Why Cholesterol Levels Have No Effect on Cardiovascular Disease [transcript]

Written by Christopher Kelly

April 16, 2018


Christopher:    Dr. Kendrick, thank you so much for having me today.

Malcolm:    It's a pleasure. Nice to see you.

Christopher:    Thank you. I'm so happy to be here in Macclesfield interviewing you in person. I have to tell you a little bit about how I got here actually. It's kind of interesting. I was being interviewed for a podcast, and it was a podcast about cycling performance. I told my story about how I'd lost my health and then recovered it using a high-fat diet. The host of the podcast, he said to me, "Oh, but aren't you going to get cardiovascular disease? Aren't you going to have a heart attack?" And I said, "No, I don't think so because I don't think there's any connection between cardiovascular disease and saturated fat intake." And he said to me, "Okay, so if that's true, what does cause cardiovascular disease?" And I said, "Diabetes causes cardiovascular disease." When I said that, what I was thinking was I had a chart in my mind and along the X axis there were risk factors, and then on the Y axis there was a hazard ratio. So if you were to put all of the things -- high blood pressure, smoking, all of that stuff, where you're from -- then diabetes would look like, you really don't want to get diabetes if you want to avoid cardiovascular.

Malcolm:    Absolutely, yeah.

Christopher:    But I realized that it was a very unsatisfactory answer. There was this one nebulous thing that caused cardiovascular disease, and then I had just given you this other nebulous thing that caused cardiovascular disease. I found out about your work through Tommy, who's written about your work in a highlight's email series, and then Jeff Gerber, who I interviewed fairly recently also mentioned your amazing series on what causes cardiovascular disease. So I had to come here and interview you. I'm delighted to be here. Maybe my first question should be, how did you first become interested in cholesterol and its relationship with cardiovascular disease?

Malcolm:    I do get asked that question quite a lot.

Christopher:    I would imagine you do.

Malcolm:    Yeah, and [0:01:54] [Indiscernible] facetious I'm feeling at the time, but I did start I graduated in Scotland in medicine in the year 19 oatcakes, some time ago. At that time, Scotland was reported to have the highest rate of heart disease in the world. Whether it did or not is a moot point, but it was definitely very high. In fact, it was a big issue within Scotland and why do Scots -- men especially -- keep dying of heart disease at a young age. I started looking at it. I had no preconceived ideas particularly. I also had spent some time in France. I traveled there, going skiing, et cetera. I knew that the French had around about a fifth or sixth, maybe figures vary, but a lot less heart disease than Scotland. And I thought, well, what's different? I started looking at the risk factors, and what I found was that their consumption of animal fat, saturated fat was slightly higher than Scotland. They smoked more. In fact, if you took all the risk factors from France and put them into a risk calculator and the same for a Scotsman, they should be about the same. In fact, the Scots should be slightly better. I know everyone says that a Scot's diet is terrible, but when you look at it, you can't really pin that down.

    So I said, well, here we have two countries where the heart disease in France is about a fifth or a sixth as it is in Scotland with the same classical risk factors. There is something else going on. And I started looking at it. At that point, I'm thinking, I wonder what that something else is.

Christopher:    Okay. And so what did you learn? Where did you start your investigation?

Malcolm:    Well, I started scientifically incoherently by saying, well, I think the French eat their food slowly. I think food is very important to them. They eat with the family. They sit around and have a nice and relaxed meal. And perhaps the process of how they eat their food rather than what they eat might be important. Now, I still think that probably is partly the case because clearly if you eat in a rushed fashion and you gobble it down and then you rush around immediately afterwards, your body is not in the correct metabolic rate to digest your food.

Christopher:    Rest and relax.

Malcolm:    Rest and relax. Interesting that I was looking at some studies from Japan where they got people to eat a meal whilst being read a boring lecture and asked to eat the same meal whilst a comedian was telling jokes . And when the comedian was telling jokes, the blood sugar level was considerably lower.

Christopher:    That's amazing. It's what the word "restaurant" means. It's totally lost in America, by the way. They rush you through when they give you the bill without you asking for it and all of that. It's like the word rest and relax is lost in the word restaurant.

Malcolm:    Well, absolutely. I mean it's what I'd call -- well, also the Scots were [0:04:30] [Indiscernible] five o'clock classically has to get home from work, where is my dinner? Buy and eat out to the pub. It was food is fuel rather than food is an enjoyable and relaxing thing. I knew that French didn't do that. So I thought, well, are we looking at the wrong things? Should we be looking at, for instance, what's happening with stress hormones? Should we be looking at the sympathetic nervous system? Which got me into a whole world of looking at, if you like, stress. I don't like that word now, but I use it shorthanded. Does stress cause all sorts of metabolic problems that could be causing or associated with heart disease?


    I've been down that route a long time, and I've looked at all sorts of issues. So I did start thinking, well, if you're stressed, your insulin levels are high because your stress hormones counteract insulin. Your blood clotting factors are high because when you're under stress, you're ready for fight and flight. People become centrally obese because the energy storage changes its function, if you like, from being in a rest situation to I'm ready to rush around and attack people situation. In fact, I still strongly believe that chronic negative stressors are definitely something that can create a metabolic and physiological mayhem to your body, if you like. You can see this quite clearly when you look at the research.

    So that's sort of where my thinking had been going for a long time. I was sort of saying, well, we're not looking at stress and we're not looking at anxiety. I've looked at some countries and fascinating work from -- you may have seen the graph from Lithuania looking at heart disease since 1980 as part of a World Health Organization study, the MONICA study. And what you can see is from about 1980, the heart rate is quite high in Lithuania, but it's  dropping gently. And then you get to the year 1989 and suddenly you see Mount Everest appears, a huge peak of death in cardiovascular disease. So you say to yourself, what happened in 1989? Well, 1989 is Soviet Union collapsed. And you can see the same pattern in almost all of these European countries, although interestingly, Poland suffered this jump about ten years previously. So you'd say solidarity and all this social upheaval that went with that. And then you look at Russia.

    So I started looking at these things. I was actually at a meeting. I was in Saudi Arabia, if you can imagine, talking about heart disease. A chap I know well, very brilliant guy, he ran the American Society of Stress, Paul Roche, said, "It's very interesting but how is actually? What is the process?"

Christopher:    Right. What happens in those final seconds and minutes? That's the question I'm interested in.

Malcolm:    Yes. What is going on? Of course, the current idea is you've got a high cholesterol level. In its simplest term, you eat fat. The fat level in your body rises and sticks in your arterial walls and they narrow and thicken and then eventually have a clot and then you die. Of course, when you start looking at that, you think, well, this is actually just nonsense from start to finish. But you have to ask yourself is the question is what's actually happening? Why are you getting these thickenings or plaques, the atherosclerotic plaques in your arteries? What could possibly be causing that? Because there is fat in there or lipid or whatever word you want to use for it, but there's also some other things as well. So you start then looking down in every process. And as you know, I've now written a gigantic series on what causes heart disease, telling everyone there's no cause. There's a process, and you have to understand the process, which is a slightly different way of looking at it. I think the desire of people to say there's a cause, this is the cause has led to some of the huge complications because each time you try and find a cause, you end up with this, well, how do they all fit together? What's going on? Because you're right, diabetes increases the risk of heart disease by between 300% and 500%, something like that. So it's clearly we're looking at a cause here.

    What's it doing? What's happening there? So people will say, well, if you got high glucose level, well, what does it do? What is it doing?

Christopher:    I can't answer that question.

Malcolm:    What does it do? Well, then you have to start looking at the structure of the artery, what's in a plaque, and you end up reading papers that you wish you'd never started reading and going to down vast channels of stuff and try not to get lost in the massive information. And then you say to yourself, right, okay, the first thing that must be happening, that must happen is there must be some damage to the arterial wall. Now, the arterial wall is lined by a single layer of endothelial cells. Within the endothelial cells themselves, there's a thing called the glycocalyx, which most people have never heard of, which is like a forest of the little hairs that stick out. If you try and pick up a fish that you just caught and you hold it in your hands and try and squeeze it, what happens?

Christopher:    It pops right out.

Malcolm:    It pops right out.

Christopher:    Like a bar of soap.

Malcolm:    Bar of soap. The fish is glycocalyx that lines its cells, makes it slippery, makes it able to move through the sea presumably quicker. It also acts as a protective layer. Well, all your endothelial cells also have a a protective layer inside them as well, and that's quite an important layer. Most people have never heard of it, but it contains a whole range of different chemicals and what they call glycoproteins and all sorts of complicated things. It also contains nitric oxide which is a thing that we had talked about earlier. Nitric oxide is the chemical that relaxes arteries and makes them open up, signals the arteries as well to relax, and also in the system it creates more what they call endothelial progenitor cells which are the cells that float around in your bloodstream that are attracted to areas of damage and cover them up.


    So nitric oxide is a really important substance, first discovered, although inadvertently, by the workers of Alfred Nobel when they're making dynamite and they were stirring nitroglycerin. You have to stir it very slowly; otherwise, you blow up. And if you fall asleep, you blow up. So there's a lot of blowing up involved. You worked in a little individual sand dunes so that if you blew up, you didn’t blow the person next to you. Well, what they found was that the man who was stirring the nitroglycerin, if they had angina, it went away. They didn't know why, but they said, "Well, let's make nitroglycerin. We won't call it nitroglycerin because people don't want to take nitroglycerin." So we called it glycerol trinitrate. It's the same thing. Put it in a tablet, you put it under your tongue, it goes into your system, opens up your blood vessels, your angina goes away. And you think, oh, that's absolutely fantastic. But what is it? Well, only about I think 20 years ago they discovered that the actual substance triggers the manufacture of nitric oxide.

    So nitric oxide is an absolutely key molecule that keeps everything healthy. And I would say in the research I've done, any substance you can find that increases nitric oxide reduces the risk of heart disease. Viagra is a well-known example of a substance that increases nitric oxide. It was designed as an anti-angina drug. They gave it to army volunteers who didn't give the tablets back at the end of the trial.

Christopher:    Oh, really?

Malcolm:    Because they taste nice. It was then discovered that it caused the erections because they increase the nitric oxide in penis and sustain erections. So that was  of interest. I don't think they knew at the time or why it worked, but that's how it works. So the nitric oxide thing is interesting because if you give nitric oxide to men with diabetes who use Viagra for erectile dysfunction, it has been found to reduce the risk of heart disease, heart attacks by about 200% to 300%, and that's only occasionally taking Viagra. These are observational studies, but they're really quite powerful.

    When you start focusing down, you say, well, nitric oxide, okay, you've got this chemical, this very amazing little chemical. What else is it doing? Well, I became interested in looking at sunlight as a healthy thing. I believe that sunlight is very good for your health. But one thing that sunlight does do, when the sunlight hits your skin, not only does it produce vitamin D, which is heart protective, it also stimulates nitric oxide synthesis. It lowers your blood pressure, it improves heart health, and it appears to have significant benefits for cardiovascular disease. So you start focusing in and you start seeing, well, here's a mechanism. What else is going on? Well, you realize that nitric oxide, if endothelial cells stop producing so much of it or the production goes down, this is a sign of ill health of endothelial cells. So a healthy endothelial cell is one producing nitric oxide. And an unhealthy one, although you can't really measure that very easily because you can imagine you have to stick a probe into an artery and it's basically impossible.

    So you then start focusing on endothelial cell and you say, okay, the signs of health and damage. So what happens when you really damageendothelia cells? Does this increase the risk of heart disease? So you start looking at things that can damage endothelial cells. One of the things that can damage endothelial cells is a condition called vasculitis which you may not know is basically inflammation of your vascular system, which basically means damage on endothelial cells. So there are some conditions that do this. So you have, say, systemic lupus erythematosus, which is a widespread kind of immunological condition, usually treated with steroids and things like that, but it causes quite a significant vasculitis. And in young women, it increases the risk of heart disease by 3,000% to 5,000%.

Christopher:    Wow. So that's causal at that point when you see a risk factor like that?

Malcolm:    It is causal. So you look at other vasculitis. There are other things that we call vasculitis, many of which you probably never have heard of, but rheumatoid arthritis causes vasculitis. That's now listed as one of the risk factors of what they call the QRISK calculator in the UK as is SLE. You say, well, what else can damage endothelial cells? I looked at a very extreme example which is sickle cell disease and it has benefits to health. But sickle cell disease, if you get the homozygous type, it's from both mother and father, you get quite severe sickle cell disease and that increases the risk -- if you're under 25, that increases the risk of stroke by 50,000%. That's a proper increase in risk.

    There's probably a couple of explanations for this, but one of the things, I was looking at the case history of an eight-year-old boy with sickle cell disease. His three-year-old brother had already died of presumed heart attack. He had gangrene of his foot due to one of his arteries in his legs, his popliteal artery, being virtually blocked. So there was no blood supply to the foot, so it became infected. It became gangrenous and had to be removed. And they did a CT scan of this leg, and every single major artery in his body was highly calcified with atherosclerotic plaque. You say, well, they're very simple, although almost you just like to say oversimple things.


