Written by Christopher Kelly
Sept. 2, 2019
[0:00:00]
Christopher: Well, Malcolm, thank you so much for hosting me here again in Macclesfield. I’m very excited to be back. Last time we spoke was 2017. I think my five-year-old daughter says that you’re the best podcast guest ever because I have not shut up talking about you since 2017. It really was a very special interview and I’m sure that many people listening to this episode have heard that one.
Since then, you’ve written a new book. I believe you’re in the writing process again, as we speak. Is that right?
Malcolm: Yeah. I’m writing my decree that’s going to be my final book on heart disease. I think I said that last time but this one is moving on I feel like into -- well, the one I’m writing is moving on, it’s the same. Well, if it isn’t cholesterol, it isn’t diets, and isn’t all these things that people say it is. Well, what is it?
In fact, that’s really been my, I feel like, life’s work. Although, I suppose you can say I also do work but my life’s interest for the last 35 years is just saying what actually does cause heart disease, cardiovascular disease, whatever term you want to call it.
That has been a journey in which I’ve taken three steps forward, 50 steps back, maybe sideways, or maybe snakes and ladders would be the best thing. Sometimes, I think yes, I’ve got it, I understand it and then suddenly, I find something and think, oh, I don’t understand this at all. It’s completely collapsing. I decided I would try and invent an antigravity machine or something easier.
Christopher: Something easier.
Malcolm: Create world peace, fasten light travel, because finding out what really did cause heart disease was just really, really difficult. But I think finally, I feel I’m on the right track with it or I do think I’ve kind of worked out at least insufficient detail, never say you’ve worked anything out because you’ll always be tripped up.
What actually we are talking about when we’re talking about cardiovascular disease and what -- I always hesitate to use the word causes because we talked a bit just before the podcast saying we need to move away from looking at causes to processes, what’s the process of heart disease because until you can understand that, you can’t really fit anything causal into the model.
You end up discussing the meaning of words sometimes. I feel like Bill Clinton, what is is, you know. What is a cause? What is a disease? In fact, that’s a very difficult one to answer. From that perspective, try to keep it both simple and sophisticated enough.
That’s really my interest because a number of people have said to me well, you just keep being negative and saying, it’s not this and it’s not that. Well, what should I do? What can I do? What does cause it? I thought you’re right because in the end, you have to try and say here’s something in its place.
I think, as I said to you, the problem we’ve had with the cholesterol, the saturated fat, whatever type of disease you cause, or sometimes it’s a bit like it’s the only planet in space and if you blow it up, it just reforms because there’s nowhere else for the thinking of the matter.
There’s nowhere else for anything to go, where people to go, and say well, come on then. What causes it? Extremely, I’m willing to say that to anybody before being at least 90% confident. I think I’d got some sort of other way of looking at it.
That’s really where I’m at the moment although, as you know, the latest book was just called A Statin Nation, which was more of the -- it’s not to do with cholesterol, it’s not to do with this, it’s not to do with that. Stop talking nonsense and stop telling 90% of the population to take their medication. That’s really for the vast majority, normally to provide any significant benefit.
That’s where I am at the moment.
Christopher: I’d love to get a history of how you began to think like this. I heard that your dad once ripped a page out of a textbook. Can you talk about that?
Malcolm: He did. It was actually mathematics of which I’m terrible, and he was very, very good. We were reading a text. He was trying to help me to get through exams by giving me crib sheets. This is how you do a differential equation. A what?
At one point, he just read a page in this textbook of mathematics and said, well, that’s wrong, and just ripped it out in shreds [0:04:04] [Indiscernible] throw it in the bin and I suppose you think [0:04:06] [Indiscernible] a textbook is wrong.
Christopher: It could be wrong. Is that a thing or is that possible?
Malcolm: Could it be possible that thing written down in a book can be wrong? I think that that gave me a sharp lesson in it’s not always -- I mean, now, we’ve got all fake news and fake this and fake that. It’s things are written down, things are accepted as being absolutely true and we have a tendency to do this so I think it’s whether a human thing of we follow authority, we know that we do. Questioning authority is difficulty and once something has been part of the curriculum and it is being taught, it’s wrong.
I mean it’s a classic statement when people enter medical school. They will say 50% what we’re going to teach is wrong. The problem is we don’t know which 50%. This has been said and yet, despite the fact that everyone says this, the idea that you could actually ever say well, this is a part of the 50% that’s wrong. Don’t be stupid. It’s been written down and everyone says it’s true.
Challenging, it is still really, really, really difficult because medicine is an incredibly conservative profession. It’s highly hierarchical. It’s rules-based, experts are experts, et cetera, et cetera. Guidelines are guidelines.
[0:05:18]
We have all these very, very sort of authorities of certain organizations like the British Medical Association and the General Medical Council. It does become a very difficult hierarchy to go against and even to think against it. When I first came out of medical school many, many years ago, I thought well, yes, I lived in Scotland. Why does Scotland have the highest rate at heart disease in the world? Oh, it’s the terrible stuff with diet, deep-fried Mars bars and all this.
You think oh, well, what does that do that raises your cholesterol level and then the cholesterol gets absorbed in your arteries and your arteries thicken up? I mean that is an absolutely simple and easy to understand idea of why would you question it? I feel very clever people, scientists have been looking at this for years and laboratories and white coats and professorships.
It is difficult to turn around and say you know what? This just doesn’t make any sense. I can’t figure it. Luckily, well, apart from my father ripping pages out of textbooks, in fact, I had a lecturer at Aberdeen University where I went to university, who, at one point, was doing a tutorial on heart disease and she was a cardiology student researcher. I didn’t know that at the time.
She made a statement to this group. It’s almost like somebody opened up a little world into her parallel universe and she said, LDL which is low-density lipoproteins, the thing we call cholesterol, cannot get through the endothelium. Again, that don’t mean much to many people but the endothelium is the single cells that line blood vessels.
It didn’t mean much to me at the time because I didn’t know what LDL was and I didn’t know what the endothelium was. But there was something about the way that she said it that I thought, that’s very important to her. That’s really, really important.
Christopher: You could just see in the emphasis.
Malcolm: Yeah. It was almost, in retrospect, maybe it’s in retrospect I realized how important it was but I do remember thinking why did she say that? What was that that just happened? Like you have a little glimpse of something, something catches your attention and I thought, well, I’m going to find what LDL is and I’m going to find what the endothelium is.
I later find out, there was articles written by E. Smith from Aberdeen about a completely different hypothesis on heart disease and how it happens. I didn’t realize it was Elspeth Smith. I thought it was E for Edward or something because you never thought women did research, and you never thought women were doctors at the time, and you never thought they were cardiologists. She was a rare member of the tribe.
In fact, I was set on the direction although I didn’t realize it. This is going back to 1980, give you some idea.
Christopher: Right, wow. Is that woman still alive? Have you gone back and found her?
Malcolm: No, she’s dead. In fact, a very interestingly, somebody reads my blog who was actually called Huxley, he was related to the Huxley, said that it was her great aunt -- no, her aunt. She said she’d died some time ago. Otherwise, yes, I would have been in contact with Elspeth Smith who, in fact, and along with a number of researchers who you don’t even know exists because this is another thing.
Once the theory becomes dominant, it’s dominant. Everything falls around it and all the thinking and all the ideas and people would have another idea, you kind of fall out of even the history of it. You can find these people. I call them ghosts in the machine. They’re there. You can find them. They’ve been talking.
There has been an alternative way of looking at heart disease. Actually, since it was first recognized as existing, there’s a researcher called Rokitansky who actually published a paper in 1842 discussing an alternative way of looking at cardiovascular disease. He called it the Encrustation hypothesis and wrote about it and in fact, he was trumped by another researcher called Rudolf Virchow who’s much more famous.
There are Virchow institutes in Germany because he was the first researcher to discover the cell. He was just a brilliant, brilliant man and because he was so brilliant, so authoritative, his ideas, knocked Rokitansky on the head but Virchow in this case was wrong. He wasn’t actually completely wrong but he was the first to see cholesterol in artery walls and therefore said, he just mentioned that we’ve got cholesterol in here, guys.
I’m always impressed [0:09:38] [Indiscernible]. I didn’t think that was cholesterol. How did they even know it was there when -- I’m just amazed at the genius of these people and they knew it was there.
Anyway, he said, there’s cholesterol in there. That point became the point -- and this other one did anything for the next 50 or 60 years. Virchow’s observations of cholesterol in the artery wall could’ve set the thinking in that direction. That’s where we went. Whereas Rokitansky’s ideas which were in fact, what he was looking at was he thought he was looking at blood clots in artery walls.
Virchow said to him, well, you can’t get a blood clot inside an artery wall. That’s impossible because it’s covered by this single layer of endothelium which they could see, so how do you get a blood clot inside an artery wall? Rokitansky had no answer to this. So his idea went of sideways.
[0:10:30]
The answer is, we now know there’s an answer to that. Had Rokitansky known what we now know, he could’ve said well, this is how you get it. But he couldn’t answer that question, and Virchow was more authoritative and had much more status. His ideas became the colonel of the whole cholesterol hypothesis.
If you look through the history, you could see that in 1912, I think the researcher is called Anitschkow, Russia fed rabbits a high-cholesterol diet and then cholesterol appeared in their arteries sort of. If you look at it, that’s not really what they did but that’s now the story, if you might.
And then over a period of time, people said well, look, we’re finding fatty cholesterol-y stuff in artery walls. Where’s it going to come from? Well, it must’ve come from the bloodstream because anywhere else it could’ve come from. Therefore, if you raise the level of fat and cholesterol, I mean people didn’t know that it was how it worked in those times.
That was the answer. It’s what we need to do. The diet hard hypothesis has been around for a long time. But no one really paid much attention to it until sometime after the Second World War when the heart disease rate in America had apparently gone through the roof. It appeared to have appeared from nowhere. Suddenly, middle-aged American men were just dropping dead of heart attacks and they haven’t before.
Then when Eisenhower had a heart attack, it suddenly became the thing and no one knew why for sure, but there were people who had been looking at this stuff for years and along came a man called Ancel Keys who said, I know what causes heart disease. It’s because you eat too much cholesterol. The cholesterol level in your blood goes up to cholesterol deposits in your arteries which is exactly the same as everybody has been saying anyway.
Unfortunately, for him, he discovered fairly quickly that if you feed people cholesterol, it makes no difference to your blood cholesterol level and so he changed the hypothesis of that point too, well, it’s not cholesterol, it’s saturated fat or fat, you never really define what sort of fat it was. Probably, saturated fat, but maybe some of those types of fat. If you try and pin anyone down, you’ll never get an answer to this. That became the dominant idea.
Then they started looking at this in studies and it just rolled on as people discovered that there were people who had naturally high cholesterol levels genetically and they had high rates of heart disease and that appeared to, if you like, put the cream on top of the cake and that was the answer to that.
And then along came statins that lowered cholesterol levels and reduced the rate of heart disease and so the answer was there. You can present the story so that it looks perfect. Every t crossed, every i dotted. Every part of it is apparently inarguable.
To an extent, that’s why we’re where we are. The story is very simple. You eat too much fatty gunky stuff, fatty gunky stuff appears in your arteries.
So you can see why people have accepted it so easily and rapidly because it’s not just scientifically that’s different but emotionally, it fits as well because we don’t like fatty gunky stuff, and the idea that fatty gunky stuff is therefore bad for us is emotionally satisfying as well.
It’s been very difficult. You look at most people and they look at you and say, actually fat is good for you. They look at you as if you must be mad. How can fat be good for you? It’s so disgusting and yucky. It must be bad. [0:13:52] [Indiscernible] and trying to actually convince people, you know what? This is just not right. It doesn’t work. It’s not correct.
You can come up with other facts. They’re absolutely 100% contradictory that you can say the French eat the most saturated fat in Europe and guess which country in Europe has the lowest rate of cardiovascular disease? France. When they still publish data that we’re looking at the Ukraine, Ukraine and Georgia, I think. Lowest saturated fat consumption in Europe, guess which countries have the highest rates of fat disease in Europe. Well, yes, the Ukraine and Georgia.
You can find absolutely contradictory data such as this. In fact, I’ve done a graph and I’ve showed it to many people which is the four countries with the highest saturated fat consumption in Europe have, on average, one-sixth the rate of the countries with the lowest saturated fat consumption in Europe.
Then you can start measuring cholesterol levels. Not all countries have done cholesterol levels. Not all countries measure LDL levels, at least not in the same way, so the comparisons can be quite complex, if you like.
[0:15:00]
But you can find example of example of example of it’s just not working. You can find examples a year ago, published a paper alongside a few of the other people in the International Network of Cholesterol Skeptics. We took all the data that we could find looking at LDL which is low-density lipoproteins which is the form of lipoprotein that we tend to call cholesterol or bad cholesterol. This is the one that causes heart disease.
We said, well, forget about saturated fat or forget about overall cholesterol levels, forget about all the other forms of lipoproteins that exists. We’ll focus on this one because this is the one that’s supposed to be killing people. We got all the data that we could from all the studies that have been done around the world and we said well, let’s see what the relationship between the LDL level and the death rate from cardiovascular disease is.
We found that there was no association at all in any studies. In fact, the only association we could find was that in fact, a higher LDL bad cholesterol level was generally associated with a lower risk of cardiovascular disease. In an older population, this finding became stronger.
This, by the way, is the most downloaded paper that there has been for the last year. A lot of people had read this, and yet the impact was precisely zero. People just said, "Well, they're just wrong." Well, here’s all the data. Here’s all the data that there is, so how can we be wrong if all the data says, there is no association?
The counterargument was oh, well, statins lower cholesterol and statins reduce the risk of heart disease. Therefore, the case is proven and you think right, well, I’ve gone through this one with people many times and said yes, statins do lower the LDL level.
Interviewing: There’s no denying that.
Malcolm: They’re designed to do it. They do it. However, statins also have many other effects. These are called pleiotropic effects, that’s the technical term, off-target effects.
For instance, aspirin was used as an anti-fever and anti-inflammatory drug when it came out and then it was found to reduce the risk of heart disease because it has other effects. Aspirin doesn’t reduce the risk of heart disease by lowering LDL levels. Aspirin reduces the risk of heart disease by being anticoagulant. It stops your blood clots forming. Statins do that as well about the same as aspirin.
The counterargument which is very straightforward is well, statins almost certainly don’t work by lowering LDL. They work through other effects. They have many other effects which is -- I’ll have time to go into all that in a moment. The fact is that it’s a bit like I’ve used the analogy of 12 Angry Men. I don’t you know if you’ve seen the film, the movie.
Christopher: I will now.
Malcolm: But it’s a famous -- it’s a McCarthy thing. It was actually done in the 1950s. It was a play and then turned into a very famous film with Hendry Fonda. But basically, there’s a black youth accused of killing his father. You sort of see the ending of the summing up before these people go into the jury room and they say, well, he had this very unusual knife that was found in the scene and no one else has this knife and someone shouted, “I’m going to kill you” and somebody saw him go into the apartment. The evidence appears utterly conclusive.
But actually, when they get into the jury room, one of the jurors says well, the first thing he says is well, I went into a local store and I found exactly the same knife. People then think well, each piece of evidence is actually creating this absolutely 100% conclusive evidence that this boy killed his father just disintegrates other scrutiny.
But it’s not really about that. It’s more about people have their established views at the time. He was a black youth. That’s what black youths do. It was probably him, why look anywhere else?
Christopher: It’s a confirmation bias.
Malcolm: Confirmation bias. I mean it’s --
Christopher: Narrative fallacy.
Malcolm: It covers all these issues of people just deciding that they know what the answer is and then fitting all the facts to match their answer. We have the same thing here I believe is that we’ve decided we know what the answer is and then every fact is just fitted in a particular way.
