Tag Archives for " the clot thickens "

March 14, 2022

Is there a new villain in the mystery of heart disease with Dr. Malcolm Kendrick

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For decades, the effort on solving the heart disease mystery has been focused on one villain, cholesterol. But what if cholesterol is the red herring?

In his book, The Clot Thickens, Dr. Malcolm Kendrick brings forward a new hypothesis and shows us how it might just be the key to solving the mystery of heart disease.


Let's Say Hello

[00:01:10.750] – Allan

Hey, Ras. How are things going?

[00:01:12.800] – Rachel

Good, Allan. How are you today?

[00:01:14.860] – Allan

I'm tired.

[00:01:17.350] – Rachel

I bet. You've been busy.

[00:01:19.470] – Allan

I've been busy. Yeah. We're moving the gym. We've talked about this a few times on the show, but yes, this weekend was when the rubber hit the road and got a crew together, loaded up almost all the equipment, put it in there. And I'm kind of particular about certain things in the gym, so I want to make sure this stuff makes sense. And there's not one piece there and then the other piece there. So if someone wants to work legs, it kind of works. If someone wants to work with the dumbbells, it kind of works. So putting it in and a lot of people helping. And it's great to have a lot of people helping, but sometimes it's also not so great to have a lot of people helping. You're like, okay, I got to figure things out, and I don't want a lot of people standing around. So it's like, okay, so everybody got all the equipment in there, and just so there's a stack of shit stuff. Okay, I am sorry. Stacks of stuff everywhere. And I'm like, okay, I'm going through it, putting it where I want it, assembling things that weren't assembled or had to be unassembled to move and got everything kind of where I want it.

[00:02:30.960] – Allan

And then today was just working on taking the camera system down. And it's kind of surprising. I'm generally fit, but I'm apparently not walk up and down a ladder a lot of times and move the ladder and up and down again and walk the ladder. That kind of worked out.

[00:02:55.530] – Allan

I'm fine. Just let me pull stuff around and just pick up dumbbells and go around. I can do that all day long, but that up and down the ladder thing is just man, that's a workout. Yeah. So if you want to work out, just grab a six foot ladder, open it up, set it up, just walk to the top of it, reach up to the wall, grab something, touch them on the wall and then come back down, move the ladder again and go up again. Just do that about 50 times.

[00:03:24.850] – Rachel

Sounds like you have a new piece of equipment you could add to your gym.

[00:03:28.510] – Allan

Yeah, ladders. Well, there is actually a piece of machinery called a Jacob's ladder. And it's basically these rungs that just go and put them on a machine like a treadmill, and you reach up and you grab one of the rungs and it just goes. And so it's like you're consistently climbing up a ladder at about a 45 degree, maybe a little bit steeper than a 45 degree. So there's a little bit of upper body strength because you're not just pulling yourself, but you're sort of also having to support a little bit of your body weight at that angle. And then, of course, most of it, if you're doing it right, is with your legs. So, yeah, there is a Jacob's ladder. That's an exercise piece of equipment or torture equipment, if you will. Yeah, you can do the same, but just go to Home Depot and buy a six foot ladder.

[00:04:15.670] – Rachel

Oh, my gosh, that's a workout.

[00:04:18.830] – Allan

Yeah. So how are things up there?

[00:04:20.640] – Rachel

Good. It's funny you say you're tired. I was going to say the same thing. My trainer calls this month the monster month, which is very appropriate. I did a 16 miler or the other weekend and 18 after that. And this will be a cutback weekend, and after that will be my 20 miler. So that's a monster month. That's a lot of miles. And I'm tired.

[00:04:45.010] – Allan

I never did 20 miles ever training for any of the races, even the ultra that I did, I'd never done a 20.

[00:04:51.750] – Rachel

What was your highest?

[00:04:52.760] – Allan

I think I did an 18 when I was training for the ultra.