    Sickle cells are sharp and pointy and as they travel around the bloodstream, they're banging into endothelial cells and damaging them. What appears to be happening is that the endothelial cells are being stripped off in a high rate. The endothelial cells, once they've gone, that triggers a blood clot to form at that area because, obviously, you have to stop blood from escaping from the blood vessels. A blood clot forms on top of it to stop the bleeding and then stops growing. But, of course, if you get a clot in an artery, it can't just break off and travel down the artery which is going to jam further down. So what happens is things go to endothelial progenitor cells which are immature endothelial cells that are present in the bloodstream come all over, find the area of damage, stick to it, grow over it, and then form another endothelial layer. Therefore, what you then have is a blood clot within the arterial wall.

    Now, that helps to explain a problem that many people have had. Well,  how can blood clotting be a cause of plaque forming and growing when we find it underneath in the endothelium? We say, well, yes, you did find it underneath the endothelium. It's just that the endothelium wasn’t there when all this happened, and it's now regrown over the top. It's almost like a magic trick. Once you understand the answer is very simple, but if you don't know endothelial progenitor cells exist, the explanation doesn't exist, and so you can't go down this route.

    So people over many years even in 1852, a man called Rokitansky, he looked at plaques and said, you know what? These are like blood clots in different stages of repair. Another doctor, Virchow, who was more famous than him, said, "Well, don’t be stupid. Blood clots can't form inside an arterial wall." And Virchow went, "Well, you're right, but I think it is anyway." So the argument kind of went away. So other people in the Second World War after the Second World war, there were various people saying, "Well, we're looking at blood clots here. We're looking at blood clots." Some people say, "Well, don’t be stupid. These blood clots are inside the arterial wall. It can't be. There's no process by which you can get a blot clot inside the arterial wall." They say, "Well, no, you don’t. The blood clot forms then the arterial wall forms on top of it."

    So once you understand that that's a possibility, you start saying, well, okay, so we look at endothelial damage. We then look at blood clots forming We then look at repair. And what we're looking at is blood clots in various stages of repair. This is what they are. And other people come along and say, "Well, don’t be ridiculous because when we look at them, there's no certain things you find and blood clots aren't there." But if you are repairing, it won't be there. In fact, in most cases, it's probably completely got rid of. It's only when this thing happens repeatedly. So what we're looking at is not necessarily endothelial damage because I'm sure that's happening in all our blood vessels all the time, but we are just preparing them. Normally, they get prepared.

    Another reason why this might be what's happening is because you never get atherosclerotic plaques in veins ever, never ever, not even in sickle cell disease. And you say, well, why not? Well, you could say, obviously, the blood pressure in veins is about 30th of that in the arteries. The blood is moving more slowly. The biomechanical stress on veins is much less. The current idea is that, well, it's all due to cholesterol or LDL leaking through arterial walls. Well, that's fine but why doesn't it leaks through vein walls? Vein walls are exactly the same arterial walls. They're a bit thinner because they've got resist less pressure. And we know that atherosclerosis can occur in veins because if you take a vein out of the leg and use it for a coronary artery bypass graft, they very rapidly develop atherosclerosis. I mean within seven years is the average time from bypass graft to --

Christopher:    Let's say that. I've got one on my neck.

Malcolm:    Well, unless you do something to stop those things happening, unless you've done the right things. The average time is seven years. So we know that veins can develop atherosclerosis. Why don't they develop it normally? What's the explanation? Well, it seems to be staring you in the face. It's due to whatever word you want to use and people have criticized me for using biomechanical stress, but it's the sort of shorthand for damage to the endothelium that is occurring due to a number of different factors. So you can look at, say, pulmonary blood vessels, the vessels in the lungs, the blood pressure there is a lot lower. Normally, you will never find atherosclerosis in pulmonary vessels. You will find it in sickle cell disease. There's one or two other conditions where it occurs.

    So clearly, there's something about the blood pressure and stress that places on the blood vessel. That seems blatantly obvious. You can also do a thing called the arteriovenous fistula which is where you stick a vein into an artery, so you create a kind of area where you can use it for things like dialysis so you can get a needle into it much more easily. These quite rapidly develop atherosclerotic plaque, the vein part of it as well.

    So we can see all these things happening and then you say, okay, well, it seems reasonably clear. The endothelial damage is required for plaque to start. Therefore, we just have a completely different answer on our hands, if you like. What's the current answer? LDL leaks into arterial walls. Well, I've been looking at this and I can see no process through which that can occur.


Christopher:    Right. And then for context, what's the risk factor? You talked about some risk factors in the thousands there. So what does having an elevated level of LDL or total cholesterol or anything else I find on the lipid panel, what's my risk factor there?

Malcolm:    Well, you can read different things. One of my bibles on it is a paper from 1991. It's actually the conference where they decided to look at whether low cholesterol could cause cancer and things like this. They found that when your cholesterol level is low, the risk of cancer went up, but they decided that wasn't causal for reasons that escape me. But even when you looked at those figures and they had over a million people they looked at, this is a time before statins which is quite good because that means no one's cholesterol was being artificially changed, if you like, to any great degree.

    So you're looking at a kind of native population, untreated population. And in women, as the cholesterol levels went up, the rate of heart disease remained unchanged. In men, as it went up, it went up in the highest group which is the above six and a half, I think as memory serves, to 10% increase which is pretty vanishingly small. And whilst it did exist, it's a very small effect. I mean 10% versus 50,000% versus 3,000% versus 5,000%, with diabetes 500%, and yet we focused all of our activity in everything that we do on to this ridiculously minor if it exists because there is very strong evidence -- I mean I discuss this with people all the time -- that people who are under stress will have higher cholesterol levels because when you're under stress, your cholesterol level does go up. This is the old yellow fingers lung cancer thing, if people with yellow fingers are more likely to die of lung cancer. Yellow fingers don't cause lung cancer. It just means that you're also smoking. So it's the smoking that causes the yellow fingers and the lung cancer. Well, the stress can cause cholesterol to go up and you'll find it in men rather than women, and it then causes the heart disease.

    So what we're looking at is we're looking associations and claiming the positions. This is the whole of cardiovascular medicine is full of people finding something associated with heart disease and going, oh, it causes it. You go, no, a little premature, don't you think? I mean I was part of a paper that was published in the BMJ a couple of years back now where we looked at LDL, not cholesterol, total cholesterol, LDL only in the elderly population over 60, and what we found was that those with the highest LDL levels had the lowest overall mortality and lower cardiovascular disease mortality.

    The effect is vanishingly small, equally you possibly don’t know. No one has yet found -- I've never found a single paper from anywhere demonstrating that raised cholesterol is associated with stroke, for example, and yet we're all advised to take statins to reduce the risk of stroke. And then you say, well, it's not a risk factor of stroke. So how can lowering your cholesterol have any benefit on it? And yet you'll be told in no uncertain terms, if you don't take statins, you will die of a stroke if you don't take it, which, of course, is complete nonsense. But, of course, of interest to me, it can't be working by lowering LDL because it's not a risk factor.

Christopher:    Right. They may have misunderstood the mechanism.

Malcolm:    Well, I think they have because statins, at the moment, even in the mainstream are saying, oh, statins reduce the risk of heart disease. They've got this other effect on inflammation. They say that inflammation is -- well, I call healings and let's move away from slightly. But what statins do, which most people don't know but there's paper after paper demonstrating it, is they increase nitric oxide synthesis and they are anticoagulant and they lower the blood pressure. So when you look at the effects of statins which any and all effects could be explained by that effect on nitric oxide synthesis. There's no need to look for anything else. There have been plenty of other agents over the years, 15, 20 agents that lower cholesterol and had no effect on cardiovascular disease or overall mortality or anything and yet statins did. They lowered LDL and they had a benefit. All the other things, lower LDL had zero benefit.

    So I think that it depends on your -- there is a way of looking at things where you can look at things from one direction. At the moment, the direction is it's cholesterol, it's LDL, whichever term you want to use. It leaks through the arterial wall. It triggers the whole process. We need to look no further than this. I could say, well, look at SLE, systemic lupus erythematosus, 3,000% to 5,000% increase in the risk of heart disease. No increase in other risk factors. What's your explanation? Is this a different disease? It's not, it's the same disease. So the current ideas just don't actually work because you can find exception after exception. You can find different mechanisms.


    If you're going to come up with a hypothesis, it has to explain everything. The LDL hypothesis explains almost nothing. And if you look at it from a different perspective and say, well, let's look at endothelial damage. I was looking at lead poisoning and there was the suggestion that lead damages the endothelial. Therefore, it would cause heart disease because the endothelium would be more easily damaged, more easily break down, there would be more blood clots, blah, blah, blah. And then a paper came out last week showing that lead poisoning, according to their figures, has been responsible for as many deaths as smoking. People say one of the reasons why heart disease rates have been falling over the last 30, 40 years, well, they've taken lead out petrol. Now, that may not be the answer. It may not be but at least it's a possibility.

    Now, I came up with the idea that removing lead from petrol was one of the reasons why the heart disease rate has been dropping in most of Western countries a year ago. And now a paper has come out saying lead is much more damaging than we thought. So as an extent when something like that comes, I go, yipee! No, all these people died, obviously. But because I predicted something. My hypothesis had predicted this and then it happened. A predictive hypothesis is a good hypothesis.

Christopher:    Because you can test it.

Malcolm:    Well, you can test it. It's very difficult to test heart disease stuff because testing things in humans is tricky stuff. But you can look back and say, well, what happened? Why did this happen? Why has this happened? What's likely to happen? If there's a hundred things that can be responsible for damage in the endothelium, there's probably another 200 more I don't even know. So there's a lot of variables here. But you can look at the major ones. You can say, what's the major ones? Well, smoking damages the endothelium. High blood glucose levels damage the glycocalyx quite severely and just strip it away. And most people with diabetes have increased blood clotting factors, stress hormones like cortisol.

    You can give people stress hormones. You can give them corticosteroids, prednisolone which you may have heard.

Christopher:    Of course.

Malcolm:    It's used in a lot of inflammatory conditions like asthma, Crohn's disease, rheumatoid arthritis, SLE. Maybe that same part why they get high rates of heart disease because of the steroid. So steroids are all called steroids because they're corticosteroids and corticosteroids are steroids made in the cortical region of the adrenal gland, cortisol being the one the human body produces naturally. Now, if you give people cortisone, you can't give people cortisone. Don't think you can give a straight drug. But people who have Cushing's disease who produce too much cortisol have an increased risk of heart disease of 600% to 900%. And if you give people steroids, oral steroids, not inhaled steroids where the doses are much lowe, if you give people  oral steroids, it increases the risk of heart disease by 400% to 500%.

    Now, that might in part be also because corticosteroids increase blood clotting mechanisms. So when you start looking at the blood clotting, you say, well, if you form a blood clot, if it's a big nasty blood clot, it's likely to be more of a problem than if it's a small gentle blood clot. So I looked at the research on hemophilia where they have a blood clotting disorder. Before the clotting agents came along, the risk of dying of cardiovascular disease in that population was 20% surrounding population. There's also another condition called Von Willebrand disease that you won't of heard of, but it's another blood clotting disorder where you're more likely to bleed. It's a form of hemophilia. They have a 60% reduced risk of dying of heart disease.


    So when you look at blood clotting abnormalities themselves and then that moves us slightly back into the light lipoprotein area because interestingly, there's a friend of mine who you may have heard of, Dave Unwin, who's a big high fat, low carb man. He was asking me about HDL. And I told him, well, high density low protein, a.k.a. good cholesterol, is quite a potent anticoagulant agent. In fact, that's one of its major actions.

    So when you start looking at the liproteins like LDL as well, there's very strong associations between LDL and blood clotting factor abnormalities. Work done on familiai hypercholesterolemia was found that if you have -- I'll simplified this down to its bare bones -- if you have a high LDL and no blood clotting problems, your risk of heart disease is unchanged. If you have a high LDL and you have these blood clotting abnormalities associated, then your risk of heart disease is very high.

Christopher:    And how much higher is LDL in familial hypercholesterolemia?

Malcolm:    In heterozygous from one parent, it's around about double-ish. Well, it's the LDL that goes -- so your LDL is normally three. It would be up to about five or six. If you get as high as homozygous, your LDL can be up to 20, 30. This is where part of the strongest argument has always been was these children die much more rapidly of heart disease, and it's true they die of clogged up arteries, although their arteries look very little like the arteries of normal atherosclerosis is a different process going on here. But, of course, these children are gigantically pro coagulant. Their blood really clot. You can imagine just filling out with ten times the amount of lipid and the association with all the other clotting factors is, in fact, blood clots are formed on lipids, lipoproteins. So there's a  very close association here. You could say to an extent in some people with familial hypercholesterolemia, the risk of heart disease is higher. Yes, but it's only the ones where you can also see the blood clotting factor abnormalities.


Christopher:    It's necessary but not sufficient.

Malcolm:    What's necessary, necessary as in if and only if this is present, you will get something happening, the raised cholesterol is not necessary because you can get it and nothing happens.

Christopher:    The endothelial damage is.

