the thoracic duct into your vein vena cava and and this is a huge like lipoprotein called a chylomicron. It's everyone's going, "Oh my god, chylomicron." But a chylomicron say 20 times the size where it's like a a beach ball rather than a tennis ball or something of that sort of size. It travels around the body and it loses its fat and then what's left the tiny little remnant is absorbed into your liver. So fat actually has no impact on VLDL. And VLDL is the only source of LDL. And yet when people say if you eat too much fat your LDL level will go up. And I go okay talk me through the process and he'll go what are you talking about? I said well you can't make statements like this without there being some evidence behind them and there is no evidence for this.

And then you people will say and the question you ask is this interesting one is there are some people called lean mass hyper-responders all right now 15 years ago I was discussing this with Dave Feldman right before anyone else knew that he was on this sort of track and uh and I didn't I said look I understand this happens but I I disagree with your mechanism of action right um but what happens with some people and it's unknown why there's a small proportion and I don't know what that proportion is who are quite lean. They don't they're not fat at all. They eat a very high or they eat a very low carb diet. Quite what else they eat is a bit unclear sometimes. And their LDL your LDL goes up quite dramatically in some cases. And then people might say well well okay so you're talking nonsense. So fat obviously it does make your LDL go up. I said I said no. I said that's it does but it's not through any sort of mechanism you would you thinking of. All right. But what's actually happening in this case is because most of the you're eating a high-fat diet, the fat is just traveling through your body getting absorbed by your cells that need it. It's not going into the liver at all. All right? So, the liver has no need to send out VLDLs because it doesn't need to get rid of this excess carbohydrate that's been turned into fat. So, the VLDL level drops down. All right? And you think, well, that would make the LDL level drop down. No, that's not what happens at all. Cuz what happens is is the body needs the LDL. Well, it doesn't need the LDL. It needs the protein attached to the LDL to stick it onto the side of a VLDL. Cuz this is like a it's like an identification thing. They have these really complicated proteins stuck to the side of these uh proteins that are stuck to the side of lipoproteins that identify them as that lipoprotein so the body can recognize them. So that protein is and that's a really difficult thing to make. It's a hugely complicated protein. So the the liver rather than making new ones says I'll just use the ones I've already made earlier and I'll take them off the LDL, stick them onto the VLDL, send them out, lose my fat. So that turns round and round. If the liver is not making VLDLs, it doesn't need the protein from the LDL. So it doesn't bother reabsorbing it. So the LDL level goes up because the body's like, "Well, I don't need you, if you like, to make my VLDLs. And if that sounds complicated, I know when I say to people, they start blanking over. I just say, look, take it look at it this way. The the reason why the LDL goes up is not because of the high fat intake. The reason why the LDL goes up is because of the low carbohydrate intake, right? It's the exact opposite thing. That's why it's going up.

And then people say, "Oh, but that leads to high LDL. So that means that if you don't eat carbohydrates, then you you'll die of heart disease." No, it's like no. And they've done they've done the recent studies on people to say is there evidence that if you have these lean mass hyper-responders and their LDLs are going up like threefold say from 5 to 15 or whatever it is or 3 to 9 or whatever that level is has does that have any measurable effect on the progression of the disease in the arteries that we call heart disease? The answer is no. But of course, this doesn't surprise me because I don't think LDL has anything to do with heart disease. I've never believed this. And I know that puts me in a minority of the world because everyone else goes, "Oh, it does cause it." I'm going, "No, it doesn't."

I had a a man recently. It was two years ago from the States. No, three years ago. Time flies when you're having fun. He um had an LDL level of 19. All right. Which is Yeah. Whatever that is. The average being three, it's like seven, six, seven times as high. And he told me, "I have no evidence of any heart disease." He's 72. They've scanned me. They've looked at me in every possible way. I have no um damage to my arteries. No thickenings, no atherosclerosis, it doesn't exist. All right? And he knew this because he had well this is called familial hypercholesterolemia which he'd actually be called familial hyperldlemia but that's even more of a mouthful. Anyway he uh because of this he was put on statins when they first came along but he couldn't tolerate them and they tried other things and he couldn't tolerate that. So his LDL's always been way up here and his doctors have been sort of studying him and going we must get your LDL level down and sort of 25 years later there is no evidence of heart disease whatsoever. Well, I thought, well, people do write to me quite a lot, and I think, well, maybe. And then he turned up in the New England Journal of Medicine as a case history, this guy, right? And everything was as he said, right? And and the evidence, the explanation for the authors was he must be protected against his LDL in some other way, right? So, when you get an absolute, you know, there's this thing of called a black swan. I don't know if you know a black swan is started with Nassim Nicholas Taleb who I like but not everybody does but anyway he said if your hypothesis is that all swans are white finding more and more white swans has very very little impact on your hypothesis once you find one black swan your hypothesis is dead right now I find black swan after black swan I find people like this man with 19 people write to me all the time saying my cholesterol my LDL is 12 which is four times I have no heart disease. I'm 90 years old. All right. Um and when you start looking at the whole thing of this is to an extent what's kept the hypothesis going for so long is familial hypercholesterolemia which basically means a very high LDL level. I mean very high. So we're talking sort of three four five six seven times as high as as normal. All right. And all the medical literature will say, "Oh, yep, these people die very young of heart disease and the rate of heart disease in young people is 400% higher than it is in the surrounding population." Now, uh, this is one of these weird areas where say, "Well, that's true, but it doesn't actually mean anything." All right. Well, the first thing is when they say the rate of heart disease is four times as high in the 30 to 39 year olds, you go, "Well, what's the average rate of heart disease in that population?" And it's virtually zero. And in the UK they have a thing where they me they monitor people with familial hypercholesterolemia and they found yes there was a 400% increase in in death rate in that population but in that population that meant four people four people that was it and that is is considered statistically significant. But when you look at overall life expectancy, when you look at familial hypercholesterolemia and you say, "Yeah, but what happens to people throughout their lives with familial hypercholesterolemia?" The answer is they live slightly longer than everybody else on average. They live longer than everybody else. And I know people go, "Oh, that can't be true." I go, "That is true." And I have the papers. I have the studies. I can There's a huge study that's been going in Norway for years and years and years. And in fact, most interestingly, the population aged between 60 to 80, which is where a lot of heart attacks and deaths happen with heart disease. If you have familial hypercholesterolemia, you are 40% less likely to die of a heart attack. So, well, this is that'd be like saying to someone, if you smoke when you're 40, you'll die of lung cancer, but if you smoke when you're 70, you're much less likely to die of lung cancer. By the way, smoking causes lung cancer. you go, "Well, that's just rubbish, isn't it? That's just not You're talking nonsense. How can this thing be a risk factor when you're one age and stops being a risk factor when you're another age?" The answer is, and I've written papers on this with other authors, that some people with familial hypercholesterolemia have another problem, a genetically linked problem. There is a few of these people, and these are the people that have the heart disease. It's got nothing whatsoever to do with the LDL. It's like looking at people with red hair and saying that they die more of heart disease and you'll go, well, that's fine, but the red hair is not causing heart disease. It's something else. And what something else is actually that people with red hair are more likely to have a Neanderthal genetic um DNA incorporated into them. And these people are more likely to get heart disease. So we're looking at we're looking at LDL and deciding it's causal and we're just sort of saying well that's causal because we know it's causal and it's like no it's not.