[00:04:57.230] – Rachel

That's a very common point to stop at. Some people do 18 or 20. Other people might do 22, but usually 18 is the magic number. So there's really not a whole ton to gain with just two more miles that might be just anywhere from…

[00:05:14.890] – Allan

You are pushing past what would normally be the bonk for most runners. And so, yeah, the 14 to 18 miles. And anyone doing a marathon or planning to do a marathon that 14 to 18 is about the time when your body starts telling you, hey, we've done enough of this. It's probably time to stop. And so the individuals that can mentally push past that point can actually potentially go forever. Not true, but in a general sense, there's a mental aspect of every mile after 14 that's very different. And for every person, it's a little different. But I just know that if you get to a marathon by mile 14, I'd say probably 90% of the people doing that marathon are walking at that point. So they might have started a little faster than you. But if you're still basically even doing a job, you're going to see a lot of walkers after mile 14, and a lot of people bailing out at that point, too. So maybe pushing yourself just a little bit past bonk in a training run is actually good from a mental fortitude. If nothing else.

[00:06:30.930] – Rachel

That's what I was going to say, 20 is my preferred number for me. It just makes me feel a little better, a little more accomplished, feel a little bit more confident. And so for some reason, for no reason, really physically, it's just for me, that's the mental part where okay, I know I got this.

[00:06:49.990] – Allan

How many weeks out are we from the run?

[00:06:52.430] – Rachel

Oh, gosh, I think we are five weeks away. It's early April. Coming up fast.

[00:06:58.220] – Allan

So is this a long taper or are you going to have a monster and then a couple of other really tough days?

[00:07:03.970] – Rachel

I don't know, because I only get two weeks of my schedule at a time. And the reason why we do that is because it could change based on how I'm feeling. I might progress faster or need some more recovery time, but I suspect that I will probably have roughly a two week taper. So to the 20 miler, it will probably be my last hard effort, my long effort, and then it'll just be kind of fine tuning little stuff after that, probably some more Hill and speed work.

[00:07:31.170] – Allan

Speed work.

[00:07:32.650] – Rachel

Always the fun stuff. Fun and fast.

[00:07:36.550] – Allan

All right. Well, are you ready to have this conversation with Dr. Kendrick?

[00:07:40.720] – Rachel



[00:08:16.810] – Allan

Dr. Kendrick, welcome to 40+ Fitness.

[00:08:19.990] – Dr. Kendrick

Thanks for inviting me. Thanks for inviting me. Looking forward to it.

[00:08:23.340] – Allan

Yeah, well, I'm 56 years old, male, Caucasian, and so anything that does with heart disease kind of comes top of mind as the number one killer for guys like me and ladies of my age as well. It's become a thing that we all know is actually the biggest killer for most of us. And so your book, The Clot Thickens, the Enduring Mystery of Heart Disease. Well, of course I'm going to want to read that mystery because it's a murder mystery. It's a big one. I'm really happy to have you here today. The one thing I'll start this out with is while I do consider myself somewhat of a health and fitness geek, I'm not anywhere close to the running in the running for Cardiovascular Research Geek of the Year, as you are. So I have to tell you as I was reading the book, one, it's fascinating. I'd love to sit down in a bar and have a beer with you because you just seem like that kind of fun guy that I would enjoy that time with. But beyond that, I think you opened up a whole different layer of the onion and then literally just started chopping it up deeper, deeper, deeper.

[00:09:43.070] – Allan

I thought I knew a lot because I've talked to a lot of people and I've studied this. And like I said, I consider myself a geek. But then you started really going deep into some of these concepts that quite frankly, it's deeper than I could wave and understand all the time. So I'm going to tell you, you left me alone sometimes, but you always seem to come back. And it was just this layering of understanding that when you get to the end of it, you're like, well, okay, that actually makes sense. And that's why they say this and they do that. So I want to get into that in a little bit later. But I want to thank you for this book because I do think for anyone who's concerned about their heart health or anything cardiovascular health related, this is a great book to read.

[00:10:29.810] – Dr. Kendrick

Thank you.

