Episode Transcript
[00:00:00] Speaker A: Hey, guys. Dr. Ben Edwards here. Welcome to another episode of youf're the Cure. Gonna be a great show today. It's one of my favorites, actually, and I recorded it a couple of years ago. It's Dr. Malcolm Kendrick, who wrote the book the Clot Thickens.
A little play on words there, but it's all about heart disease and stroke and really the root cause of heart attacks. There's still a great misunderstanding. People think high cholesterol causes heart attacks, and that's not the case. And we're going to talk about that today. But the reason I wanted to replay this was because it pairs really nicely with an interview I did a few weeks ago with Dr. Hans Vinck and Bob Long. They talk about the glycocalyx. You need to know that word.
It's the inner lining, the smooth, slick inner lining of the blood vessels. And when it is damaged, that protective layer is missing and you're more likely to form blood clots.
The spike protein tears that glycocalyx up, as does smoking, sitting sugar, seed oils, lack of sunshine, stress, all the things we preach around here.
And now we have a way to actually measure that. There's a little camera you put under the tongue, and it takes videos of these capillaries and it's able to measure your glycocalyx. It's called the Glyco Check. And we have acquired one of these cameras at Veritas. So you're welcome to come do that. You can email any infoeritasmedical.com and scan your glyco calyx and see how healthy it is.
And you can measure that again and again over time as you implement diet, lifestyle changes and or supplementation. There's this great supplement called Revasca. We talked about it in that podcast.
[00:01:42] Speaker B: A couple weeks ago, so you can.
[00:01:43] Speaker A: Learn more about that there. But I just wanted to replay this because it's still a constant theme of new patients that come in and think high cholesterol is a problem. It's not a problem.
Inflamed cholesterol is a problem. In fact, there's a study, British Medical journal, open in 2015, where they reviewed the cholesterol data and the conclusion was clear. It was actually the exact opposite of what people were thinking.
And this study showed that people over age 60 that have the highest cholesterol, lived the longest, had the best mortality outcomes.
[00:02:16] Speaker B: Fascinating study.
[00:02:18] Speaker A: Journal of American College of Cardiology.
[00:02:20] Speaker B: Dr.
[00:02:21] Speaker A: This was, I believe, August of 2020, they did a review study on saturated fat and it concluded, saturated fat does not cause heart attacks. There was a study out of the, out of jama, this was March of 22 I believe. And it concluded statins, the drug to lower cholesterol, they don't do anything for mortality. A reduction of 0.8% only. Anyways, not going to go down those studies. Dr. Kendrick will talk about a few of those as well. I've done a whole course on this, the heart disease course. It's on the website if you're a member. You can go to the educator meditation course tab and go find that course. It's an hour long course and I go through probably a dozen or two dozen studies on this very thing so that people can understand that cholesterol is super important. We need it every cell. Your body needs it, your hormones come from it, your brain needs it, your immune system needs it. So cholesterol is a vital nutrient we need or vital part of our physiology that we need. And if you don't eat enough, your liver kicks in and starts to make more.
So enjoy the show today, guys. Sorry, it's replay. I've been busy, been out of town, traveling, going to some conferences. We've got some great shows coming up here. Here in the near future.
We've got Nerissa Jones. He was on 13 medications, super sick. And Jesus healed her, set her free. And once she figured out her identity, I met a lady, Misha Tate. Didn't even know who she was. If you're an MMA fan, mixed martial arts, you'll know who she was. She's world champ.
I was on a stage with her, shared on a panel and, and got to meet her, became friends with her. We're going to have her interview coming up here in a few weeks. But it's about her identity. When Jesus showed up and saved her. In regards to her identity, you know, Texas just passed, voted to pass the constitutional amendment, $3 billion. Texans are just voted to spend over the next 10 years for dementia, dementia research, $3 billion. We're going to talk with the one doctor that I can find in the published literature who's actually showed clinical outcomes positive with his dementia protocols, meaning people's dementia gets better and even resolves early stage dementia. The only doctor I know producing these results. So we'll see if he gets some of that $3 billion. That's Dr. Del Bredesen in his book the End of Alzheimer's. So some great shows slated for the future, but today's show, a goodie. An oldie but Goodie. So enjoy. Dr. Malcol Kendrick.
[00:04:49] Speaker B: So heart disease is the number one killer in America. Every year, 600,000 plus will die from heart disease.
And that's a new phenomenon.
Dr. Chris Kenobi, his research showed us that In Boston in 1811, there were no heart disease deaths recorded.
In the entire 1800s, there were eight worldwide reports of heart attack in the entire world in the entire century, the 19th century.
In 1897, Sir William Osler reported six cases of angina, no myocardial infarctions. That's 1897. By 1900, 12.5% of deaths were due to heart disease, quote, unquote. But it was valvular, not coronary.
John Herrick published his first known case of myocardial infarction in the United States in 1912. The first identifiable case of myocardial infarction. 1912, John Herrick published that.
And today we're at 600, 000 plus.
So is it possible something's gone on over the past hundred years that's driving this? That's not saturated fat and cholesterol related. Dr. Malcolm Kendrick wrote a book called the Clot Thickens where he.
In the subtitle, the Enduring Mystery of Heart Disease.
So we need to just start at square one. And I think this is where we'll ask Dr. Kinder to come in and kind of explain why he would even consider looking at some other theory of heart disease. Why, why would he propose a different mechanism of heart attack than what the standard cardiologist around the Western world proposes as the cause?
So, Dr. Malcolm Kendrick, welcome to the show. Thank you for joining us today.
[00:06:45] Speaker C: Very pleased to be invited. Thanks very much. Yes. Hopefully people will be interested in a subject that people talk a lot about.