You can see that with the statins. Yeah, well, of course, there was a researcher in the UK called -- it’ll come to me as I speak -- who is very much against the hypothesis and the whole cholesterol hypothesis and was quite big reputation. When statins came out, he changed his mind, he said lower people’s cholesterol now.
That was what happened. All resistance crumbled. Before statins came out, there was an awful lot of people starting to question it because there had been other cholesterol-lowering agents that hadn’t work or increased the mortality. They’ve been other studies that had not worked and increased the mortality, and then statins suddenly just all the debate and all the discussion, it just went --
I think that was the point really at which this really became a powerful idea and an unquestionable idea and the idea that anyone could even question it. Well, you’re just an idiot. You don’t understand science. You don’t understand anything.
I think that going back to your initial question, before I started waffling for ages, was how did you get into this? Well, I got into this by being questioning. I think that’s my natural character. Some people have, some people haven’t. My father was an actual questioner and then I was set on a different direction by Elspeth Smith. I’ll raise her name up because she and others had really worked this out some time ago.
[0:20:09]
To an extent, I’m only just -- I’m standing definitely in the shoulders of giants here because I didn’t sit there in a vacuum and think, oh, this is the answer. I just thought right, well, if that’s the case, how does it work and her ideas, Rokitansky’s ideas do get -- a few others like Robert Ross [0:20:26] [Indiscernible] hypothesis. There have been people like they’re a different world. I don’t if you’ve seen Stranger Things. No, you probably --
Christopher: No.
Malcolm: The Upside Down is a different world. It’s upside down from ours. It’s just underneath our world. There’s a whole bunch of researchers who have been in this Upside Down world but no one wants to speak to them, no one wants to pay any attention to them. They have managed to breakthrough into our universe but they’ve all been, in my opinion, right.
There is a different hypothesis, and it works. It makes sense. It fits all the facts about what actually does cause cardiovascular disease. Believe me. I spent the last ten years trying to pick it apart, trying to look for information that says, this doesn’t fit. It doesn’t work. This can’t work.
The purpose of science is, first of all, to create a hypothesis. The second purpose of science is to destroy the hypothesis. There’s no point coming -- you can come up with any ideas like the 12 Angry Men. I can come out with -- I’ve seen people come out saying, oh, it’s all due to infectious diseases. You go well, actually, that doesn’t work at all. You even find the evidence that that doesn’t work.
You can make quite a good hypothesis for infectious diseases. I’ve seen people say oh, that’s all due to vitamin C or it’s all due to vitamin D or come out with an idea well, it’s all due to the lack of sulfur. They can give you a very convincing hypothesis and then you say all right, let’s try and find a country [0:21:47] [Indiscernible] and it quite rapidly emerges.
But then you speak to these people and they come up with these most convoluted ways of saying well, why that’s not. And you think, okay, you’ve already decided you’re not going to change your mind. Some of them are people who are the International Network of Cholesterol Skeptics who say definitely isn’t cholesterol and then they say, but it’s definitely this. If you challenge this --
Christopher: This is different --
Malcolm: Exactly. What you have to say is, you have to look at it all the time, I think, and say does it fit? Does it match? Can I find contradictory evidence? I say to people say the infectious disease hypothesis, which makes a lot of sense. There’s this thing of if you have gingivitis or gum disease, you’re much more likely to die of heart disease. This is true. There’s a reason for that.
I could say, Elspeth Smith and these people we’re talking about, that fits. It works, but it doesn’t mean it’s the cause. It means a cause. It’s one of many possible causes for this process.
I’ve tried to use -- some people have discussed this. I’ve tried to use the analogy of rust in the paintwork of a car. Now, normally, if you’re going to get rust, although I did have [0:22:59] [Indiscernible] when I was younger and that rusted just automatically. It had a tinkling in its own as it rusted. But normally, nowadays, you’ve got to damage the paintwork before anything will rust. And then once you’ve damaged the paintwork, water and salt get in and will accelerate the process. But without any damage, nothing is going to happen.
You say, well, what can damage the paintwork on your car? Well, I can think of 500 things on the top of my head. You can reverse into a wall, another car can barge into it, you can drop some shopping or a tin of baked beans on the side of the car, a sharp stone can jump up, something can fall off the side of the -- you can keep going.
Now, they can all damage the paintwork on a car. There’s nothing else about them that is the same. So say, a stone chip and a tin of baked beans falling out your shopping, what relates these two things? Nothing.
Christopher: Apart from?
Malcolm: Apart from what they do. It’s not what they are, it’s what they do. When you say if, I haven’t explained any of this up to this point to anyone who’s listening, if the starting point of the development of a thickening in your artery wall which is a atherosclerotic plaque is that you have to damage the artery wall in some way.
Then you have to ask yourself the question, well, what can damage an artery wall? What things can do this? And then once you start thinking this way, I could give you 50 off the top of my head. I can give you -- systemic lupus erythematosus, if you’ve never heard of it, don’t worry, and I can give you Kawasaki disease. I can give you bacterial infections. I can give you diabetes. I can give you smoking. I can give you air pollution. I can give you poisoning.
Christopher: Sickle cell.
Malcolm: Well, we did talk about sickle cell which I think -- to me, this is the ultimate example. Sickle cell disease, so called because your red blood cells are sickled, they look like a sickle shape. They’re like the moon in a sort of wedge shape, and they’re very sharp at the end. I mean really, we’re talking sharp. If you’ve got what they call homozygous from both your parents, the gene for this, you have a lot of sickled cells.
Obviously, a sickle cell charging to an artery at high speed has got a sharp pointy end rather than it’s round and looks like a donut, is bickering up against the artery walls. As it does so, it’s going to cause some damage. It’s going to damage the -- when we talked about the endothelium, the single lining of the cells, as Elspeth Smith said, well, these endothelial cells are being constantly battered by sickled cells.
[0:25:25]
I was looking at case history of a 14-year-old or maybe he’s 12, 12 or 14-year-old boy who’s admitted to hospital with gangrene in his foot. He had sickle cell disease. They found the gangrene in his foot, because the circulation to his foot was severely compromised. He had severe atherosclerosis in the arteries in his legs supplying his foot which is why it became gangrenous because of little blood supply.
They had to actually amputate his leg. They did scan him and found that every single artery in his body was calcified which is late stage atherosclerotic plaques in every artery in his body. His brother had died age three and he’s already had a stroke. As I said to you earlier, people with sickle cell disease, the increased risk under the age of 30 of having a cardiovascular event is increased 50,000%. That’s proper cause.
There is an issue to those sickle cells clumping and causing strokes so they tend to have more strokes than heart disease and any of these things. Then you got to say to yourself the other thing about case history was this 12 or 14-year-old boy had no other risk factor for heart disease. He didn’t have high cholesterol levels. He had nothing. He didn’t smoke.
You have a case of severe atherosclerosis at a very young age, in a 12-year-old boy, every artery with atherosclerosis, and the only explanation is that you got sickle cell disease. If you’re going to explain cardiovascular disease, you have to explain how could this disease cause thickenings and narrowings in your arteries around your body? How can that possibly be?
The only answer, and in fact the answer the paper itself said, mechanical damage to the artery wall lining is probably causing underlying disease. It didn’t explain how. But then you go back to Rokitansky. Rokitansky said well, what I find is I find blood clots in arteries.
That’s what I’m looking at, that’s what I think I’m looking at. Virchow said well, you can’t find blood clots in arteries because the endothelium is sitting on top of them. Imagine if the endothelium had been stripped off. The endothelium is stripped off and then immediately after that, a blood clot will form because as you can imagine, the body doesn’t like having exposed blood vessels. It thinks they’ve been damaged and will immediately charge to the rescue and form a blood clot on that point.
Once you take the endothelium off any blood vessel, the blood clot will instantaneously form. Now, the whole process is gigantically complicated and of course it then stops forming. But then you say well, what happens to that blood clot? You got a blood clot stuck to your artery wall. Okay. Now, it may not be very huge. Probably quite small. But if that blood clot -- imagine you scratch your skin on the back of your hand, what happens is it bleeds.
Christopher: It eventually clots and stops.
Malcolm: It clots and stops and your left with a scab and that scab will fall off because in your skin in your hand, the cells underneath, several layers of cell that grow up form the surface layer, and they will eventually push the clot off and it will drop to the floor.
Imagine if the cells in your artery did the same thing and it pushed the clot off, what would happen to it?
Christopher: It would be floating around in your bloodstreams.
Malcolm: Yeas, and causing strokes and heart disease, and heart attack. So your body can’t allow that to happen. What does it do? What it doesn’t do is it doesn’t -- it can’t grow up from underneath anyway because it’s only a single cell layer and there’s no endothelial cells underneath so it can’t grow from underneath. There’s no underneath cells. So where does the cells come from that we could cover over a blood clot. Where does it come from?
No one knew this until about 1997. Well, it’s discovered there’s a thing called endothelial progenitor cells. They’re produced in the bone marrow. They float around in your bloodstream and when they find an area of damage, they stick to it. They grow from endothelial progenitor cells which are fairly undifferentiated into fully-fledged endothelial cells and hey, presto, your blood clot is now underneath your endothelium. That’s what happens to it.
Now, we can see this happening. This was seen by researchers in the 1960s. I was looking at researchers who’ve done experimentation on pigs because pigs are about the same as us. They don’t normally get heart disease. What they did was some pretty horrible things like open them up, open up their arteries and scrape a bit off, stitch it all up, and then two days, three days, a week later, kill them and see what happened.
They saw these spindly strange almost like endothelial cells sitting on top of the blood clots that they produced. They didn’t know what they were and they couldn’t explain their existence. You feel like saying, you were looking at it. You didn’t understand what you were looking at.
Anyway, endothelial progenitor cells in the bone marrow, cover over the clots within the artery wall. So then what happens? Leave a blood clot that’s sitting within your artery wall. In general terms, the body doesn’t like areas or things of damage kicking around, so it sends in the cleanup squad which are called white blood cells, which are called monocytes and macrophages, and they just get rid of it.
[0:30:19]
This is probably happening, I hate to say this to you people, but it’s probably happening in your arteries as we speak. However, if your clear up squad, if it’s not happening that fast and if your clear up squad are clearing things up well enough, they will just be got rid of. There’ll be no sign that there was anything there in the first place.
Of course, if you’ve got sickle cell disease, your arteries are getting continuously damaged as they’re clearing up, the repair systems can’t keep pace of it. If your repairs feel like sometimes there's potholes on the road, nowadays in Britain, we drive on the roads, there’s potholes everywhere. Well, we lay the tarmac over it, and over it, and then the rain gets on it and the cars bash up and down it, and a pothole develops. We would then cover it over. Of course, this is not an automatic process. Someone has to say there’s a pothole. Let’s cover it up and put a patch on it that’ll last about two days, and then it falls off and then it’s all there again.
It’s like pothole development. If we don’t spend enough money on pothole clearing up, the roads will end up in a bloody mess. Now, the repair systems in the body are obviously continuously repairing things and doing the damage, getting rid of the damaged areas.
But if your damage is going faster than your repair, then these potholes eventually become major things that then become almost impossible to clear up. That becomes the plaque and that is now is an irreparable thing. The system just gives up. As you can see, it happens because -- and this is moving slightly sideways but there is another animal species apart from us that doesn’t produce vitamin C. Another thing, where is he going with this?
Vitamin C, we don’t make it or synthesize it ourselves. We can’t. Almost all other animals can, and we can’t. Great apes can’t and various other animals can. Guinea pigs can’t. Why can’t guinea pigs manufacture vitamin C? Who knows? They can’t. Fruit bats can’t either.
If what you do is vitamin C is essential for the structure of almost everything in your body because it makes collagen. Collagen is the background support. It’s a bit like the steel reinforcement bars and concrete, if you like that analogy. I’m not sure how good it is. But anyway, without collagen, your body starts to break down. Now, one of the first things it starts to breakdown is your blood vessels because the collagen behind that keeps your blood vessels strong and well made.
If the vitamin C drops, the collagen starts to fall apart and then your blood vessels start to crack and they start to bleed. When people get scurvy or used to get scurvy -- I used to get bleeding gums. In fact, death was due to chronic blood loss, we just bled to death slowly. So that sounds terrible. It’s not a very nice disease, scorbutic.
There is a patch system that we have that helps, if these little cracks appear, we have a patch system. This patch system is called LPA, Lipoprotein(a) which is exactly the same as LDL except it’s got another protein attached to it and that protein is attracted to areas of damage sticks to it, blocks the area of crack and stops the bleeding, or at least not entirely but it’ll keep you alive a bit longer if you become vitamin C deficient.
Some people have said a lack of vitamin C causes cracks to develop in the artery walls then these LPA molecules attached to the area, and because they’re part of the blood clot and formed internally into the blood clot are the underlying things that causes the plaque to develop.
Someone in the ‘60s made guinea pigs vitamin C deficient. Within two days of becoming vitamin C deficient, they start to develop atherosclerotic plaques in their arteries. When they gave them back vitamin C, the atherosclerotic plaques disappeared. This is a perfect model. But if you left them longer than about a week, then the plaque areas, they couldn’t be got rid off, they just stayed there.
We had an experiment in the ‘60s, an animal experiment which showed that if you damage the artery wall, you get cracks, you get plaques developing and you can get rid of the plaques. We had this model. This model works so we can see it. So it’s a bit like the pothole analogy.
Then you say, okay, not everybody’s got vitamin C deficiency. In fact, Linus Pauling, you may have heard of, won two Nobel Prizes. His idea was heart disease was chronic low-level vitamin C deficiency. We should all take lots and lots of vitamin C all the time and we would never get heart disease.
For people who’ve got this LPA in their blood, yes, you want to be taking vitamin C and don’t become vitamin C deficient. It’s quite difficult to take too much vitamin C. If you’re worried about that, take vitamin C because then your arteries won’t crack, blood clots won’t form and you won’t get atherosclerotic plaques. However, that’s a cause of heart disease. It’s not the cause of heart disease.
Here’s another problem. [0:34:58] [Indiscernible], Linus Pauling, this was their idea. That was the cause of heart disease. We’ve worked it out. It’s this one thing. No. How do you explain heart disease and sickle cell disease then for instance? There’s no vitamin C deficiency here. You have to explain everything. You can’t just explain something. You have to explain everything. Otherwise, you haven’t got a hypothesis.
[0:35:16]
Anyway, go back to that. I know I go off on these tangents to pull it around, but essentially what we’re saying is that you have to damage the artery wall, and if you damage the artery walls at high speed, then atherosclerosis or plaques will develop.
Those plaques could become permanent because at a certain point, they kind of almost seal off and then the white cells can’t really get at them and they give up [0:35:39] [Indiscernible], so they can become bigger and bigger and bigger and eventually they can block your artery and eventually that’s what kills you.
Then you start saying well, what other things can cause rapid damage to endothelial cells? One of the things you’ll find well, smoking. Smoke one cigarette, this thing called microparticles. If you can measure them in your bloodstream -- if you’ve got microparticles in your bloodstream, it means your endothelial cells are breaking down at high speed.
Christopher: Are these the metabolites from cells themselves?
Malcolm: The metabolites from the cells. It’s like measuring liver enzymes to see if you got liver damage because once the cells break down, the enzymes spill into the bloodstream and you can measure the level, so that’s how you do these things.
If you start destroying endothelial cells in a high level, you’ll find high level of microparticles in the bloodstream. Smoke one cigarette, and you can see microparticles in the bloodstream for the next 30 minutes so you’re actually wiping out endothelial cells. Air pollution, you can see the same effect. Air pollution, weakens and damages endothelial cells. It’s not the stuff in your lungs that gets into your bloodstream and actually damages your blood cells.