[00:10:31.490] – Allan

Now, of course, most of us were in our 50s, 40s, 50s 60s. We go into the doctor, they take a little bit of blood beforehand, and then they go in there and shock and awe, oh, my God, your cholesterol is so high. How are you still alive? We've got to get you on a statin, and a lot of that comes back to this, I'm going to call it a cholesterol hypothesis. But to be fair, anyone on that side of the argument, they don't believe it's a hypothesis anymore. They believe it's a law, a law of heart, if you will. This cholesterol. Can we talk a little bit about why this became so contentious? Why is there no debate beyond this is what happens. And then a little bit about why there might be a crack in the armor for this cholesterol hypothesis.

[00:11:29.930] – Dr. Kendrick

I think you go through this and you can go through it in different ways. The sort of question of why does it just become the same questions back to the first law of statin dynamics or whatever we call it. It's quite interesting, but I am interested in looking at how ideas take hold and become incredibly widely believed based on very little. In this case, it was more than very little. But the idea itself was in a way, I think it's taking hold because it's so simple, although it keeps changing. So the original thinking was if you eat too much cholesterol or diet high cholesterol, this will raise your blood cholesterol level, and then this excess cholesterol will be deposited in your arteries that will cause thickening and narrowings. And then eventually one of the thickenings will fully block and you'll have a heart attack or stroke. So it's incredibly easy to visualize. And I think there's a story humans love a nice, easy story because HL Menken who said for every complex problem there's a solution that's easy, simple to understand and wrong. In this case, we have a very easy and simple to understand story.

[00:12:44.610] – Dr. Kendrick

Of course, if you go back to the man who pushed it hardest was Angel Keys, who many people have heard of. Some people think he's a hero. He's not one of my heroes, but he was the first one to really push it. And he started off by saying, if you eat cholesterol too much cholesterol, the cholesterol level rise, et cetera, et cetera. He then did experiments on feeding human beings cholesterol and find it made absolutely no difference to the level of cholesterol or at the time, the cholesterol he was measuring. I'm not entirely sure what he was measuring because no one knew was that thing called LDL. It just measured a kind of lipids in your blood. So leaving that to one side, it made no difference. And in fact, if you look at recent experiments, cholesterol in the diet makes almost no difference to cholesterol in your bloodstream. And of course, you don't even have any cholesterol in your bloodstream. So the whole concept starts to fall apart as you dig into it. But then I think it was kind of floundering a bit in about the late 70s and 80s when there had been various cholesterol which are actually LDL loadings, like protein, bad cholesterol, the term for it lowering agents, but they hadn't really made any difference.

[00:13:53.910] – Dr. Kendrick

Then statins came along. They lowered the LDL, they reduced the risk of heart disease, and they were held as the ultimate severes of mankind. And at that point, really any opposition apart from very few people, just faded away. If you have hypothesis high LDL causes heart disease, it would lower the LDL, low density of protein, and the rate of heart disease goes down. Now, that's pretty strong evidence you would imagine. In fact, most people thought it was conclusive. This is it, if you like. So I think that's kind of rushed over millions of bits in the way. But I suppose that's the kind of basic elements to it. And of course, there was a point where to research at Dulstein and Brown found that people who had extremely high levels of LDL in their bloodstream were more likely to die heart disease when they were young. They then identified a thing called the LDL receptor, which takes LDL out of the bloodstream. And people who had fewer LDL receptors or ones that didn't work properly had these extremely high levels of LDL. And then they said that a lot of them died very young. And if you like this conclusive proof, and in fact, people throw the familiar hypochosterolemia, which is a term high

[00:15:16.680] – Dr. Kendrick

It's not cholesterol, it's LDL. So it should really be called familiar high density lipoproteinmia. But if you look at the actual facts around familiar hypocholesterolemia, in fact, that argument doesn't hold up very well, but people just don't even wish to look at it. But in fact, I wrote a paper recently with a few other researchers showing that some people with high LDL at the same time have a high number of clotting factors. The two things are very often related. And in fact, the LDL receptor itself takes clotting factors out of the blood. So if you have less LDL receptors, you have both a high LDL and you have a lot of extra clotting factors. So there's two things going on. And in fact, when you look at familiar FH and you look at, say, brothers who got the gene for LDL being raised, one of them has the LDL problem and the other one doesn't, they both have the same rates of heart disease because the other one has also got the forcing factor out of the heart disease. In fact, it's almost like I sometimes use the example of Twelve Angry Men, a film which you may or may not have seen.