So. Yeah, you're asking about. I'm just going to. I'll tell you a fact. One of your facts isn't true. Herrick actually was the first physician to describe a non fatal heart attack.
Prior to that, everybody thought that if you had a heart attack, you died.
But by using early stage electrocardiograms, he managed to prove that some people had heart attacks that didn't kill them.
So sorry to. Sorry to.
[00:07:22] Speaker B: That's good, good asterisk there. Thank you.
[00:07:26] Speaker C: But yeah, no asking about this. A lot of people ask me, how did you, how did you get interested in this area of heart disease? And I said, well, I am a doctor and in Scotland, when I was at medical school, Scotland had the highest rate of heart disease, coronary heart disease or coronary artery disease or whichever of the myriad names that people use to call the same thing.
Was the Number one killer. And we were number one. We led the world in dying from heart disease. So obviously it was interesting to know why it was. And at this time we were taught. We sat in our little rows writing things down. Saturated fat raises cholesterol, Cholesterol gets deposited in your arteries, they gradually thicken up and you die of a final narrowing of a clot over that narrowed point.
No one had any reason to say this is wrong at medical school. You just write lots of things down, memorize them, and then try and regurgitate them in an exam situation. So it's like I'm not going to be questioning anything I'm taught.
So. But one thing that did interest me was, was I'd been to France many times and, and it was pretty obvious to me that in France people ate an awful lot of saturated fat. They had a lot of pate, they had a lot of meat, a lot of cheese, they drank lots of milk based products. And when I looked at it, it turned out that the French consumed slightly more saturated fat than the French. The French consumed slightly more saturated fat than the Scots. And yet the rate of heart disease was 1 5th age matched.
In fact, Scots women had twice the rate of heart disease as French men and women classically have about a quarter of the rate in the younger age groups. So I thought, well, this doesn't seem to fit.
And this kind of started me on a journey. So I very rapidly looked at the data from around the world and came to realize that saturated fat has no relationship to death rates in various countries.
And of course, once you start to question that if the reason why you have a high cholesterol level is because you eat saturated fat and people who ate more saturated fat had lower rates of heart disease, then the whole hypothesis, the diet heart hypothesis or the diet heart cholesterol hypothesis, or again, trying to pin anything down is impossible, starts to fall to pieces and just something nagged and nagged away at me and I began to become kind of obsessed into looking at it. And so that's really where it started.
[00:10:03] Speaker B: Okay, yeah, you mentioned in your book on page 12, there's really these. The government guidelines came out in 1977, but there was no evidence to support the guidelines. And that's a key point listeners need to understand. Just because a institutional body sets guidelines, we assume there's real good evidence behind that. Doctors assume that even.
But you lay out pretty clearly those early guidelines really weren't based on any good hard evidence. So could you talk a little bit about that as far as you know, and maybe it's just opinion where these guidelines even come from. Why did they come if there was no evidence for them?
[00:10:46] Speaker C: Well, I think it's a bit like many government reports. The decision is already agreed before they do the research or create the guidelines. You know, and I think a bit like a Russian show trial, your guilt will be proven because we know you're guilty if we have to step back. The idea that saturated fat causes heart disease or raising cholesterol had kind of been gathering momentum since the 1930s perhaps.
Then one man in the United States, Ansel Keys, became the absolute cheerleader for this because the rate of heart disease in the US exploded really after the Second World War, or appeared to.
And people were running around thinking, well, what's causing this? Where has this come from? And so the man who managed to grab the attention, Ansel Keys, he did a study showing that the more saturated fat you ate in various countries, the more, the higher the rate of heart disease. And, and very much if you go back, he cherry picked his countries. He ignored. He studied 27 countries and ignored all but six or seven. And the ones that didn't fit his hypothesis, he just sort of basically didn't pay any attention to. So France, for example, wasn't even part of his original seven countries and study.
But given, given the idea, I think the idea itself became quite attractive. Is this idea of, of yes, this fatty stuff builds up in your arteries and therefore it must be to do with something that you, you've taken in or eaten. And it was a very simplistic story and people just grabbed hold of it.
And essentially, yes, despite the fact that in 1977, the McGovern hearings and govern wasn't it he decided they're going to set dietary goals for heart disease. And there was only really one suspect at this time and that was saturated fat. Now no one asked the question, well, how does saturated fat raise cholesterol levels? Which is a completely different and complex area.
So they just had this one idea at the time. There were plenty of people on the committee who said, you know, the evidence just isn't there. Well, they're right. The evidence wasn't there. There was, there was no randomized controlled study at that time had been done anywhere in the world or published to demonstrate that if you increase saturated fat intake, you increase the rate of cardiovascular disease. There was none. Not one. I know people find this quite amazing and they say, well, how could this have happened? All these guidelines and we're bombarded with this absolute as a fact that saturated Fat raises cholesterol levels and causes you to die from heart disease. And yet, in fact, a colleague of mine, someone I worked with closely, Zoe Harcombe, did her PhD thesis on this, looking for the evidence to support the guidelines, and could find none. There was none. None. And so it's a bit difficult for me to talk at length about the lack of any evidence. All I can keep saying is there isn't any. And when you ask people to demonstrate, say, where has it come? Okay, show me that study.
They can't. And then say, oh, yeah, but there's been plenty of studies after that that approved it, to which you have to say is, well, actually, Zoe harcombe, in her second part of a PhD, looked at that and found there have been no studies since then either. So there is a complete and utter lack of evidence. They're just. It doesn't exist.
And I can't really say anything other than that. I just could keep repeating it for the next half an hour, but it might not really add to anything to it.