So the whole concept of LDL being damaging is wrong. So therefore whatever anyone says about oh your LDL goes up or your LDL goes down. Remember that study I talked about with Ancel Keys their LDL went down their heart disease rate went up in a kind of linear effect. In this Framingham study, the more your LDL fell, the more your heart disease went up. And if you look at elderly people that becomes more extreme, so people over 70ish, I don't like calling them elderly anymore as that age is approaching me fast. Is that the lower your cholesterol level, LDL level is, the more likely you are to die. And it's quite a dramatic difference. And so we have people aged of 70 who are more at risk of heart disease. Yes. Cuz they're older. and they're being told you must get your LDL level down. I'm going but but you know look at the look at the evidence. Please just look at it. You you you know and people just they just then withdraw in and say oh I'm not discussing this with you cuz you you're just an idiot or something like that. And I said hold on that paper was published in the BMJ. You know this is this this was not the you know 14 times the we did this research. We looked at all the evidence and from all the evidence that we can find LDL has no effect whatsoever on the risk of heart disease. It might be it's got an inverse risk. In other words, the lower your LDL level is the more likely you are to die. And that sounds extraordinary thing to say, but that is what the evidence says. That is what the studies say. I mean, I can't I'm going to hold them up in front of you here on my front of my camera. this one and this one and this one and this one and this one and this one and this one. It's just, you know, so where's the evidence the other way round? I mean I as you know I got sued well I got attacked by a major newspaper in the UK for saying such things and we then sued them for libel and won because once we went to court right and the evidence was presented to someone a judge who doesn't really actually know anything about this area it was like well yeah well yeah these people seem completely reasonable in what they seem to be saying is completely right what's your problem but the problem is of course that the the medical profession if it can be called as a single thing is absolutely wedded to this idea and so it's almost everybody else and then so everyone goes well they can't all be wrong can they well they're wrong about the dietary stuff you know that a lot of people listening to this will know they they're wrong about this stuff I mean the paleo diet the keto whatever you call it anyway they don't eat so many bloody carbohydrate diet All right. Is healthy for you. It is good for you. It is. There is no parameter that is not I mean some people are less. I look at my son and he's like a bean bowl and he eats Cheerios and and waffle. He eats every carbohydrate known to man. His diet is is reasonably healthy. But he he is like just you know I said just you wait till you're my age son.

You now as Dr. Kendrick mentions heart disease is not caused by LDL cholesterol. It is actually caused by eating too many carbohydrates. And a really easy way to fix this is to simply drop the carbs and increase your healthy saturated fats. Now, as you do this, you might experience some side effects like headache, nausea, and fatigue. Now, all this is very normal, especially at the beginning. So, what you can do is do the salt trick. Add some high-quality salt to your meals and also add it to your water. But if the symptoms still persist, I would highly recommend that you lean on a high-quality supplement, one that has sodium, potassium, and magnesium because this is so important for proper brain and body function. And that is why I have Element as a sponsor of today's episode. Now, I like to use a high-quality supplement like Element because it has a proven science-backed mix of sodium, potassium, and magnesium without any preservatives and nothing artificial. And I like to use half a sachet of the raw unflavored option every morning in my morning coffee and the other half I just sprinkle in my water during the day. And right now Element is offering my viewers this free sample pack on every order. So you're going to get eight single servings of Element to try for free. If you want this just head to drinkelement.com/theprimalpodcast.

I do want to close this argument about LDL by offering solutions to people because this is about empowering them, not giving up to the doctor in front of them. So if LDL does not cause heart attacks, can you please list the markers that they need to look at on their blood work that they can present to their doctor and say, "This is it. Look at this one."

Yeah. Well, ironically, of course, one of the markers that you they will have is where they look at and they call them triglycerides, by the way. I don't know if they do in Dubai, but they do here. Yeah, triglycerides and they do most places. So, VLDL, as I talked about, very low-density lipoprotein, for some weird reason, is called your triglyceride level, right? Although it's a fifth of your VLDL anyways, just forget about it. But, so the VLDL, the stuff that I was talking about that's produced when you eat too many carbohydrates, all right, that level is quite important. Not in so much as it causes disease of its own, but it's a marker for you're eating too many carbohydrates and that your liver is having to shove is having to convert glucose into fat and shove it out. Now, as it does that, what happens is the thing that's called good cholesterol, HDL. All right? So, people have heard of high-density lipoprotein. Again, it's a marker. All right? As VLDL come out of the liver, the HDL transfers proteins to it. All right? to allow it to be recognized around the body. It's one of the functions it has. And as it does that, the effect of the HDL level effectively lowers or it does lower, right? Measurably lower. So when your HDL goes down and your VLDL or triglycerides go up, all right, what this is telling you is you have and some people would say this is insulin resistance or a marker of heading towards type two diabetes, right? That level, that ratio is is is quite important. I mean, you could just measure someone's blood sugar level or their HbA1c or other things and say, "Well, actually, we know that anyway. You're not telling us anything new." But if that ratio improves and then some people will say that's a high cholesterol or they will say your HDL level, your HDL to cholesterol level is poor. In other words, you've got low HDL and your overall cholesterol level is high. But that cholesterol level includes VLDL in it. by the way, it's part of a just a general lumped together figure. So if that figure starts to look wrong, then you'll probably want to do something about it. And that something is to reduce your carbohydrate intake and then that will tend to normalize. Not always, but almost always, right? And on a population basis, the the most the greatest risk factor for cardiovascular disease is is um type two diabetes or which the trouble with the term type two diabetes is there's a certain point at which you're diagnosed with type two diabetes and go you've got type two diabetes and if you're like one point lower than that they go ah you don't have type two diabetes. Actually, you're on a a sort of spectrum here from your insulin and your glucose and all that is working fine to you're completely knackered and your blood sugar is too high and your insulin's way off kill. You want to keep that as low as possible all the time. So, the thing you need you need to be looking at is, you know, some people have these continuous glucose monitors. I don't know if you can get a bit obsessed by that and just constantly looking at it and warning. I don't know. I would I know I'd go, "Oh my god." that Mars bar is killing me. Um, but no, the the glucose level and how it's responding and your insulin, that's a much more important thing to be looking at for most people. It's not always the cause of cardiovascular disease but I was looking at uh India recently actually because I was doing a an interview with Indian doctor and um and it was fascinating because he he he works in in ER emergency medicine and and the rate of heart disease in India is going through the roof by the way and also interesting women have more heart disease in India than men which is another thing everyone tells you women don't get as much heart disease as men I go yes they do um if they do the wrong things basically But the reason for that often is they've got a lot of what they call central obesity in India for for whatever reason obesity in India is described as having a waist greater than 25 rather than 30 but it tends to be central obesity. So this central obesity thing having a high waist hip ratio having a what used to call in Britain a beer belly that shape is it means also it's another sign an indicator that you've got a problem with your metabolism that's going on. All right. And that that is it's the same thing as the VLDL HDL ratio. It's all telling you the same thing. Your metabolism is is screaming out in pain. All right. Do something about it.

Now, what can you do about it? Well, you can take exercise. That's fantastic. Always good. Always recommended. High-intensity exercise is the best like HIIT what they call high-intensity exercise training because what that does is it burns the sugar out of your system. You may have heard of people have heard of anaerobic and aerobic exercises, but anaerobic exercise means you're using sugar as because you you're going beyond your oxygen uptake need. So you burn sugar. Now when you burn sugar, it's not very efficient, but actually it gets rid of the sugar, which is a good thing. So if you do like 2 minutes of running on the spot or pushing heavy weights, this is good. whereas actually going for a long run, slow run, although it may use up more energy, that's using up fat and fat's got much more energy in it and blah blah blah. So high-intensity exercise is good and then changing your diet is good and eating less carbohydrates is definitely good and whatever. But don't eat nothing but people think, oh well, if I'm going to reduce my carbohydrate, I must eat fat protein because fat's bad for me. No, it's the opposite way around. You can't eat too much protein. It's not good for you to eat too much protein. Again, too much protein in a diet, not good. I recently saw a young man of about 20 who was doing bodybuilding stuff and trying to make himself look like Arnold Schwarzenegger and he was eating his protein shake shakes, all these things. Uh and and he he actually died because of kidney failure because the protein gets broken down, goes into your kidneys and right. So, I mean, you'd have to you have to eat an awful lot of protein to do this, but I would I was going to say that that would be like a lot of protein to cause that damage. But I just want to preface that if someone is doing carnivore or keto diet, you can't eat that much protein cuz typically people might eat 100 grams of protein roughly which is not too much for them and men and women need to eat enough protein.

I do just want to summarize what you mentioned cuz my question was the markers that people need to look at. So what are the numbers that people need to attain for HDL and triglycerides?

Well, it tends to be a ratio actually um that they have here which is the ratio of and it's normally it's in the UK because everyone uses different measurements and everyone has a different way of looking at this here. All right. So what you can do I think your best one of the tools that you can use and it's available to everybody. All right. Is a thing called Qrisk. It's called Qrisk 3. And if you type that into Google it will come up. It'll show you um a little algorithm it puts in what's your risk of heart disease. Now, I don't agree with a lot of it. All right. Some of it's nonsense, but it does have things like smoking and diabetes. Um, but it it has these this ratio thing on it. All right. And you can put your figures into that and it will tell you whether that's a poor, good, or otherwise ratio. So, that's quite a good little tool to use, I think.