[00:16:30.450] – Dr. Kendrick

But it starts in a courtroom where a young Latino man, this is 1940s, is accused of murdering his father and all the evidence has built up that it looks like it couldn't possibly be anybody else. It's got to be him. He was seen holding an unusual knife. Somebody shouted, they heard him shouting, I'll kill you, et cetera, et cetera. And the film is basically somebody picking every single piece of evidence apart to the point where you end up saying, well, actually, yes, he couldn't stab his father because the person who apparently heard him shout was deaf and it was an alt training going past at the same time. And the person who thought they saw him stabbed him, wore thick glasses and couldn't possibly have seen what was going on, et cetera, et cetera. All those are very simple things. But the central theme of the film was actually that once you've decided someone's guilty, you create all the evidence and you just bring it around and everything is made to fit to this action. Whereas if you sort of come back and say, okay, let's see if anybody else could have committed this murder, let's look at what actually happened.

[00:17:32.350] – Dr. Kendrick

And to an extent, that's kind of where I took it, which is you almost can't talk about heart disease without talking about LDL and cholesterol because that's the playing ground field, if you like. And as I said to many people, I discuss it. I've tried to say, if you play on that playing ground, on the playing field, the referees belong to them, the ball belongs to them, the Stadium belongs to them, they write all the rules and you can't win. So what you have to do is say, well, I'm not going to play that game in that place because I can't win there because you'd end up talking about cholesterol all the time, but I don't want to talk about cholesterol because it doesn't make any sense. So I've tried in this book to sort of say, leave it aside. Let's look at it from another perspective. Is there another way of looking at heart disease with ignoring LDL cholesterol and all that, that actually fits the facts better than the cholesterol hypothesis? And in fact, I believe that almost anything fits the facts better than the cholesterol hypothesis, because beyond the things that I've told you, some of which are not even true, there isn't anything to sustain it.

[00:18:36.730] – Dr. Kendrick

People say, I would use an example sometimes I say, well, smoking a cigarette, what does that do to your LDL level? Nothing. So what's the connection between there was an advert in the UK at one point showing people smoking cigarettes, and as they smoked cigarettes, and a sticky Goo came out at the end of it and they were trying to say, if you smoke a cigarette, the sticky Goo goes into your arteries. Well, there is no sticky Goo in a cigarette. So where does the sticky Goo come from? Within the cigarette? There's nothing there to associate with, say, the LDL. So there's a very important factor. And what makes it has absolutely no connection with cholesterol or LDL. And if you look at, say, diabetes, which probably from a population perspective, and the fact that there are more people with diabetes, there's millions of people on a population basis. Diabetes doesn't raise your cholesterol level, nothing to do with your cholesterol level. So it's obviously operating through a different mechanism. So when you start looking at the things that can cause heart disease and say that we know cause heart disease, there are some things that we say cause heart disease and they don't.

[00:19:44.860] – Dr. Kendrick

But smoking definitely does. Diabetes definitely does. And you look at those two things and say, well, let's try and relate them to the LDL hypothesis. Well, I can't. There's nothing there nothing to grow up all of. So something else is happening in this case. Something else is causing a heart disease with these very highly increased population levels. But if you look at even raised blood pressure, which does increase the risk of heart disease, again, what's that doing to your LDL? Nothing. So when you start looking at all sorts of factors, the most important factors, if you go to your doctor and they say, let's look at your risk of heart disease in the UK, they have a thing called Q risk. It's about 20 factors, of which none of them are LDL. Actually, it doesn't even figure in assessing your risk. So the more you look at it, the more you think it just doesn't work.