[00:14:22] Speaker B: Well, and we will move on, but I encourage everybody to get the book because when you see this stuff written in black and white, I'm going to read a quote here from Dr. Salem Youssef. This is from your book.
And Salem was replying to someone at a conference.
We got brainwashed by a very questionable study called the Seven Countries Study many years ago, and it was ingrained in our DNA and generations of us were brought up with that.
Somebody said that you need to wait for the guidelines committees to die before you can change the guidelines committees again. So maybe that's where we're at. We've got to wait for some of these guys to die off before the truth can come. But. But. Or we can get the book. The Clot Thickens Again is the name of the book. Dr. Malcolm Kendrick, could you spend just a moment educating our audience? You do a great job in the book talking about ldl. I tell people, patients all the time, why would our liver make a constantly make LDL particles all day long? If that's what kills us, why are we making something that would kill us?
And you talk about cells need LDL and in fact they put out a receptor on their cell membrane for that ldl. Why would a cell put a receptor on its cell membrane to say, come kill me, but talk a little bit about, we don't spend a lot of time, but what is ldl? Where does it come from? Why? Why does the body need it again? You do a great job in the book of that, but a little brief summary there.
[00:15:56] Speaker C: Okay, well the reason why people talk about a cholesterol level, but we, we don't have a cholesterol level because cholesterol doesn't dissolve in blood.
So you have to carry it around in a little lipoprotein. There's plenty of different lipoproteins of different sizes.
LDL is low density lipoprotein. It's not actually made in the liver. The liver produces, synthesizes cholesterol and it synthesizes saturated fat from carbohydrate.
And if it's got, once it's got enough of these, it packs them into this thing called a very low density lipoprotein, which would be say the size of a, of a basketball versus an low density lipoprotein being the size of a tennis ball. Maybe not exactly at that scale. Anyway, the VLDLs have come out of the liver. Another word for vldl is triglyceride. You may have heard of triglycerides. For some reason we use the word triglyceride to define a very low density lipoprotein. And we call a low density lipoprotein cholesterol or a low density lipoprotein.
People will be confused by the nomenclature because it's incredibly confusing. Anyway, stick to this vldl. Very low density lipoproteins come out of the liver, they travel around the body losing fat as they do so, mainly fats, and they shrink down and down. They become an intermediate density lipoprotein, then they become a low density lipoprotein. About 95% low density lipoproteins are then taken back into the liver and recycled. Those that remain in the blood cells that need cholesterol. And cholesterol is essential for cellular function. Stick an LDL receptor out into the bloodstream, wave it around. Well, actually not quite like that, but anyway, they stick out an LDL receptor, the LDL locks onto the receptor and the whole ldl, LDL receptor complex is pulled into the cell. The whole thing is broken down and then the cholesterol is used for various purposes around the body. As you say, why would the body produce cholesterol and or LDLs if they were damaging? The answer is clearly that they would not. And in fact, if you eat a normal diet, your liver will be constantly producing, Synthesizing, manufacturing about 10 times as much cholesterol as you will ever take in from your diet. You'd have to eat about 25 eggs, egg yolks a day to bring in as much cholesterol into your body as the liver naturally synthesizes.
Another point I'd just like to add in here is that there is no connection between saturated fat, no direct connection between saturated fat that you eat and is absorbed and ldl. Because when you eat saturated fat it's absorbed into the bowels. It's packed into another type of lipoprotein called a chylomicron which would be the size of a beach ball or maybe even bigger. This is released directly into the bloodstream, it travels around the bloodstream losing its fats content until it shrinks down and shrinks down. So it becomes about the same size as an LDL molecule at which point it's taken into the liver, the liver breaks it down and the cholesterol that's in there is used to manufacture new VLDLs.
So there isn't actually a connection between saturated fat and LDL levels that they are unrelated. They go down completely different pathways which, which is another thing that I find to be interesting. But you won't read that anywhere in a textbook.
[00:19:36] Speaker B: Yeah, well I want to point out because you do another great job in this book. You summarize so many of the old studies and you mentioned the seven countries study, that was a cherry picked data and therefore corrupted study. But right after that the Minnesota heart study where they replaced this traditional saturated fats in the diet with these polyunsaturated fat vegetable oils. And what they found was a decrease in the ldl, no change in cardiovascular disease death rates and an increase in all cause death rates in the group that use a polyunsaturated fatty acid. But more importantly this study done by Ancel keys of the seven country study, they didn't publish it for 40 years. They did not publish that study.
Quick comment on that. The unpublished study and the corruption in evidence based medicine in general. We'll do a little tangent here on that.
[00:20:35] Speaker C: Well, I think that there were two studies. There's a Sydney heart study which was a smaller study which again the data on actually cardiovascular deaths was buried and was published about 40 years later by the same group of researchers who then discovered that the Minnesota coronary experiment which had been done by Ancel Keys also the data existed, he actually found the son of.
I can't remember who was the other lead investigator who said, he said oh I believe your father did a study on this. And he said yeah, and all the data is still in my garage in kind of floppy disks or whatever it was, or magnetic tape. So they got hold of the magnetic tapes, they read Them. And so the people that did the study never published it. It was other people who found the data and then published it. And what they found was that yes, if you, if you replace saturated fat, polyunsaturated fat, the, the LDL level, not the cholesterol level fell, which you may say goes against what I've just said. But actually there's a complication to the switches. If you have polyunsaturated fats, they also contain other things with polyunsaturated fats which are called stanols. And plant stanols are the plant form of cholesterol. And if you absorb a plant stanols into your system, this causes the body to readjust and not absorb cholesterol and the overall LDL level drops. So it's not as saturated fat reduction that causes the LDL to fall, it's an increase in plant stanols that causes the LDL level to fall. Anyway, that's a sort of an aside. This is a problem with the whole area gets more and more complicated. But anyway, the cholesterol level fall and the more that the LDL level fell, the higher the rate of mortality. Overall mortality. So for about a 30 milligram per deciliter fall in cholesterol LDL, the mortality rate went up by 20%.