Malcolm:    Endothelial damage I think is the only necessary -- I  wouldn't call it risk factor. It's not really a risk factor. I think if you're looking for causes, sometimes it's a bit like if you want to get rust on your car, you first of all have to chip the paint. Now, the paint can be chipped by someone could scrape a key on it. A chip could come up from the road. You could bang into another car. You can bang your shopping into it. Many, many things can do it, trying to say, well, a tree branch and a large hill stone, they seem completely unrelated things, but actually they're related when they hit your car. So it's this thing.

    So what are the things that can damage the endothelium? Well, sickle cell disease and SLE don't look very similar diseases, but what they're doing is the same thing. So you can look at, say, Kawasaki's disease, which you may or may not have heard of, is a disease that youngsters get more commonly in Japan than anywhere else that's why it's called Kawasaki's disease. They get severe vasculitis, and these children can die aged four or five of heart attacks. Now, what seems to be happening is they're getting a very severe endothelial damage but occurring only for three to four-week period, and during that period there's a lot of damage to the arteries is occurring. And I've seen pictures of children who got over the Kawasaki. They're getting angina. And there's a picture of a coronary artery in a sort of eight-year-old that looks like someone's showing the dye and it's huge dilated area the size of a tangerine or something. His artery just got a huge aneurism.

    So my interpretation of that is they got the vasculitis. It was very severe for three to four weeks. A lot of damage occurred within the artery and its cell. But then, obviously, it settled down. So what you're seeing afterwards is a kind of the aftermath of a very short but very violent endothelial damage war. When you see that, you think, I think I know what's going on here. And it's only recently been found that these children are more likely when they grow up to start running into other problems, but they're not quite the same problems as prolonged slow grade atherosclerotic plaque buildup. It's kind of like very short bang.

    So this vasculitis thing again we see here, so again Kawasaki's disease, SLE, there's a drug called Avastin which is designed to treat cancer. What it does is it interferes with new blood vessels being grown because cancers like to get blood supplies, so they actually trigger their own blood supply growth called angiogenesis, development of new blood cells. So this Avastin is the vascular endothelial growth factor inhibitor. Basically, it knocks your nitric oxide down. It stops new endothelial cells growing. In some studies, if you take this drug in a higher dose for two years, it increases your risk of dying of heart disease by 1,200%

    So we're looking at cause and effect here. I think earlier on before the interview, I was talking about to you about thalidomide and saying it's interesting, thalidomide caused this horrible limb shortening, and people are uncertain how on earth that happened. But as it turns out and it's not through the same process but similar process, when you get thalidomide, it stops angiogenesis which is why thalidomide is also used in cancer. And it's also used in leprosy and other diseases where there's increased blood vessel creation going on. If you give thalidomide, the blood vessels can't grow so the limbs can't grow so they're horribly foreshortened which some people disagree, but that is the main thinking as to how thalidomide did the damage. With animals, they've got animals pregnant. They've given them thalidomide and they get the same malformations as you get in humans. But if you give them Viagra, then they don't get the malformations. Viagra, as we said, increases nitric oxide. Since this is essential for new endothelial cells to grow, and therefore you are countering the affects of the thalidomide.

    So it looks like we have cause and effect here. So you do end up going a little around the world here. You say, well, I'm looking thalidomide, Viagra, sickle cell disease, rheumatoid arthritis, systemic lupus erythematosus, Avastin. How are these things connected? If you can't connect these things and they all cause heart disease or prevent disease, then you don't know what you're talking about, because you have to be able to connect these. There's a process going on? What's the process? How do these things fit in?


    In the UK, we have the QRISK3 calculator for heart disease which gives you 20 factors that you can put into the calculator and then it will say your risk of having a cardiovascular event in the next ten years. There's some suspiciously accurate figure like 7.2%. I've used it myself and I was at 9.7%. I then changed my sex to female. It went down to 4.6%. And I go, well, why? I've got the same risk factors. I'm now just a woman instead of a man. You've got to explain that. Now, this is a much more complicated explanation. I'm not going to go in it. But the risk factor calculator also has SLE and rheumatoid arthritis in it. It doesn't explain them. It also has using high-dose steroids. It also has severe mental illness. It also has use of atypical antipsychotics which are all, if you like, stress hormone related because people who have severe mental illness have enormously switched on sympathetic nervous system. And if high levels of cortisone, adrenaline and everything going on in their body and these people, their life expectancies are horribly reduced.

    Severe mental illness is probably the single most life expectancy reducing thing you can get. And something may be of interest to you, if you get severe depression, you can develop Type 2 diabetes because severe depression is also associated with very high cortisol levels and insulin resistance. When the depression goes, those things go away. So even if you start looking at mental illness, you can see the connections coming in here.

    So I think what's happened is the world's become focused on one cause, cholesterol, LDL. Everything else is a kind of add-on, but this is the center. This is what I sometimes call the geocentric view of the solar system. The Earth is at the center and everything rotates around it. You can criticize anything, but you must have cholesterol at the center of this universe. It must be there. You can't get rid of it, and you must explain everything in relation to that factor being it at the middle. Well, if you take it out and say, well, it might have some small part to play somewhere, but it really is not the central thing that's going on, things start to fit. They start fitting together or then it's like the jigsaw puzzle theory where you've got a piece of a jigsaw puzzle and you've decided it sits in the middle and you've got it upside, but you've got it there and you're not going to move it, and every other bit doesn't really fit. You can sort of hammer it in and you can pretend it fits, but it doesn't fit. So you just take that bit out and then get all these pieces and say, well, how do they fit? How does all this fit together?

    I can tell you that although I'm making it I hope simple even if everybody will object to every part of it and tell me I'm talking rubbish, but you can follow these things around and you can look at this and you can say, well, what's that doing there, and what's that doing there, and why is this here? I think we have to move away from this causal model of here's a cause, here's the disease to a what's the process going on? What's actually happening? Can you explain that? And then you can say, so how does this fit? How does that fit? How does this fit? So you can find other things.

    I was looking at a map result which you probably have may not heard of. It's what they call a PPI inhibitor. It's for reducing acid secretion in your stomach and stopping you getting ulcers.  You might have heard of omeprazole and lansoprazole, anything in razole is a PPI inhibitor. I was looking at some research to show that actually it interferes with nitric oxide synthesis and endothelium through a pathway, complicated biochemical pathway but it's there. And I said, well, if it interferes with nitric oxide synthesis, it will increase the risk of heart disease. And then lo and behold, it does increase the risk of heart disease. It doubles it, maybe triples it which is rather worrying since every patient I see who's over the age of 65 is on a long-term PPI.

    But then you start saying, how are you going to explain that through the cholesterol hypothesis? It didn't do anything. Doesn't have anything do with cholesterol or lipids or blood pressure or it doesn't make you start smoking, it doesn't give you diabetes. Yet here we have why it does this thing? Why do statins increase? Nitric oxide synthesis is just an unrelated effect. It's just something that happened to do but it does. And you say, well, it does that and it reduces the risk of heart disease.

    Viagra increases nitric oxide synthesis, so it should reduce the risk of heart disease. Well, look, it does. Explain that some other way. Well, you can't. Well, you can't explain it. It's a current idea. It just doesn't fit. So you rather just say, well, it's not important or it's a paradox or whatever the way they have your immunization, you know, this is what Karl Popper called immunizing contradictory information which is say, well, it's not important. We don't understand that but we understand why that doesn't work. You see this happening all the time and one of your questions you asked me earlier was why don't people see this? Well, because history is full of people not seeing things.

Christopher:    Right. And what about inflammation? Does an inflammation cause heart disease?


Malcolm:    A lot of people say this. I've stopped banging my head off the wall on this one, and I just now smile and we'll have a cup of tea instead because I call inflammation healing because that's what it is. Generally, it's the body trying to heal itself. If you see a lot of inflammation going on, it means there's a lot of damage going on. If you go to the thing that's doing the damage, the inflammation would disappear. There is no such thing as spontaneous inflammation as if somehow a finger is pointed at you and you will become inflamed.

    Yes, in some cases like systemic lupus erythematosus, which is an inflammatory condition, but there is a cause. What is the cause? Well, I don't know what the cause is because no one knows what the cause is. We know that we can dampen it down with immunosuppressants and steroids. So we know that in some cases, the information itself can become more damaging than what's ever causing it. So we call autoimmune disease when the body starts attacking itself. Yes, inflammation in these cases are damaging. Why, however, is the body attacking itself? Why is that happening? The suggestion here, therefore, would be that cardiovascular disease is an autoimmune disease. The body's attacking itself.

    Well, I can see no evidence for that. You can see that inflammatory markers are higher in people with high risk of heart disease. So that's what you expect because as I've said to you, if you get damage in the endothelial cells and then you get a clot forming and then actually looking at guinea pigs experiments where they removed vitamin C from guinea pigs -- guinea pigs can't produce vitamin C -- within a few days, they developed atherosclerotic plaques. When you then give them the vitamin C back, the atherosclerotic plaques disappeared. What made them disappear was the macrophages which you may have heard of white cells that clear up the debris in your body. The macrophages came. They engulfed all of the plaque that was formed and took it away. That's their job. That is inflammation. If you cut yourself, if you cut your hand, then it will go red. I mean sometimes it gets infected, that's a different thing. But even if it's not infected, it will go red, it will swell up because that's all the clear up mechanisms going to get rid of the damage, to come to help to repair it all and get rid of it all. You can call it inflammation. You can call it healing. It is healing. When inflammation is due to long-term chronic autoimmune or something triggering a system like asthma is due to the body attacking things in the lungs, thinking they're infective organisms and they're not and you get inflammation and you get all sorts of stuff and people die of it. And if you dampen the inflammation down, that's a good thing.

Christopher:    Because that's inappropriate inflammation.

Malcolm:    That's inappropriate inflammation. Appropriate information is when you're seeing a healing process operating. They had this idea that after a heart attack the myocardial cells in that area became inflamed, and so they gave steroids to try and reduce the inflammation because they thought, well, inflammation is causing further damage. So what happened was if they caused so much damage, they stop the healing process occurring. Aneurism is developing at the side of the heart will then burst. If you dampen down inflammation, as I would say, if the inflammation caused heart disease, the most potent anti-inflammatory agent in the body is cortisone or corticosteroids. They are the most potent anti-inflammatory agents that we have They increase the risk of heart disease by 400% to 500% and non-steroidal anti-inflammatory drugs and NSAIDs, which we used to call another stupid aspirin in disguise, are things like naproxen, diclofenac, you've heard of many of them, they increase the risk of dying of heart disease. So we've given people potent anti-inflammatory agents and the risk of heart disease goes up, not down.

Christopher:    So you're suppressing that healing process.

Malcolm:    You're suppressing the healing process. You're getting rid of the -- there's an interesting study on people who got ankle injuries in physiotherapy and putting ice and rest and elevation and compression.

Christopher:    That's common knowledge.

Malcolm:    Yes. And as it turns out, it makes things worse. The inflammation is the body trying to heal itself, and you're trying desperately to dampen it down. So what happens? Well, less healing occurs more slowly. We're looking at the body  is trying to heal itself. We're calling that. I mean it's like saying why did you break your ankle? Well, it got more and more inflamed and so my ankle broke. No, I think you'll find that actually it's the other way around.

    Why are you getting inflammation in your arteries? Because the damage is occurring and the body is trying to heal it. Well, let's dampen down all that nasty inflammation. Oh, look, everyone is dying. In fact, medicines full of seeing inflammation and trying to dampen it down and then people dying. There are many examples of this. There's a horrible tendency to look at the thing and decide that the thing you're looking at is the cause of the thing. It's a circular logic thing that goes on and instead of saying, why is that there? Why is it happening? What's going on?

    So the inflammation thing I think is just a sigh in despair when people tell me it's due to inflammation. The spontaneous inflammation monster that comes out of the ether and it makes you inflamed.

Christopher:    You remind me of the conversations I have with my four-year-old daughter where she says, "Oh, why? Why is that? Why does that happen?" And then the reason she's asking that is because you've not satisfactorily answered her question. For some reason, adults they stop doing that. Why do they stop doing that?


Malcolm:    Well, it's boring. People start hitting you after a while for walking away. And they feel they don’t have to. They say, "What is this?" It just is or they actually don't know and then they can't tell you, so they don't want to admit that I don't know why that happens. I can't tell you why that -- I can't tell you how does LDL get through the arterial wall? It just does. Well, it must do because it's there. There's another explanation. It gets through and, in fact, the focus on LDL is like you're saying, the only thing in the plaque is LDL. Well, that's complete and utter nonsense. What do you find an atherosclerotic plaque? You find fibrin which is an end result of blood clots forming. You find red blood cells. You find everything that you can find in a blood clot you can find in a plaque. Now, a lot of it is gone in a late stage plaque.

    Well, unsurprisingly, I just told you that macrophages come and clear all the way, but they don't clear all the way. What you're left with is a kind of central core goo that it ends up. And then they say, oh, look, at all these macrophages. You find these dead macrophages around, oh, must be dead macrophages that cause plaques to form. No, they are just the ones that -- another interesting thing about macrophages -- well, I think it's interesting -- is the endothelial progenitor cells do not just become new endothelial cells. They can also become monocytes. Monocytes can become macrophages. Their fate is not fixed. Once they arrive at the scene of the accident, they can form themselves into many different things.