[00:20:36.920] – Allan

Basically, the way I look at it is you ask someone, where did you find your keys? And the answer is, the last place I looked. And so if you think you have your answer, you stop looking. And if we did that in other aspects of science, we would still be saying the Earth is flat. We would still be saying the stars and the planets circle us and we're the center of the universe. And I don't mean that in a soft way. I'm just saying someone had to be the heretic. Someone had to step out on a ledge and say, well, there's a few bits and pieces here that just don't seem to make sense. They don't line up the way that you say they do. And here's this other hypothesis that seems to line up more of them. And that's the hypothesis you brought forward in the book, the Thrombogenic, or I'm going to call it from going for blood clot, because that rolls off the tongue a little easier.

[00:21:35.590] – Dr. Kendrick

Thrombo just means blood clotting and generic just means the initiation of where it comes from anyway.

[00:21:44.470] – Allan

Right? Exactly. You get into medical terminology a few times in the book because a lot of times the same words are used for different words are used for the same thing. And sometimes the same words are used for different things where you're talking salts or you're talking this or that. So the reality is it gets very complex sometimes just the terminology that makes it that way.

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[00:24:10.090] – Allan

In The Blood Clot Hypothesis, can you kind of give us a general, high level overview of what that is and how that's different?

[00:24:19.510] – Dr. Kendrick

Yeah. Well, essentially it's very I try to keep it as simple as possible, is that all your blood vessels are now just starting with a point that obviously this atherosclerosis, which is a thickening in your arteries, it only occurs in your arteries, larger arteries in your body, never in your veins, and never very rarely in the blood vessels in your lungs, which are called pulmonary circulation, which is one of the first things you look at and say, well, why there? But anyway, all of the blood vessels in your body are lined by a thing called endothelial cells, a bit like tiles on the wall, although they're obviously a lot more complicated than tiles on your wall. And so you have the flexible tiles on all your blood vessels called endothelial cells, and they have many different functions. I like to think of the endothelium as like an organ of your body. It's just so huge and complicated, so many mechanisms, it does so much. These cells are like, just unbelievably complicated. But anyway, outside of all their functions, one of the clear functions that they have is to stop anything sticking to them. So they are like Teflon.

[00:25:33.190] – Dr. Kendrick

So blood flows through them, it doesn't stick to them and it doesn't form clots on them. And there's all sorts of things that I say in the book that all these endothelial layers are actually covered by a very Teflon layer, not really Teflon. It looks like a lawn under the electron microscope. Little tendrils and tendrils of sugars and proteins that stick out and they contain them. Within this forest are anticoagulant factors and factors that make the blood vessels contract and expanded hugely complicated system going on in there. But essentially there's a very strong do not clot here message going on in all blood vessels. But if you damage this called glycocalyx, which is a term that most doctors have never heard of. But if you damage the glycocalyx and you expose the endothelial cell underneath, you start to lose this anti coagulant layer. If you strip endothelial cells or damage them, then you expose the underlying artery wall. And then that's a very big mistake, because lying in there are like factors that are incredibly potent blood clotting agent or tissue factor, which is basically like the red alarm signal. The moment tissue factor is exposed, the blood hits that point and just goes, bang, I'm going to have a blood clot.

[00:26:51.950] – Dr. Kendrick

Of course, if you take off one endothelial cell, we're talking about something that's 100 in the thickness of a human hair. So this is not a major blood clot we're talking about, but if you do, say a thousand or however many it is and damage them in some way, the blood clot will form at that point. Now, this is probably happening, I hate to say it in your blood vessels. Most of the time, we are continuously having points in our blood vessels that are doing a lot of stress and damage and blood clot forming. Mostly what happens then is the blood clot stops growing, because for every factor that says blood clot start here, there's another 20 factors going, stop, stop. We don't want this going too far. It's a tremendously complicated feedback system all the time. It's just mind bogglingly complicated. But anyway, so clot forms, there stops forming, it shaved away through various mechanisms. And something that people couldn't understand for many hundreds of years was how do you find a plaque which some people have said was a blood clot underneath the endothelium? Because surely if the clock forms, it must form on top of the endothelium, not underneath the endothelium.