Air pollution causes damage to the endothelial cells in the same way that smoking does which is why they now say air pollution’s totally dangerous. They don’t really seem to understand why it is. I can show you that.
Christopher: Right. They’re just looking at epidemiological data.
Malcolm: Yes. They are just looking at epidemiological data and a bit like the smoking.
What else can damage an endothelial cell? Well, the other thing that can damage an endothelial cell is a high blood sugar level. What causes high blood sugar level? That’s diabetes. Risk of heart disease in diabetes is three to five times as high in a normal population and therefore you can say, okay.
We’re starting to see that you can actually bring these things altogether and say, well, the first thing you have to do is damage the endothelial cell and there’s many things that can do that or many conditions. There’s a condition called Kawasaki disease which I think I mentioned it to you. Kawasaki disease is an inflammatory condition affecting young children. It’s called Kawasaki because it was much common in Japan. That's where it came from.
You can die of a heart attack at age four if you have Kawasaki disease. You say well, how can that possibly cause heart disease? Well, with Kawasaki disease, the other name for it is vasculitis. Vasculitis, vascular means blood system, itis means inflammation. Like tonsillitis is inflammation of your tonsils, and appendicitis is inflammation of your appendix. Vasculitis is inflammation of your vascular system which basically means damage to your endothelium.
If you get Kawasaki disease, you get this severe and acute vasculitis that strips your endothelial cells off and then that causes rapid damage, so rapid that you can get what you call aneurism so it balloons in the arteries which is normally a very late stage of atherosclerosis. It’s not quite the same thing that kills you as an older person.
The vasculitis is inflammation of the vascular system. The other thing is we get an infection, an infectious disease that gets into your bloodstream like sepsis which is the most extreme example of that. What kills you in sepsis? What kills you in sepsis is that the bacteria releases a high level of exotoxins which is the toxins that are just released from the bacteria as they multiply. This is kind of poison.
Christopher: This is different from endotoxin, is that right?
Malcolm: The complexity of medical terminology. These are two things that are completely different but we call it the same thing. An endotoxin just means the toxin is within you. An exotoxin is a thing that the bacteria produces. Exo, outside. Endo, inside.
Exotoxin’s produced by bacteria. What they do is they attack the vascular system. They kill all of the endothelial cells and what you get then is what they call disseminated intravascular coagulation because blood clots are happening all over your body and because blood clots are happening all over your body, the blood supply to your organs and you die of organ failure. But what’s happening there, an acute example is basically, damage to the endothelium at a really high speed.
Interestingly, if you give people vitamin C at very high levels, it can reduce the risk of dying from sepsis considerably, which is very interesting research, which is completely ignored by the --
Christopher: I was going to say that’s controversial, isn’t it?
Malcolm: Well, there shouldn’t be nothing controversial about it. Vitamin C can’t do you any harm and it could reduce --
Christopher: Well, it’s controversial that it’s not standard of care.
Malcolm: It’s bonkers if it’s not standard of care. It’s just ridiculous. I’ve been banging on about this to some people for some time saying, why can’t you just try it as is in some studies have reduced mortality from 40% to 8% which is, for the risk of what, it costs nothing. It can cause no harm and it could reduce mortality by 500%.
Christopher: It don’t get better than that.
[0:40:15]
Malcolm: Nothing is better than that. Anyway, this is the conservative medical profession. Oh, well, it’s not properly studied and done.
Anyway, so in a lower level, if you get a chronic gingivitis or a gum infection or any infection, any infection can cause a vasculitis because obviously, any bug that’s floating around in your bloodstream, any bug is usually producing exotoxins and otherwise, nasty chemicals. Those exotoxins directly hit the endothelial cells and directly damage them.
You’re increasing the rate of damage of the endothelial cells if you have chronic low-grade infections. Virus is different than bacteria but viruses obviously can’t produce the exotoxins because they’re just viruses and they don’t do that but bacteria can.
Of course the other interesting thing which I haven’t mentioned at all up to now, and this is something no doctor that I’ve ever spoken to has even heard of, is that you know if you try and pick up a fish, what happens?
Christopher: Slips out of your hands.
Malcolm: Slips out of your hands.
Christopher: We talked about this last time. The glycocalyx. I’ve not shut up about the glycocalyx since you mentioned it.
Malcolm: Oh, right. I mentioned that before. The glycocalyx. No doctor I’ve ever spoken has ever heard of it. You’ve heard of the heart, you’ve heard of the lungs, here’s something of equal importance. It’s called the glycocalyx which is kind of a slippery gooey lining that lines all your cells that’s made up of protein and sugar. It’s called proteoglycans or glycoproteins. It’s like a little forest.
If you see it, it’s like a forest sitting on top of your --
Christopher: Yeah. It reminds me of the villi that sits on top of epithelial cells.
Malcolm: It is the same thing. They are same. It’s just a different version of the same thing. Their job is in part, is to stop anything clotting because blood clots [0:41:56] slide past quickly and there’s also chemicals inside.
In fact, sitting within the glycocalyx is the enzyme that produced nitric oxide which you may or may not have heard of but nitric oxide is an amazing chemical that causes your blood vessels to dilate. In fact, it’s the active substance from you might’ve heard of GTN to help stop angina. You pop one under your tongue, it used to be pop one under your tongue. They come in different versions now.
Because it’s a nitrate, it stimulates nitric oxide production in your endothelial cells, it causes your blood vessels to dilate increases of blood supply to your heart and gets rid of the angina. The other thing about nitric oxide, it is the most powerful anticoagulant agent known to man. It stops blood platelets and all other things in your blood clotting.
If your nitric oxide production is good and high, then you won’t get blood clots forming and blood clots so you see the final event in causing heart attacks and strokes so it’s all kind of interrelated.
Another thing that’s very good for nitric oxide synthesis and production is sunshine. Go out in the sun and your body will synthesize nitric oxide and it lowers your blood pressure by more than most blood pressure lowering tablets and we’re told it’s bad for you but complete nonsense.
Sunshine is about the most fantastic medication that you can have. Go out in the sun, increases your vitamin D, yes, but it’s an awful lot more than that. One of the things it does is it stimulates nitric oxide synthesis which is why if you look at the rate of heart disease deaths in the UK, and I’ve done it with [0:43:29] [Indiscernible], it’s like looking at a wave form. Wintertime, up, summertime, down, wintertime, up, summertime, down. Why? Because the shiny things in the sky stops us from dying. Get out in it.
You ever heard of evolution? We’ve been living underneath this thing for all of life developed for this thing was shining upon it apart from your volcanic events under the sea. The idea that this is harmful to us, and we should hide away from it, we obviously don’t believe in evolution if you believe that’s the case.
You don’t think we’ve evolved to operate and to think with that shiny thing up there. You’re not thinking it might do us some good, yes, don’t burn yourself to smithereens but otherwise, it is healthy. Anyway, that’s nitric oxide.
When you’re saying to yourself is essentially the process, if you like, that I’ve been looking at is to say that if you damage the endothelial cells, this triggers the process. It doesn’t necessarily cause it which is one answer as to why do you never get atherosclerotic plaques in veins ever?
Christopher: Difference in blood pressure.
Malcolm: Well obviously.
Christopher: Oh, because the level of cholesterol are different in veins.
Malcolm: Well, they’re not. They’re exactly the same as is everything else. There’s only one difference. We call it blood pressure. We call it biomechanical stress. An artery is having the blood whooshing at high speed, at a high pressure, at high levels of turbulence whereas the vein is a bit like a slow-flowing river as it reaches the sea is kind of going along very slowly. Well, where’s the pressure? Where’s the biomechanical damage going on there? Well, there isn’t any, is there?
[0:45:02]
Essentially, that’s why you never get atherosclerotic plaques in veins because there’s never enough biomechanical stress. If the blood pressure’s high, if the blood sugar is high, smoking, all of these things. They’re not enough. That’s why you never get atherosclerotic plaques in your lungs either because people are going, oh, it’s about oxygenation, the blood in your arteries is more oxygenated.
Christopher: I’ve not heard that.
Malcolm: People come up with all sorts of -- you’re never going to get more oxygenated blood than you are in your lungs, are you? And you don’t get atherosclerosis in your lungs unless you develop pulmonary actually among hypertension and then you can occasionally.
In fact, this case, this boy I was telling about, 12-year-old, he had atherosclerosis in his lungs, and that’s something you usually don’t see but because of these arteries being so significantly under pressure with the sickle cells going past them.
The current ideas cannot explain to you why you don’t get atherosclerosis in your veins because veins are exactly the same structures are your arteries. They have one layer of endothelium and then --
Christopher: Do they have the glycocalyx and all of that?
Malcolm: They have all of that, yeah. They have everything. What they don’t have is a hundred millimeters of mercury on average blood pressure to deal with plus blood flow going 16 times faster or whatever it is and so nothing happens. If you get a vein in your leg and use it as a coronary artery bypass which happens, within five to seven years, it’ll be blocked up completely.
Nothing else has changed except you stick it in where our artery should be and it rapidly develops atherosclerosis. All the other veins in that person’s body will be atherosclerosis free as they always are. You’ve changed one thing. You’ve changed the biomechanical stress, the potential for damage on that blood vessel. Suddenly, it’s developing atherosclerosis.
How else can you explain it when everything else is the same? Well, the answer is you can’t. Well, I suppose a lot of people do develop atherosclerosis, most of us do which is the way that we develop.
Christopher: We don’t dive it.
Malcolm: We don’t dive it. We dive at something else first probably. That’s why, if you like, age is the number one risk factor for dying of cardiovascular disease because in most people, it’s building up let’s say speed x. If you smoke, it’s building up at speed 2x. If you’re smoking, you’ve got diabetes, it’s building up at speed 4x. If you’re smoking, you got diabetes and high blood pressure, it’s 6x.
When people say heart disease is multifactorial, i.e., there’s lots of factors causing it. Well, actually, well, that’s sort of true but it doesn’t mean anything. You got to understand how they all fit together. My general idea about heart disease is say there’s 15, 20, I don’t know how many things that generally could be causing a problem. If you got one, nothing actually is going to happen. If you’ve got two, nothing actually is going to happen.
There comes a point where suddenly, the damage that you’re causing overwhelms the repair system. Where does that happen? It happens at different speed in different people because the other -- if you look at it from the repair point of view is saying, well, what interferes with repair?
One of the things that interferes with repair is if you take steroids, steroids are anti-inflammatory. Inflammation, in my world, equals repair. People who take oral steroids have a 400% to 600% increased risk of dying of heart disease because steroids are -- they’re anti-inflammatory, anti-repair, so you’re knocking the repair systems on the head.
One of the other things that will cause repair is -- and this is relatively technical. There are drugs used in cancer treatment. They’re called vascular endothelial growth factor inhibitors. As you can imagine, the vascular endothelial growth factor is something that makes endothelial cells grow, also increase nitric oxide synthesis and it’s a good thing.
Now, if you don’t have VEGF, your endothelial cells can’t grow, can’t repair themselves. In fact, the bone marrow production of endothelial progenitor cells is really reduced. So you got to say well, why would anyone take a VEGF inhibitor? What’s the purpose of that?
Well, actually one VEGF inhibitor is thalidomide, and no one knew for a long time why does thalidomide cause arms and legs to be very short and not form and not grow? Well, the answer was in the womb, VEGF causes blood vessels to grow and develop. The thalidomide blocked that from happening. The blood vessels didn’t grow and develop so the arms and legs couldn’t grow and develop.
That’s why they have short legs and arms and that’s what thalidomide did. Thalidomide is actually used as an anti-cancer drug now because of its VEGF function, because blood tumors as they grow create their own blood vessels, stimulate their own blood vessel formation to feed them with enough blood supply.
If you can stop the formation of the blood vessels, the tumor won’t grow and would die, so it’s actually quite an effective treatment. Another thing that causes problems is if you got too much VEGF or whether you got the right amount, you get macular degeneration. Have you heard of macular degeneration?
Christopher: Yes, yeah.
Malcolm: There’s two different forms but the most common form is too many blood vessels are forming in the macula behind your eye. Therefore, that starts to cause damage and you lose the central vision in your eye. What you do is you inject a vascular endothelial growth factor inhibitor into your eye which is -- we called it Avastin, which sounds rather unpleasant. It works.
[0:50:11]
Christopher: Is it localized?
Malcolm: Well, it hits into the bloodstream. But these are very small doses. But there’s another drug called -- the Avastin can also be used as an anti-cancer drug and is quite a commonly used anti-cancer drug and as a VEGF inhibitor, so it stops the blood vessels from developing and growing stops, repair the blood vessels and reduces the production of endothelial progenitor cells in the bone marrow.
Guess what impact you think it may have on heart disease. It increases the risk of dying of a cardiovascular event in the next two years up to 1,200% so it causes atherosclerosis. In fact, it was almost a [0:50:51] [Indiscernible] huge increase in risk --
Christopher: It's that kind of switching problems.
Malcolm: Well, in fact, all chemotherapeutic agents because they stop turnover and growth of cells generally, that’s how they work, are becoming more sophisticated nowadays, will increase the risk of cardiovascular disease. That’s one of their adverse effects.
The interesting thing is that in order to reduce the risk of causing cardiovascular disease by taking Avastin which is a vascular endothelial growth factor inhibitor is you give a drug called an ACE inhibitor which is used to lower blood pressure.
Christopher: How does that work?
Malcolm: Well, because one of the other effects of ACE inhibitors is that they increase nitric oxide production in endothelial cells. That’s one of their effects. In my opinion, that’s how they work. You know another thing about statins do --
Christopher: They increase nitric oxide.
Malcolm: Statins increase nitric oxide synthesis. Therefore, that’s how they protect against heart disease. I hope I don’t become too gigantically complicated in explaining this. I hope it’s clear but what I’m trying to give is the sense of the interconnectedness of all of these things such that you can understand -- if I was going to say to an average fellow GP, how do you think Avastin increases the risk of heart disease and atherosclerosis? I mean they would just look at me blankly. They would have no idea. Initially, you would think well, there’s no connection here. What’s the connection?
But once you understand the process which is endothelial damage, formation of a blood clot, then repair, then you’re saying we have a three, if you like, we have three arms to this process and if this go out of culture, so we need to say well, what conditions increase risk of blood clots? Well, there are a few.
There’s a thing called Hughes disease where genetically you’re more likely to blood clot and these people have a really vastly increase risk of dying of heart disease and then you look at things and say well, what about -- well, I was looking at hemophilia which is due to a lack of blood clotting agents in your blood. Prior to the blood clotting agents, the synthetic new ones coming along. The risk of dying of heart disease in hemophilia was reduced by about 500% didn’t get really dying of heart disease.
Once you start looking at heart disease as a process, an interlink process of damage, clotting of hair, you can then take any factor that increases the risk and say well, plug it into the model, does it fit? And which is what I’ve been doing over last probably five to ten years is looking around for -- and then people come out and saying things come out here sideways and you think, here’s a thing called Losec which is a thing to reduce acid in your stomach which is used for ulcers which is called -- I just forgot the name. Omeprazole. You may have heard of it.
Christopher: Is it a proton pump inhibitor?
Malcolm: Proton pump inhibitor. You say that increases the risk of dying of heart disease. You go, why the hell does that increase the risk of dying of heart disease? Well, actually, if you look into the biochemistry of it, it reduced nitric oxide synthesis in your endothelial cells. It does it through a really complicated pathway but it’s a well-established pathway and then you think okay, I can understand that it fits in absolutely perfectly to this differential model.
You say how does omeprazole cause the same disease as sickle cell disease or a low-grade gum infection or Avastin or smoking or diabetes?