Christopher:    That's amazing.

Malcolm:    At one stage, when people found these endothelial progenitor cells on damaged areas, they said, well, we're finding these white blood cells. We don't know why we're finding them here, but they're stuck to the area of damage, and they're forming a kind of layer. Why are white blood cells doing this? The answer is they're becoming endothelial cells. They are going down a different route. So when we find these dead macrophages, they could well have arrived as part of the repair package. In fact, they probably did. And some of them just got stuck in there, and then they died as they do.

    Again, we have to thing that we find something in a plaque and go, well, it's a cause. They are trying to clear up, you idiots. Why can't you see this? This is just the right way around. Again, if you go cholesterol, then you can't explain this in any other way. So you're stuck with this cholesterol-centric view of everything. And again, when you call it a fatty street, this is the first thing you can see in an atherosclerotic plaque is a fatty street, well, there's not very much fat in it. There's quite a lot of fiber in there.

    There's an awful lot of things that are actually not LDL. In fact, LDL is a minor part of it. And as we talked about before, there is another LDL and it's called lipoprotein(a) which 99.99% of doctors have never heard of. But Lp(a) is LDL. It's an extra protein attached to it which is very interesting because this is why the vitamin C feeding experiments because it was hypothesized that if you don't synthesize vitamin C and you get vitamin C deficient, your arteries start to crack because the vitamin  C is essential for the production of collagen. Collagen holds arterial walls together.

    So when your collagen level is down, your artery will start to crack open, you start to bleed. In fact, the final cause of death in vitamin  C efficiency is you bleed to death. Your gums start bleeding. You bleed into your eyes, and you bleed internally then you're dead. So someone hypothesized, well, actually this lipoprotein(a) seems very interesting because what happens is it's attracted to areas of arterial damage. It sticks to them and it forms a very tight plug because the protein, the Lp(a) protein, is designed to attach to proteins in the arterial wall.     

    And the other fascinating thing about that protein is its identical in structure, virtually identical part, from one fold the difference to a substance called plasminogen. And as some people may have read my stuff, plasminogen is converted to plasmin by tissue plasminogen activator and tissue plasminogen activator triggers plus. And once the plasmin is triggered, it becomes an active enzyme that breaks apart fibrin and breaks apart blood clots. If you've got lots of Lp(a) and you have blood clot, it can't break it apart. It acts as a tPA inhibitor.

    So those blood clots stay where they are. Well, that makes sense because you don't want people just keep cracking and bleeding. In general, of course, you have to have a part of the blood clot that remains stuck to the arterial wall because if the plasmin just gets sort of the whole plaque, then all you've got is an exposed area of non-endothelialized arterial wall and the clots is just going to form, it's going to break up. So a certain part of the clot has to remain stuck to the arterial wall. That's the bit that gets the endothelial and stuck back on top of it, which is why most of the blood clot, by the time it's involved, drawn into the arterial wall, is effectively not viewed as blood clot, if you like. It looks like you've got fibrin there, a few bits and pieces of other things, something like proteins mixed up in the whole works.



    So that is a kind of explanation. So when the guinea pigs, they give them scurvy, their blood vessels crack, they develop atherosclerotic plaques very rapidly. They give them back the vitamin C, everything repairs and the whole process just wipes out. So there are some people who say that if heart disease is due to chronic vitamin C deficiency, so our blood vessels are cracking open slowly and gradually but fast enough that the turnover of the clot is not cleared away quickly enough and gradually the plaque develops, and so therefore you should take lots of vitamin C.

    I believe it makes sense as a hypothesis.  It's quite nice. It's very elegant. But again, I can find you 500 other causes of heart disease that have got nothing to do with vitamin C. I think it is a possible cause. It is not the cause, and it is something that if you've got a high lipoprotein(a) level, you may want to look at it because some studies have shown, if you feed people lots of vitamin C, their opioid level drops, although it doesn't seem to be consistent finding. It seems to be that level is just set. You either go to high level or you not. But it's very interesting area to look at.

Christopher:    Where are we there with respect to -- so an elevation of Lp(a) in your blood, how does that compare to the sickle cell anemia say?

Malcolm:    Oh, it's much, much smaller. There is a consistent relationship, but it's maybe off the top of my head you're looking at 20%, 30%, 40% potentially. So it's something kind of LDL range of risk if you like. So we're looking at, say, you've got diabetes. You got 500%-ish, something like that; raised LDL in younger men, 10%-ish. One of the interesting factors, one of the things that first triggered me to the whole clotting thing was the Scottish heart study that showed if you had a high level of fibrinogen, which is the precursor to fibrin which is a clotting factor, we're looking at 300% to 500% increases in heart disease risk. These are consistent findings.

    So there's another condition I was looking at, antiphospholipid syndrome, if you've never heard of it, Hughes syndrome. Again, it's supposed to affect one in a hundred people. Every time I look at the rare condition, affects one in a hundred people. There are 10,000 rare conditions. So we've all got a thousand or however many is. But people with Hughe's syndrome are vastly increased risk of dying of heart disease and stroke, and it's a blood clotting disorder. It means they're more likely to be clotty. So slightly different end results. More often they have strokes, less often they have heart disease, which kind of figures because the heart disease risk thing and I won't go into that too much detail, they're also more likely to get what they call deep vein thrombosis and things like that, which are an association but it's not quite the same condition we're looking at.

    So I think again if you look at anything that reduces the risk of blood clot formation, anticoagulant, that reduces the risk of heart disease. In fact, when you look at what happens to people after they had a heart attack, you give them tPA which is the blood clot buster, to open up the blood clot this form, it will then be put on clopidogrel which is anticoagulant. It's virtually blood clot management to keep heart attacks.

Christopher:    What about aspirin?

Malcolm:    Aspirin is anticoagulant. It's anti-inflammatory but it's actually more powerful anticoagulant. There are two basic parts to a blood clot. There are platelets which a little cells, there are millions of them floating around in your blood, that when they see an area of damage start clumping together very quickly, and they form the kind of plug along with the Lp(a). And then the fibrinogen is a small strands of protein floating around and the clotting cascade and all of those things, you've heard of Factor VIII, IX, X, XI and all that stuff, they trigger fibrinogen to become fibrin which is like long, thin, sticky fishing line that then wraps itself around and tightens it up and holds it really tight together. So once your platelets are stuck together and your fibrin is formed, that blood clot is quite a hard thing to shift for obvious reasons. The thing that will shift is plasmin just slices the fibrin apart and then the whole thing just starts to be disintegrated.

    So fibrinogen is a risk factor. Anything that increases clotting factors is a risk factor. And in fact, in diabetes, some things you probably don't know, the thing called plasminogen activator inhibitor is higher. So the inhibition of plasminogen activation is quite high. It's more difficult to get rid of clots in diabetes. So it's a pro-oagulant state.

Christopher:    What about triglycerides?

Malcolm:    Triglycerides are procoagulant, quite strongly procoagulant. If you drop triglycerides into blood sitting on a Petri dish, it clots. Bang!

Christopher:    Wow. It's starting to make sense. So what other things can make platelets stay together?

Malcolm:    Well, damage to arteries, obviously. Actually, toxins, bacterial infections. In fact, you're heard of sepsis, this is the most extreme example, in sepsis, first of all, the endothelial cells are damaged and triggers a procoagulant state, and then everything starts sticking together. So in sepsis, actually things that kill you is little millions of blood clots forming all around your body that block all your organs up and then you die of multi-organ failure. That's what actually kills you. But if you've got like gingivitis or chronic abscesses in your teeth and things like that, that increases your risk of heart disease because these bacteria are triggering blood clotting processes are going on all the time in your body. So long-term chronic infectious conditions are likely to cause stickiness of your platelets. That will happen.


Christopher:    What about anti-toxins that may be translocated from the gut, so lipopolysaccharides, for example?

Malcolm:    This is a big area at the moment. I have been looking at it. I know the whole microbiome stuff is very important. I think that what you can see is that if you have damaged gut flora and you have almost like semi-inflammatory bowel condition, actually the epithelium rather than endothelium within your bowel you have epithelium, which normally stops and anything get --

Christopher:    Why do they use different words for those cells? Are they the same thing?

Malcolm:    Well, I suppose endothelium, epithelium, I've seen them used interchangeably, but epithelium tends to mean the cells lining  your gut. Endothelium tends to mean the cells lining your blood vessels, although I have seen theme used interchangeably, but it's like arteriosclerosis, atherosclerosis, I mean I don't know what the hell the difference is, but people seem to use these words interchangeably. So if your epithelium becomes leaky, if you got leaky gaps, if you like, in your gut, then things seem to leak through. And yes, this is not a good thing. So you find that in things like Crohn's or ulcerative colitis or IBS or any of these conditions where there's what they call leaky gut syndrome and the stuff gets into your system. You don't want stuff in your system basically because it will be procoagulant. It will be damaging, quite high damaging. I don't know, some people say opens up the blood-brain barrier and allows things to get into your brain that you don't want because normally they would be prevented.

    So once you've attacked this endothelial barrier and opened it up in any way, bad things happen. And that's clear, if you like. So chronic infection, leaky bowel, the thing is speaking to you, you could probably stand here and read through a textbook of things you've heard of and I say, well, that damages, that damages -- they're all that.

Christopher:    It's a mess.

Malcolm:    It's like there are 300 things doing this and 200 things doing that and 100 things doing this. There are some that are absolutely really disastrous like smoking, cocaine use, it's horrible for endothelium lead poisoning, mercury poisoning, fluoride poisoning. All of these things, they damage your endothelium. If you think about nasty things that people do to themselves, they do this air pollution, endothelium damage, all of these things. So if you like, in my world, it's like a constant battle between repair and damage. There's a dynamic going on. Things are constantly being damaged. Things are constantly repairing. If you push the system too far towards rapid damage, then bad things happen. You've got to try and rebalance or get rid of as many things as you could think of damaging your endothelium.

Christopher:    Talk about what happens when you remove lead. I know there are some studies that --

Malcolm:    Well, there's that layer of endothelium, one cell thick. Sorry, what do you mean by --

Christopher:    Chelation therapy, for example, if you remove the lead contaminant, what happens?

Malcolm:    Well, it improves things. Chelation therapy, which I still don't fully understand but I sort of read about it, appears to be putting things into your bloodstream that will absorb heavy metals and then it will be excreted presumably by your kidneys. I presume that's about the only place you excrete or sweat, you can sweat things.

Christopher:    Yes, that's right. You can sweat stuff out.

Malcolm:    So chelation therapy, when I first heard of it, I thought this is just the biggest load of nonsense I've ever heard of.

Christopher:    It sounds super woo-woo.

Malcolm:    It is. The woo is still the woo. And then someone did a study to prove it didn't work and find it worked. Ooh, that's interesting. So yes, you can apparently remove heavy metals through chelation therapy. I'm not going to talk about any detail because I don't know exactly what you give people.

Christopher:    This is interesting to know. You have this prediction that maybe these environments or pollutants are causing the problem, and then someone does an experiment to see whether reducing the environmental pollutant makes things better and it did.

Malcolm:    And it did, yes. So it's a kind of a nice model and it works. I think is relatively common in the US, isn't it? I don't know anyone who does it in the UK maybe just because I don't know, but I've never heard of it being offered. And I'm sure if I set up a clinic and said chelation therapy here, roll up, roll up, I'm not asking for 100 pounds, I'm not asking for 99 pounds, your hair will grow more lustrous, I'd probably get reported to the GMC or something and struck off.     

    There's a few things I wouldn't mind trying nowadays. I'm busy in other things, but the more I not look at things, I think the vitamin stuff I know it's not the same thing, but there was a study Cambridge -- or was it Oxford? --  where they gave people high doses of vitamin B6, 12, and folate and reduced the risk or in fact stopped Alzheimer's disease progression in its tracks. And I thought, well, that's interesting. How much interest this had been from the mainstream medicine? None. This is like, oh, well, we're still looking for treatments for Alzheimer's.  Hold on. These people just found one. It doesn't reverse everything, but it stops the progression and it appears to be very beneficial, and yet no one is remotely interested in. You think, surely you might be interested in it. I mean vitamin C as I just looked at, if you give people with fulminant sepsis, which is really horrible, kills lots of people, if you give people vitamin C, it reduces the risk of death from 40%. So people with fulminant sepsis, four of ten will die. If you give them high dose vitamin C, 0.8 out of ten will die.


Christopher:     So it sounds like a cure.

Malcolm:    Not a cure cure but it is fantastically beneficial, and it's been found in study in America. It's been found in the study in India and somewhere else. I looked at it and I said, well, how can this work? It appears to work because vitamin C protects endothelial cells from being damaged, and so the exotoxins don't strip them out, and therefore you don't get the disseminated intravascular coagulation so people stop dying. There is a mechanism.