So, people can use the Q-risk tool. someone I tend to go to, if you like, when I'm looking at figures that I if I'm starting to try and recalculate into milligram per deciliter and millimole per liter and and what what they're saying in Dubai, what they're saying in the UK are and the US are all different. All right. So people might get rather confused, but if you want to use one tool, it's a reasonable one and that will tell you. You can see that's the ratio. So the ratio of 3:1 is healthy and 4:1 is on borderline and 5:1 is unhealthy. All right. So the actual absolute figures are not necessarily important particularly it's the ratio in this case that is actually important.

Makes sense. So I will put that link uh Qrisk in the description so that if somebody has their blood work and they see the two numbers just plug them in and they can get the ratio. The ratio is important. Yeah. You might have to do a convert. If you risk 3, you'll be using millimoles per liter. But you can find a conversion if you do cholesterol conversion on Google. You can put in your figure in milligrams per deciliter and it will convert it immediately to millimoles per liter. All right. On the screen and then you can do that and then you can put the figures in. All right. That's what I tend to do because when I see American figures I'm always thinking what does that mean? What are they talking about? I do see people in in the comments and I understand because I I have a global audience if it comes from the US or people in Australia or maybe the UK and they're like dang why don't you give me the numbers for my own country. So the ratio that you provided maybe is an easier solution. But how about uh so HbA1c or blood glucose and your insulin you mentioned those as things to look at as your risk factors for heart disease. So can you give me some targets or numbers for those so so people can attain those?

Well again we've just changed in the UK for our HbA1c figures are now changed again. All right. Um the figures that will you will get in your own country. I mean it used to and it still is although it changed it now your fasting blood sugar should and it is using millimoles per liter between four and six is fine right um although if it's approaching six it's probably getting a little bit high so if you're at seven you'll be going oh my god if it gets above that but what people tend to look at they know the HbA1c is a kind of more general measure because over a 30-day period your red blood cells before they die pick up glucose and become glycated is the term for that. And so the more glycated they are, the more your blood sugar has been high during that period. So that's more of a kind of average period over 30 day kind of period. And that's probably a more useful one because obviously if you take blood sugar when you're fasting, you don't really know what's happening when you're eating. So your blood sugar might be doing this, you know, and it might be up there for quite a long time and then you come to the doctor and say, "Oh, we'll do a fasting blood sugar test." But I spend none of my life fasting, so I have no idea what that means. as most people are snacking all the bloody time, you know. So, so actually the Hb hemoglobin part A1c is just part a protein attached to the to the to the red blood cells and that is where the glucose sticks. Now, that figure I would go to your own country and go what's what's considered high? And and these are quite reasonable figures. I'm not going to disagree with them, but the lower the better essentially is always the question. So someone says you know it's 30 or I think it's if it's say 40 it's okay in Britain it's 45 you're considered to be moving into diabetic but I'm not sure how you translate that into Dubai or Australian or American figures I I'm not sure of the conversion in my head I can't remember what it is so I would go to your own country but again that's another marker that's very important and another increasingly important one and this is this is where I have to take a deep breath there is a version of LDL right and it's called Lp(a) and it's going to become well heard well there's going to be a lot of noise made about it in the next year because the drug company has worked out how to lower it. Previously no one managed to do this. All right. Lp(a) is a form of LDL. All right. But it has another protein stuck to the side of it. It's an additional protein. Another protein called a lipoprotein A. Um, now I'm not going into an entire sort of medical hoo-ha about this, but that actually is an important thing and it increases your risk of heart disease by quite a lot in some people and your Lp(a) is quite an important thing to know the answer to. All right. Now, it mostly is not measured by anybody. You'd have to go and ask them to do it and most doctors would just look at you blankly and go, "What's that?" you know um but it is of the lipoproteins it's the one that might be actually directly causal. All right. So it in my view that's an important one and people should be looking at that one and the the sort of fascinating and irritating thing is when when when they measure your LDL if you get an LDL result from the lab it will include Lp(a) in it but they won't differentiate it. They will just say it's LDL. All right. So if your Lp(a) was very high and comparatively and your LDL was normal in inverted commas they tell you you had an high LDL level. You don't. you've got high Lp(a) level which is more important. All right.

It makes sense. It's kind of like um you know I have a carnival group so we have a lot of people they do carnival and this is why I ask you the question first straight about LDL cholesterol because believe it or not that's the main question that I get why has my cholesterol and we have doctors like you that come on each week to answer the questions and then the doctors try to answer them but you see that is the main thing that people look at LDL and then we always talk about there's different types of LDL so you have the large buoyant you have the small dense even now you're saying the the Lp(a) so but basically in In the whole grand scheme of things, it's not just LDL. There is that component that you mentioned the Lp(a), but the bigger picture is to zoom out to understand HbA1c, insulin, triglycerides, and your HDL.

Now, I want to move on to understanding what would happen if somebody would actually increase their fat and do high fat for 30 days. So, by that I mean increase butter, increase beef, and lower their carbs. Some people might even do zero carb. What's going to happen to their heart? So my question for you, if somebody was to adopt a high-fat diet just for 30 days, what would happen to their heart just say for example in the first three days?

Very little, I would imagine. The the other thing is of course that what we're talking about with heart disease is not a disease of the heart. It's a disease of the arteries supplying blood to the heart. The heart itself isn't actually diseased unless you have a heart attack in which case parts of it are killed. So the disease we're talking about here is a disease of the arteries and the disease is called I call it atherosclerotic cardiovascular disease ASCVD which is the term that actually is now more widely used throughout the medical community although most GPs that you went to for instance wouldn't use that term. They'd still talk about heart disease or something anyway. So it's a disease of the arteries and that disease is a is a thickening of the artery wall and a thickening and narrowing of the artery wall. Now that process in theory and probably is true can take decades to go from nothing very much to fully blocked. I mean you can talk 50 years for that to happen. So it's obviously not happening very rapidly. Although that's not quite true because what happens is it's a process of a very rapid thing happening and then nothing happening for quite a long time. So actually when you look at people's arteries and they've done these studies but they've looked at people's arteries and done and who've got heart disease and they can see the blockages and then then next year they can come back and they get the same thing done and they can see the blockages are still there and then one year suddenly it will be bigger. All right. So, so what doesn't happen is that the thickenings don't just gradually get bigger. One time I tried to do an impossible mathematical equation was what's the size of an LDL molecule? How big is an atherosclerotic plaque? How many LDL molecules are there in each atherosclerotic plaque? If that was to be the case and it ended up with so many zeros in the end, it became meaningless. But so what actually happens is is is the thickenings jump in size. So, so what is actually happening is you can get sudden jumps and what that represents is you know if you've read my stuff is there's a blood clot forms at that point on the artery wall and that's what makes the size of the apparently the size of the thickening jump because they are the remnants of blood clots that are formed on the artery wall.

So what's happening in the heart if you have um is is you know a high-fat diet is is nothing really although because your heart tends to use um free fatty acids for energy not carbohydrates. So it will use those anyway. Whether there's any switch in metabolism from free fatty acids which are basically fats um fatty acids fats the same thing. You want to try looking at lipids fats. No, use one word and stick to it. You know, triglycerides, that's a fact. Yeah, it's a fact. What's a triglyceride? I thought that was a VLDL. No, it's not. It's like you couldn't create a more confusing nomenclature if you'd set out to do it, I don't think. Anyway, so would your would your heart change its its uh energy substrates? No, I don't think so. Would your arteries thicken up? No, they wouldn't. Would your blood sugar go down? Yes, it would. So a very important thing that might well happen in your arteries is

Because all your arteries and only the tubes and all your blood vessels are actually lined, they're lined with a little furry lining, a bit like a little forest. That's called the glycocalyx. Glyco, glucose, protein strands. They sit and they waft about. You know, if you try and pick up a fish, it will slip through your fingers. Very slippery. Why is it slippery? Because it's covered in glycocalyx. That's the slippery thing. It's like nature's Teflon. It's really slippery. It's the slipperiest thing you can imagine.

And so the inside of your blood vessels is all really slippery and it's all anti-clotting. All the anti-clotting substances sit there and say, "Don't clot here, don't clot here, because I don't want to clot here." And and those, those little strands are that thick normally. All right. I don't, they're very thin, really, as you can imagine. And then if they become that thick, then you are more likely to damage the blood vessels.