Christopher: Chronic stress.
Malcolm: Or chronic stress which raises your cortisol level which partly increases blood coagulation, damages the glycocalyx and reduces the repair systems. If you stop looking at heart disease as this is the cause, you say no, this is the process.
Then you can start to say, well, I can understand therefore how does exercise protect you against heart disease? Well, because it increases nitric oxide synthesis in your endothelial cells alongside a few other things and it reduces your stress hormone levels generally and reduces your sympathetic drive.
The stress thing which I was most interested. Well, how does stress do this? Well, you start looking at stress, it’s just like it’s a bombshell inside of your cardiovascular system in many ways. Under stress, your blood becomes hypercoagulable. In other words, much more likely to clot. It damages your high levels of stress hormones and sympathetic tone, what we call sympathetic tone is the flight or fight thing. If a lions walks in the room, we'll sort of evacuate our bowels.
[0:55:21]
Christopher: Right, you liquidate your assets in many ways.
Malcolm: Yes. Our heart rates go up and our blood vessels contract and our blood pressure goes up and our endothelial cells are [0:55:30] [Indiscernible], all sorts of hormones are triggered. It’ll just do damage all through the cardiovascular system. What you don’t want is that system chronically activated. It’s built like taking a steroid, damaging your cardiovascular system. Be constantly under a low-grade stress or chronic stress or being strained, as I thought.
You can see exactly how all that fits together. To my mind, and this is the process thing, this is what Elspeth Smith was talking about, she was looking at blood clot, she was looking at LPA, she was looking at endothelial damage, she was looking at all these things. She was saying well, even if you look at people whose arteries normally look quite healthy, what you find in them is the remnants of blood clots.
If you think blood clotting is a very complicated system but take it to a simplest level, little cells called platelets which are floating around in your bloodstream, they all stick together to form a kind of block, then all the other cells and everything else in your bloodstream gets involved as well.
But then along comes a thing called fibrin which is made from fibrinogen which is a long sticky strand of fishing line that wraps around everything and holds it really tight together, makes it very difficult to break apart. Fibrin is made by this what they call the clotting cascade or the clotting factors you’ve heard of sort of end up being fibrin.
If you look at arteries of people, they’ve got fibrin in there. They’ve got the remnants of blood clots which would probably it’s been cleared up. How else are you going to get these things inside an artery wall?
It’s when Rokitansky said, I’m looking at blood clots. He was looking at blood clots in different stages of development and repair. He was right in what he saw. I have spoken to pathologists who chop people up after death and stuff like that. A lot of them said you know, that’s what we see. This is what we see but no one’s ever -- well, why don’t you say it? Why don’t you say it to people? This is what you see.
Everyone says, oh, well, you get cholesterol inside. You get cholesterol crystals inside an atherosclerotic plaque. Where does a cholesterol crystal come from? Must be due to cholesterol in the blood. Well, that’s exactly where it can’t come from. That’s precisely the wrong interpretation.
The only tissue or part of the human body where the free cholesterol is high enough concentration to form a cholesterol crystal is, you won’t know this, no one knows this, is the membranes of red blood cells. The red blood cells, in fact the highest concentration of cholesterol in your body is the lining of the red blood cells, the thing that -- the donut cover.
You will never find a higher cholesterol concentration anywhere else in the body. The reason for that is very complicated but it’s because of the oxygen going in and out and the fact that cholesterol’s required for all of that. If a red blood cell gets incorporated into a clot --
Christopher: I see. That’s where it came from.
Malcolm: That’s where it came from. It came from red blood cells because it can’t have come -- you know, LDL, it does carry cholesterol around and it carries fats around. The fats and cholesterol are combined and then they are called a cholesterol ester. You don’t need to know, but if you stick a cholesterol molecule to a fat molecule, that’s called the cholesterol ester. Esters are a combination with alcohol and a fat and that’s why some people say cholesterol is an alcohol. Structurally, it’s an alcohol in some ways.
Anyway, cholesterol esters are how cholesterols coming around inside LDLs. You can’t make a cholesterol crystal from cholesterol esters. It’s not chemically possible. You can make a cholesterol crystal from pure cholesterol and the only place you find pure cholesterol that is any source of that is red blood cells. I’ve read research where people have said we found pure cholesterol crystals and this must’ve come from red blood cells. This research is published. I’m not just making this up.
You have to go and research really, really, really heavily to find these stuff because you’ll never find it -- if you write in atherosclerotic plaque cholesterol, you’ll get 600,000 papers saying atherosclerotic plaque that’s full of cholesterol, that must’ve come from LDL. They’re all wrong because that’s not physically, chemically, scientifically possible. It can’t have come from there. It’s impossible that it came from there so it must’ve come from something else.
There are some researchers have gone off, seen the cholesterol crystals, and thought actually, no. In fact what Virchow saw when I said, how did you know he saw cholesterol? He saw cholesterol crystals. Otherwise, he wouldn’t have known it was cholesterol. Because if he’d seen a cholesterol ester, he would not have known more chemically. He saw cholesterol crystals and said, that’s cholesterol. He was right. It was cholesterol crystals.
Ironically, the only place you could possibly have a cholesterol crystal in it is if there were blood cells in it. The only way there could’ve been red blood cells in it was it if it was part of a blood clot because red blood cells are essential for blood clots to form.
Once you start looking at this stuff, you think no, how on earth did this ever, ever get designed? Red blood cells, when they become incorporated into a blood clot contract down into polyhedron shapes. They attach themselves to strands of fibrin while they’re doing it in order to pull the whole blood clot tighter.
[1:00:27]
Red blood cells are essential to create tightly bound blood clots. They are part of the blood clot. They’re an essential motor and driver of it. When people say what does a blood coagulation system consist of? It consists of everything. There’s nothing in the blood that doesn’t have a role or a part to play in blood clotting.
You have mentioned to me triglycerides which are called very low-density lipoproteins. If you take the VLDLs, very low-density lipoproteins, triglycerides, and drop them into blood, they will act as a focus for blood clots to form. They are procoagulant and in fact, they’re procoagulant because the surface, the lipid surface of the VLDL, the triglyceride, is the surface upon which blood clots are formed and HDL, high-density lipoprotein, good lipoprotein is actually anticoagulant. That’s one of its functions.
LDL has got functions in the creation of blood clots. What you get to say to yourself as I said to your earlier, LPA, Lipoprotein(a) is LDL with an extra protein attached to it, an extra protein that’s attached to it called the Lipoprotein(a).
That’s why it’s called Lipoprotein(a) because it’s LDL with Lipoprotein(a) attached to it. That protein, apart from one amino acid, is identical to protein called plasminogen which won’t mean anything to you but if you have a blood clot or a stroke or a heart attack before the new fancy techniques came in, you used to be given a clot buster.
A clot buster is a tissue plasminogen activator. It’s an enzyme that can converts plasminogen, and the plasminogen snaps the fibrin apart and breaks clots apart, slices them apart. That’s why if you’re having a heart attack or a stroke, you may be given TPA, artificial, breaks clots apart.
Now, the protein that’s touched the LPA and plasminogen are identical apart from one amino acid, but if you’ve got this protein in your blood clot, it stops tissue plasminogen from working. It stops blood clots from being broken apart.
Once you got a blood clot with a little of LPA in it, it’s basically not going to be broken apart very easily and it’s locked on. You got to ask yourself as why did the body decide to stick Lipoprotein(a) to LDL because LDL has its part in the blood coagulation system.
Everything is connected to everything else in this world and anyone who wants to give you a simplistic answer is going to be wrong because the more you look into it, the more you realize what we have here is just mind boggling and complex.
Christopher: Do you think you would’ve considered cholesterol, HDL, LDL, triglycerides at all had you sat down and attempted to understand this system from scratch? Imagine you were a detective and some pathologist called you in and said oh, this guy died of something. What do you think it is? You just start from scratch. Do you think that you ever would’ve been in a position where you’re explaining the role of these lipids?
Malcolm: Well, no because if Rokitansky had known about the endothelial progenitor cells, we would never have found a cholesterol hypothesis, in my opinion. We’d have gone down the right route. We’d be treating people correctly. We’d understand this disease. It would’ve been understood in 1960.
But we’ve gone down the wrong way and so what you have to say to yourself is of course these things have become -- I was looking at familial hypercholesterolemia which is where LDL is taken out of the bloodstream by at thing called an LDL receptor. That’s the most simple thing. I don’t know if you’ve seen the old trains with the post on it, we come whooshing through the station and then a thing would stick out and there will be a bag.
Christopher: Oh, yeah, I know what you mean.
Malcolm: Then the bag will be drawn into the train or something like that would happen. It didn’t need to stop. LDL is floating around your bloodstream and if the cell needs cholesterol, it will stick the thing out, grab hold of it and pull it into the cell. Cleary, if your body doesn’t produce so many of these receptors, and the LDL doesn’t get pulled out of your bloodstream so your LDL level goes up. That is familial hypercholesterolemia. Now, there’s about 600 different versions of the hypercholesterolemia.
But when you start looking at the LDL receptor itself, what you realize is this is a fairly ancient thing and it also has important roles as a blood clotting system. The LDL receptor itself also takes what we call Factor VIII out of the blood, removes excess Factor VIII which is an important -- it’s one of the most important blood clotting factors.
If you don’t have, and this is not true of all forms of FH, but it’s true most forms of FH. If that isn’t pulling Factor VIII out of the system and the LDL receptor also has all sorts of complicated -- gene locus is right next to LDL and many other blood clotting factors. In fact, these things are all interconnected.
What you can find is if you -- I’ll see if I can explain this. I sometimes struggle to explain it to myself. You can have brothers. One of him, because it depends if you got the genetic -- one of them can have FH and the other doesn’t have FH or they don’t have the right cholesterol. They can both have exactly the same rate on risk of dying of heart disease.
It’s because it’s the clotting factor that they share, not the LDL that they share. It’s LDL that is the clotting factor abnormality that they share that is the thing that causes them to die of the heart disease, not the LDL.
[1:05:39]
Once again, what people have said is all people with high FH, high levels of FH are more likely to die of heart disease when they’re younger, this is true but not everybody with FH is. It’s only the ones who’ve got the dual clotting factor, LDL abnormality that are at risk.
The interesting thing about FH is once you’ve reached the age of about 50 to 60, everyone studies at different ages so you can’t be absolutely clear. I’m not being deliberately disingenuous here. Some studies looked at people up to 50s and looked at 60 or 65 and above. Once you’ve reached the age of about 60, people with FH are less likely to die of heart disease because it’s the age when you’re most likely to get heart disease.
Christopher: Why is that?
Malcolm: Because LDL doesn’t cause heart disease obviously. But when they say increases your risk of dying of heart disease when you’re like 30 or 40, that’s true but the rates of heart disease in these populations is very, very small.
Say your risk of dying every year when you’re 30 is one in 50,000, so if four people died instead of one at that age, that would be considered a vast increase in the risk. That’s still a very, very small amount of people dying. But you get to the age of 65, one in a hundred are dying. If you can reduce the risk at that age, that’s far more significant.
Obviously, I don’t want anyone to die at this age when they’re younger but what they’ve done is they’ve taken very small populations and it said oh, look at the increased risk, it’s huge. The increased relative risk issue, absolute risk is minute.
When you get to the population age when they’re like 60 or 70, these people have 50% of the risk of heart disease and they relative to different populations with FH over hundreds of years had come back and looked at gravestones and tracked people genetically. What I found is that familial hypercholesterolemia, people with familial hypercholesterolemia live just as long as everybody else. There’s no reduction of life expectancy.
Everything that appears to be absolutely sorted is not sorted. This is confirmation bias in all those other things to the power of a hundred, but people are absolutely convinced by it and yet, we don’t say they’re all wrong and I’m right. I’m not the only person thinking this stuff but they are all wrong at the moment, we’ve got the wrong culprit, we’ve stitched it up, we’ve got it behind bars.
It’s guilty and it’s not and you can explain the role of LDL in FH and all these things in a completely different way. My fear is, my great fear is there’s so much money and everything behind all this is maybe never going -- the right answer is will never be widely believed.
Then we’re going to be continuously going wrong on this, what’s the market -- I mean statins have gone off patent so there’s no money to be made out of that particularly for the pharmaceutical industry but the new cholesterol lowering agents have come along. We had one called Repatha. It’s out there. It’s a monoclonal antibody you inject it into people. It lowers cholesterol more than statins.
In the trial was they claimed it’s a great success. The total number of cardiovascular deaths was greater in the Repatha group than the placebo group. Now, if that doesn’t give you pause for thought, nothing will. It’s a whole other group of agents that were called the imabs or whatever they call it. Anyway, there's about four drugs that were actually designed to raise your HDL cholesterol and they did so by about 140% in one case and they lowered the LDL cholesterol by more than statins in one case.
There was a drug that raised HDL by 130% lower than LDL by 40% and the total effect on the cardiovascular disease was zero and in one case, it went up with one of these imab drugs, and it still didn’t cause anyone to say -- so I suppose my great fear is there’s so much money, so much reputation behind it, so much guidelines and everything behind it that maybe it’ll never change. Maybe a few people listen to me and that’s fine but the great majority of people are just stuck with this and maybe we’re stuck with it forever.
Christopher: That’s really frightening, isn’t it? I’ve just finished listening to my neighbor’s book. His name is Dave Deamer [Phonetic]. He spent 50 years, so he’s in his 80s, spent 50 years doing basic research on the origins of life. Something really caught my attention that he said at the end of the book, and he teaches this to his students, is that the first thing that you should do when you discover a new hypothesis is oh, because you can celebrate finding it just for a couple of days, you can tell us many papers you like. You can enjoy that moment but then your job is disprove it, is to shoot it down.
The reason that you should do that is so that you could move on and find a better hypothesis. I think this thinking was inspired by Karl Popper. I think that was the original source that he cited.
[1:10:04]
Malcolm: He was a reputation man. He was a black swan and it’s difficult to be as absolute as Karl Popper. The black swan. All swans are white is your hypothesis. You find one black swan, your hypothesis is gone. But in the medical world, you can say smoking causes heart disease. Does that disprove your hypothesis? It’s much more difficult than that.
In fact, Bradford Hill came out with his [1:10:29] [Indiscernible] which is like things like strength of association and reproducibility, and it’s about nine canons which you have to look at and he says it don’t matter. If you got two, does it matter? Which one’s stronger? It much more vague than that if you know what I mean, in that you’re never going to be absolutely sure.
But I mean kick someone out of an airplane and drop 20,000 feet to the ground, they’re going to die. In medical stuff, you’re not going to get a level of certainty like that but it’s so much like weather forecasting. Can you tell me where the raindrop’s going to fall in 2:30 pm to so many variables? It’s difficult to understand all the variables and therefore, you can’t be -- I would say to people, I can’t tell you how to avoid heart disease completely. I can tell you how to change your odds.
I’m never going to get to 100%, 0%, I might get it to 90%. I’m hoping to get to 80%. I’m not going to get you to 100% because there’s obviously things out there that I don’t know of because sometimes I’ll just think bloody hell. I’ll read a paper and think, bloody hell. It’s like ten years ago, I never heard of the glycocalyx and I thought, what’s a glycocalyx?
Christopher: Yeah. Well, I never heard of it until you said it two years ago on the podcast.
Malcolm: I know. Bloody hell. Well, actually, there’s quite a lot of things, isn’t it? Oh, from that perspective, it’s going to be something. I mean, the sickle cell disease, I wasn't looking around for. Is there any situation where you can get atherosclerotic plaque in your lungs? That’s when I hit on sickle cell disease. Sickle cell disease increases the risk of heart disease by 50,000%. That’s something that I thought I should know about. The systemic lupus erythematosus, that increases the risk of dying of heart disease by 5000% if you’re a woman under the age of 40. Why don’t I know that? Well, the medical database out there is now the size of a planet. Well, it’s the size of the universe actually. There’s stuff in there.