    There's a famous case of someone in New Zealand whose family pleaded with the doctors. He was dying of flu, influenza, and they him a really high dose of vitamin C and he recovered completely. Well, that's a relevant. Weird, you get things that chelation therapy works. What's the interest? None. Vitamin B works. What's the interest? None. Vitamin C works. What's the interest? None. It seems like if you mention the word "vitamins," the mainstream medicine just goes, oh, vitamins are just, you know, we're just not interested. That's not proper medicine. It hasn’t been studied properly. And the counter-argument is, well, there's no money to be made in it, so it's not going to be promoted, is it?

Christopher:    I did want to say that, but you said it now. I have to say there's a lot to love about the -- I'm going to call it the Kendrick protocol, what we talked about. We talked about sunlight. We talked about Viagra.

Malcolm:    Yes. Viagra, what could go wrong?

Christopher:    We talked about stress -- of course, that you can't really monetize stress management.

Malcolm:    You can't. Maybe you can find some way of doing it, let me know.

Christopher:    We talk about alcohol. I know you've got some interesting thoughts on drinking, how that might be affecting all this.

Malcolm:    Well, my main thing about alcohol is it makes people relax, and it does have an impact. Moderate -- whatever you call moderate alcohol consumption, I've never worked that out, it does increase nitric oxide synthesis in the endothelium, whether that's because people are relaxed and their cortisol levels drop or whether it's a direct effect because there's all the stuff about red wine which is completely baloney. In fact, when I've looked at it, any alcohol in the same amount of units or however you wish to measure it has the same effect. The red wine stuff is -- and I say to people when I started looking at France, I said, what do the French do? Well, they sit outside and they have their family around and they have wine with the meal. Maybe a few variables going on you're not just capturing. The red wine is maybe associated with family drinking, good social occasions because the Blue Zones, which you've probably heard of, the areas of the world where people live longer than anywhere else, the outstanding factor is good social relationships, good sense of community, strong sense of family, sense of purpose, sense of belonging. And that tends quite often to be associated with eating and drinking together as families and groups and drinking wine rather than the more solitary, like myself, whiskey drinker sitting gloomily in a room.

Christopher:    That's not what we're talking about.

Malcolm:    No, no, no, these are de-stressing. I try to look at where is the evidence for increased life expectancy? What are the things that you can do? What are the things that damage your life expectancy? First of all, mental illness and depression and whatever. Also, looking at groups like Australian aboriginals who have a life expectancy 20 years less than the surrounding population. There are lots of indigenous populations like North American -- what do they call them? I think they're called aboriginal Americans, Maoris. They have had their society stripped apart. Their life expectancy is very low.

    In the UK, I've said to you, we laughed about postcode being a risk factor. Well, if I moved this conversation ten miles into the center of Manchester and put postcode in there, it would reduce our life expectancy by up to ten years, more in some cases. So that social thing, I like to consider health to be physical and psychological and social. You have to have all these things working together. And the social is important as anything else, possibly more important than anything else. If that's wrong, you're in trouble. If that's right, it's helpful. It keeps you physically healthy. It keeps you psychologically healthy.

    So what's the other thing? Smoking reduces your life expectancy by up to eight to ten years. Lack of exercise can reduce it by six to eight years. Lack of sunlight can reduce it by as much as smoking. So if you avoid the sun, you're stressed, you don’t have friends and you smoke --

Christopher:    It's a recipe for disaster.


Malcolm:    Well, you're going to get to about 60.  That's about what people do, isn't it?

Christopher:    What's going on around here? So I've come here for sunny California to Doncaster and then Macclesfield. I was standing outside the railway station, and I was just completely shocked by how many people were smoking. Literally, there were more people smoking than not smoking.  I rented a car to drive here, and it smelled of cigarette smoke. What the heck? I have not seen that in California since I've been there 15 years ago.

Malcolm:    The smoking rate in the UK has dropped, but one of the problems is nowadays you're not allowed to smoke in public places. So if you're at a station, all the smokers will be standing outside. If you go to a hospital, the first thing you see are people  standing around and smoking. It's like everybody smoked in hospitals. No, you're not allowed to smoke in the hospital ground, so the nearest point is like -- the problem where I work in the intermediate care is there are about 20 or 30 nurses and health care workers and quite a lot of them seem to smoke, but they all stand outside because they're not allowed to -- it's very visible like five people smoking away all dressed in nurse's uniform, you think, this looks good.

    So yes, smoking has reduced in the UK But I think there's an element of certain groups and populations are more likely to smoke. They tend to be disadvantage to people, this kind of, well, I might as well just smoke, I might as well just drink attitude. I think that's almost a sign of psychological despair, isn't it?

Christopher:    Right. You are a practicing GP, so how you help people with social support network? It's not an easy problem to solve.

Malcolm:    No, it isn't. On an individual basis, I advise people to join rambling clubs and walking, join a gym and find something they enjoy doing that's physical. I have a few things saying, there's a dancing club and some people enjoy dancing. I would say to people, if you don't enjoy your exercise, don't bother because you'll never continue with it. You can't force yourself to do something you don't want to do year after year unless you have iron willed and most people are not. So if they can find something -- golf, walking, dancing. There are parkruns in -- they've got them in the US as well I think, maybe they don’t, where they organize five-kilometer runs and anyone can go along. It's all very much some people are quick and some people are very slow, but it's quite sociable and people quite enjoy it.

    So I think this enjoyment thing is gigantically important. I don't say to people, get down to the gym and raise your heart rate to 153 beats per minute. It's never going to work. It just isn't. It's not their life is never going to be. So I think you advise people to -- I have spoken to people and say, well, you must raise your heart rate. You must do four and a half hours a week and I think that's a lot. I just don't see most people doing this at all.

Christopher:    It's completely arbitrary.

Malcolm:    Well, who knows? I'm sure exercise is better than no exercise, but if you're going to put people off because you're saying to them you've got to push yourself into even bleed from your lungs before it's doing any good, people just aren't going to do it. People are not going to do it. It would be nice if we had walkways and people could walk places around without having to feel they -- America is the worst in that. I went to the hotel there and the shopping mall across the road a hundred yards away --

Christopher:    You can see the [1:06:58] [Indiscernible] on the crosswalk.

Malcolm:    I said to the guy at the hotel, "How do we get across there? How do I walk across there?" He said to me, "You don’t walk. You get a taxi." It's only a hundred yards away. So I decided to walk and I wish I hadn't. I found myself walking at this little sort of only drive-in entrance. There wasn’t a walking entrance. So I got a taxi back. So we need that, I can individually do. What I can say to people  is it would be nice just to stay here, have walkways designed through it, one next to my house. And then they basically just allowed them to extend their gardens so you can't walk through there anymore. So even right here, it was designed for people to be able to walk around, you can't.

Christopher:    Right. You need to exercise your freedom to roam.

Malcolm:    Yes, well, exactly. Well, like walk up [1:08:47] [Indiscernible] which are nice and beautiful walks and I enjoy that, but not everybody does. How do you get people  to do it? How do you involve it into people ? And also the general healthy things. How do you increase the social networks of people? I can't do that for them.

Christopher:    Right. It has to be intrinsic.

Malcolm:    Well, it's a shame, I mean [1:09:08] [Indiscernible] I suppose. And there's hardly anyone goes to church anymore. If you look at it, people who go to church live longer than people who don't. That's just a fact. But I think if you look to people who belong to golf clubs, they probably live longer than other people as well. So I don’t think it's not necessarily the religious aspect of itself, but also that thing of having somewhere where you can meditate a bit and take yourself out of yourself and not just be on you all the time. These are important things. The French are very good at this. They shut the shops at lunchtime and [1:09:39] [Indiscernible] stuff. This is it.

Christopher:    Yeah, I haven't thought about that but you're right.


Malcolm:    You go there on holiday and then say,  "Is this place open?" "It's a holiday." "Well, it's a holiday. We're shutting. It's our holiday too." Whereas over here it's like, we all best be working and working and working and constantly working. You think let's have a bit of relaxation, guys.

    So I think how do you tell people to do these things? You will relax or else you'll be beaten to a pulp. Things like mindfulness, yes, but again it's very hard to keep the motivation going, to keep doing it, isn't it. So you need to find things for people that they can build into their lifestyle, and I suppose we need to look at -- you need to speak to governments and say wellbeing. I was just looking at America where there are certain electoral registers where people living 10, 15 years shorter than other places. This is not anything to do with the health service. The health service has nothing to do with this. This is how people live their lives. We know ourselves. You'll drive through certain cities and certain parts and think, this is not a very nice place. It just looks depressing and soul destroying as well, isn't it? And you think, well, surely we can make these places lift the soul a bit, make ourselves feel it would be a nice place to be, a bit green and a bit something, especially in Scotland, in the West Coast of Scotland, there are housing estates that are just designed to make you feel like life is not worth living. Let's just immediately commit suicide.

    I think it's important that we do look at things not just for material side. On whatever we do, we have to look at things more. We have to start changing our way of looking at how we can help. There are people that do have okay lives and sort it out. We don't need to help them. They've already done it, if you like. We need to stretch out a lot more to -- I hear there are parts of Manchester not far from here that are just grim. Is it because of the people there? No. They don't want to have grim lives, but it's very difficult to get stuck in those places, and we have to work out ways of improving that definitely.

Christopher:    Talk about statins. W haven't really gone there yet. So what's going on there? I don't understand. Why do we continue to take them? Why do they continue to be prescribed if they're not helping?

Malcolm:    Because the opinion leaders tell us they are magic and wonderful. And if you don’t take them --

Christopher:    Why are the opinion leaders not enamoured with Viagra if that's going to be a better solution?

Malcolm:    Well, there's a whole series of different questions within that question, aren't there? It's a question with many layers. Why do people keep doing stuff that doesn't work? Why do people get attached to a certain idea and will never get rid of it? Because they do, because they've been told, because the statins are making huge amount of money. There has never been such a push on a group of drugs to prescribe them as there have been with statins. The publicity --

Christopher:    [1:11:21] [Indiscernible] you prescribe a drug for somebody that didn’t actually have a disease.

Malcolm:    Well, I don’t know.

Christopher:    Or is high cholesterol a disease?

Malcolm:    Exactly. That's another question. I mean it's funny in a way because you can never -- as a doctor, you prescribe statins. You've never seen any one's life being saved by them. I sometimes joked with my colleagues. We talk about statins. Bring me someone who will be dead who is still alive because they're taking a statin. Of course, they can't because that's impossible, and yet strangely normally doctors like to give somebody an antibiotic who got just infection, they get better, you can sort of see that happening. With statin, you can't see anything happening, nothing happens, if you like. They're still alive. It must be working.

    So what they do is fool themselves. I mean I've spoken to fellow doctors and said, well, okay, if you took statin in secondary prevention that has already had a heart attack or a stroke so that high risk and you took it for five years, how much longer do you think patient will live for on average? They often say to me three, five years or something. I say, well, the correct answer is 4.1 days. That's what the research tells us. And they go, "No, that's wrong." No, that's correct, four days. So that's less than a day a year for taking statin. We don't know what happens after that because the trials haven't lasted any longer than that. There have been ridiculous studies come out saying, well, we've followed up patients for 25 years. The statistics behind that are so ridiculous that I can't go into them here but just believe me, no.

    If you ask an average patient, they think virtually the -- because they do say to them if you take statin, it will reduce your risk of heart disease by 36% or whatever it is. That sounds incredibly impressive. You strip that apart and you realize that actually it's just weird how reducing the risk of cardiovascular disease by 36% can end up meaning also the same thing as increasing your life expectancy by four days but it does.

Christopher:    That's just the way they purported the numbers, relative risk.

Malcolm:    Relative risk. I have never had a single doctor and I've asked this question of maybe hundred doctors, you know, you have conferences or meeting or a chat. I said to them, "Do you know what the difference is between absolute and relative risk?" And do you know how many have been able to give me an answer?

Christopher:    You would expect all of them.

Malcolm:    None. I have yet to meet a doctor who knows what the difference between relative and absolute risk is.

Christopher:    Is it maybe not fair to ask them to understand that?

Malcolm:    I don't know. Maybe it's not the right question. I have no idea what the right question is. Maybe it's unfair because you could ask me something I thought I knew and when I'm asked on the spot, I think, oh, I don’t really know. When I've explained it to them, they go, "Oh, is that what it is?"

Christopher:    They're not dim --

Malcolm:    No, they're not dim but they don’t have --

Christopher:    [1:14:48] [Indiscernible] understanding it.


Malcolm:    They don’t have time to go into this.  In fact, I was giving medical students a lecture on this sort of stuff. I hope I did explain to them. And they would come up and go -- a couple of them would come up and said, "Oh, people have tried to explain this before and I've never understood it." I said, well, okay, I start by using it and say, so say you have a blood pressure lowering drug and the placebo and you give a hundred people the blood pressure lowering drug and a hundred people the placebo. And after the end of the trial, one person has died on the drug treatment arm, and two people have died in the placebo arm. So there's two who died in one arm, and one died in the other arm. That's a difference of 1%. It's also a difference of 50% because one instead of two, right? So let's say you do the same study and it's a thousand people and two died in a placebo arm and one dies in the treatment arm. That's two to one.