So this stuff called glycocalyx, which I haven't spoken to a single doctor in my day-to-day work that's ever heard of it, it's the most important thing in cardiovascular medicine, the glycocalyx. Anyway, this protects all your blood vessels. It's hugely important. It's anticoagulant and it's that thick. Now, if you eat fat and your blood sugar level goes down, your glycocalyx might be that thick. And if you eat sugar and you keep having high blood sugar levels, your glycocalyx will be this thick. And that is why diabetes causes heart disease, because diabetes causes your blood sugar level to be high. This damages the glycocalyx. This reduces the protection to the artery wall, and the artery wall becomes damaged.

And this also happens in the very small blood vessels, because your capillaries, which are, if your artery was this size, the capillary would be this wide, you know, it'd be really, really narrow. That's got glycocalyx in it too. If the glycocalyx is damaged in the capillaries, well, obviously you can't get an atherosclerotic plaque because a capillary is this size and a plaque is this size. So, you can't get a plaque building up in a capillary because there's nowhere for it to be. What happens instead is the capillaries are damaged and they break down and they burst.

So, when you have diabetes, you know, the people look at the back of your eyes and they go, "Oh, you've got diabetic retinopathy." Well, retinopathy just means damage to the retina. What that means is the capillaries in the smallest blood vessels are bursting. So you get little hemorrhages and they're blocking, and so your blood supply to your retina is being damaged and you get blind if you're not careful. So that's, it's exactly the same process that's happening in these little tiny blood vessels as is happening in the big blood vessels of glycocalyx damage. The end effect is obviously completely different because large blood vessels don't burst, or you would just be dead.

The same thing happens in your kidneys because your kidneys have got these little tiny little blood vessels that make them work in the nephrons. If these start to be damaged and break down, your kidneys start to fail because your kidneys don't work. So when you get diabetes, you get retinopathy. You get nephropathy, which is damage to your kidneys, and you get neuropathy, which is damage to the very small nerve cells in the tips of your fingers, for instance. Now, why do you get that? Because if you've ever looked at a picture of blood vessels in your hands, it's like there's just trillions of them. If they start to break down and die, then the nerves don't get the blood supply they need and they start to break down and die. So you lose your sensation in your fingers.

So whilst nothing might be happening to the large blood vessels in your heart necessarily, in fact, it won't happen immediately. Although it could happen immediately, you might get a blood clot there. Back. You're dead. All right? And that's less likely to happen if you're eating a high-fat diet than if you're eating a high-carbohydrate diet. The other thing will definitely be happening is you'll be reducing damage to the blood vessels in your fingers and everywhere else, your kidneys and your eyes. So, you will be coming healthier over a 30-day period. That will be improving your health.

As Dr. Kendrick mentions, following a high-fat diet can heal inflammation, lower blood sugar, and also reverse insulin resistance in the longer term. So, it's really important to remove all the toxins from our lifestyle. And this also includes the toxins that you put on your skin, because whatever you put on your skin penetrates what's called the blood-brain barrier, and that can go into your cells causing disease. And when I heard about this, that really made me stop and think because I have followed a high-fat carnivore lifestyle for the past few years, and it has helped me heal so many different chronic health conditions. But I still didn't realize I was still exposing myself to chemicals through my skincare. And I used to use 10 different skincare products. But now I only use one. It's 100% chemical-free tallow balm.

Now, you might be thinking, Reena, why would you put a tallow balm on your skin? Well, this has helped my skin so much. It's improved the hydration and my skin texture, as I generally have very sensitive, acne-prone skin. And that is why I created the Primal Tallow Balms as a chemical-free solution for your skin, but also for my skin. The Primal Tallow Balms naturally contains vitamins A, D, E, and K2. It is made from 100% grass-fed, grass-finished tallow. So, what does that mean for you? Well, you might experience better skin texture, better hydration, and better moisturization. And the best thing is there's no nasties, there's no preservatives. It is just 100% pure tallow. And I like to use this unscented balm every single day. Just 10p lasts me 24 hours. So if you want to be chemical-free from the inside out, pick up a tallow balm. Just head to shop.primal.com and get 10% off your next order.

So basically, in the first 3 days, your blood sugar is going to decrease, and that has major effects on your whole body. As you mentioned, it improves the glycocalyx layer, which then supports and protects the artery wall. So that's going to help with your arteries. But then also your whole body is going to feel maybe healthier. You might get more energy. Your insulin levels then, for example, might come down.

So, let's go into 30 days. They just mentioned 30 days, but I really want to give people hope to try high-fat, low-carb, or zero-carb, because there's major effects just in 3 days or even 30 days. So, now 30 days, what are the things that we could see, for example, with your triglycerides? Could they be coming down? Uh, they should be coming down by that point. Yes. I mean, there's a kind of, there seems to be quite a lag between what your liver gets up to and what you eat, possibly because there are stores all around your body and it takes a while for them to kind of outbalance themselves. I'm not sure exactly. It gets very, very, you can imagine, complicated. This is this is complicated, but yes, that will be happening. Your triglycerides should come down, your HDL should go up. Your ratio should narrow. What happens to your LDL? I don't care, but probably nothing, I would imagine. Well, in some people, if the fat is all being diverted outside of their liver, the VLDL will be dropping down. Your liver will not be needing the LDL. So that, some people there, the LDL might be going up. That doesn't happen in everybody, but it happens in some people. But all these ratios are improving. That's just a sign.

But insulin itself, I've just been reading a whole bunch of papers showing that insulin is really quite damaging to your blood vessels. Not, not in normal physiological levels, obviously, but when your insulin level goes up. And I was just looking at that with regard to type one diabetes, people getting high insulin inject, you know, they get injections of insulin all the time, and they looked at the blood vessel damage, and it is damaging independently of the glucose level. So if your insulin and your sugar are down, you are improving your blood vessels. That is happening. Yes, your energy, um, your, your sense of having energy should be improved, in part just because you start to lose this sort of wave of sugar going up, insulin going up, driving it down, and your whole metabolism is kind of going, "What are you doing to me? Stop it. I need energy, and you're knackering me." So, yes, that will improve for people, and they demonstrate that it does. And so it's overall, you should feel more energy. You should feel a bit better. Definitely do a lot better. People, especially who have high blood sugar levels, which may seem to make people feel very tired. I'm not sure why. And your blood vessels will be a lot more healthy. Your kidneys, your eyes, and your peripheral nerves will certainly be thanking you for it because they got a chance to recover, because very small blood vessels can regrow. I mean, there is a system for that. That happens in your heart. If you block an artery in your heart, that doesn't mean no blood gets down past that artery. The body will have created what they call collateral circulation, which is little blood vessels, a whole network of little blood vessels that will bypass the blockage. I've seen people walking around quite healthy who've got no, got all of their coronary arteries are fully blocked. They are surviving on collateral circulation. That is the creation of new small blood vessels. Your body can do this, and it will do it better if your blood sugar level and your insulin levels are down, because there's more chance of them being healthfully created. So there's all sorts of positive benefits going on here. Perfect. Just after 30 days. So this is to motivate people to just give it, be consistent for 30 days. 30 days. Well, you've read that book or something. I've read it once. It was if you do something for 30 days, then it becomes routine, and then it's much easier. Yeah. So, if you can get someone to do something for 30 days in a row, then they're probably going to keep doing it for longer, which is quite right. It is a thing. Well, I just picked the 30 days because it's quite interesting just to give it that snapshot. But I do have a question about a year. Because when it comes to arteries and then the the arteries and the plaque, people are very concerned about that. So, if you were to do high-fat, low-carb, or zero-carb for a year, do you think that you could get some plaque regression, especially if it's soft plaque? I don't know. Oh, I think what you're, what I don't know because, and don't worry, I have tried to know this. All right. And I've spoken to interventional cardiologists. I've looked at the scans. You know, the important thing is to stop it progressing. All right? Because they've done a work with what they call CAC scanning, coronary artery calcium scanning. If a plaque's been in your heart for a long time, it actually, in the end, it calcifies, right? As does do other areas of damage in your body. So if you can see a lot of calcium in your arteries in your heart, it means you have had a lot of atherosclerosis developing. It doesn't tell you it's happening right now because it can't, right? Because this is a process that takes some time. But if you get people who have, even people who have quite a high calcium score, and you stop it progressing, and I Cummings, who you may or may not have spoken to, who's done a lot of work at this in Ireland, shows that your risk reduces to the same risk as people who don't have a lot of calcium in their heart. It's not the amount of calcium that's damaging. It's the fact that that's just telling you you're getting ongoing damage in your heart. You've had it. You've got to stop it. And if you can stop it, then it really doesn't matter if it progresses or not, because your risk reduces to down to what it would have otherwise been with areas of damage. I think generally overall over time, if things aren't progressing, the body will be just gently kind of chipping away at them. So there will be some reduction. That's my own belief, by the way. That's not evidence-based. That's just what I think happens. All right. Um, but but there is evidence that if you stop the progression, then it doesn't really matter if you get regression, right? Because you don't need to regress. You know, I would sort of say, and then people might say, that's a bit depressing. Once the damage is done, it's done. Yes, that's true. But so long as you haven't dropped dead of a heart attack.