I’m sure there’s stuff out there that just will change, I won’t know but never heard of, don’t know exists. Someone pointed me at this PBI [Phonetic] stuff and I thought, I didn’t know that. Where did that come from? Oh, there’s a whole enzyme system in your -- anybody says I can tell you for sure. I can’t. I’m actually speaking to a guy in the States. I'm thinking of working with him. He’s doing epigenetic screening work there. He’s doing all sorts of screening of your genes and then trying to say that you don’t need to worry about this but you need to worry about that, you should do this and you shouldn’t that.
Christopher: So he’s looking at environmental factors as well of the genes.
Malcolm: Well, the epigenetics is obviously the switch on or off of the genes. We might have a genetic susceptibility just [1:12:52] [Indiscernible] but actually, we’re never going to do anything that triggers it because -- and certain things also need to happen. I suppose this is an attempt to greater certainty.
Like I said to you, why do some people who smoke not get lung cancer? Because they do have a gene, though I can’t remember which one it is, that means that they convert something to something else which reduces the risk by 95%. It’s about like altitudes. Some people could go up to 20,000 feet, they’re okay. Some people go up to 10,000 feet and they’re struggling because they’ve got a different enzymatic system.
I think we’re going to have to move to -- we’ve got this genetic information. We’re going to have to try and use that. I’m interested in what he’s doing. He’s doing it very high end at the moment, and say to people, because the whole dietary thing, should we eat carb, should we eat fat? The information seems contradictory.
But I’m sure that what we’re going to find is some of us can deal with carbs, some of us can’t, some people deal with fat and proteins differently. Until we know that, I can’t say you should do this and everybody should do this because I know that everybody shouldn’t do this. I think Michael Mosley, he’s a stiff on getting fit and he found that -- actually, he doesn’t become -- he exercises, it doesn’t actually make him any fit which is bad for him.
Christopher: I spoke to him recently actually.
Malcolm: Did you? He seems to be a nice guy.
Christopher: He’s at the Real Food Rocks Festival.
Malcolm: All right. I think we need to -- I can’t say the absolute way to avoid everything is x for everybody because that might be doing some people some harm actually, rather than good.
I think the next stage of medicine is going to be figuring out you rather than everybody, what’s good for you rather than everybody. I think that that will be where we’re at I think in the next world. That’s why I’m moving into this world a bit with -- just the company in the States calls it [1:14:36] [Indiscernible]. He was a surgeon. He’s moved into this optimizing human health. It's a bit American for some of it for me, but I do think that this is right and I think that therefore, it’s a bit like the vitamin C thing or the LPA thing, I was talking about.
Some people have high levels of LPA. They should be doing different things than people who got low levels of LPA. Therefore, I can say I know these things generally are better things to do but if I was going to say someone, you for you, the way you’re going to avoid heart disease or any type of disease or as many diseases as possible is this is your lifestyle thing. I think that we will be moving more into this.
[1:15:11]
Christopher: The thing that worries me about that is that the pillars of health are the same for everyone and the temptation when you talk to people about whole genome sequencing and maybe you have a slightly different carbohydrate tolerance. You get into what people might call marginal gains and what Simon likes to joke and call marginal brains.
Malcolm: Marginal brains.
Christopher: Kind of the relentless pursuit of the unimportant and then ignoring the things that really matter.
Malcolm: Well, I mean, clearly, the very important is do some exercise, remain calm, reduce your stress, good relationships, blah, blah, blah. I mean there are pillars that are going to give you 80% to 90% but what you don’t want to be doing is saying to people do this or do that, and it’s the wrong thing for them.
Yes, I agree that you can salami slices do ridiculousness if you’re not careful, but I think equally you can see that some people are going to react differently to things in other people genetically. So just want to make sure we’re not giving -- what I don’t want to do is say to people, you must do this and find it’s just the worst thing for them because they’re different.
It’s not going to be the answer to everything but I think it can help to fine-tune in a bit. On the bigger things. I mean as you rightly say, you can spend your whole life sequencing everything and then spend your entire life with a mass spectrometer beside you making sure you got the correct amount of the saturated fat and whatever fat. There’s more to do in life than that, that’s for sure.
Christopher: What do you say to people that accuse you of statins nihilism? Is it an internet cult with deadly consequences?
Malcolm: Well, obviously. I’m 100% convinced by their argument. But no, it’s the shutting people up thing, isn’t it? If you haven’t got any other argument, just say you’re killing thousands of people or you don’t understand science. It’s just ridiculousness. I mean not one of these people who have made these arguments could explain what really causes heart disease.
For example, none of them have had the original thought in their minds ever. I mean they’re very good at understanding some of the science, but they’ve never had -- so the cholesterol hypothesis was your idea, was it? No. so you’re just going on what other people have said. Have you ever looked at it? Have you ever actually really sat down and looked at it?
To be frank, these people are paid vast, in the majority, paid vast some of the money by companies in whom is their financial interest to crush debate. It’s the opposite of science. Instead of saying, oh, you’ve got some interesting ideas, which they should say, even if it was wrong, they should say, well, let’s have a discussion about this. I was invited to a meeting a couple of years, probably more than two years back now, talking about statins and blah, blah, blah. One of the great statin promoters, Professor Sir Rory Collins from Oxford was invited. As soon as he found I was there, he just wouldn’t debate.
Christopher: Oh, really?
Malcolm: Yeah. I mean they won’t debate because I think they deep down know that they’ll just be kicked and defeated because I was at a debate on is the English breakfast good for you with a guy who’s a professor in nutrition. He’s written many papers and blah, blah, blah. The British Chemical Society having this [1:18:15] [Indiscernible]. At the beginning, most of them were convinced that fat was bad for you. But at the end of it, not one of them thought it was bad for you just because stuff that I presented them. What can you say?
Well, I think, my general view and I say to people from [1:18:30] [Indiscernible] when the flack is at this greatest, you know you’re always a target because they know they’re under attack and they know they’re not going to sustain their arguments, so they just try to silence you. That’s what they’re trying to do. Another philosophy I have is the angrier someone gets, the more likely they’re wrong.
I’m encouraged by these acts. It means I’m getting at them and what was it that Gandhi said? First they ignore you, then they laugh at you, then they attack you, then you win. I said, there’s four stages. I’m at stage three. Next stage is then you win. But it is worrying because of the amount of money and power and prestige and authority on the other side. Even if you win, no one’s going to even notice because they will just close it off.
Christopher: You should give people a sense of how much money is involved. You wrote about that in a book. How much is the statin business worth? How much did Pfizer earn by their -- ?
Malcolm: Well, what’s it worth? Estimates, they made a trillion dollars in profit from statins. There’s still profit to be made but it’s not in that level. Pfizer are making I think $39 billion a year from their one statin. I mean these are some of the money that -- that would be a vast company all by itself. That will be the world’s biggest company where actually just one statin, one company.
The sums of money are mind-boggling. Some of the money just in the dietary stuff, the low-fat stuff. I was looking at it recently and so they reckon the market for low-fat stuff is $1 trillion a year.
Christopher: That’s like margarine. So sad.
[1:20:06]
Malcolm: Interesting, in fact, I was speaking some other weekend, because we’re on this boat and so we got flour. I said it’s interesting. I said you can’t get margarine anymore. They went, what? I said well, look at this flour. It says buttery, and it says low-fat something. It doesn’t say margarine. You can’t buy margarine anymore. It’s gone.
It’s like the Invasion of the Body Snatchers. No one’s noticed. They still talk about margarine. So go on, find margarine in the supermarket. You can’t. It’s not there. Why not? Because margarine is created to be [1:20:39] [Indiscernible] healthy or not.
When they first created margarine, it was colored pink because it was unfit for human consumption, pink margarine. How they make it or how they made it, I’m not sure how they make it now, I can’t find this at all, it’s very complicated, was that in order to make an oil which is a liquid fat into a solid fat you can spread, you have to change the structure of it chemically and you have to turn it into a trans-fatty acid which you may or may not have heard of.
Trans just describes bond, shape, which instead of being wiggly and V-shaped and wobbly and round, this actually becomes a solid kind of overlap bond. Anyway, it doesn’t bend. Because it doesn’t bend, it doesn’t wobble, and because it doesn’t wobble, it’s not liquid, it's solid.
You turn chemically using 5,000 degree centigrade, you can turn healthy oils into trans-fatty acids which then you can spread on your bread or use for cooking instead of lard or whatever and it has been discovered that trans-fatty acids are actually damaging and unhealthful and [1:21:45] [Indiscernible] bans their use in several countries. They’re banned.
Ironically, by trying to get rid of saturated fats and turn them into unused polyunsaturated fats, because it’s still called an unsaturated fat even though the bond is weird and not to be found in nature. All of nature is used to things called cis bonds. That’s how our systems work. That’s what we’re designed to work with. Trans bonds are very rare in nature so our systems are enzymes are not designed to cope with them.
If you start filling your body up with trans fats, the structure of our cell membrane starts to become weird, the transmission of neurotransmitters become weird the way that everything operates and stops --
Christopher: You’re made of the fats that you eat.
Malcolm: Well, of course. The fats that we eat, of course the greatest irony is if you eat carbohydrates and your body has to convert into fats, the fats makes them into saturated fats and the common fat is palmitic acid which is the one that we’re all told is unhealthy.
Our body naturally produces palmitic acid which uses this bond's shape. The trans-fatty acid, you don’t want them in your body, nor do you want sterols in your body, healthy sterols or your cholesterol level.
Cholesterol is a sterol which is a different type of sterol. Plants have sterols and they use them in their cell walls which are solid because cells have cell walls and animals have cell membranes and our membranes are all wiggly and wobbly and do lots more things in cell walls.
Essentially, cholesterol is a thing that actually makes cell membranes’ structure work, function, controls them, all that sort of stuff. If you put sterols into our cell membranes and try to turn them into cell walls, well, surprise, surprise.
Christopher: It doesn’t work.
Malcolm: It doesn’t work. We’re not designed to be plants. We’re designed to be animals so we need animal-y things. The animal sterol is cholesterol and plant sterols are [1:23:42] [Indiscernible] or horrible things that you can’t even pronounce. We don’t want those in our body.
Of course, it will lower our blood cholesterol level because these fat things are replacement, just the ridiculousness of what we’re trying to do. We’re designed as an animal to eat other animals. We’re designed to have saturated fats in our body and we’re trying to replace some of the polyunsaturated fats, sterols, trans-fatty acids.
It’s like this institutionalized stupidity. What should you eat? You should eat this stuff that is out there that we’ve been eating for the last god knows how long. That’s what we’re designed to do. Start making artificial shit and not surprisingly, it’s made to have adverse effects upon us and that’s what we’re doing. It’s just bonkers. Well, that doesn’t mean plants themselves are unhealthy but specifically sterols --
Christopher: Right, they’re tinkering.
Malcolm: Tinkering with what diet veganism -- well, I’ve been attacked by vegans. I have nothing against veganism. You need to take supplements or you’re going to die if you’re vegan but people who eat vegan diets seem to be perfectly healthy. People who eat vegetarian diets seem perfectly healthy. People who eat high fat diets are perfectly healthy.
I don’t see diet as a particularly important area actually. Although I think processed foods, high carbohydrate foods just becomes food that people eat too much of then because I think if someone told you to eat half a pound of butter, you could get about a third of the way through.
Christopher: And the same as sugar, right? You tell them to eat the contents of your sugar bowl, I wouldn’t get that far.
[1:25:10]
Malcolm: I know. If someone says here’s 16 packets of crisps, you can sit there all --
Christopher: Yeah, or even if you just combine the fat and the sugar and whip it in the bowl, add an egg.
Malcolm: I know. We’ve done the dietary thing. We’ve got [1:25:24] [Indiscernible] systems aren’t telling us you’re having too much and I’m worried that we’re having too much and that’s causing part of the problems and that in part has been because people have said stop eating fat and eat carbohydrates.
Well, they’ve taken the fat out and replaced it with sugars. We’ve turned our diet into a battle ground and the enemy are winning the battle, if you like. This area is particularly fraud, isn’t it? Everyone is just battles away.
Christopher: Yeah. I think you’re right and you touched on something there which is it’s kind of a distraction. It’s the thing that everybody wants to talk about. I mean Michael Mosley gave a talk at Real Food Rocks and it was pretty good but he didn’t say anything about sleep. It was a talk about the pillars of health. And yet, sleep was missing.
He wants to talk about the Mediterranean diet and fasting and high intensity interval training and all this stuff. He didn’t say anything about sleep. Wait, hang on a minute, Michael, we’re going to take a top-down approach here. Shouldn’t we say something about sleep? People want to talk about the Mediterranean diet.
Malcolm: Well, [1:26:22] [Indiscernible] achieved anything, it was that it changed the whole debate into health is about food and nothing else is important and heart disease is about food and then people argue about which type of food? It’s sort of saying, well, forget about food. As you say, sleep -- Phil Hammond, I was speaking to him at a conference. He’s big into sleep. You may not know who Philip Hartman is.
Christopher: No.
Malcolm: He’s a doctor. He writes for Private Eye. He also does some comedy stuff. He’s a nice guy.
Christopher: Oh, this sounds like someone I’d enjoy.
Malcolm: Well, he has this thing called what he calls CLANGERS. I’ve got one of his cards. It makes sense about how our health and sleep is big for him. He’s very keen on the importance of sleep and yes, I agree. There’s a whole lot more important things than what you eat and how you eat but we seem to have just become that’s it.
If I write a blog on -- I did write a blog and it said, I can’t find any particular diet is particularly good or bad for you to any degree that’s worth bothering about, you know, outrage ensued. Well, okay. Then show me the evidence. Show me the evidence that one particular form of diet to heart disease is better than any of the diets or worse than any other diet.
Yes, trans-fatty acids, artificial fats. Outside of that, I can’t see it. Believe me. I have looked. I can’t see any patterns emerging. The Loma Californian palmitic acid Seventh-Day Adventists group, yeah, they live a long time and they’re vegetarians. In fact, they were the creator of -- Kellogg was a Seventh-Day Adventist.
There’s a religious movement actually to not eat animal fats and things because it would raise lustful thoughts. It’s really weird stuff. They’re a very important and very powerful group actually, hugely influential that have been behind the guidelines that have been created around the world so don’t cross the Seventh-Day Adventists or they’ll have you and the vegans will have you as well because they got me removed from Wikipedia.
Christopher: Oh, is that who he did it?
Malcolm: Well, I’m told. The problem with the internet is don’t believe anything anyone tells you so I’ve reached the point of people saying, I know who it was. It was this guy here. It turns out that was rubbish. But I believe it was the vegans who get together and --
Christopher: Ha. That’s interesting. It wasn’t someone that was promoting statins.
Malcolm: No. Well, maybe it was. I mean they pretended it was somebody else. I mean I don’t know this is the --
Christopher: The problem is everyone’s anonymous. Sure, there’s a revision history on Wikipedia but you don’t know the identity of the person that made that edit.
Malcolm: Well, you don’t. You can’t find it out. I’m out there. I tell everyone who I am. I hide -- well, there’s a few things I don’t want people to know about it. I think it’s outrageous that I say this is me, I live here. Here’s my name, here’s my blog, here’s who I am, here’s the books I’ve written. People can attack you and you just have no idea who they are. That’s just ridiculous to me. I mean I think there should be a law passed.