So in other words, the polyunsaturated fats significantly increased mortality in the people that took them, which is the exact opposite of what they wanted to find. So then you say, well, I wonder why they never published this study. Well, have a wild. Yes. Ancel Keys, who staked his entire reputation on the fact that saturated fat causes, is bad for you and causes cardiovascular disease, suddenly finds that when he did this experiment on about 9,000 people, one of the very few randomized control studies, it actually went the exact opposite direction than he intended it to. So he basically buried it. There is no other explanation you can make for this. And of course if people bury all the data that they don't like that doesn't support their theory, then your evidence base is, is turned into meaningless mush. You can't, I can't tell you how many other studies were done that weren't published because clearly I don't know they exist. This one was only found by accident. How many more of them were out there? I don't know.
[00:23:44] Speaker B: Yeah, well, another study you, you talk about on page 30, the Norway study. It was a 10 year study. 50, 000 people.
And in a nutshell it showed the highest cholesterol folks live the longest. The exact opposite.
[00:24:02] Speaker C: In fact. The Researchers contacted me at one point, I never heard of their study, I say, called Hunt 2 and said, oh, you might be interested in our study. And they looked at, yes, many more time, a lot more people than were in. This was not a randomized controls trial. It was looking at people over a 10 year period looking at their LDL. This was LDL levels and looking at deaths from cardiovascular disease, not overall mortality in this case.
And what they found was that with men, the higher levels of LDL were associated with no increase in cardiovascular mortality. But in women, the women who had the highest LDL levels and that was over 300 had the lowest rate of cardiovascular disease. It was 40% lower than the women who had what we call a normal cholesterol, this LDL level.
So the studies keep using LDL and cholesterol and then they change back and forward. So I sometimes have to be careful, I'm not mixing it up myself. But anyway, this study just showed the exact opposite of what was supposed to be found, which namely raised cholesterol levels or LDL levels increase your risk of cardiovascular disease. And I can find you many, many studies, big, huge studies in Japan that show exactly the same thing.
I peer reviewed a paper recently from Taiwan where they looked at LDL levels in diabetes and found that the lower the LDL level was, the more likely people were to die prematurely. And it had no impact on cardiovascular disease. So these studies are all out that there's many, many, many, many, many, many studies out there.
[00:25:44] Speaker A: There.
[00:25:44] Speaker C: It's just that if you provide a study or produce a study showing that LDL has no association or a negative association with cardiovascular disease, you get, you just really struggle to get it, get it published.
So it's very difficult to analyze the evidence base here because it's utterly biased in one direction.
[00:26:05] Speaker B: Yeah.
And you talk about in the book, I mean there are other doctors who've done this, even groups, the thinks group, but have looked at, they've done reviews, papers, they've looked at all the data, they've gone back historically, they've summarized everything and consistently find what exactly what you're saying. And you talk about on page 37 that a quote here. Unfortunately, none of this has had any discernible impact, meaning all the evidence that points to the exact opposite of what mainstream cardiology is telling everybody.
The evidence is there, the papers, the review papers are there, but it's just not moving the needle.
Before we go to our break and on the other half of the break we're going to really talk about the point of the book the Clot Thickens about blood clots in the arteries and could that be what's causing heart attacks? And. But I just want to wrap this part up with.
Just giving you a moment to just share with.
Well, I think what the audience is thinking at this point. How could this be? If all this evidence is there, it's been published, the review studies are there, it's clear just what's your opinion on what's, what's, what's the deal?
Why are we still walking in the dark on this? I'm talking conventional medicine and, you know, the statins are being pushed so hard, it should be in the drinking water, etc. What's your thought there?
[00:27:28] Speaker C: Well, I think there's two things thing. One is that opinion leaders, what you call key opinion leaders, which you'd always call experts, or whatever term you have for them, all tend to share the views at the top. And the view is, amongst cardiologists, cholesterol saturated fat hypothesis is correct and their reputations rest upon that.
So the people at the top of the conventional research world who are on the committees and run the American Art association and such like, really are not keen on any other idea damaging their position and reputation.
The second thing is just the natural inertia. Just someone sent me a paper showing that new ideas in cardiovascular in medicine, on average, if they are taken up at all, take about 20 years to actually come into general sort of clinical practice. There's a huge inertia. And the final thing is, of course, in this case is just gigantic amounts of money.
Statins have been around for some time, they're off patent, they're not making huge amounts of money now, but during their lifetime they made approximately $1 trillion in profit.
There are new cholesterol agents coming along and they are enormously expensive and gigantically profitable. And then we have the food industry, which has been promoting the low fat, high carbohydrate approach to health and cardiovascular disease specifically. And that's another trillion dollar industry.
So there's a vast, vast commercial world that's built up around this hypothesis. And I would include in that the world of diabetes, because when people said you should stop eating saturated fat and instead, well, what else are you going to eat? You're going to eat more carbohydrates because most people don't eat more protein. So essentially the Dietary Guidelines changed the world to a higher carbohydrate eating, higher sugar eating and the rate of diabetes. If you look at a graph that runs from about 1960 to 2020, the year, virtually the year that the guidelines came out, the government guidelines came out, the rate of diabetes started on its upward inexorable trend.
And then of course if people become more diabetic, there are vast, vast amounts of money to be made in the medications used for lowering blood sugar and treating in a vertex diabetes. So that's another trillion dollar industry. So we have a huge, really, really huge commercial interest here at state to maintain the diet heart cholesterol hypothesis. So yes, there's an awful lot of different factors at play to stop this from being changed.