The first person to notice this was actually George Mann, who studied the Masai villages of Kenya for a long time. They ate no carbohydrates, well, at least they claimed not to. And he thought they didn't. They ate their diet consisted of cows, cow's blood, and milk and yogurt. And there was, they didn't eat carbohydrates, and they had very, very low rates of heart disease. I mean, he didn't even find anybody who'd had a heart attack and died, right out of that population. Um, and what he did find, though, is they had quite a lot of calcification in their arteries. All right? Because these were hyper-exercising people. They would run, you know, they 20 miles a day or whatever it was, chasing whatever they chased or running away from things that chased them. But they, so they had a very high-fat diet and blood and whatever cholesterol. They actually had lower than Western LDL levels and cholesterol levels. They had actually measurably quite a lot of calcium in their arteries and no heart disease. All right? So you have to bear in mind that this is not a, this is not a simplistic, you can't look at this as this is bad, this is good. All right? If you look at high, high-performance triathletes, and they, they've got quite a lot of damage to their arteries. What you'd call damage in their arteries. Is it damage? Or is this just what happens if you live that lifestyle where you're doing a lot of exercise all the time, really heavy, intense exercise? Is actually not very good for you. But at what level does it become not very good for you is very difficult to define.

So I should probably explain what regression means. So regression is when the plaque is reversing. You're getting less plaque seen in the arteries. So what Dr. Kendrick is saying that as long as it's not progressing, getting worse, that's okay. In some people, we have seen a regression. I've seen that from interventional cardiologists have told me in the carnivore space because they look at these people on high-fat diets. Sometimes it regresses, but the main thing, as you mentioned, is that it doesn't progress. So, we know now what's going to happen when you do a high-fat diet. Some amazing things. I've got a bit of a game for you. Listing some foods here, and you tell me in one word, good or bad for your heart. So, if somebody was to eat a lot of these foods, is it good? Butter, is it good for your heart? Neutral. Now, a lot of these we say good or bad. All right. It compared to if you're stopping eating something else, good. All right. So, butter is good. The the the study that showed that the consumption of the highest saturated fat is coconut oil. And they did that study. It was actually Michael Mosley, who you may remember him in the UK. He, um, they did a study where they kept everything the same and gave people coconut oil and butter and something else with, I think it was olive oil. No, it wasn't olive oil with saturated fat in it. But the one that had the, the one that that did was looked the most beneficial was actually the one with the highest saturated fat, which was coconut oil. Whereas butter apparently did nothing one way or the other, as far as I can remember. But you're saying good or bad, I'd say butter. If you're stopping eating a muffin and eating butter, good. If you had the choice of not eating the muffin or not eating the butter, stop the muffin, eat the butter. Yeah. Well, maybe I should have prefaced my question by saying eating your fat but going dropping your carbs, or maybe zero carbs. So, what I mean by that is no muffins, no pasta, no bread. So, butter, okay. Okay. Coconut oil, okay. Okay. What about bacon? Yeah, it's fine. It's good. I like it. Ribeye, fantastic. Avocado. I don't like it very much, but I don't like avocado. It's good for you then. Oh, okay. Okay. Uh, what else? Peanut butter. I don't know actually. I would suggest, I would think, thinking about it, I think it's not very good for you. Yeah, it's not very good because it's high in omega-sixes. So the foods that we listed there, so people, if they eat more of those foods, and that just happens to be what they call the carnivore diet or a keto diet. And I know for you, you don't advocate a diet per se. You like real whole foods. But in this day and age, I see people just need a little bit more prescription around how to do things and what to omit. And because, as you can imagine, there's so many people talking about different things. Lately, there's a sugar diet, and people saying that I'm eating less sugar, I eat more sugar, less protein, and that's good for my health. Who knows where the heck that comes from. You have done a lot of work understanding the real cause of heart disease. Now, it's called the thrombogenic hypothesis. Can you explain it to me like I'm a child? Because I am a child and in my brain. Well, we all are. And that we like, yeah, we like a thing to be, we like a story. Uh, we like it to be simple, which is really where the cholesterol thing started off. I think you eat too much cholesterol, your cholesterol goes up, it gets deposited in your arteries, king. Easy to understand. As H.L. Mencken said, "For every complex problem, there is a solution that's simple, easy to understand, and wrong." That's wrong.

What's right is that your arteries are basically, um, as you can imagine, there's all sorts of stuff flowing through them at high speed. So, the first thing to the first simplistic thing that I say to people is, you know, plaques or atherosclerotic plaques or whatever term you want for them, which is a thickening in your arteries. All right? Why don't you get them in veins? Well, you never get them in veins, and you never get them in the blood vessels in your lungs. All right? Now, they're all the things that flow through your bloodstream, surprisingly enough, flow through every part of your body because it's all connected. We discovered that, you know, 400 years ago. Um, so your cholesterol levels, the same, your blood sugar levels, the same, all the things in your bloodstream are the same in your lungs, in your veins, and in your arteries. Maybe it's tiny fractions different. So why aren't you getting plaques in your veins and your lungs? Why doesn't that happen? And I ask people this question. They look at me like, well, what does that matter? Well, it sort of matters because if you take a vein out of your leg, which has happened, and you put it into the heart and make it become a coronary artery, as in a coronary artery bypass graft, it very rapidly develops atherosclerosis. These things block up after about seven years on average with atherosclerotic plaques. So veins can develop atherosclerosis, but they don't develop them when they're being a vein, but they do develop them when they're being an artery or acting as an artery. And in fact, they develop them faster. Why is this? And if you can't answer that question, the cholesterol hypothesis doesn't even consider that to be a question to be asked. It says if the cholesterol level is high or the LDL is high, it it is somehow or other absorbed into the artery walls and thickens them. Well, why doesn't it do it in vein walls? And why doesn't it do it in the walls in your art in your lungs? Well, they have no answer to this. They just sort of go, well, they don't even, I mean, they don't even try to answer this question. They don't even think it's a question, right? I thought it was a question. Said, if it's a question, and so, oh, it's it's because it's higher pressure or something. What do you think pressure pushes LDL through an artery? Whoa. It's come on, go on, talk me through that. Give me the physics for that. Oh, you can't, because it's nonsense. So I thought, well, clearly therefore something is happening because if you do get high blood pressure in your lungs, and that happens, there are conditions where you get bypasses from your left to your right side of your heart, and your blood pressure in your lungs can become quite high. It's called Eisenmenger's syndrome. Doesn't exist so much nowadays because people get operations which they couldn't have done 50 years ago because there was no heart-lung transplant. So you can get plaques in your lungs if the pressure is higher. So you think, okay, so it's blood pressure then, isn't it? Well, it is and it isn't. But you obviously are looking at something quite fundamental here. And when I started looking at it, I thought, what is going on? Why this? Why this? And when you start looking at it in more detail, you realize that of course arteries are under much greater, what I call biomechanical stress. So your coronary arteries, which means the arteries of your heart, are being compressed tightly when the heart contracts. In fact, your blood doesn't flow to your coronary arteries when your heart contracts because it shuts them. It's only when the heart relaxes that the blood flows through. So a coronary artery is being squashed like that all the time, 60 times a minute for all of your life. So you can imagine the lining of your blood vessels there is getting under quite a lot of squishing and squishing. And also in your neck, you've got carotid arteries that come straight up from the aorta. That's an area of high pressure and high turbulent flow. So I'm not the first person to think this, by the way. I thought this is an area where there's damage is going to be occurring to the lining of the, if it's going to be occurring anywhere, it's going to be occurring here. Right? So you're going to damage the lining. What happens when you damage the lining to an artery? And that's when you open the box, if you like. You go, "Crikey, what happens?" Is that will create a blood clot, as it must. Because you can imagine, the body's quite sensitive to damage to the lining of a blood vessel. Suggests the blood vessel has been damaged, which suggests we might be about to bleed to death. So there's all sorts of systems, vastly complicated systems that when you damage the lining of a blood vessel, you get a blood clot. Bang, straight off. Now, obviously, it can't just completely continue to be a bigger and bigger blood clot, otherwise, the time the first time we had damage, we'd have a one big blood clot and we'd be dead. So, what happens is at the same time as that blood clot is forming to cover over the area of damage, it's being stopped. So, we have this. Anyway, the last time I looked, there's 53 factors that make blood clots happen and 53 that stop them or pause them or control them. You can't believe how complicated this system is. I look at it again and again and think, how did this ever happen?