If you were going to try and attack and insult people, then you must say who you are and you must be contactable because this anonymous attacking is just outrageous, I think. I don’t know who these people are. I do get [1:29:20] [Indiscernible] that’s a wonderful thing you’ve written and blahdy blah. My mother’s got this problem and she’s got a high cholesterol and she’s done this and what do you think we should do?
I don’t know who you are. I never give advice over the internet partly because some of them are clearly an attempt to entrap me.
Christopher: Oh, really?
Malcolm: Oh, yeah. I know that’s the case. I have some proof that I believe is absolutely incontrovertible that yeah, there are people who want me to give advice over the internet, and if I do, they will have me. I know that. There’s some ways of telling where it’s just ways that things are written as well that make it very clear that specific trigger things that I know if I made a comment on that that I would be -- I’d be reported to the GMC and my license to practice medicine would be removed.
[1:30:08]
Also, in the other side, there are people who are trying to attack you, they wouldn’t tell you who they are or people who are just trying to rile you and there are people who try to praise you to get you to say something you shouldn’t.
I try to be polite and I’m normally sort of polite-ish kind of guy, at least in public, and make no comments like that and give generalized advice. I just say generally, once you read my books, you’d probably know what I think about it or stuff.
There’s a guy who contacted me and at least it turned out it was true, but of course I didn’t know. He said I live in the states and my LDL level is 18 which is six or seven times normal. I’m a 70-year-old man and I’ve been investigated for the last 20 years and can’t really take statins and I have no detectable heart disease at all.
I thought that’s interesting. I’m not going to write about this guy because he might not exist and then there was a case history done and it was this guy who then told me and it was true. He’s a 72-year-old man, LDL level of 16 which makes him super high from hypocalcemia, no detectable heart disease, he’s under investigation. Well, why is this man protected against heart disease?
I wrote him and said, there’s a reason. Because LDL doesn’t cause heart disease. He’s not protected against anything. Of course, that comment which is completely and utterly dismissed out of hand. I said, well, that fits for all the facts, doesn’t it? Even the hypothesis, my hypothesis is LDL doesn’t cause heart disease.
He fits my hypothesis perfectly and he doesn’t fit yours but no, they’re just trying to find some genetic thing that they could find. Ah, look, he’s got a PYX 93 chromosome difference in LY-6 locus on his chromosome 73 or whatever. That’s the reason.
I mean you see this happening because there’s a population -- HDL is supposed to be protected against heart disease for reasons that we can’t understand. But anyway, they found a population in Italy with very, very managing low levels of HDL, and no heart disease in this population. This is a genetic group, somewhere near Milan.
They called their HDL ApoA-1 Milano. All right? And then synthesized it and then try to inject into people, because it was especially good at taking cholesterol out of plaques. When it first came out, lord, it was fantastic and the plaques disintegrated and reversed and the company was sold for a billion dollars to Pfizer, and then they did some further studied on it and found it doesn’t actually do anything at all, which kind of got swamped and no one’s heard of it anymore.
People come out with these things, and they have an explanation and they interpret it and then you never hear anything more of it but it kind of immunizes the reputation for a while. Oh, yeah. That’s been explained. They’ve got a special different form of HDL. Did you follow the story through? Were they actually then did a proper clinical trial on it? And nothing happened.
Oh, we didn’t know that. No, you wouldn’t because there was no noise about it whatsoever. So you find these things out for instance, the HPS study, Heart Protection Study in the UK. Lord, this is a wonderful trial, proving the benefits of statins and benefits on heart disease and everything, and overall mortality.
Some years later, because I tried to found out, well, what was the impact on women in the HPS study? Silence. And then the journal of [1:33:19] [Indiscernible] left toe nail removal, published the female mortality rates and they were unchanged. You won’t hear about this.
All we get is statins work equally well for men and women. The first study, 4S study came out, which was the one that really changed, Scandinavian Simvastatin something study. Again, the mortality rate, far fewer women, the mortality rate for women went up in the 4S study. Where do you see this? Where did you hear this?
And then the other big study that changed everything is called the WOSCOPS, West of Scotland cholesterol something, something, Pravastatin something study. I mean the acronym has been impossible to remember after a while. No women in that study at all.
So we have 4S where it went up. WOSCOPS, there was no change. HbS, there was no change, and statins work just as well for men and women. Well, that’s not what your studies say. And then you come across -- I can’t remember the exact figures. It’s been like 25 major placebo control statin trials done all by the pharmaceutical industry, all positive.
And then along comes a study done with the National Institute of Health called ALLHAT-LLT, lipid lowering -- anyway, it doesn’t matter, but it was a big study done and they did the study and which it was found that statins had absolutely no effect on cardiovascular disease whatsoever, that started in that study.
You’ve got 25 positive studies by the pharmaceutical study, one negative study by the non-pharmaceutical industry. Well, what conclusion can you draw from this, my friend? Well, I know what conclusion I draw from it. Because the other thing is the regulations guiding clinical trials have changed in 2005. Prior to 2005, if you did a study, you didn’t even need to tell anyone you were doing it. If it was negative, you could do this thing called don’t bother publishing.
Christopher: Right. I love that one.
Malcolm: Which has happened a lot. How many statin trials, big statin trials have not been published? I don’t know because they wouldn’t have been published. Now, we do know with the antidepressants because that came out as a big hoo-ha.
The antidepressant studies found that, and I can’t remember the exact figures but it’s something like 74 studies have been done, 36 studies were published as positive although something like 12 of them weren’t positive or published as positive. None of the negative studies -- one of the negative studies was published.
[1:35:31]
It’s like saying how many times does my coin come up heads or tails? And only counting it when it comes up heads. You got all 50 heads in a row. What about the tails? Tails? I didn’t see any tails. That’s what we’ve been doing with clinical studies.
Christopher: That’s SSRIs you’re talking about specifically.
Malcolm: No. The other ones, the SNRIs. They're not SSRIs.
Christopher: Okay. And then so why all of those papers have been published?
Malcolm: Well, they now have been made public and the overall effect is now zero but they’re still being widely, widely prescribed. It’s like it never happened. It’s just weird. Anyway, the regulations change. Well, they did this thing where they said you got to register in an old trials thing and you have to say what your trial’s going to be, what you’re going to study, what your end point’s going to be, what your statistical analyses are.
All right. Some people do it but that first happened in the US in academic institutions are not necessarily pharmaceutical companies and they did the studies that were produced before, and this was 1999 and this happened earlier. There’s 56% of the cardiovascular trials were positive before these regulations came out and after these regulations came out, 8% were positive.
If you look at the statin trials prior to 2005, apart from the ALLHAT-LLT, they were all positive. After 2005, nothing positive at all. So what does that mean? Well, one explanation would be we’re having to study more and more these groups of people so we’d expect less positive results.
The other one is well, as soon as you got nailed down and you had to actually publicly state what you were doing, all the positivity turned to nothing because we have the whole -- I mentioned in the book, the MCE study done was the Minnesota Coronary Experiment study which was a study whereby saturated fat was replaced polyunsaturated fats. It was done between ‘68 and ‘73. The idea was going to be 10,000 people. Really big study.
The idea was going to be replaced polyunsaturated, the cholesterol levels fall and the rate of heart disease would fall. What they found was they replaced saturated fat with polyunsaturated fat. Cholesterol level did fall. I’m not quite sure why that happened.
For each 10% fall in cholesterol level, there was a 20% increase in overall mortality and no change in cardiovascular disease. It was a complete failure. In fact, an absolute contradiction of the hypothesis, and this study was never published. It was held in the garage.
The data was in someone’s garage. I think someone was speaking to someone who said, “Oh, I think my father did that study.” What is it really? Do you know if the data’s still available? He said, “I think it’s in my garage.” This researcher went to the garage, pulled it out, read it, and published it, like 45 years later. It was a complete contradiction of everything that was being said. And of course, do you know who’s the lead investigator of that study was? It was Ancel Keys.
Christopher: No way.
Malcolm: He disproves his own hypothesis and buried the data.
Christopher: Why would he do that? It’s so weird.
Malcolm: Well, of course, why would he do that? Because his entire career -- his status and his power and his authority depended on being right. He did that because he’s both a cheat and a liar. I can say that because he’s now dead and you cannot libel the dead. I think I would’ve said it had he been alive as well, in fact, I would have. That was ridiculous.
We do know that negative data are hidden away. We know that outcomes are manipulated. We know all these things go on. I gave a talk about this about three weeks ago and I’ve seen another researcher came up and was very angry with me for being -- so you’re telling these young doctors that they can’t believe it. What is your purpose? What is your function?
I said well, I said my purpose and function is to highlight the fact that actually, the research database that we can’t have is I think irredeemably corrupted and cannot be relied on anymore and that we must change things. We must change this because if I read a paper and I can’t believe it, I’m doomed.
Christopher: Right, you got nothing.
Malcolm: I’ve got nothing. I read many papers and I know they’ve been manipulated. This is a terrible place to be. I’m very concerned about it. I said so you’re getting angry with the wrong person here. You should be angry with the fact that what I’m telling you is true. [1:39:40] [Indiscernible] 2005, most read paper in the last 15 years.
Why most published findings are false. It’s true. Well, if we’re in that situation, I mean Richard Horton, editor of The Lancet. He says, 50% of what is published is not true, 50%. Well, how do I know which is the 50%? How can anyone know?
[1:40:05]
If that’s the database upon which our guidelines are being written, our guidelines are crock and shit as well. This is a terrible situation. It’s beyond terrible. If the database of medical research cannot be relied upon to be at least, I don’t know, 98% accurate, 95% accurate. I mean there’s got to be errors. Of course, there are. There’s going to be things that people find things and they aren’t true. I don’t know what level but it’s systematically being corrupted. This is not a mistake.
Christopher: This is in addition to what you already said about heart disease being a process. A clinical trial is designed to see the effect of one particular variable, right? But there may be hundreds, thousands, who knows how many different variables --
Malcolm: Well, if you think you’ve got an important variable and you change it, you should see some benefit or some harm. There’s never been a clinical study on smoking and heart disease but I’m pretty convinced. There’s never been a clinical study on exercise and heart disease but I’m pretty convinced. He struggled to convince me otherwise.
Christopher: nbsp; What’s the solution with the clinical trials and publications going missing and if you have any ideas? I mean I know it’s a big question.
Malcolm: Well, there is a solution but it’s so gigantic. It’s rip it up and start again or the other problem is what they call reproducibility and we're stuck with that as well because reproducibility is okay, you’ve done a study that's shown x. Can anybody else find this?
Christopher: How the hell would you fund that though? It’s hard enough to get funding for the first go.
Malcolm: Well, not only could you not fund it. You wouldn’t be ethically allowed to do it because if I show that stay statins prevent heart disease in 50-year-old men with one leg or whatever or whatever group I decide to study, I now then say well, I’d like to prove that’s right or wrong. The ethics committee will say, well, this study proves it’s beneficial so you’re withholding a medication for people as beneficial so we won’t give you ethical approval to do it.
Once the study’s been done and dusted and proven positive, you can’t ever do it again, so reproducibility is not only going to be vastly expensive, it’s actually going to be illegal. We’re going to have to hope that all these studies were correct, because if they’re not, no one’s ever going to do them again. So then what? Where are we then? We have a database that I think is a crook that could never be challenged or reproduced.
We just got to hope the hell it’s true. I know it’s not true. I know that studies have been done that are manipulated. Everybody knows. I’m not saying something controversial here. Richard Horton has written 50% of the published data are not true.
I’m not standing at a weird limb here being some kind of [1:42:32] [Indiscernible]. Marcia Angell who’s the editor of the New England Journal of Medicine for 20 years have come to the conclusion, I can’t remember the exact words, reluctantly and slowly that most of what is published is not correct.
She was the editor of the number one medical journal in the world for 20 years. Richard Smith, he’s utterly scathing. He said, "I don’t even bother reading it anymore." He edited the BMJ for about 15 years.
The major editors, long-term editors of the major journals have lost faith in medical research which is just -- it’s like they’re saying, I don’t know what would be another example. It’s just beyond disastrous really, that I should be able to read a clinical study and say all right, the only purpose of the people writing this study was to try and establish as well as they could the truth of the matter. I can’t do that.
Christopher: Do you think this highlights the importance of ancestral health? I can’t help but think that when I’m sat here listening to you tell me this. We’ve been trying to establish what works and what doesn’t work.
It seems that that system is hopelessly broken but you look backwards in time and you look at the inputs that your genes were expecting, as you mentioned earlier, sunshine, unprocessed food, plentiful sleep, appropriate stress management, exercise, these types of things.
Like you say, I cannot necessarily produce a study that shows that that’s true but it must’ve been at some point in the past.
Malcolm: Well, you’re never going to produce a study that’s going to prove that’s true because no one’s going to fund it because there’s no money behind it.
Christopher: Right, you can’t make money out of it.
Malcolm: There are different ways of studying things. The problem is we become trapped in a paradigm which is the only evidence that matters is called a randomized controlled study which is bollocks, essentially. There was never a randomized controlled study in smoking and lung cancer. That never happened. They just said let’s look at people who smoke, doctors that smoke, doctor’s that don’t smoke and see what the difference is. Well, the difference was there was a 16 times increase in the rate of lung cancer in people who smoke.
Christopher: Which is what you would say is a proper increase in [1:44:26] [Indiscernible].
Malcolm: Well, you can’t say -- statin people say the observational studies have no value. In other words, you can’t do -- it’s only randomized controlled studies that can control things properly. This is nonsense. If an effect is large enough, you don’t need to do a study. This is the argument used by epidemiologists is I don’t need to study the impact of parachutes on injuries after jumping out of an airplane at 10,000 feet.
Christopher: That’s a great paper.
Malcolm: It's used for the wrong purposes very often anyway but that’s true. I know if I jump out of an airplane at 10,000 feet. I don’t have a parachute, I’m going to die. If I do, I’ll probably not.
I’m not going to do a study on that because it would be unethical to do so because benefits are so obviously great. Certain observational studies probably don’t need to -- I don’t need anyone to tell me to take an exercise and go outside and that stuff is good for me. You’d have to do the opposite and disprove it. So you’re right in that aspect.
[1:45:16]
But when it does come to an extent like if an effect is so small, you need 20,000 people in either arm to prove the statistical significance. It probably wasn’t worth it anyway.
Christopher: Right, we’re in the marginal brains territory again.
Malcolm: Yeah. When antibiotics came along, they didn’t do any randomized controlled studies. They just said, oh, somebody’s dying of infection. No, they’re not. You didn’t need to do a whole bunch of studies on it. The reason why we’re doing huge studies on things is because the effects is like that which is probably not worth it anyway.
People say well, that study was too small to prove anything to which my argument is that study was too big to be worth doing. Do you need that many people? Forget it. Who cares?
Benefits that are major are pretty bloody obvious. Benefits are minute. Well, that’s where they make their money. They’re just trying to prove damage or harm which is where I discussed with you the vaccine thing. There’s never been a randomized control study in a vaccine.
There’s never been a study in harm or potential harm or anything like that. The assumption is that they’re beneficial. If you’re going to do something new to people, if you’re going to do something that hasn’t happened before, the onus should be on you to prove it’s safe.
Christopher: I totally agree with that.
Malcolm: If you’re not going to do anything, that’s fine. If you’re going to say go for exercise, and eat natural food, and go in the sunshine, have good relationships, I don’t think you need to do a study on this.
Christopher: Especially if you’re doing it to everybody, right? Then the precautionary principle should be applied.
Malcolm: I will say it makes everybody sterile and no mankind dies out. We never thought that would happen. Okay. Fine. Well, you might’ve thought as a possibility if you’re seeing any signs of it, any warning signs. Medicine’s got itself in a funny place, a bad place in my opinion. I don’t know how we get out of it at the moment.