[00:30:21] Speaker B: Yeah, well a trillion dollars is a pretty good roadblock to truth, I would say. And for that trillion dollars I might add. This is Jama.
3-14-2022.
The name of this, the title of the study evaluating the association between low density lipoprotein cholesterol reduction and relative and absolute effects of statin therapy. A systemic review and meta analysis. Again, that's Jamaica, March 14, 2022. Basically, in a review like this they go back and look at a lot of data, a lot of studies and they summarize all these statin studies. It was 21 randomized clinical trials that they summarized.
Drum roll please. The overall effect of a statin to reduce total mortality and cardiovascular outcomes. Absolute risk reduction for a trillion dollars, 0.8% reduction of all cause mortality.
That's a hefty bill for a 0.8%.
And they want to put it in the drinking water. I mean I have patients who, their doctors scold them, yell at them, elevate their voice and even threaten to fire them from the practice for not being on a statin.
I mean it's absolutely. So my answer to those patients is well, go buy a copy of the Clot Thickens, wrap it up in a nice little bow, nice little sweet loving note on there on your cardiologist's birthday. You send it to them, you have them read this book by Dr. Malcolm Kendrick.
We're up against the break. Dr. Kendrick, what's the best way for people to follow you? Or do you want people to follow you? I know you wanted to read the book, I bet, because you want the truth to be out there. But what's the best way for people to look at your work?
[00:32:16] Speaker C: Well, obviously I've written three or four books and I do run a blog. I've been a bit, bit reticent on it recently for, for other reasons.
One of those reasons being an upcoming court case where I'm suing the, the, the Associated Press in the UK for publishing stories that I consider libelous. So we have a very large court case going on at the moment. Reliable.
And that's taking a bit of my time. But yes, I, I do a blog called Dr. Malcolm Kendrick. It's on WordPress and you can see my ramblings that have been going on for many years, a lot of which are to do with heart disease. But other topics emerge from time to time. So that's just. Dr. If you just put Dr. Malcolm Kendrick into Google, you'll find all sorts of things, some of which are not necessarily particularly, particularly complimentary. But there we are.
[00:33:09] Speaker B: Well, and I'm going to highly endorse your writing. And another part besides just the truth in your book is your writing style. And they're very good sprinkling of humor throughout. So it's a great read, easy read.
It's probably the best summary, I would say.
I haven't read all the books out there, but this is my go to when I'm trying to open someone's eyes to the truth on heart disease and cholesterol. When we come back from the break, we'll continue with Dr. Malcolm Kendrick and we'll talk about, okay, if it's not cholesterol, then what is it? What's the deal with all this heart disease? 600,000 people a year plus in the United States dying. So y' all stick with us. We will be right back. And as always, these shows are archived on our website, veritasmedical.com also on Apple iTunes.
We'll be right back. I'm Dr. Ben Edwards. You're the Cure.
Okay, everybody, we are back. Dr. Malcolm Kendrick is with us. The book the Clot Thief Thickens the Enduring Mystery of Heart Disease.
So I think we made a pretty good case in the first half of the show that it's not saturated fat and cholesterol that's causing heart disease. So, Dr. Kendrick, I'm just going to give you the remainder of the show. Take it any way you want, but talk, talk to us about what you discovered in your your journey to find out what's causing heart attacks.
[00:34:30] Speaker C: Well, thank you very much.
What I have to say is, and I say it to everybody in my attempts to be modest, which my, my family always say, you're not modest at all. What you're pretending for is that there has been an alternative idea about cardiovascular atherosclerotic cardiovascular disease, which has actually precedes, predates the cholesterol hypothesis.
So it's kind of like I can't remember who came up with the Phrase ghost in the machine, which is this idea that there are things in there. If you look back, you can find that although you think there is one idea, there will be lots of other ideas, but they all just kind of get trumped and they get silenced. And the Ghost in the machine is kind of the remnants, if you like, of thinking that's never quite managed to get out into the public domain. So the Ghost in the Machine was first proposed in 1852 by Carl von Rocket Tansky.
It's a fantastic name. But.
And he was working in Vienna and he looked at arteries in people who have died of other things, usually accidents or infections, very common causes of death. So he was examining plaques. So people who say there was no heart disease in the 19th century, I have to say, well, they were seeing a lot of plaques in the 19th century.
But moving on, what he said when he, when he examined them, he said, what I'm seeing here, when I look at plaques, thickenings in the arteries, I'm seeing blood clots. I'm seeing the remnants of blood clots in various stages of what he called metamorphosis or change, because he saw what they call fibrin, which is a. Which is a protein that wraps around all blood clots and makes them very, very different shift. He saw blood red blood cells, he saw platelets, which are small cells that start the blood clot in the first place.
And he basically saw everything that you see in a blood clot. Although in some cases, if they were. If they were clearly old and been there for a long time, they had changed such a lot that many of them had become calcified, which is kind of the end stage process of many areas of damage in the body. They become calcified and look white and sometimes actually have almost like bony tissue within them.
Other people disagreed.
And really the discussion was not fraught at that point because not many people were or did not appear to be dying of heart disease. It was only in really the 1930s, 1940s, when heart disease started to become a major recognized killer again, that people took interest. And there were researchers in the 1940s dug it.
A bunch of researchers from, I think it was Harvard who again started looking at plaques and really said, we seem to be looking at blood clots here or the remnants of blood clots, or we're seeing what seems to be clotting.
But this idea never took off. And one of the reasons why, and I think it never took off, and I've been trying to explain this again to people, is obviously Blood clots form within the blood itself.