Christopher:    It's still 50%.

Malcolm:    That's 0.1% absolute risk reduction, 50% relative risk reduction. Do it with 10,000 people, two to one. So you can keep doing this. You can do it for ten million people. So the absolute risk reduction become 0.000001, and the relative risk reduction remains at 50%. So unless you know what the absolute risk is, the relative risk is meaningless. You don't know what that means. If the absolute risk was 50% to start with, then it's quite a reasonable thing to reduce it by 50%. If the absolute risk was 0.0000001 at the start and if you reduce it by 50%, you wouldn't even know there's a difference. But people use this relative risk and they use it in all sorts of different areas, and therefore you're left with this, oh, 50% reduction, that sounds good. No.

Christopher:    And a newspaper title.

Malcolm:    Fifty percent reduction in death of stroke. But the risk there was only two people died in the last 500 years. Now, one person is going to die in the last 500 years. That technique is used in all sorts of areas, but it's the other way around. So if a side effect is caused in -- if there's a sort of adverse effects --

Christopher:    I'll stop you there. Explain the difference between a side effect and an adverse effect.

Malcolm:    Well, I'm a bit pedantic but a side effect is anything that the drug can do that is not its central effect. So it could be positive or negative. So with Viagra, the erection was a side effect. Some effect some people might call it an adverse effect. Some people call it a beneficial --

Christopher:    It depends on the point of view.

Malcolm:    An adverse effect is something that you would all consider not a good thing. So it might cause a  severe headache or it might cause a skin rash or something. So a drug-related adverse effect is the correct term for nasty things drugs can do whereas the side effect could be positive or negative. In general, people use side effect when they mean drug-related adverse effect. The other one people have trouble with is serious adverse event. So a serious adverse event is something that your drug should prevent. So a serious adverse event could be a stroke or a heart attack. So you would hope statins would reduce strokes and heart attacks. But the trouble is people think that an adverse event is a bad thing, preventing them. So people get themselves mixed up. So when I say to people, serious adverse events are things you need to look at as well. You're not just looking at death, so you're looking at strokes. And other adverse effects could be an episode of depression or getting hit by a bus.

    That may sound facetious, but in the early cholesterol lowering trials, the risk of accidents was increased by people who lowered their cholesterol levels to the extent that people thought this might be a direct effect. In fact, it is a direct effect but not the way they think it is. So you look at all the adverse events that occur, serious adverse events and you say that statins should reduce serious adverse events because if they're reducing non-fatal strokes, non-fatal heart attacks, et cetera, et cetera, then the serious adverse event rate should go down. But when they've looked in it, there's been no difference in serious adverse events between the statin and the placebo. So in other words, for everything, nasty thing that statin is preventing, something else is happening.

    Now, this is one of the areas [1:18:28] [Indiscernible] by many people. And it's also an area where the researchers that have hold the data will not let anyone else see it, which is another worrying thing is that the cholesterol treatment trial is collaboration. They're not sort of -- although there's serious adverse event and adverse drug event data. And they won't let anyone else see it.

Christopher:    Oh, really? Can you not get that under Freedom of Information Act?

Malcolm:    No, you cannot. I don’t know how you can't get it under Freedom of Information Act but you can't. I think it's because they're a charity and charities are exempt from Freedom of Information, at least in the UK they are So you can't get it. People have asked for it. People have asked for under Freedom of Information. The Cochrane collaboration are trying to get it and they won't get it. They can't be shown it, so they see it. Now, I think this is absolute outrageous. I think people should be waving banners around and saying to their own peep that no one seems to care. And yet you think, well, surely that information should be public domain but it's not. Journalists don't believe me when I tell them this until I show them the actual thing saying we don't release this information.

Christopher:    Do you understand some of the pharmacological mechanisms that statins might be causing problems?

Malcolm:    Well, there's a bazillion possibles because they prevent cholesterol from being synthesized in the liver or any cell in the body. Cholesterol is a 37-step process, but it's not just cholesterol that appears. There are about six other important chemicals, most all of your sex hormones like testosterone and cortisol, et cetera are on the head as well. And possibly the most important single thing that it blocks is I think called coenzyme Q10, which again no one's ever heard of. It's also called ubiquinone. But it's actually a co-factor in the production of ATP we call it, which is ATP is the substance which when it's reduced to ADP powers all the processes of energy in all your cells in all your body. That's the final result of eating food. Clearly, that's quite important because if you didn't have any of that, you'd immediately stop working and you just die.


    So coenzyme Q10 is reduced about 50% when you take statins. Obviously, high energy cells like muscle cells and heart cells are powered by ATP. So if you knocked CoQ10 down, you might expect damage to occur. And we can see that that damage does occur. When you see people become fatigued. Research in Austria on athletes, athletes who took statins just had to stop taking them because it can run as fast.

Christopher:    I mean I've heard reports of people not being able to get out of bed.

Malcolm:    I think there's a degree of (a) some people are more affected than others, and (b) depending on your level capacity, if you're a 20-year-old athlete, you probably could knock 50% of your coenzyme Q10 and to all intents and purposes of the people would see nothing when your times might have gone from ten seconds to eleven seconds, but most people aren't running or exercising at that level. Once you start getting older, it might be the difference of being able to get out of a chair or not, get out of bed or not or all sorts of things or not. So yes, some people are more affected. I mean I look at what's statins do and think ,how can anyone take these without collapsing in the heat?

Christopher:    You've described a mitochondrial poison, haven't you?

Malcolm:    It is a mitochondrial poison. Of course, pharmaceutical companies knew this. When statins were first about to come out, Merck filed a patent for staitins to be given with CoQ10 supplementation. They didn't act on that. But you should ask yourself the question, well, why did they do that? Well, they'd seen the results and I have seen the results in animal experiments where the CoQ10 went kaboom on high levels and dogs and whatever it was that we're using it on, poleaxed, and in human beings and then they have the cheek to say that statins don't cause muscle pains and aches. Anyone who's talking to anyone taking statins, you speak to a hundred people, you'll find at least 50 will tell you they get muscle aches and pains.

Christopher:    Could that be due to the nocebo effect? As you probably start by explaining the nocebo effect.

Malcolm:    The no-brainer effect. Placebo is you think you might be getting better; therefore, you get better even if you're not getting better. It's kind of fooling yourself aspect of thing. Nocebo effect is you think you might get a side effect; therefore, you get a side effect.

Christopher:    Because it's written on the label.

Malcolm:    Because it's written on the label, right, yeah. A number of people who read the label would be zero. I mean this idea that doctors are telling patients they might get muscle pain when they take it, I don't know a single doctor that tells patients this. Almost no patients even know they have any adverse effects because what most doctors say is these drugs do not cause any adverse effects, and that's the message they get or they say, well, it's on the label but actually we don't really see that.

    So the idea that they are suffering from a thing they think they're going to get because they're told they're going to get it, well, first of all, they're not told they're going to get it in the vast majority of cases or it's diminished that they're told don't worry about it. So that's nonsense. There was a study published recently saying it's all due to the nocebo effect which I did sort of dismember but I haven't got too far with doing anymore with it, it's just start to finish nonsense. I mean the nocebo effect exists. There's no doubt that it exists, and there's no doubt that some people will complain of an adverse effect if they've seen that they think they might suffer from it. That's true. I mean we know if you give people painkillers that are placebos and say, it will be very effective but it might give you a pain in your ear or whatever you decide to say to them. The patients will say, it was very effective but I did get that pain in my ear, doctor. That does happen.

    The nocebo effect is real in that you can convince people -- as a doctor, we've done many things we probably should be less than telling people about in case we get sued, just having a laugh for ourselves, but patients can be very suggestible. They can be very malleable. That's true. In this case, it could explain and then they suggest to explain something like 0.25% adverse effect, and yet an RC study is showing 70% of people stopping taking statins after a year. Sixty percent of the 70% saying because of adverse events. I've spoken to people that were like, "Oh, it could just be due to the statin. Oh, I didn't know." I mean if you said that, you might as well say, all adverse effects of all drugs are just a nocebo effect, so we should just ignore everything everyone says to us. I mean what's that about in medicine? We were supposed to pay attention to our patients. If they say, "I'm getting muscle pain," you don't go, "No, you're not. You're just making it up." I mean, oh, look, they've just died of rhabdomyolysis. I never expected that. It's such a ridiculous place to be. If people say this to me, I just look at them and go, "Have you ever seen a patient in the last 20 years, Mr. Research person?"


Christopher:    Okay. I get that. What about this new class drugs, the --

Malcolm:    PCSK9?

Christopher:    Yeah.

Malcolm:    Yes, they are fantastic things that really lower the LDL level to previously never seen levels. What they do is they normally if an LDL molecule is taken out of the system, it attaches to a receptor. The receptor in a molecule pulls into the cell, and the receptor LDL complex is broken down by an enzyme. That must be something to do with PCSK9, but I can't remember which one it is. An inhibitor inhibits this enzyme so the receptor is not broken down so it starts to back out so it picks up another LDL and pulls it back in. Essentially, more LDL is being dragged into cells than otherwise would have been. As I say, that just proves how healthy cholesterol is because you've got all these cells full of cholesterol and you're saying it's good for you because, obviously, you can do any damage while it's floating around. It can only damaging when it's in the cell and this stuff makes more if they go into cells. So that shows it's healthy. But anyway, that's how they work. It's an injection. It's every about a week or two weeks. It costs about in the UK 8,000 pounds a pop a year.

Christopher:    Okay, a year.

Malcolm:    A year, sorry. And if everybody taking statins was put in a PCSK9 inhibitor, it would cost the NHS 86 billion pounds a year. So that would be the end of the NHS. Anyway, they're not aiming for that everybody market. What do they do? They did a study and they didn't want to do a study, but they did a study and they lowered the LDL by down to lower than one millimole per liter on average. There's actually 30 milligrams per deciliter in American vernacular. And the end result of the study was that there was a slight increase in deaths from cardiovascular disease.

Christopher:    A slight increase?

Malcolm:    Yes, and a slight increase in deaths from overall mortality. So slightly more people died and slightly more people died of cardiovascular disease just by having their LDLs lowered to unforeseen lower levels. And it's been hailed as a success, of course.

Christopher:    Because it lowered the LDL?

Malcolm:    No, because it had impacts on other outcomes. You think the most important outcome would be dead or alive. Next most important would be died of heart disease or didn’t die of heart disease. No, no, no, don't be silly. They measured five different outcomes. You're going to get, off the top of my head, there was nonfatal MI, nonfatal heart attack, PCI intervention to put statin and a couple of other things that I can't remember off the top of my head now.  However, these went down but you've got to say is that an intervention procedure to put statin is not clinical end poi. It's the decision to put a statin. And that was the one that changed the most, obviously. What you also have to know because I was at a meeting where one of the chief investigators was talking, and he said he spoke to people and this chap said to him, "Well, I knew I wasn't on the PCSK9 because my LDL didn't go down." "All right, how do you know it didn’t go down?" "Well, the doctor told me." But also if you go in and you're on a medication and you're part of a trial and you speak to the clinician, you have to let them know you're part of the trial, so they will know and they will know what your LDL level is. So they will know if you're getting the treatment or not.

    Effectively, these are unblinded trials. The decision making -- somebody had a stroke, I got a bit of weakness in my arm, doctor. This is stroke. I got a bit of weakness in my arm, doctor. No, it's nothing Don't worry about it. You can decide. You can make decisions as to what the diagnosis is. And if you know somebody is taking the drug, you can decide to have it or don't have it. You'll say, I want you on unblinded trial. So what are the two hard endpoints? You're dead or you're alive. You died of a heart attack or you didn’t or a stroke. Those two endpoints were made worse by lowering the LDL to levels that which -- we are assured cardiovascular disease should not occur anymore. What were the ones that changed? Nonfatal stroke could be quite a major serious stroke, but it could also be -- I've got patients myself who I've been leaning over to the right a bit and speech is a bit slurred for a couple of hours. What do you think? I don’t know. Was it a stroke? It might have been. I've had two or three before. They seem to be all right now. They're perfectly normal again.

    So you have to be very careful of what people are measuring. So did they work or did they not work? In my world, they didn't work because the two hard endpoints went worse. And if your hypothesis is LDL causes heart disease and heart disease, death, and you find it increases those things, you really have not convinced me in any way, shape or form of the value of doing this. Others are convinced. They're out trumpeting this wonderful new drug. This is a wonderful sort of savior of humanity. Well, they would, wouldn't they? It's quite a lucrative thing to do.

Christopher:    And it really just come down to profit. I have to be like a conspiracy theorist, but is it --

Malcolm:    You don't have to be a conspiracy theorist because there is a conspiracy. It's called let's make enormous amounts of money. I don't mind people getting involved in clinical trials. I don't mind people standing up saying it's wonderful. What I do mind is that these are the same people that get put on the guideline committees, on the NICE committees, on the FDA committees and decide whether or not drugs should be promoted because these people should be told, no, that's fine, you can make your millions doing the research and doing the publicity and attending meetings. That's fine, we have no problem with that, but you're not going to decide on how to treat people because you are irrevocably biased. And yet we still seem to let these people be the same people. I think, what? Really? And the trials themselves, can you trust them?