Christopher: Here’s a final important question for you. Does this mean people listening to this, they’re probably thinking screw that? I’m never going to do the doctor again. Do you think that should be the takeaway message? Do you think that mainstream medicine should be avoided completely?
Malcolm: Of course not. I mean you broke your leg.
Christopher: Right. It’s a stupid question but people do think like that.
Malcolm: Well, of course. If you got a serious infection, take an antibiotic. There is no doubt especially in certain things, trauma, disease, appendicitis and blah, blah, blah, anesthetics, operations, antibiotics, sterile techniques.
We are, and should be eternally grateful that the stuff is here for us. If you’re in real trouble, things are going shit wrong, you need to go to a hospital and get seen by doctors and patch you up. Where our medicine has gone wrong primarily is preventive medicine. Preventative medicine. I don’t know which one it is.
Christopher: You use this term in the book, bloody monkey medicine.
Malcolm: You say marginal gains. There’s a guy called Rose [Phonetic] who wrote basically that. Yes, the effect on any individual might be small, but over 20,000 million people, we might save 20,000 lives. Well, then again, you might not. I think by the preventive medicine idea which is driving an awful lot of Western medicine now, the basic concept it's better to stop people getting unwell in the first place, true. But that’s not the same as screening because screening is a different thing. Screening is picking up disease early, preventing or delaying. That’s a different thing. That’s about making people generally healthy but we’ve mixed up the two things and we’re saying that screening is prevention. It’s not. It’s detecting things early. It’s not the same thing.
I detect you’ve got early stage cancer. People say, well, that’s a no-brainer. Oh, I detected you got early stage cancer and we’ve operated on it, and we’ve got rid of it, and you’ve been cured. That is a good thing. Well, if it worked liked that, it would be a good thing but it doesn’t work like that. It works nothing like that.
It’s again, it’s a bit like the cholesterol idea. Superficially, it’s very simple and inarguable when you actually start looking at the downsize, you start seeing it in a different way. You think, okay, that doesn’t work as well.
There’s a thing called, sorry to open up the discussion when we’re closing it down a bit. Think about sensitivity and specificity. When you’re looking for cancer, you don’t ever want to miss it. The thing is it has to be 100% sensitive is what they’re going for. The problem with that is whenever you go for that level of --
Christopher: And to say yes every time. Yes, you got it.
Malcolm: Yeah, and we do every time, you say you got it. And then there’s this specificity. How many people are being told they got cancer when they haven’t because say the natural population was one in a thousand people are likely to have cancer if we screen them and we picked it up perfectly?
Well, that’s fine so we pick up one in a thousand. So we pick up -- probably picked up and just likely to have it, but then we’re also told 100 people they’ve got it when they don’t. Is that without harm? Well, they might get secondary operations and might be getting further this. They'd be getting anxiety.
Christopher: Well, you already said yeah, the psychological stress is a major contributing factor to cardiovascular disease. Maybe they don’t get cancer, but then they die of --
Malcolm: Yeah. That's actually where we come in bits because of that [1:50:04] [Indiscernible] screening which is like very early stage, probably doesn’t mean anything, but they now believe and absolutely certain they’ve got cervical cancer and they’re going to die and that’s not what that says at all. So you have to be very careful about this stuff.
[1:50:20]
And then secondary operations, you can do the -- possibly, when you take the cervix away and then a woman may not be able to actually become pregnant because the cervix is not strong enough and you’ll get lots of pregnancy early stages, so it doesn’t come -- these stuff doesn’t come without cost.
It comes with quite high cost. It’s very expensive anyway. We’re doing all these things and we’re just throwing them at the public and saying oh, yes. Cancer screening is a fantastic thing. Well, prostate cancer screening, every time one looks at it, actually, you know what? We can’t really see any benefits from this. We can see quite a lot of harms from it.
If you could have a screening technique that every time somebody had a disease, picked it up, and you never got it wrong, and you never said to people you had it when you didn’t, and the treatment was 100% effective which we don’t know these things, and, and, and, provide it, provide it, provide it. Of course, you can’t object to that.
What they do in the states now, they do whole body MRI scans on everybody, just the screening thing. On average, they find the cause as incidentaloma which is like something we’ve just found, we don’t know what it is but we found it. So you find a thing in the lung, and it looks a bit like it could be something or maybe it’s nothing.
You find on average, seven incidentalomas if you do a whole body scan on people. Then what do you do? Operate in each one of them? It would scare the shit out of them.
Christopher: Yeah. We’ve had a physical therapist on the podcast talk about this recently with MRI scans of the back, right? You go get an MRI scan. They find all these stuff and it’s oh, we found it you can just throw anybody in an MRI scanner by the time -- so maybe some sort of degenerative disk disease begins at 20 years old. So you throw anybody in an MRI scan and you’re going to find things that reflect an abnormality.
Malcolm: Well, I mean they did a study in Australia where they looked at a woman who died in accidents and other things, and then examine the breast tissue, very detailed, and found that 40% of women had what you could diagnose as breast cancer. And yet, about 4% of women get breast cancer.
What were these other things? Were they all going to kill him? No. Will they ever grow? Maybe. What are they going to receive? We don’t know what the natural progression of most of these things are going to be. And then we’re going to say that we found breast cancer. This thing, ductal carcinoma in situ, you can find it in [1:52:29] [Indiscernible] of women.
Was it ever going to turn into something nasty, it was going to kill them, when in a vast majority of cases, no. You can’t then say to the woman, “Oh, well, don't worry if we find cancer, but it’s probably all right.” You’re then forced to remove the breast or something. That’s a huge amount of harm that you’re going to cause to people which you probably didn’t need to.
So you’re finding things and then you’re stuffed and then you’re operating, and then operating can kill people, and they can get infection and then they can lose the other breast. I’ve had letters from a woman who said, well, I had this and then got an operation. It got infected. And then I got necrotizing fasciitis and then I had to run a skin graph put over and I nearly died.
These things happen and that would never have happened. Probably, who knows? And you say, oh, well, we can’t risk it. You’ve have to take some risk. Nothing’s going to be 100% risk free. But this idea that some of our medicine’s going to pick up absolutely everything that could be possibly wrong you and sort it out. Well, that’s not going to happen. I'm going to pick things up with you that aren’t even things.
Probably more than we -- so what I say is yeah, if you’re acutely ill, go to the doctor. For screening purposes, they did a survey of all cardiovascular screening programs that we carried out over the years to find out what the benefit has been from cardiovascular screening programs done throughout the world.
You know what the finding was? The total benefit in reducing cardiovascular disease from all these screening programs was zero, .0 -- in fact, they said one was the average risk. The confidence is were .99 to 1.01. That may not mean anything to you.
What that means is it was bang on zero with no possibilities that it was wrong. So these screening programs didn’t do anything at all. Now, we have [1:54:12] [Indiscernible] you must do more cardiovascular screening. Based on what? You have no evidence that they work. In fact, all the evidence says they don’t work.
Christopher: It’s definitely in the details here because it depends on the test that you’re talking about so the coronary artery calcium scan.
Malcolm: Well, maybe. We don’t know. You’re again making an assumption that we picked that up and we could do something about it.
Christopher: Yeah. There is that. I mean so it’s generally true, isn’t it, with problems like once you know you got a problem then the solution then materializes, right? So you know you got a problem.
Malcolm: I’d advise you to read [1:54:43] [Indiscernible] who I think is still alive. He must be about 100 by now, who is a cardiologist who works in the States for a long time. Brilliant man. Brilliant, brilliant man. My hero.
When he was working in the States earlier on, he was a [1:54:55] [Indiscernible] doctor, and when he had a heart attack, the advice was -- it wasn’t an advice. It was recommended to lie in bed and move after six weeks. If you needed to have a pee, you pee in a bottle, if you need to have a crap, you crap in a thing that slither under you. You can’t move muscle. Everything had to be done for you.
[1:55:08]
He thought, you see men lying there getting more and more worried. Well, we now know if you lie in bed for six weeks, your chances of getting a DVT and dying with pulmonary embolism are through the roof.
This must’ve killed millions and millions and millions of people. What did kill millions and millions and millions of people? Telling people to lie in bed and move after six weeks will have killed tens of millions of people. There can be no doubt about this. He said this is just ridiculous.
So he sat them up at the end of the bed, at least they were sat up and looking around and felt they’re in charge of their own density. Fellow doctors from other wards sent medical students around with coffins on their shoulders writing killer on the side -- no, I think it was murderer. He was correct.
He then tried to look at coronary artery bypass grafting because he wasn’t sure it was -- problems with the angiograms are causing people to have stroke and things. He tried to do a study on whether they worked or not. It was a big operation. It was making millions. Everyone was having coronary artery bypass.
They have this thing where they do an angiogram which shows up your arteries and die. Your major artery is with your left hand because it sends blood to you left ventricle which is the one that does the biggest pumping and if they add an obstruction of more than some 50% or whatever it was, they used to call that the widow maker, can you imagine?
Obviously, the moment someone said you’ve got a widow maker, you need a coronary artery bypass. Afterwards like, yup, I want one. He was saying, well, can’t we not just see if it worked by saying 50% of people don’t have it and see what happens.
Of course, you couldn’t get anyone to agree to not having [1:56:33] [Indiscernible] eventually manage to work out because you did an ECG various other tests that you could establish that they had one of these or not. Not entirely sure. I do remember going into some details. So then he manages to say we’ll do medical treatment for half of them and you had an operation for half of them.
His findings were that the coronary artery bypass graft provided no benefits overall. They couldn’t get published for four years or whatever. He just again, it seemed like it must be an obviously a beneficial thing to do. You’ve got a blocked artery. We must put extra veins around it and get the blood supply.
Well, it doesn’t work like that because the heart produces a single collateral circulation whereby if you block one artery, the other little arteries take over the blood. In fact, that’s more likely to save you because that fully blocks then these little extra arteries will keep you alive and you won’t die whereas if you bypass it, if you then have a heart attack, so it’s bad for you. The operation itself had a 4% mortality rate and doing the angiogram can cause strokes.
If you take it altogether, it’s like no. But I mean, again, there’s huge difficulties you have in getting published. Again, it was like murder and everything like this. You just think we’re up against this world of we don’t understand what we’re doing in the human body enough to do these things.
It’s like the hearts are pumped and these are pipes, and different pipes block other pipes. Do you really think that’s how the human physiology works? Do you have any idea how complicated all this shit is?
They used to give people steroids after a heart attack because you get inflammation in the area where there’s an infarct. So this [1:58:05] [Indiscernible] the inflammation. They’re wonderful. Inflammation equals healing. These areas weren’t healing. They were turning into big aneurisms and bursting. We’re killing people again. We don’t know what we’re doing well enough to interfere for everybody, for everything like this. We don’t know yet.
This ridiculousness that we’re doing that everyone must have statins, everyone must have this, everyone must have that, everyone must be vaccinated against everything known to man. I’ve seen studies showing people who got measles and rubella and whatever, the reduction in risk of having heart disease when they’re older reduced it by 40%.
We know that if we keep people in entirely sterile environments, it’s incredibly unhealthy. You try and grow animals in germ-free environments, they die very quickly. So our systems are designed to react against the surrounding environment.
If we try to make everything too sterile and too healthy, will this result in [1:59:02] [Indiscernible]? Do we know this for sure? Can you reassure me that if we get none of these childhood diseases that have been around for hundreds of years, that there will be no downside to this whatsoever?
Christopher: Right, or you get asthma and allergies instead.
Malcolm: Or you get asthma and allergies and god knows what. Do you know these things for sure? You don’t. You don’t. You’re just telling me I must believe that we do. It will just be beneficial.
Christopher: A solution will emerge and it will be wrong.
Malcolm: Anyway, I don’t wish to sound too nihilistic. I think more than Western medicine is great and it does fantastic things. I had appendicitis. If it weren’t for modern Western medicine, I’d be dead. My father had rheumatic fever and got their heart valve replaced and lived for another 15 years after that. Fantastic, brilliant, and astonishing things.
Christopher: I’m the same with my motor bike accident tearing the arteries out, I would’ve been dead within minutes.
Malcolm: Yes. And now, you’re alive. I would like to say to people, the overall effect of modern Western medicine has been gigantically positive but we’re moving out into areas where we’re trying to control things that we don’t understand. We’re trying to change everything for everybody.
Preventive medicine, we don’t understand enough about pathophysiologies, how diseases work, and how everything works interacted together just trying to pick off targets one after another and saying that we’re going to provide benefit because we don’t think it was there.
[2:00:27]
The hubris is just -- if anything I've seen from reading about medicine and the wrong ideas that are taking place and the damage that they’ve done is -- it’s so very easy to say after it’s all well, we didn’t know. You don’t know, you don’t know now but you’ve got to be much more willing to say, could we be doing harm? Is this beneficial? Can we be sure about this?
Because until we are, as I said to you earlier, a life expectancy in the US and UK is now falling so whatever it is medicine is doing, it’s not doing it very well. Are we over treating? Are we overmedicating? Is there too much medication going on? I think we are. We have to look at these things.
I just find that we have reached a point where decent as well as being squashed. I say to people I’m critical because I want it to be better. I’m not critical in the automotive industry because I don’t give a shit about the automotive industry. I’m critical in the medical profession and the whole ancillary around this because I want it to be the best it can be.
I want to make sure we’re doing no harm. I want to make sure we’re doing good. I want to make sure the evidence is there. I don’t want stupid ideas to be damaging people. I want the debate to be there. I don’t just want to be shut up and told oh, you’re a statin denier. We should just ignore everything you have to say because call me a statin denier, I mean the word is deliberately --
Christopher: Yes, loaded.
Malcolm: I’m critical of statins because I think that in many cases, doing more harm than good, and that we shouldn’t be looking to this as a way of -- what’s the future of everyone just [2:01:57] [Indiscernible] statins from the day they’re born. That’s where we’re going to end up. It’s just madness. We have to question, we have to question. I think that’s sort of all I’m trying to do. Maybe I’m wrong, then prove me wrong. Don’t just tell me to shut up and go away.
Christopher: Don’t just delete my Wikipedia page.
Malcolm: Don’t pretend I don’t exist. I’m very important. I’m not just a number. Don’t do these things. These are stupid. This is not an argument or discussion. This is like Hong Kong where they’re now sending in people with iron bars to beat up protestors. You won’t win in the argument. You’re just trying to make sure that no one ever protests ever again. In the end, when the final protest comes, it will be total annihilation of the Chinese state if you’re not careful. You have to listen to people’s concerns. Do not just beat them with iron bars, which is intellectually the same thing, calling someone [2:02:53] [Indiscernible]. Not good, not good.
Christopher: That’s a teary place to wrap up. Can we talk about some of the [2:03:01] [Indiscernible] -- actually, let’s tell people what we told them. I think that’s an important thing, right?
I think one of the key things that you talked about was that cardiovascular disease is not caused by a single thing or even a collection of things or rather we need to stop thinking like that and thinking about the process that leads to the disease. There’s lots of things that contribute to that process and the commonality is not what they are or what they do.
Malcolm: Absolutely. I think we have to look at it that different way around. I think medical thinking sort of started in the mid-19th century when they started to find these single causes for complicated diseases and that model has sort of become almost part of the background. I hate to use the word paradigm but I would use it in this case.
People don’t even think outside of their thinking. They don’t realize that that form of thinking has blocked from actually moving away from that. The search for the lost cause. We will find a cause. You know you won’t. You’re not going to get any satisfaction that way.
It’s almost like it's place that you’re aiming for, desperately trying to reach. It’s not even there. It’s around everything else so you have to look at it in a different manner and therefore you’re going to say I’m not going to find you of course because there is no a cause, there’s a process. There are things you could plug into that process. I think you just have to look at it in that different way. I’m sure cancer’s the same.