And when you look at a plaque, an arterial plaque, is thickening in the artery. It's beneath the lining of cells called the endothelium, a single lining bit like wall tiles, though not exactly like wall tiles. And essentially what they were finding was blood clot underneath the wall tiles.
So at the very early stages, Burkha, who worked alongside Rokatanski, said, well, they can't be blood clots because they're underneath. Well, they're in the artery wall, and they're underneath a lining of cell.
So what Rokatansky didn't know, what Verkhow didn't know, in fact, what nobody knew until the mid-1990s, is that we have circulating around in our bloodstream a thing called endothelial progenitor cells. They're made in the bone marrow. They circulate around in your blood. And if there's an area of damage to the lining of your arteries, the endothelium, they're attracted to that area. They stick to it. They grow together and form a new layer of endothelium. And in this way, any. Any blood clot that forms on an archery wall, that will get shaved down and down, but the. Finally, it will be covered over entirely and will be drawn into the artery itself. So I sometimes think, well, if Rokitansky had known this, he would have been able to say, well, obviously, this is what's happening. The blood clot forms. The blood clot cannot be allowed to just break off and travel down the artery because it will just jam up somewhere further down, causing a thing like a stroke or a heart attack. And that does actually happen in some cases, still happens. So the body has to have a protection mechanism. It can't just, you know, say if you scratch your skin badly, then you get a. It will bleed, and then it'll stop bleeding, and then you'll get a scab, which is basically a blood clot. Then the skin will grow underneath the scab, and the scab will fall off.
That process cannot occur in the artery for the reasons I've just outlined, because if the scab just fell off, the scab would travel down the artery, into your heart, up into your brain, and you'd have a stroke. So there has to be a mechanism to stop that happening, and that mechanism is endothelial progenitor cells. They cover over any blood clot that forms on any blood vessel wall. It is then effectively drawn into the blood vessel. In most cases, that will be broken down by the various repair systems and it will disappear completely and you'll never know it happens.
However, if that point is not fully repaired and that happens sometimes, that then becomes a vulnerable area where a blood clot is more likely to form again.
So another blood clot is likely to form on that area, and then you can get blood clot after blood clot after blood clot after blood clot, and eventually this causes the artery to narrow and narrow at that point, and then you'll get a final blood clot over that vulnerable point which will fully block the artery and cause, say, a heart attack or a stroke or whatever.
All the strokes have a slightly different etiology. So that's the basic mechanism that's going on. That's going on inside your body, inside your arteries is happening. And. And, you know, people are saying, well, well, you know, well, how can that happen?
I say, if you look at it, every single part of that process has been identified. We know that certain things damage the lining of your artery, such things as smoking. So if you smoke, nanoparticles, called nanoparticles, are released to get through your lungs and into your bloodstream. Once they're in your bloodstream, they travel around and they damage and destroy endothelial cells.
And we know that this is the case because if you get a healthy volunteer to smoke one cigarette, then you can measure a thing. There's another thing called micro particles, which are released by endothelial cells when they die. So you get someone to smoke, smoke one cigarette, then all of a sudden the blood is not full of, but has a number of microparticles floating around, which says endothelial cells have died. At the same time, the bone marrow increases its production of endothelial progenitor cells, so the areas of damage are covered over and repaired.
And so that's the mechanism we can see happening in smoking. You can't explain why smoking causes heart disease using the cholesterol hypothesis. Hypothesis, because there is no relationship between smoking and cholesterol in any way, shape, or form.
So then you look further and say, well, what other things like smoking cause heart disease? Well, we now know that diesel particulate air pollution causes exactly the same problem, because small particles from diesel engines, nanoparticles, get through your lungs, they go into your arteries, they travel around your bloodstream, killing endothelial cells, and then you get lots of little blood clots forming. They are usually fully repaired, and nothing happens. But of course, if you smoke and you expose yourself to diesel fumes and then say you've got a raised blood sugar level with Diabetes, you say, well, how does a raised blood sugar level cause a problem? Well, just to make the explanation slightly more complicated, all endothelial cells have a little forest on top of them.
I sometimes say, if you try and pick up a fish, it slips through your fingers. It's very slippery because it's covered in a thing called glycocalyx. Glycocalyx is just a fancy word for protein, glucose strands. It's like a little forest. And within that forest sit anticoagulant agents that stop the blood from sticking and clotting at that point. So they say the glycocalyx was an inch thick, which it's not. It's so small you can't really see it.
But if the glycocalyx is thinned, then the endothelial cell beneath becomes vulnerable to attack by various substances in the bloodstream that it would normally not be vulnerable to.
So you can actually see if you raise somebody's blood sugar level very high artificially. And then you look at the glycocalyx, it is thinned, it often almost completely disappears in some cells.
So blood sugars being high causes the same problem as smoking and diesel fumes. So you can start to see that essentially we can already see that anything that damages the lining of your arteries will and can trigger blood clots to form. And if those blood clots are particularly big and difficult to shift or grow larger than they normally do, then you've got another problem.
And if the repair systems that would normally get rid of all these, get rid of all these things have been, have been, have been damaged in some way, you'll have another problem.
And although this seems like a complete switch round, I find it interesting. I was looking at what things can damage the repair systems, and one of the things that can really damage the repair systems is a thing called Avastin, which is actually an anti cancer drug.
And I know you're going to say, well, where does this come from?
Avastin is used to stop new blood vessels being created by cancer, by cancer tumors. But one of the ways that tumors grow is that they release a thing called endothelial vascular endothelial growth factor, which is an end hormone. This triggers the body to produce more little tiny blood vessels and therefore the tumor can then feed itself with blood and oxygen and grow and grow and grow.