Christopher:    What would you predict is going to happen in the US where the insurance companies are running the show?

Malcolm:    I predict they'll think this is too expensive with PCSK9s. I think they've already had said it. Of course, they come at a huge pressure because there's an enormous pressure put on them by various people, the pharmaceutical companies, lobbyists, the senators and the congressmen. Senators and congressmen lobby the FDA and and they lobby the insurance companies. So if your insurance company says no, the next thing you know you probably get a little knock on your door from Senator, "Well, gee, Chuck, I've known you for 20 years. We played golf together. You know what you're saying, you shouldn't be using this drug. Well, you know what I think, well, you really should." "Oh, you think so?" "I really do think so because you know your golf club membership is coming up for renewal next year." You know when you have to be voted back on to the committee. I mean all these things you'll never know what's going on and maybe some things are, a bit conspiracy theorist, but the game is the game. The pharmaceutical companies, they spent I think the figure I'll say and this may be wrong because I may be remembering it wrong was $20 billion lobbying Congress last year. They don't do that for nothing. Of course, they don't. They want return on their money. They've got to be getting at least $20 million back because they won't be doing it.

Christopher:    It's terrifying.

Malcolm:    The whole system is on [1:31:33] [Indiscernible] -- I mean the FDA, the Food and Drug Administration, is primary money source. It's a pharmaceutical company. They're the people who pay for the organization that's supposed to be monitoring them. What do you think? Well, really? This seems a bit strange. I worry less because this study came out showing it didn't achieve that. So they can't be doing that much fiddling with the figures. If they're really fiddling the figures, you wouldn't get a result like that. It's a bit like is there cheating in horse racing? Yes, there is? How much? Well, not enough that no one will ever bet on the horses again. There are people  who whistle blow, because in the States, if you whistle blow, you can get $100 million. So it's quite lucrative whistle blowing in the States. Anyone working in industry you think they've seen something that's really dodgy probably would think, you know what? I quite fancy $100 million for whistle blowing this company. So in the UK, you just lose your career and never work again. But in the States, it's quite worthwhile doing it.

    So I don't think it is -- it's mainly the presentation stuff. How did you set it up? How did you present it? They don't want to go after overall mortality. They don't want to go after cardiovascular mortality because they know they're not going to show it. So they start looking at things like interventional cardiology interventions and nonfatal this or stuff like that. So they can manipulate trials in certain ways to get the results they want. I don't think that they actually just make up the results because if they did, they wouldn't get the results that we see.

Christopher:    Well, maybe this would be a good time to summarize all the things that do work. I think there's a lot to love about what you're recommending. Can we go over some of those things? How do I not die of cardiovascular disease? What are the  things? So I need to worry about my endothelial function. How do I --

Malcolm:    Yeah, contemplate your endothelium, all 2,000 square meters of it apparently.

Christopher:    Oh, wow!

Malcolm:    There's lots of it. Be nice to it and hug it. And I would hug it by the sunshine is good for it. The sunshine and relaxation is good for it. Exercise is good for it. I suppose things like mindfulness, joining clubs, all these sort of things are good for it.

Christopher:    Social support.

Malcolm:    Social support, all those things are good for it. Certain food stuffs potentially. You may have heard of L-arginine, citrulline which increases the synthesis of nitric oxide, things like that. I wouldn't necessarily say take Viagra but depending on your situation. I wouldn't run away from it.

Christopher:    Is there a downside to that?

Malcolm:    Is there a downside?

Christopher:    If there is, you don’t know it.

Malcolm:    That might break up a few relationships here and there. I haven't seen any particularly maybe if you take ten at once, I don't know what happens then. Your blood pressure drops or hypotension. So things like that. Make sure that you've got --I always say to people, I take vitamin D in the winter. That is endothelial protecting. I take Vitamin C just year-round just because --

Christopher:    I talked to a doctor last night who saw scurvy in his practice very recently. He couldn’t believe it at first, then he realized what it was.

Malcolm:    That's what it is, yeah. I know. Well, I don’t think we're in danger of too much of scurvy, but you can keep your vitamin C up is a good thing. I mean you go into supplement after supplement after supplement, and I've kind of said your magnesium -- if you're on certain medication, your magnesium is important because some people's magnesium drops through their boots. I would say look at your medications. If you're on lots and lots of medications, if you're on PPI, I mean the average person over 50 is now on five different medications. Should you take aspirin? I don't think so. I don't think it is worth it because it can cause bleeding in some people and dangers and things like that.


    So when it comes to food, you're saying and I think the focus here is if you've got problems in your blood sugar and you're spiking it up, then I think you should look at your carbohydrate intake and reduce that. Some people seem to eat carbohydrates that's coming out of their ears, it causes no problem. Other people do have a problem with that. So I think the carbohydrate reduction. I know some people who completely don’t eat any carbohydrates. I think it's very difficult. Most people aren't going to do that. Equally, I don't think it's necessary for most people. If your doctor said, oh, your blood sugar is up a bit or you maybe got pre-diabetes, whatever that is, or diabetes, then you need to be looking at high fat, low carbohydrate diet because the evidence, as I see it, is the problem I've got it I haven't seen any mortality improvement data. I mean everything says it should be beneficial, but I haven't seen anyone say, look, people are living five years longer or three years longer, whatever. I haven't seen those data. I mean I don't know who's really calculating it. The pharmaceutical industry isn't going to be funding those studies, and it's very difficult to get the money to do them in other ways. But definitely the dietary thing I think is important as well.

Christopher:    Chronic sources of inflammation, so you have to look after teeth.

Malcolm:    I would say look after your teeth. Yes, if you've got gingivitis or anything like that, definitely look at those things and try and get them sorted out, absolutely.

Christopher:    And then xenobiotic metal exposure, what can we really do to avoid environmental pollutants?

Malcolm:    Well, I don't know because I don't know how you know you're exposed to them. Should you be doing blood tests, say what's my lead? What's this?

Christopher:    But that's really acute exposure.

Malcolm:    Well, I think it's chronic exposure with some of the heavy metals because they don't come out in your system very easily.

Christopher:    When you do a blood test.

Malcolm:    When you do a blood test, things we talked about, I could mention every vitamin virtually. I could mention almost a bazillion supplements, and I'm not sure on those things. I think it could become awfully complicated. You could look at magnesium. You could look at calcium. You could look at lead. You could look at this. You could look at that.  Where would you draw the line? I don't know. I don't know the answer to that I think I would say to other people.

Christopher:    Is there anything you do or recommend to your patients to avoid exhaust fumes, particulate from buses, that type of thing?

Malcolm:    Pollution is pretty difficult to avoid.

Christopher:    I know. That's why I'm --

Malcolm:    What do you do? You go cycling, that's even worse.

Christopher:    Yeah, it's really, really hard.

Malcolm:    You're breathing really hard. There's a bus next to you and it's blowing stuff into you. Go walking in the hills.

Christopher:    Right. Go mountain biking in the woods.

Malcolm:    Go mountain biking in the woods. Those would be definitely okay things to do. I think a lot of the pollutants are leaking out. I think one of the things that Eastern Europe has still seen very high heart disease rates, and I think in part that's because those countries were polluted to death. I think a lot of these pollutants are still over there. When you look at  places like Czech Republic and East Germany, just almost all festering sores I think. What can you do for that? I don't know. Should be chelate ourselves? Should you once every two years say, let's check these things? Quite difficult things to check. I think it's a tricky one.

    The other ones may be more specific. I usually say to people, potassium is good. The study in Scotland showed that greater potassium ingestion reduced the risk of overall mortality by 250%.

Christopher:    And is that supplemental or just dietary?

Malcolm:    Just dietary. They just measured potassium in their urine and said if you got more, you're eating more basically. That was the thing. That same study found that salt had absolutely no effect on anything except slightly reduce your mortality rate. I've seen again the anti-salt stuff just forget about that. Ignore it, irrelevant.

Christopher:    For all people, I've had some people say they offer some people the salt thing is relevant --

Malcolm:    I think if you got high blood pressure already, check --

Christopher:    You’ve got to find why it’s high, right?

Malcolm:    Well, it's a good idea. The only evidence I've seen of salt is actually if you try and restrict salt, it's bad for you. I've never seen any evidence that high salt intake is damaging. Maybe there are some people who are particularly salt sensitive or whatever. You got to remember, if you lower your salt intake, your body system triggers in to keep your blood pressure up, and the trigger is a thing called the renin-angiotensin system. And you know what's really damaging to your endothelium? Renin-angiotensin. Yes.

Christopher:    Oh, no! That's amazing. Okay.

Christopher:    Quite damaging. Well, they probably put stress on them when they're interacting with nature. There's no such thing, so there's no big surprise that if you try and force your blood pressure up, you're narrowing your blood vessels. Well, how do you know your blood vessels -- you're knackering your nitric oxide synthesis. So you're damaging your endothelial cells. A study also from the States, people with really highly salt restricted who already had heart failure probably had a bit knackered arteries. We were talking a 400% increase in mortality in salt-restricted diets. Of course, what's the mainstream response? All these studies weren't carried out properly. What studies have you done that were carried out properly? None. You haven't done any. You just looked at observational data and said, "Oh, look, the jungle dwellers of Brazil eat barrels of salt and they don’t die of heart disease." Yeah, and do you think there might be other few other things going on with them versus an industrialized Western person living in Chicago, for example?


Christopher:    Right. I think you'll find this a bit more complicated than that.

Malcolm:    I think you will and then you look to Japan and find, well, they eat tons of salt. It's not doing it to them. They say this counts and that doesn't count. This population is important. That population doesn't matter. They explain everything away with ridiculousness. So forget about it. Eat more. Eat low salt if you want that, KCl instead of NaCl, which is good for you.

    So there are a few things. My main thing started out with, well, don't worry about all these things because actually an awful lot of things we're told to worry about we don't need to. A lot of the drugs we're told to take we don't need to take. There are things like worrying about salt, we don't need to. Staying out of the sunshine, a lot of rubbish that is. We've given almost all the wrong advice. Avoid heart attacks by eating carbohydrates and not eating fat. Wrong. If you've got diabetes, eat carbohydrates. What? You've got a problem controlling your blood sugar level, eat sugar. Come on, guys, that's just --

Christopher:    Avoid skin cancer by staying out of the sun.

Malcolm:    Yes, stay out of the sun and die of skin cancer. Apart from exercise is smoking. Those are two things you actually get right. Everything else is the wrong way round and just more damaging, more harmful than good. And yet somehow people sustain this ridiculousness with no data either. All I do is look at the data and say, that makes sense, that makes sense, well, that makes sense. Oh, I can see how this works. We have this gurus of health or whatever they call themselves. Still will not change their messages because their status is -- you know, people say conflicts of interest. I say conflicts of interest is not just money. Money is important. If you give someone a million dollars, they're likely to say what you want them to.  But equally, a lot of these people would have said that anyway because they believe it because they're part of the tribe that believes it. The status, the authority.

    I know one thing, I'm never going to be in the guidelines committee. I'm never going to be given money to speak at a conference. I'm never going to be part of the cardiology community. I will be a hated outsider. That's what I am. And a lot of people can't deal with that. I don't mind it. I just wear a little bit of a badge of honor. The more you hate me, the happier I am.

Christopher:    Pretty easy, Malcolm.

Malcolm:    You say, well, these people should be on committees because you can't just have everybody agreeing with each other. This thing of group think, cognitive bias and all these things that are just so hugely important for people. We're social animals. We want to be part of a group. We want to be part of a thing. You don't want to say to your colleagues, you know what? The cholesterol hypothesis is bunk if I was the head of the ACC. In fact, Alderman, who was a salt guy, who was the Chairman the American Society of Hypertension and the World Health Organization and said the salt thing is rubbish. He is now a persona non grata. People won't speak to him. He doesn't get invited to conferences. His friends aren't his friends anymore.

Christopher:    That's a powerful disincentive to be the guy that stands up and says, "This is nonsense."

Malcolm:    Yeah. Well, it's like being in [1:43:02] [Indiscernible] and somebody saying, "You know what? I think Man city are better." I am going to support Manchester city. "Well, you can't sit here any longer. Get over there."

Christopher:    It makes so much sense when you look at it through the evolutionary psychology lens, right? What happened to you if you weren't part of tribe, if you're on your own in the words? You die. You need your people.

Malcolm:    Yes, you need your people. Most people do need their people. And that's why so many things are difficult to change because who's going to be the first to break ranks? Maybe they're all sitting there going, "You know what? I don't believe it. I don't believe it."

Christopher:    I'll cover you. You go first.

Malcolm:    You go. You say it. And they say it and you say, "You shouldn't say that. That's terrible." Who's cheering? We  are very driven by these things. So I would say that financial conflicts of interest are almost the least important why things don't change. We have this peer review, don't we? Peer review, the halo process of peer review. Well, who are your peers? They're all people you know they agree with you. So if I wrote a paper saying it's all bunk, guess what?