Anyway, so what happens is, step one, you damage the lining of the artery in some way. Now, if the glycocalyx is thinner, then it's less protected. Now, other things can damage it. High blood sugar levels can damage it. Smoking can damage it. There's also, there's a million things that can damage the lining of your artery wall. Once it's damaged, the blood clot forms, then it stops. Then you have a problem. You have a blood clot stuck to an artery wall. Now, if you scratch your fing, if you scratch the back of your hand, obviously you get a scab. At time, the scab falls off. But if a scab fell off your artery wall, it would just get stuck in your brain. So, you can't have that system happening. So, you can't have the same system occurring. All right? So what happens is the body has to cover it over with a new lining, a new arterial lining. It's called the endothelium and the glycocalyx. It's the lining of your arteries. And that's what happens is you get a lining area covers it over, and then the blood clot is drawn inside the artery wall. That's the only system that can happen. And then your repair mechanisms come along and chomp away at it and get rid of it. Until they don't. Because if that keeps happening at the same point, then you will get a buildup of damage, and each recurrent area of damage becomes a new layer, if you like. And if you look at plaques and people have, they find that very many of them are still sort of semi-intact, show layers like tree rings, where there has been a repeated episode of something happening at that point, like 30 layers of thing. The only explanation for that is possible is that's a blood clot. Another blood clot, another blood clot, another blood clot, another blood clot, another, you know, when I said about phasic, this is what's happening. You are getting a blood clot at that point. It's then repaired. It's covered over, and in most cases, it disappears completely because the repair systems get rid of it. So this is happening, unfortunately, in every one of us all the time. It's like our skin isn't constantly being scratched and damaged, and you look at it and it looks completely normal, doesn't it? You don't say, "Oh my god, I'm covered in scars." What you say is, "Oh, look, you get a really bad cut and it will cause a scar, but most of the minor abrasions just disappear completely." So, most of the minor abrasions disappear completely. So when they, they got volunteers to smoke one cigarette, healthy volunteers to smoke one cigarette, and they measured the breakdown products of endothelial cells, they actually, you could see endothelial cells were dying and breaking up around the body. You think, "Oh my god, one cigarette." Luckily, when you do that, the bone marrow produces more endothelial cells or pro-pre-endothelial cells to cover over the areas of damage, and it's all gone. So that's one of the reasons why as you get older, you get more of a problem, because the things that when you're younger get repaired, as you get older, the repair systems start to get a bit creaky, and so when you get an area of damage, instead of it being just got rid of, it starts to get a bit more, less likely to be got rid of.

So what you're looking for is basically, so that's the process essentially. You damage the endothelium, blood clot forms, it's repaired. Well, that's happening to everybody all the time. And if you inhale diesel fumes, the nanoparticles get into your bloodstream and damage the blood vessels. You can see these things. These have all been measured, right? But what happens is if you increase the rate of damage, then you might have a problem. If you increase the size and scope and make the blood clot more difficult to break down, that's going to be a problem for you. And if you interfere with the repair mechanisms, then you're not going to get rid of the plaque. So, simp. So essentially, it's a, it's a three-process thing. More damage, bigger and more difficult to shift blood clots, damage to the repair system, or interference with the repair systems, and you will start to develop plaques that will grow faster and faster, and it will overcome the body's ability to get rid of them. All right. And that's it. So when you're saying what causes heart disease, you say, does it damage the endothelium? Yes or no? If it doesn't, it's not a cause. So, we have, I mean, in the back of my head, I've got, I can give you a list as long as you like of things that I found that can damage the endothelium, and it's rather scarily long, right? Anything to do with inhaling smoke, for instance, that's really bad. So, wood fires, unfortunately. Well, I love a wood fire. Really? A wood fire? Yeah. Yeah. Wow. So, so just a question. So in, instead of people thinking that butter or bacon is going to cause them to get a heart attack, you're saying that inhaling smoke like wood fire is actually going to cause a heart attack? Yes. Can do. Yeah. Well, that's like, people are not going to not think about that. They can think what they like, you know, but it's true. Uh, that that's the fact. Once the particles are small enough, called nanoparticles, your lungs are relatively leaky. Things can leak out of your lungs and into your bloodstream. And once they've leaked out of your bloodstream, these particles are quite toxic to your bloodstream, your blood vessels, and they start damaging. So smoking is obviously one way of putting smoke into your lungs. And and people say, well, how does smoking cause heart disease? You go, well, it raises your cholesterol. No. Raises blood pressure. No. It doesn't do anything that you can measure. Why is it causing heart disease? And what is it actually, what is actually happening? What is actually happening is the nanoparticles of smoke get into your, out of your lungs into your bloodstream, go around your body killing off endothelial cells. That's what happens. All right. That's what happens with wood smoke as well. That's what happens with diesel fumes. Why do you think, you know, that's been found, diesel fumes are particularly small particles compared to other forms of fuel. That's what causes that. The miners, coal miners used to have heart disease. Yeah, of course, their lungs were destroyed, but actually they had terrific rates of heart disease, and that's because they were breathing in crap, if you like.

So what about lead poisoning? And people's, this is another thing I was looking at a paper which again gets undermarked, is that in America, they found that that lead, not poisoning, but high levels of lead in your blood, in your body, caused, and this was going back say 10 years, 250,000 deaths from heart disease every year, more than smoking. And I said, well, how does lead, how does lead do it? Well, it's very simple, because lead is one of the most damaging things to your endothelium. And they've shown this, you can demonstrate it. It strips your glycocalyx. Heavy metals, terribly damaging. You know, they used to put lead in petrol. OMG. And we said it was perfectly healthy. And lead pipes and all that. Now that these are going, this is one of the reasons why heart disease rates are going down, have gone down in the Western world. And you can look at, say, I looked at one which was, the single disease that causes the highest increased rate of heart disease death is sickle cell disease. Right? How can sickle cells cause heart disease? Well, a sickled cell is kind of that shape with sharp, pointy ends rather than a nice round donut shape, normal red blood cell. Can you imagine a sharp, pointy red blood cell hammering through your blood system? That's going to be stripping your endothelium apart. And it does. The increased rate of heart disease. I mean, children used to die very young from severe sickle cell disease. The average age of death was two. So obviously, they weren't dying of heart disease at that time because they just weren't. But now that they treat that, you can be treated and get transfusions and things, and they live, they live a lot longer, thank goodness. Um, but they still, the rate of heart disease is astronomical. And people just look at it and go, why is that? And instead of saying, this is a 50,000% increase in the risk of heart disease at that age, these ages, 50,000% increase. You're looking into the heart of the matter at this point. You can't explain it any other way. They don't have any other risk factors that you can identify, and yet their risk is 50,000%. So that's telling you, it's like that is shouting at you what the cause of heart disease is. It's screaming at you. It's going, it can't be anything else. This is it. You found the answer. And in fact, the people who authored this paper said it themselves. They said, "The reason this is happening is because of the physical rigidity of the sickled cells causing damage to the lining of the blood vessels." They said it, but they didn't then follow that on and go, "Oh, well, maybe that's what causes heart disease then, isn't it?" You go, "Yes, it is." Because it's so blindingly obvious. It's just, people are going, "Okay, again, explain it. You explain it. Go on." They don't. They just go, "Oh, well, it's, there's not very many people with sickle cell. I know it's probably different." And so, let me try to summarize what you've mentioned. So it's not cholesterol causing heart disease and heart attacks. It's anything that's damaging the endothelial, the endothelial cells, which is the lining of your arteries. And on top of that, you have the glycocalyx. And there's numerous things that we could mention, but anything. And Dr. Eric Berg said, anything they tell you to do the complete opposite, because it's probably good for you. So in this sense, eat more saturated fat, eat more whole foods, walk, do high-intensity exercise, get out in the sunshine, do some fasting, and stay away from all the rubbish, pollution, crap, smoking, all the other stuff. So, and it kind of makes sense, but I think that is, if we can understand that is actually the cause of heart disease and heart attacks, not the cholesterol.