What Avastin does is it knocks vegf, vascular endothelial growth factor on the head, it knocks it through the floor so that new small blood vessels cannot be created, which stops the tumor from growing and can be treated, you know, can actually cure.
Now you've got to say to yourself, well, that's fine. But vascular endothelial growth factor also means that it protects the endothelial cells, it nurtures the glycocalyx, and it also increases a substance called nitric oxide, which is the most potent anticoagulant agent known in the body.
So, not surprisingly, if you give people Avastin, vascular endothelial growth factor inhibitor, the endothelial cells around the body start to suffer.
And when they looked at the increased risk of cardiovascular disease with Avastin, they found that it was increase the risk of dying of cardiovascular event by approximately 250% over two years.
So again, if you turn this process around on itself and say, well, let's look at it from all different directions, what things can damage the endothelium? What things can cause blood clots to grow bigger and be more difficult to get rid of, what things can damage the repair systems?
And I think you can come across and if you ask yourself the question, that question of does it do one of these three things?
And if the answer is yes, then it almost certainly increases the risk of cardiovascular disease. And so, if you like, this is a kind of potted or very rapid way of looking at it, but it does explain why some things that are apparently completely and utterly, on the face of it, different.
So I have occasionally used an analogy which is if you want to get rust in a car, which is always a problem, you have to have something happen. The first thing that has to happen is you have to damage the bodywork of the car.
So that can be caused by a hundred different things. A stone ship would fly out, they could scratch it with your keys, you could drive past them, you could drive past a bush and it scratches it. There's a million things can damage the bodywork in your car.
And so you can say, well, what connects? You know, a pebble and a key and a roof rack falling on it or a shopping trolley hitting it? Well, the only thing that connects it is the action that they have, the effect that they have on the paintwork of your car.
So anything that damages the paintwork in your car can increase the risk of rust, and anything that can damage your endothelium can increase the risk of cardiovascular disease.
So when we look at something, I'll just throw one more in here and maybe you have a question or two at this point. Another thing that's recently been discovered is that, is that periodontitis? In other words, infection in your gums, infection in your teeth can greatly increase the risk of dying of cardiovascular disease. And again, how does this fit with the cholesterol hypothesis? Answer it doesn't. How does it fit with what we call the thrombogenic or blood clot genesis ideas of cardiovascular disease? Well, if you have bacteria floating in your bloodstream, they release exotoxins. A toxin? An exotoxin, just an external toxin. The exotoxins hit the endothelial cells and damage them and cause them to die. And then blood clots form over these areas.
And in fact, one of the interesting things was when SARS COV2, or COVID19, as we call it, arrived. And people were saying it looks like a lot of people are dying from blood clot related deaths like heart attacks and strokes and blood clots in general. How can this be? How can a virus cause heart attack?
Well, the answer is that the SARS CoV2 virus gains entry to cells, endothelial cells, mainly in the body.
Once it's gained entry to the cell, it then reproduces itself and then the cell bursts open and dies, at which point you have again damaged endothelium all around the body. And then blood clots form at these points.
Or the body itself decides it's going to attack endothelial cells because the immune system recognizes when cells are infected and then attacks and kills them to avoid the virus from spreading further.
So when you look at something like you say, well, COVID 19 increases the risk of heart disease and smoking does, and diabetes does, and Avastin does, and what you have to say to yourself is, well, what actually connects all of these things?
Is there a mechanism of action that makes sense, that connects them? And the mechanism of action, it does one of three things.
It damages the endothelium.
And this is why you only ever get plaques in arteries, because they are under the greatest biochemical stress. You never get plaques and veins or pulmonary lung blood vessels.
So the blood pressure has to be sufficiently high, the blood flow has to be significantly turbulent before the endothelium is under enough stress to be damaged or the blood clot that is formed is bigger and more difficult to shift. And you can see that in people who have things like that. I won't even go into high LP levels or the repair systems are damaged in some way. And if you have something that does all three, then you're in real trouble. And if you have 10 things doing all three, then you are in real, real trouble. So it's a really quite a simple hypothesis. It's been thought of by many people in different parts of it being thought of over the years.
But many people didn't have the necessary information. They didn't know there was endothelial progenitor cells. They didn't know there was a thing like nitric oxide. They had no idea that it was a glycocalyx, et cetera, et cetera. So. So without those pieces of information, how you could have any hypothesis about heart disease is fascinating, because you didn't know 90% of what you needed to know.
And yet people were very confident that LDL caused cardiovascular disease. One thing LDL does not do is it does not damage the glycocalyx and it does not damage the endothelium, which is why, you know, the idea that it causes an increased risk of heart disease is pure nonsense. Anyway, sorry, I feel I've talked probably far too long with that without somebody coming up with a question.
[00:51:35] Speaker B: No, that was beautiful. A great explanation makes much more sense than the liver spitting out ldl. That kills us a couple. We've got about six, seven minutes left, so I do have a couple questions. One, is there something that we can look at in blood work? I mean, everyone's so concerned about, I need to go to my doctor and check my blood work. And really, they're talking about their cholesterol levels.
So if we're not checking cholesterol, is there something in the blood work that a patient could go check that would be predictive in any way, or something in the cholesterol panel be predictive?
[00:52:14] Speaker C: Well, I think there's a couple of things that I. I am interested in is blood clotting factors. One of the studies that initially triggered my interest was the Scottish Heart Health Study, where they found that a high level of fibrinogen, and fibrinogen is like a little short strand of protein. When a blood clot forms, the ends are stuck together to form fibrin. Fibrin is the thing that wraps around blood clots and makes them really, really difficult to shift and tough.
But they found that a high level of fibrinogen in men particularly, was the most important risk factor for. For cardiovascular disease that they could find.
That's very rarely measured.