Christopher:    Guess what? You'd do the same to me.

Malcolm:    We write papers all the time that get rejected all the time. And on the most specious of reason. You didn't mention this study that no one had heard of. We didn’t take this into -- whatever. The editor seems to get one peer review going, "Oh, I think this is bunk. No, we can't publish it." This is the greatest system known for maintaining the status quo. We should get rid of peer review. It just doesn't exist. We just say publish it and then open it up and people outside the world can criticize and we can review it and debate it. Peer review is just ridiculous system. And yet we say unless it's peer reviewed, it's not valid. I have lots of peer reviewers' comments. I've been asked to give judgments on some  papers, and I've seen some of the comments that are just not -- this is just rubbish. You haven't even read the paper, have you? You don't even know what it said. You just decided you don't like it because you've looked at one of the authors.

Christopher:    Oh, wow.


Malcolm:    Yeah. It is that level. Because if you are dealing with the complaints about a paper just put in at the moment, and the complaints don't make any sense at all. You said things that we've said that we didn't say. We didn't say that. This is just made up. He's not read that. You can't have read it in the paper because we didn't say it.

Christopher:    Well, and it is going for something you said previously or --

Malcolm:    Yeah. You said that once before, didn't you? Well, maybe I did. But in this paper, it does not state it. Or they'll say you've mentioned something and you haven't. And you think, well, you just haven't read it. There was a paper written some years ago where in the methodology section the author had written, "If you read this sentence and phone this telephone phone number, you will be sent a great champagne." And it was published unchanged. No one had changed it and no one phoned the telephone number. Then one person phoned the number and the guy said, "You're the first person who's ever phoned this number. Have a great champagne." That paper got all the way through everything and no one did anything about that sentence.

Christopher:    Wow! That tells you something.

Malcolm:    Well, it tells you no one reads the methodology section.

Christopher:    It's true. I don’t read the methodology section. It's all I have to say. I don’t often understand it.

Malcolm:    Well, they're designed not to be understood. They're also designed to be written in such a way that you just fall into deep sleep when you try and read it because it is terrible stuff. Sometimes I do read the methodology section. Sometimes I do read all the stuff because I'm saying, I can't believe you got this. How did they get it? Quite often, the abstract doesn't match the text. Quite often the conclusions don't match what they found. Or if they found something -- what's the latest one I read about? We have discovered this and that, but this should make no difference to how anyone does anything. It's quite a common one where they say, well, we couldn't find any benefit from cholesterol in this population, but we should still lower the cholesterol level.  

Christopher:    Or they call it paradox.

Malcolm:    I love a paradox. A paradox is a contradiction that we don't want to pay any attention to. It's a paradox. It will be discovered that it's wrong at some point. Right now, we just ignore it. This is what happens all the time. We have seen papers where they found that people with low cholesterol level were more likely to die of heart disease. And then they said, but what we did was we took out the first two years, and we excluded this group and we excluded that group. We excluded the next group and we did this in the next thing. And the conclusion in his paper was that people with low cholesterol level were less likely to die of heart disease, which actually contradicted what they'd actually found. But then they just did this thing where they just fill it around with the data until they get the result they want.

    Is that lying? What is that? That is just we can't accept our findings. We won't accept our findings. I've seen people almost pleading saying, "Well, I know we find this but we didn’t find it. We didn’t really want to publish it." It's just amazing, some of the stuff that you come out with and you think, how did they do this? How did they do this in their brains? What's going on inside their brains where they've seen something black and white and they're just ignored it?

Christopher:    Right, rationalization. They're doing back flips inside their --

Malcolm:    Well, they're doing something, aren't they? I just think, well, maybe I've got a brain that when I see something, I just think, well, actually that seems to be contradictory and actually that means I'm wrong. You can't just give up the ghost because sometimes there are explanations that explain why you fail to see something, the pleiotropic effect of drugs, this drug does this. Yes, it does but it also does this. So it could be that it's working like rather than like this. You can say to people, here's the pleiotropic effect of statins. And if they want to believe it's all to do with LDL lowering, you just go, well, that's just irrelevant. It doesn't matter. Well, I just say, the LDL lowering is irrelevant. It doesn't matter. You can't say that. Well, you can't say that. You can't say that. Where do you get to? You're wrong, I'm right. No, you know, I'm wrong. My dad is bigger than your dad. Where does that argument go? It's just funny but -- so I just say -- I know you're trying to wrap up a bit earlier on, but essentially --

Christopher:    This is good. I'm having fun.

Malcolm:    Essentially, yes, it's a lot of lifestyle stuff. It's got very little to do with drugs. I think there are certain things you can take should you be looking at all of these factors I've talked about, possible chelation therapies and things. I suppose you should. Potentially, I haven't got as far as to be able to get all this written out, and you should do the following 123 things. I don't know if it would ever come to that that you would say that. I think that you can say to people, these are all the things that potentially could be dangerous.

Christopher:    A checklist.

Malcolm:    A checklist. And say, well, you may have none of these things. You may have one of these things. You may have ten of these things.

Christopher:    It's about modulations and predispositions.

Malcolm:    Well, a lot of these things, as I say, is this healing to damaging thing? If you're doing more healing than the damaging, carry on. If you're doing more damaging than healing, change things over until something shifts. You're out of that because we are all different. We are genetically different. Our response to injury, our white cell count, our immune systems, our repair systems, our susceptibility to damage -- these are all different things. I mean some people smoke all their lives and never get lung cancer. Some people smoke for ten years and die of lung cancer. What happened there? There was something different going on.

    So I think yes, of course, these are general issues. Some of these are specific issues to you. Maybe it is that you are vitamin C deficient. Maybe you're not taking enough. Take more. It's not really hard to do, isn't it?


Christopher:    It's not really a downside to that.

Malcolm:    I can't see any. I mean the pharmaceutical industry tells us, oh, my God! Vitamins are the most dangerous things that mankind has ever taken. You'll kill over and die. And now there's statistics for -- I think it's 2008 or something, there was not a single death through vitamin that had been identified anywhere in the US. At the same time, that year there had been 120,000 deaths from correctly prescribed medications. It's like 120,000 versus zero. Which one should you be looking at? Well, let's look at the zero and tell everyone that's really damaging. Some people go bonkers and they take too many, and it's completely pointless. I think there's one or two vitamins that potentially I've seen some downside to.

Christopher:    B6 maybe.

Malcolm:    Yeah, perhaps, those things. You don't need too much of these things.

Christopher:    Copper.

Malcolm:    Copper, yeah. There are some clear cut ones like vitamin C. It would be bloody difficult to take too much of that.

Christopher:    I don't think you can. I think it just gets --

Malcolm:    It just goes and you get fed up with taking it.

Christopher:    Yeah. It's like 20 grams is --

Malcolm:    So I think that mainly you're not going to just see any harm with various supplements other than knock your backbones down a bit. Are things good for you? Vitamin K2, magnesium, yes. Potassium, yes. I'm just slightly reluctant making a list of 120 things you should take in, being worried that people will then take 120 things and --

Christopher:    Focus on the minutia and miss the big picture.

Malcolm:    Yes, the big picture, mental wellbeing is so important. Yes, some exercise and some sunshine and these things are really important. I've just finished the -- I have a book coming out, A Statin Nation, which is coming out in about three months' time. And I'm writing another much more technical one. This is it. This is my attempt to say to you some of those things we talked about, these things we talked about in a coherent message and just say, this is how it all fits together. This sort of works. And a hypothesis,  it's not going to cover everything. The big things I didn't even know and just to find I was unaware or got wrong. I think it fits better. It fits almost everything I think, and it's also predictive. It's not just a reactive bunch of things that just people have added together, but the current hypothesis is on diet and on cholesterol and LDL. They just don’t fit. They don't work. They don't fit from also sorts of perspectives. So I hope it dies as a hypothesis. But at the moment, it's still looking pretty robust.

Christopher:    So it's going to be two books you say, a technical one --

Malcolm:    Yeah, the first one is coming out in July 12th I think it's being launched, A Statin Nation, which is a not so technical. It is more of an update in a previous book that I wrote but covering more of the stuff we've talked about here. It's a bit more analysis of things and here are some of the things you can do.

Christopher:    A prescriptive.

Malcolm:    It's more prescriptive side. Here are some of the things that there's really good evidence for of improvement in health and life expectancy. I just try to cover all those things as concisely as possible so that it's not an absolute checklist. I have said the ten things you can do to avoid heart disease but that's slightly artificial, but I think I've tried to get it to that here are the ten things.

Christopher:    So if there is a Pareto principle there, if I can do 20% of the things and get 80% of the benefit, then --

Malcolm:    Yes Well, absolutely, you do any of these things, you get benefit. But do them all and would you definitely then avoid dying of heart disease?

Christopher:    There's no guarantee in anything in life.

Malcolm:    It's about shifting odds, isn't it? At the moment, your odds are 50%, I'll shift them to 10%. I can't get rid of --

Christopher:    Yeah. I'll take that.

Malcolm:    You take that. Well, I don’t know exactly what the shifting of the odds is, but I would hope that I could get people to shift their odds 20%, 30% at least in the beneficial direction. That would be something that I would be very happy about.

Christopher:    Well, I hope people listening will get behind you and buy multiple copies of your book.

Malcolm:    Thousands of copies each.

Christopher:    Yeah, exactly, and then send them to all of your friends. You may be doing all of the things that we've been talking about already, and so you think you don’t need the book. You do need the book because unless people buy the book, it doesn't become well known and then people don't find out about it.

Malcolm:    That's the thing is that making the noise amongst all the noise, enough noise.

Christopher:    Right. If this gets to become a New York Times bestseller, then people have to take notice.

Malcolm:    Yes, it's that messaging thing that gets out there and that's the important thing.

Christopher:    I will mention this book again once it's out in July, but what's the best way for people to get it up the charts? I've heard some people talk about how you need to go into a bricks and mortar bookstore and buy a paperback copy or something. Is that true?

Malcolm:    No, if you buy it on Amazon, Amazon takes 60% or whatever is the sales price, which makes me --

Christopher:    No one gets rich writing books.

Malcolm:    No one gets rich writing books, yeah. Well, some people do but most people don't. It's described as a -- someone told me about pop groups and they said there are two sorts, those that make not as much as you might think and those that make more than you could possibly imagine. But the vast majority are in the you'd do as well working at MacDonald's with the amount of time or the amount of hours you spent on it. But it's not for those reasons per so although you need to eat and things, but it's the message out to people that I'd like to get. And if I can improve people's sense of wellbeing or just enjoyment in life, make it a bit more -- I'd like to say enjoyment makes you live longer. I do believe that is true. I think we need to stop worrying and pulling in on ourselves too much and all these medications and all these tests and all this stuff. I just think it's becoming negative. It shouldn't be negative.


    I say to people, "Go out and get suntan." They're like, "Oh, my God! Everyone is going to die." No, they're not. Stop worrying about it. It's just good for you. Does it feel good for you? Do you enjoy it? Of course, you do. Well, do it. Does it feel good taking exercise? Well, it does afterwards. I feel morally superior. And it does feel better to do these things. These things I think are generally things that would make people feel better to do, and that's one message is enjoy it. And actually, you're not harming yourself. It doesn't have to be about grinding yourself into pulp, crushing yourself and doing everything as prescribed. We need to make it fun as well.

Christopher:    Fantastic. Well, Malcolm, thank you so much for your time. I'm incredibly grateful for you. Keep up the good work keeping a squeaky wheel. Where are the best places for people to find you online?

Malcolm:    Well, I've got a blog, drmalcolmkendrick.org, which is quite an easy place to find me. And if you just type in my name into Google, you'll find stuff and things that I've written and whatever. But the blog is probably the number one place. I mean there are other bits and pieces around, but I'm hoping to try and put a couple of online kind of YouTubey type things on.

Christopher:    Oh, wow, okay.

Malcolm:    And just sort of see how they fly, if you like, just because people like their information in different ways, the blogosphere and whatever is important.

Christopher:    I must admit, I did have quite a hard time reading the blog post because I'm so used to getting my content in audio format now through my podcast and then audio books as well. So it's a consideration.

Malcolm:    I'm old-fashioned. I still write "Dear Sir" or "Madam" on emails, "Yours faithfully."

Christopher:    It's amazing.

Malcolm:    Your correspondence is important to me. But sometimes the discipline of writing a thing out is trying to make it clear. When you're speaking, you sometimes wander all over the place a bit.

Christopher:    Exactly, you condense it down.

Malcolm:    Condense it down, yeah. Well, it's nice to have chat to you and hopefully we can make a difference.

Christopher:    Absolutely. I will, of course, link to everything that you mentioned in the show notes, including as many of the studies that Dr. Kendrick mentioned. We do a really good job I think now of hunting those down and excising everything. So if you like to follow up and read the references, then you will find those in --

Malcolm:    Dr. Kendrick made-up paper.

Christopher:    -- the show notes over at nourishbalancethrive.com/podcast. Well, thank you very much.

Malcolm:    Okay. Nice to meet you.  Cheers.

[1:57:34]    End of Audio

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