Now, I want to move on to statins, because this is a big topic. Do you think statins prevent someone from getting a heart attack? This is, I've been sued for this. Um, and I've, anyway, no. Well, and then the cholesterol lowering bit has got nothing to do with it, right? Now, you remember talk about the damage to the artery lining and all that I've just been going on about and going mad about. All right? Well, there is a substance called nitric oxide, and it is the world's most, it's the single most important molecule for your cardiovascular health. Right. It's anti, it's the most potent anticoagulant known in the world in nature, and it stimulates the body to produce new endothelial cells, and it, it also exists within the glycocalyx and health, and it makes the, it just is a, anyway, having a high level of nitric oxide is the most important thing for your cardiovascular health as a single thing. All right? Statins increase nitric oxide synthesis. Okay? Now, they do it through a complicated method, but they do it. All right? Now, they don't do it a huge amount, but they do do it. All right? So, that is a potential benefit of statins. How large is that benefit? It's not very large. It's pretty darn small. All right? But it's got nothing to do with the LDL lowering. It's just an unpleasant and unfortunate adverse effect of the statins. The benefit is something else that they do. So, when I say to people, do they can prevent heart disease? Yes, they can. But at very high cost, in my opinion, of adverse effects and damage. Right? So I tend to say to people is, I use one statistic, which is, and this is from the papers themselves, this was not my paper, it was published by somebody else, Christensen, and he looked at what is the average increase in life expectancy from taking a statin for five years, using the data from the clinical trials themselves, the big clinical trials, the ones that are used to promote statins. And the answer is, if you have not had previous heart disease, in other words, they call that primary prevention, stopping a first thing happening, is that your risk, your increased life expectancy is three days. All right? That's for five years of taking a statin. Okay? And if you've had a heart attack or stroke or diagnosed heart disease, it's 4.1 days. So that's the increase in life expectancy that you can gain from taking a statin. And in the end, that's what you're trying to do. It doesn't really matter what you die of, particularly, just are you going to live longer or die of something else instead? Is not really worthwhile. So that's 0.6 of a day per year of taking a statin, according to clinical trials. You may or may not wish to believe that they are unbiased. Or 75 if you've had a heart attack. So you can make that decision. The people can make that decision themselves. Is it worth it? I would say I wouldn't do it for that, because you'd spend at least 0.6 of a day going to the doctor, getting your cholesterol measured, getting the statin, taking it, getting worried about it, then getting a whole bunch of adverse effects from it. Forget it. All right. I just, they are held as the miracle drugs. If you ask a doctor, and I've done this, if you, and others have done it as well, if you ask an average doctor, how much longer do you think a patient will live if they take a statin for five years having had a heart attack? All right. They will normally reply something in the region of two years. All right? That's the sort of figure they've got in their head. I say to them, it's, it's actually four days. And they go, that's rubbish. So, well, where's your evidence? You have none. I can show you the papers. I have evidence. All right. They still just go, well, you know. So you have to make your own mind up. The doctor will have in their head, you will live about two years longer if you take this statin for five years. That's the figure they have somehow or other. Some will be shorter, some will be longer, but they all think they're miracle drugs, right? I went to a meeting. It's the thing they do in the UK where they educate you on the latest developments and stuff, right? You know, so I spend most of my time going, "No, God." Um, however, they taught this, they sort of about things you could do after a heart attack or whatever. And then they talked about giving it was it a heart hug? A heart hug. All right. They said statins give you a heart hug. This is a scientific meeting. All right. I thought, right, get me out of here now if we're starting to use terminology like this. But there is this thing, they are seen as the benevolent wonder drugs that are just, they have no adverse effects. They are just beneficial. People should just be taking them anyway, whether they've got heart disease or not. That's the medical profession, honestly to God, thinks this, most of them. Um, so you will get a very big bad pushback from the doctor who just thinks you're an idiot. You don't understand. They're, you're going to die of a heart attack. You'll be dead tomorrow. You, you know, blah, blah, blah. It's like, take a deep breath. It's nonsense. All right. It's four days if you've already got heart disease. If you have a day's worth of adverse effects a year, it just cancels it out. All right. And I've seen people, quick short ironic story, the newspaper, the Mail on Sunday, that decided to attack a few of us for being anti-statin and said we were mad and we were murdering people and whatever. All right. At one point, and we know because we've seen the background information, they went around trying to get case histories from people who'd stopped taking statins and then had a heart attack. So they could say, "This is someone who heard what Dr. Kendrick said and he had a heart attack and blah blah." They didn't find anyone, by the way. What they did find, the first two case histories that came back to them were two people who started taking statins, suffered liver failure due to it, and died. All right. And what the comment of the editor of the newspaper who was doing these articles was, "Well, I don't think this is the type of case history we're really looking for." And the other thing he said is, "Since we put out this call, we've been inundated, we've been inundated with people telling us they've stopped taking statins and feel much better." Right. So when he put out the call, he got the exact opposite of what he was looking for.

I have a thing I say to patients, which is, if you stop, if you take a statin, um, it adds 15 years to your life. And they go, "Oh, that's fantastic." I said, "No, you're probably misunderstanding me. I don't mean it'll make you live 15 years longer. I mean it will make you feel 15 years older." Right? Because they have this effect. Because another thing that they do, I mean, they raise nitric oxide, is that they, they don't just block cholesterol production in your liver, they block, or other cells in your body, they block the production of a thing called co-enzyme Q10. No one's ever heard of it. You quickly know co-enzyme Q10 is a really important chemical in, whatever it is, exactly what you term it, that works with the mitochondria to produce ATP. Right? ATP is the end result of all of what you eat being produced into energy. ATP converts to ADP. That's how your body has energy. That's your petrol, if you like. If you're a car, ATP is your petrol. It's your rocket fuel. All right? And it's been shown that statins reduce co-enzyme Q10 by 50% and reduce the amount of ATP in your body. Now, that was known very early on, because when they were about to launch statins in 1985, Merck put out a patent for the, that when they give people statins, they would take co-enzyme Q10 at the same time. All right? So they knew, they knew that it did this. All right? They knew all this stuff. They always do. But then they decided it wouldn't look very good giving the antidote to this drug at the same time, as it would mean it probably was considered not that healthy. So they got rid of that idea, but they'd done the experiments on dogs, and dogs were particularly sensitive. They virtually died when they took statin because the co-enzyme Q10 in dogs went to virtually zero. They had no energy reduction. They just lay there and presumably everything just stopped. So yes, we know that statins have these, they do these really bad things as well. And that's probably not such a problem if you're 40 years old or something, and your production of co-enzyme Q10 and ATP is probably reasonably high. But as you get older and older, obviously you, you can reach a point where your reserve is, is at its kind of met, and then suddenly you drop co-enzyme Q10. The number of people I have spoken to who became virtually bedbound through statins, who couldn't get up, who were weak, who had muscle pain, and they're going, "Oh, statins can't cause muscle pain." I said, "But we know that statins reduce co-enzyme Q10. We know exactly what that does." Big surprise. It makes you knackered with muscle pain. Well, yes, it does. Exactly. Once you understand all the processes, and I kind of do, you go, well, it's going to cause that, and it's going to cause that, it's going to cause that, and it's going to cause that, and it's going to cause, and it causes all these things you would expect it to cause as adverse effects. Drugs do not just pinpoint one thing in the body and go, bing. Nothing does that. They do all sorts of things all over the place. Statins do most unpleasant things in your body. Really unpleasant things. Beatrice Golomb looked at amyotrophic lateral sclerosis, which is Lou Gehrig's disease in America, which is basically one of the most horrible diseases you can get. All right. And she found that atorvastatin and simvastatin increase the risk of ALS by 50-fold. 50 times increase in ALS. All right. That's published. I've got it. Can you just give the brand names for atorvastatin and the other statin that so that people understand? Lipitor is atorvastatin. Simvastatin. I can't remember what it's called here. We just call it simvastatin. It used to be something else. And there's a lot of statins. Rosuvastatin, pravastatin, simvastatin. It used to be cerivastatin. They're all basically the same. Right? Um, some of them are what they call lipid-soluble, which means that they can get into the brain more easily, and they seem to be the ones that are more likely to cause neurological problems. Surprise, surprise. And your brain is 25% made of cholesterol. So, imagine blocking cholesterol production in your brain. What do you think that's going to do, gentlemen? Uh, well, it's going to be absolutely fine. Don't worry about it. Right? You know, Duane Graveline, who I knew at one point, who's

Now, died. He was an astronaut, trained as an astronaut. Um, he took statins and had an episode of what they call transient global amnesia, which is basically you just forget everything completely and you can't remember anything virtually. He thought he had had a stroke. Turned out it was a statin that caused it, right? Cuz he did this challenge-rechallenge. He restarted the statin. Same thing happened to him. And he was an aeronautical physician, so he's dealing with pilots. He was rather concerned that if a pilot was taking a statin and they suddenly had an episode of transient global amnesia and forgot how to fly a plane, that wouldn't be a good thing.