But obviously, the more fibrinogen you have, the more fibrin is going to be created and the more bigger and difficult plots are to shift.
Another thing, another disease that most people have never heard of, and yet it's relatively common, is called antiphospholipid syndrome, sometimes called Hughes disease. I don't know what they call it in the U.S. but one of these two things, the problem with Hughes disease or antiphospholipid syndrome, is that the body decides that the membranes of endothelial cells is a bit alien and they start to attack it. And in fact, although, in fact it's maybe 1 in 100 people, maybe less than that, I'm not sure. It's difficult to know.
It causes 50% of known strokes under the age of 50, and so it's therefore very damaging. And it causes something like 25% of cardiovascular disease, cardiac coronary artery disease in those under 50.
And people aren't screening for it. They're not looking for it.
And another thing I look for is the level of lpa, which I talk about at some length.
LPA is called, is lipoprotein A. It's another form of lipoprotein. Actually, it isn't. It's ldl, but it has a specific protein attached to it called apolipoprotein A.
And some people have a high level of this, and some people have a low level of this. It seems to be almost entirely genetically determined.
But if you have a high level of it, the, the actual, the protein Apologin A actually acts as a blocking, a blocking agent to another substance called plasmin, which slices apart fiber and breaks down clots.
And if you have lots of LP in a clot, then the fibrin slices doesn't work, and the clot becomes bigger and more difficult to shift. Now, it's not a, it's not a cause of endothelial damage, and it's not really a cause of a breakdown in the repair systems. But what it does do is it causes you to have really quite difficult to shift blood clots.
And, and even the mainstream is beginning to recognize that this is an potentially important factor. So those are all, if you like, clotting factors.
And, and they, they, they are things that I would tend to look for.
Sorry.
[00:55:18] Speaker B: Yeah, very good. A couple minutes left. I want you to get to commenting on a beautiful studies you put here in the back. Back in the page. 207. Sunbathing adds 10 years to longevity, and statins add three days to longevity for every five years that they're taken. Found that to be fascinating. Another study on page 262 you quoted sunlight.
Different studies, 3 to 8 to 10 years added to life expectancy. So just comment a little bit about things. I'm assuming that some sunlight somehow is improving the glycocalyx maybe, or adding some protection and if, if it's not doing that, could you comment on what do you know does keep the glycocalyx healthy and prevents that blood clot from even starting so we don't have to worry about our lpa.
[00:56:11] Speaker C: Well, within the glycocalyx is actually the substance that nitric oxide synthesize, which synthase, which is the enzyme that makes nitric oxide in your, in your body.
Sunbathing actually causes the body to release nitrates which get into the bloodstream and increase the nitric oxide level. Sunbathing reduces blood pressure by doing this because it causes the blood vessels to open up. It also protects the glycocalyx because nitric oxide is the, is quite a strong glycocalyx protective agent. It also protects the endothelium.
So anything, not anything, you don't want to overdo that nitric oxide to a ridiculous degree, but anything that increases nitric oxide is good for you. And, and things. Some people said certain foodstuffs like beetroots and with nitrates in the, stimulate nitric oxide production. But, but sunlight is probably the most single effective way of doing that. There's also sunlight increases vitamin D, which is also protective to your, to your, to your vascular system.
So you sort of protect your, your glycocalyx by a, not, not, not eating too many carbohydrates and getting your blood sugar too high. And if you sunbathe and you get, and you get some nitrates in, in other ways, these are the better ways to protect your endothelium. And there's some evidence that some of the things people use to protect their, their joints are using chondroitin sulfate and higher high aleuronic acid, which is then, which is then synthesized in the liver into albumin, which is a protein, little protein bomb.
There's a huge amount of them. They float around in your bloodstream, they get stuck into your glycocalyx and they provide the protein backbone for glycocalyx protection.
So and in fact they've shown that people who have a low albumin levels are much more likely to die from heart disease. So making sure that you have the right sort of proteins on board can also protect your glycocalyx to a degree.
[00:58:14] Speaker B: Okay, just got to do one more study real quick. We're wrapping up here, but this is Journal of the American College of Cardiology Volume 76, Issue 7, August of 2020 and the name of the article, Saturated Fats and Health A Reassessment and Proposal for Food Based Recommendations A state of the art review. So another review study, they went back and reviewed all this data on saturated fat and here's the conclusion. Quote, several foods relatively high in saturated fatty acids, such as whole fat, dairy, dark chocolate, unprocessed meat are not associated with increased cardiovascular disease. End quote.
All right, so go eat your heavy whipping cream sourced from a good cow. Go eat some dark chocolate and some, some good quality meat sourced from, from a good cow. Again, eating the right stuff.
Dr. Malcolm Kendrick, thank you so much for joining us today. The name of the book again, everybody, the clot thickens. Dr. MalcolmKendrick.org is a website, his WordPress site for his blog. Check that out. Highly, highly recommend the blog.
Unfortunately, these days, guys, you've got to be informed. You've got to put in some effort to get informed, and so do physicians. They can't just listen to guideline committees, obviously. So if you want to get informed and have your loved ones informed and even have your physicians informed on the number one killer in America and what really causes heart disease, get the book, the Clot Thickens. It's in the top three of all books I give out to medical students rotating through my clinic. And, and I highly Recommend it. So, Dr. Malcolm Kendrick, thank you again for joining us today. And thank you especially for all the work and all the years and I'm sure all the ridicule you've taken, but appreciate all you do.
[01:00:00] Speaker C: Thank you very much. I've enjoyed it. Thank you. Thank you.
[01:00:03] Speaker B: Okay. All right, everybody, we'll be back next week with another show. I'm Dr. Ben Edwards. You're the Cure.