There will be some cancers where there’s a cause. There’s something [2:04:27] [Indiscernible] or whatever but we’re stuck with this inappropriate model and because of that, we’re hampered. It’s caused a complexity. All this stuff about HDL and LDL and VLDL ratios is because they find a contradiction and they just change the hypothesis and expand it and expand it in an attempt to keep it alive.
That’s where vast amounts of complexities come from ironically, by trying to keep it simple, they’ve complicated it to a degree of ridiculousness. So you just have to remove that model from your brain and say, okay, what’s actually going on here? It might be intellectually satisfying to say, I can’t tell you what causes heart disease.
I can tell you the process going on and I can tell you things that were going to influence that process and make it more or less likely to happen. In that case, it’s been more like weather forecasting. I can’t tell you it’s going to be a cloud at 5,000 feet of the exact size of this at 3:30 in the afternoon. I can say, it will be cloudy. I can tell you, the risk of rain is 15%. You might get away with it raining, you might not get away with it raining. It might rain a lot.
[2:05:27]
It doesn’t mean my forecast was wrong. It just means I can’t provide you with that level of complete accuracy. I can’t pat you on the head and say you cannot have heart disease now because you’re doing everything to prevent it so we have to look at it more in a different way of thinking. We’re looking at things that change odds and things that make things more likely or less likely.
We have to remove this if you do this, this will happen. We already know that’s not the case with infectious diseases. TB, some people get it, some people don’t. Any disease can be [2:05:58] [Indiscernible].
And a number of factors. How were you feeling on the time? Did you get exposed to it in the morning and the afternoon? Was it at nighttime? If you operate on people at nighttime, you’re more likely to die if you’re operated in the morning. Same operation, same person, different time of day.
These factors, just there’s so many of them. I think we have to be more humble about certainty. I can’t give you certainty. I can tell you this might happen if you do this because this is going to cause this to happen and that to happen.
Christopher: Just increase the likelihood of you getting the result that you want which is not just dying of cardiovascular disease but any cause, right?
Malcolm: Well, these things are linked if you look at the places where heart disease is higher, cancer is higher, all the degenerative diseases are higher. They’re not separate diseases in that degree.
There’s like what I call social health, physical health, psychological health, and you can’t -- physical health didn’t exist for that social health and that psychological health and all these few things have to be involved. If you look at areas of Britain where there’s high rates of heart disease, there’s also high rates of cancer, high rates of drug use, high rates of alcohol, you know.
Christopher: Right. Nothing happens in isolation.
Malcolm: These things are not happening in isolation. They are interconnected and so you’re right about just looking at the overall healthiness of things that you do. Guess what? If I said to you, point to places in Britain would’ve got a low life expectancy, a higher rate of cancer, a high rate of heart disease and diabetes and blah, blah, blah, and drug use and alcohol use. You would pick them up. That would be Central Liverpool, Central Manchester, Central --
Christopher: Right, it’s the poverty map.
Malcolm: Poverty map essentially. One of the things they did in the States which is fascinating was they looked at Twitter messages -- is it Twitter? I think it was Twitter, and in regions of America, countries in America, North East America. What they find is the closest correlation they can find was of the rate of heart disease was negative Twitter messages, really nasty Twitter messages, and rates of heart disease correlated [2:07:53] [Indiscernible] they’re like almost perfect. So much better than any of their CV calculators at American Heart Association.
That study’s been done. You can look at the nastiness of messages from a county is directly correlated to the rate of dying of heart disease, and it’s not absolutely perfect obviously but it works, and that’s sort of saying we should be looking at that and then say, well, that’s fascinating.
Christopher: Yeah, that’s funny.
Malcolm: That’s funny. It’s collected and corrected. If you want to be healthy, you want to live social relationships. I'll have to get you Phil Hammond's CLANGERS thing which is quite fun. We did the CLANGERS. Do you remember the CLANGERS?
Christopher: Yeah, I do. Just slightly before my time. But yeah, I do know what that is.
Malcolm: It just uses it and it’s be nice to people and be sociable and sleep and just stuff, you know, it’s all basic stuff. I think it’s probably pretty accurate. It’s not rocket science from that perspective. Of course, then people want -- the problem is people desire for an answer.
Christopher: I thought that about the book, actually. The book is a statin nation damaging millions in the brave new post-health world and I feel like maybe your sister made you write that book because I’ve been encouraging you here to wax-poetic perhaps is the right term.
Your sister’s just like, oh, come on, Malcolm. What do I need to do in order to not die of these problems? I think the book, am I right in thinking that you were trying to answer those questions?
Malcolm: Some of those questions, yeah. You’re too negative. We need to be positive. We need to give people a sense of what you can do. I mean absolutely. But those things, people have been banging on about these things for -- they’re not difficult but they’re -- obviously, there’s no money to be made in them and then there’s no drive behind them and there’s no -- what do you say to people? Just take a chill pill. Get a dog, go for a walk. Make a friend.
Christopher: Well, they’re not complex. I’d like to rephrase that. They are difficult. It’s just they’re not complicated.
Malcolm: Yeah. Well, I think we can forget about those. I mean there’s evidence that people who take statins believe they’re protected so they stop exercising.
Christopher: Oh, god.
Malcolm: That’s been proven. So actually, it stops people doing healthy things. Oh, don’t worry. I’ll just take a statin and I’ll stop. We need people to be positive. I think New Zealand’s brought in this trying to measuring things of the health country.
It’s not just, what’s your GDP? All those silly things that are -- countries got to be poverty struck are not going to be healthy at all but we need to move. I think we’re rich enough as a country to look at creating elderly people being lonely and they’re talking about building more old people’s villages, you think no, no, because the evidence is fantastic. You put nurseries next to old folks.
Christopher: Yeah, amazing.
[2:10:37]
Malcolm: The old people can go and speak to the little two or three-year-old multi-generational and they’re so much happier and the kids love it. We’re going to isolate all the elderly people in their old villages and there will be no one under 65.
Christopher: Yeah. That’s really sad.
Malcolm: You have to keep the generations together. We have to create towns where that happens or the most social structures. I mean the ‘60s where you built these horrible high-rise flats which is destroyed our soul. We have to create environment that makes people enjoy being there.
Look outside, a better greenery and stuff where we’re almost living automated lives, aren’t we? People communicating on electronic devices rather than looking someone in the eye. I’m sure I mean there’s benefits to it in ways but we’re moving away from stuff that is truly beneficial stuff.
I’m moving into something -- well, that’s been going on for a long time I suppose. You know, yes, being positive. It’s not difficult to do these stuff, make friends, have good relationships, speak to your kids, go and exercise, eat natural food stuff, don’t eat -- this has probably been negated for like --
Someone told me how many Pot Noodles are sold every day in Britain. It’s something beyond ridiculous like seven million or something. It’s millions. There was someone I knew, they worked there when they were a student and get tons of Pot Noodles. I think I’ve seen more. There’s something like 14 million Pot Noodles eaten a day in Britain. Natural food. Food that looks like food. Exercise that looks like exercise. I think these are not difficult issues to get right.
Christopher: Sunshine. Your favorite thing.
Malcolm: Oh, my sunshine, your sunshine. Sunshine, vitamin D, and you know the two populations in Britain who get the least malignant melanomas?
Christopher: The least, the people who get the most sunshine, the people that work outside like landscape gardeners or something like that.
Malcolm: Farmers and building work.
Christopher: Okay. I was close.
Malcolm: We’re all told fear the sun. It’s ridiculous isn’t it? People say, I feel much better when it’s sunny. Yeah, you do. That’s a clue. Things that make you feel better are good for you. Clearly, if you avoid the sun the whole winter and then go out the first sunny day and burn yourself to a crisp --
Christopher: Well, it is what people do. I work an office job all year round, indoors underneath florescent lighting and then I go on holiday for two weeks to Spain and burn myself on a crisp on the first day. That’s probably not a good idea either.
Malcolm: No. But it’s like anything. It’s like exercise of anything that you can see, you can overdo it. With exercise, you can overdo it, you can take yourself over the top but with sunshine, you can overdo it. It doesn’t mean all sunshine is bad for you. It’s this thinking again. It’s absolutist, isn’t it?
Christopher: Yeah, all or nothing thinking.
Malcolm: Yeah. All or nothing. A moderate amount of alcohol is not why they’re bad for you or good for you but if you drink 63 pints in one evening, it’s going to kill you. And then I hear this phrase, everything in moderation is like try botulism [2:13:30] [Indiscernible] and you won’t say that again.
Two grams would kill the entire population [2:13:35] [Indiscernible] distributed it accurately. There are healthy things, there are healthier things, and there are things that won’t do you too much bad but you might enjoy them. People say well, it’s terrible but if it makes you relax with a group of friends and have a good time in the evening -- remember, years ago, a friend of mine’s mother used to say well there’s happy drinking and unhappy drinking. Happy drinking is good and then unhappy drinking is bad.
Christopher: It’s not what you’re drinking. It’s how you’re drinking it.
Malcolm: It’s why you’re drinking.
Christopher: And why, yeah.
Malcolm: You’re drinking because you want to have a good time, or you’re drinking because you want to forget your life? I think these things, again, my attitude of enjoyment is good for you. Hedonism actually is what people say. Oh, it’s terrible. If you’re enjoying it, it can’t be good for you.
Stuff you enjoy, it’s good for you because enjoyment is good for you. Having fun is good for you. Taking pleasure in things is good for you. There’s no doubt about that. My father-in-law was a very quiet man, but he had a heart attack and then we’re still drinking red wine. It's good for you but you had to drink 67.5 mils or something. You sort of measure it out.
You could have 68, you could have 67. I didn’t really like it when you drink it because he was still -- it's good for him. I’m sure, in that case, it probably wasn’t good for them. But had he said, oh, I have a couple of glasses in, maybe another one if I feel like it. Well, I don’t feel like it, so now -- for him, it’s prescribed, and a lot of people are like this, 67.5 raises your heart rate to 126 for 15 minutes four times a day.
Christopher: Right, lost your autonomy.
Malcolm: Come on. Another thing I say to people is none of us get out of life alive so just part of it is to enjoy it, part of it is to have some fun. Don’t get too bloody serious all the time.
[2:15:11]
Have a laugh because -- I think that humor thing. These people criticize people for -- I mean, Boris Johnson like him or leave him, at least he can make you laugh. That’s a good thing. And Theresa May, I can't imagine she's [2:15:22] [Indiscernible] ever. It would be split in two and crash it to a thousand pieces.
Christopher: The face would crack.
Malcolm: The face would crack. What was the most dangerous thing or what was the most naughty thing you ever done? Running through a field of wheat or something. I said Christ, really? I’m not going to tell you the naughtiest thing I’ve ever done or top 100 naughtiest things I've ever done.
There’s more to life than just measuring 67.5 as well. I think we need to remember that is don’t get too serious about it all. Have some fun. And if occasionally you get too much to drink, well, that’s okay. Sometimes, you don’t take your 150 minutes exercise a week.
That’s an important thing as well I think for yourself. I look at people who -- there’s a place around here where I work. It’s called [2:16:14] [Indiscernible] that sucks the life from your soul if you walk around it. It’s concrete, it’s just closed up shops or charity shops or betting shops, and the people are just -- they just look like life left in them. I know what the rate there would be. You stick a pin in there, the rates of heart disease and cancer and things.
I think whether the fun has been sucked out of them or not having fun has sucked out the life out of them, I don’t really know but you just think of no, no, no. That’s usually important and I don’t know how you measure that.
But I will tell you there was a study done in Japan when you got people to listen to a boring lecture after eating and took their blood sugar levels and then you got people to listen to somebody telling jokes and having fun after the same meal and they found the blood sugar levels were 50% lower when they were laughing and having fun.
I started looking -- I looked at the French. Why do they got such a low rate of heart disease? My initial thought was do you know what? When they sit down and eat, they sit with the family, they take time, they relax, they’re enjoying themselves, have a glass of wine with the meal, it’s all a big social occasion, whereas in the west, it’s like ram it in and off you go.
I said, our system’s having fun laughing, enjoying ourselves, puts our system into yang or yin, whichever one you want to call it, and allows us to digest, to metabolize, to deal with our food better. If you’ve got a bunch of stress formers kicking around and you eat food, you’re putting insulin against --
Christopher: Oh, yeah. I think everybody knows what happens when you do that. It just doesn’t sit well.
Malcolm: Well, you can measure it and it doesn’t well, and it doesn’t do you any good. The idea that fun, enjoyment, relaxation is actually physically good for you. I’m sure that this is true.
Christopher: I think that’s a fantastic place to wrap up. I’m much happy about that than I was about the [2:17:58] [Indiscernible].
Malcolm: Yeah, in fact, the medical researchers, it’s just disintegrated. And we’re all doomed.
Christopher: Watch that link online. I don’t think I’m doing social media anymore. I'm going to link to it. You write regularly on your blog which is just fantastic. It sounds like there’s another book in the works so maybe I should link to your blog is the best for people to find you online.
Malcolm: My next one might be about vaccination. I haven’t decided yet.
Christopher: Oh, really?
Malcolm: That’s a real area of controversy but I’m just trying to open up the debate a bit because it’s becoming incredibly polarized and I want there to be somewhere where people can say yes, in general, vaccination seems to be a good thing of course.
But we must be willing to say that there could be some areas where it could be better and where are they? There’s no issue. Well, that’s a huge problem, isn’t it? I say I’m going to write about vaccination and people say you’re brave.
Christopher: That in itself, obviously, there’s a problem.
Malcolm: Yes, there’s a problem. It’s like standing up in Hong Kong and going, “I want democracy” and being hit with an iron bar. There’s a problem there that you can’t say anything. That can’t be us. We mustn’t in the Western Liberal democracies feel that there are areas we can’t discuss and that increasingly seems to be the case. That’s why I’m kind of debating it. I don’t want to get pigeonholed and people say, "Oh, he's just a -- "
Christopher: The vaccines guy, yeah, that’s a very --
Malcolm: But equally, I feel very strongly that debate is being silenced and it’s getting a bit scary so I probably will just because --
Christopher: I think it’s like a suntan, right? You don’t want to go straight into [2:19:31] [Indiscernible] cardiovascular disease first.
Malcolm: Something not controversial like global warming or the transgender movement or something like that where people get very irate very quickly.
Christopher: Well, thank you so much for your time, Malcolm. Is there anything else that people could do to help support your work? Because we really, really, enjoy it.
Malcolm: Well, send large sums of money to my bank account, details will pull up.
No, I just want people to question things and I want people to question things for themselves and I want people to enjoy thinking for themselves and try and avoid saying to people what they should think even though I know the answer to everything, obviously.
Christopher: Obviously.
Malcolm: I’m right about everything as I tell my children. They don’t believe me either. But just to questioning and be open minded and to say, well, I think you’re talking rubbish. If you think what I’m saying is completely rubbish, don’t just say it’s rubbish. Tell me why.
Christopher: Tell me why it’s rubbish.
[2:20:24]
Malcolm: Tell me what’s wrong with it then we can have a debate then that’s great and then that moves things forward. I think the greatest hope or the greatest achievement would be that people can move beyond the current thinking a bit or look at it externally or review it or examine themselves.
This is what I want, I know it, because I don’t want the silence. I want to say I’m right and if you will disprove me, you’re obviously wrong. That’ll be stupid as well. If anything, I just want a Socratic debate to be alive in this country and for people to do it themselves. I’m sure there’s people out there who’ve got better thoughts than I have and come up with better conclusions and hope that would be the case definitely.
Christopher: Well, Dr. Malcolm Kendrick, thank you very much. I very much appreciate you.
Malcolm: No problem.
[2:21:07] End of Audio
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