All right, you may remember that recent crash in India, um, where the guy switched off the fuel systems. Okay, inexplicable. Well, it would be explicable if you'd forgotten how to fly a plane and you just suddenly started moving the switches around. Is that something to worry about? At one point, I said, I'm going to ask the pilot of every plane I get onto, are you taking a statin? In which case, I'm not flying on this airplane because I don't want you to suddenly forget how to fly an airplane while I'm on it. Thank you very much. Can you imagine if somebody asked that question? I just, I just want to check if you're, if the pilots are on a statin. I don't want to fly because they're going to get some bad side effects.

Um, last question. So, and by the way, I think people do know co-enzyme Q10, and there is a pathway called the mevalonate pathway by which the statins work on. I wonder if we can show that on the screen. Um, so that people can understand that it is actually a pathway to block co-enzyme Q10, which then blocks cholesterol. Well, I, I like to think of it a bit like a trunk to a tree, and there are branches that come out. If you block the trunk here, you block all the branches as well, one of which has cholesterol, and others are created at the same time. So, you're not just blocking cholesterol production. No.

So, if somebody from this conversation is taking a statin and they're like, "But Dr. Kendrick, I'm so scared about getting a heart attack, but I'm on a really good diet. What can they say to their doctor to make them understand and give them the power to take control of their health and get off that statin?" Well, you can do what some people do and just don't tell the doctor, "But stop taking it." And then a big pile of statins at home, which I saw a lot of, by the way. Um, I think you just say, well, it's very difficult because people don't like to argue with doctors because somehow or other they think doctors know more than they do, which they do about a lot of things, but not they've got very kind of broad but thin knowledge about things. One of the things is people are getting no, or they're not aware they're getting any adverse effects. All right, so they're getting no pain, they're living their life, best life they can live, and running marathons or whatever they're doing. Um, you know, you can say to them, is it worth the battle? Well, that depends on yourself. I say to people, if you think you're getting an adverse effect, like your memory's got a bit wonky, or you're feeling weak, or whatever it is. They say, "I think it might be caused by the statin. I'd like to do a challenge-rechallenge, which is basically stop taking it for about two to three months." All right, see how you feel. If the symptoms go away, all right, then you take it again and symptoms come back, you've proved that's it. All right, that's one way of doing it. It's a challenge called challenge-rechallenge.

Could just, and then the doctor can say, "Oh, well, you should." And, and I've seen this, the doctor say, "Oh, you should still take it anyway because otherwise you're going to die of a heart attack," which is a very worrying and stupid thing to say to somebody. Um, and I don't know how you've got to be quite, got to have a bit of, um, testicular fortitude, as they say, is to do that, which is to basically tell your doctor, "We get stuffed. I'm not doing what you say." You then have a problem with the insurance companies because if you are found to have a risk of heart disease and you're not taking a statin, your insurance will go up, and they might, especially if you're going on a holiday, you might run into problems. That's there as well. All right. I think you just have to go, right, I know I'm going to be told I'm an idiot, and I know I'm going to be told I'm going to die tomorrow from a heart attack. I know all the moral manipulation and whatever is going to happen, but I'm, I'm going to do it anyway. All right? And, and can you do it? Can you not do it? It's like saying to people, LDL doesn't cause heart disease. I can. And yet you get swamped with all the stuff on the other side going, it does cause it. There's no evidence for any of this. They just say it. All right. So you just have to be confident. And I think I say, the world changes one conversation at a time. Hopefully, a conversation like this, the other stuff I've done, the other stuff I've written. I'm not alone in saying this, not by any manner or means. Eventually, the, the world will change, but you know, as, as also said, the world changes very slowly, then all of a sudden. This is going to go at some point. It will be gone in some number of years. Hopefully tomorrow, hopefully 11:43 UK time. But, um, when it changes, it will be like that. All right. And then all the people who are saying one thing will suddenly say, well, as we've said all along, it's blood clotting that causes heart disease. You know, I'm aware of that. All right. You've just got to keep pushing away because their arguments are based on nothing. All right? Their arguments are based on an idea that was first floated 170 years ago and was wrong then. It's been wrong ever since. Continues to be wrong. Um, so it's just wrong.

Carbohydrates aren't deadly substances that will kill you, but, and for everybody, this varies. You will reach a point where they will be damaging and they will kill you, right? Fat, saturated animal fat, has never been damaging, has is healthy, perfectly healthy for you, and good for you in all sorts of ways. This is just, these are just facts. All right? They are inescapable facts. I mean, people say inescapable. People can escape from facts all the time. That's a, it's a thing that people do. But science is there. The truth is there. It doesn't go away. It's there to be found. You found it. I found it many years ago. Other people I speak to know it. The people that promote the other ideas, they don't even know the facts. They don't know the evidence. They don't know what they're talking about. But the facts will not change. The science is clear. And therefore, at least, you know, you're basing on something solid. All right? They're just basing it on dogma and repeated nonsense. So, be bold. Accept this. This is the way the world is. You are going to be healthy doing this. You are saying the right things. I would say a very easy solution is go find a doctor like Dr. Kendrick that understands this stuff. Then you've got a doctor that's on your side. And we do offer a group of people like carnival and keto people. And we have 800 doctors from all around the world that people can find a doctor. I wonder if you're on that list. Probably not. But, um, they could probably find people that can help them because I don't think that you can convert a traditionally trained doctor. It's just too hard. So if you can't find a doctor like you, Dr. Kendrick, that's the way that people can probably get help.

Dr. Kendrick, if people want to see you more, where can they find you? Well, I've got a few books that I've written. Obviously, the, the last one is, it's called The Clot Thickens, which basically it gives you an alternative thinking. It tells you why the cholesterol hypothesis is wrong. I've done that before. But it also says, well, here is actually the evidence behind the thrombogenic hypothesis first proposed in 1852 in Vienna by Calvon Rocketansky. So, it ain't new and it ain't mine. All right? It just happens to actually explain what causes heart disease properly and ties most of the strands together. Doesn't give you every possible answer and maybe not the answer for you particularly, but for most people. And I think it supports the paleo carnival, whatever you want to call it, diet and tells you why that's healthy and tells you why eating too many carbohydrates can be very unhealthy for you if you are not careful. So, and I do a blog, Dr. Malcolm Kendrick. Haven't written on it too much recently because I've been worrying about what I should be doing with it. And I think I'm going to go back and just do a whole, a bit like this. We explain it for people. This is it. All right. Again, again, again, repetition might get into people's heads. Who knows? Repetition is good. It really works because sometimes if you have to unlearn what you've learned for decades, repetition helps. I'm going to leave the links for all your books in the show notes that people can click. So, if you see more clicks happening on your books, it's probably my audience because I really want to know what you're teaching. But Dr. Kendrick, thank you so much for your time. You've been amazing. Thank you. Thank you very much. Cheers. Bye-bye.

Thank you for joining me today on this episode with Dr. Malcolm Kendrick. Now, if you're learning from and enjoying these free episodes, please hit the subscribe button. That's an excellent zero-cost way to support what we do here. You can also find me on other social media accounts. I'm on Instagram and on X under the name of the Primal Podcast. Now, if you love this episode, check out this episode with Dr. Philip Ovedia. He is a cardiac heart surgeon, and he'll talk about what eating eggs and high fat will do for your heart and your cholesterol. Finally, thank you for your interest in root cause healing, and I'll see you next.