[00:28:05.500] – Dr. Kendrick

And in fact, the very first person to propose this hypothesis, called Workout in 1852. So we are going back a long time couldn't explain, he said, when I'm looking at a sporting plates, I'm looking at blood clots, I'm looking at them and they are blood clots in various stages of repair and growth and whatever. And another chap called worker who made people with horror city, but it's underneath the endothelium. So they knew there was a thing called which I'm quite impressed with, and they also knew what they were looking at. And so people who say there was no such thing as heart disease before the year 1900, I've got two guys in Vienna discussing atherosclerosis plots in detail 50 years before this. Anyway, so what they didn't realize was that, yes, you get this blood clot and it falls on this area. And then what happens? What if it just broke off and carried on down the archery? It would eventually block something further down, so that can't happen. So what happens is that there are pre endothelial cells. They're called endothelial progenitor cells. They're floating around in your bloodstream, they're made in your bone marrow and they recognize this area of blood clot and they stick to it and they form a new layer of endothelium on top of it.

[00:29:15.860] – Dr. Kendrick

And then the blood clot that has formed is now within the artery wall. This is how it happens. Endothelial progenitor cells were not discovered till the mid 19th 90s, by the way. So obviously what then happens is that little blood clot that's formed mostly repair systems come along, things called macrophages white blood cells. They tear it away, they chomp at it, they take it into tiny little bits and then get rid of it removed and it's gone. The problem happens is if you have repeated blood clots at that same point, so you kind of get blood clots, it then becomes associated with an area of vulnerability to that point where it's formed. New industry sales are not as robust. There's a bit of flat lying underneath it. It's a bit narrowed at that point. So this becomes a focus if you like a bit like a pothole in a road where a pothole forms and then somebody bumps and then bump, bump, bump, bump, bump. And eventually you get this big pothole, which is a major problem, and you've got to fill it in. I know that sometimes use the analogy, if you don't fill in your potholes fast enough, then your roads will be a disaster.

[00:30:24.410] – Dr. Kendrick

If you make sure you repair your potholes fast enough, then you will have an apparently smooth road. If you look at it closely, you'll probably see there was a pothole here once, but it's okay now. It's been repaired. And then gradually you get blood clot forming after blood clot forming after blood clot forming, the artery narrows at that point, and then it becomes a focus for that final blood clot that is big enough to block the artery fully. And then you have things like heart attacks and strokes. So it's really just the same process. And conventional medical thinking accepts that the final event is a blood clot. We all know that. There's also a pretty wide acceptance that the growth of plaques is due to repeated blood clotting at the same point. You can see this happening and you can see that if you look at some of the facts and our trees, it looks like tree rings one after the other. What they won't accept is that the first step in this process is the same thing. At the moment the idea is, well, it's LDL that gets into the artery wall and causes the initial thickening, and then another process takes over the blood clotting process.

[00:31:32.850] – Dr. Kendrick

All I'm saying all the thermogenic hypothesis of the blood clotting hypothesis is it's the same process from start to finish. The first step is damage to the artery wall, followed by a blood clot. The growth is damaged to the artery wall, followed by blood clot. And the final event is damaged to the Artery wall, followed by a big obstructive blood clot. So essentially it's just the same process all the way through. That's it. It's not a complicated mechanism. If I just want an easy mechanism, I think most people can understand it. It's not beyond that can of anybody to understand. So that really is the process of plaque initiation, growth, and then the final terminal event is all the same thing. So that's it, is that makes sense.

[00:32:23.920] – Allan

Yeah, absolutely. I'm going to jump ahead a little bit on our plan here, because I think this is actually a really good time to talk about lipoprotein A versus the LDL that we've become so accustomed to measuring. You brought up something I think that was really interesting was that I've talked to a lot of doctors and a lot of them say, yeah, there's cholesterol in those blockages. Those blockages have cholesterol in them, which you would expect if the Blood's clotting. It's pulling in a lot of other stuff with it. But in fact, what you've said in the book was that these are more like cholesterol salts, I guess. Cholesterol esters, I'm sorry, I think, is what you said. Cholesterol esters versus actual cholesterol. And that's where the lipoprotein a, which in talking to some people about blood tests, they're saying you want to add that to your lipid panel because that number might actually be important. More important than LDL? And in your book, you seem to indicate that it probably is, although we don't have a statin or something we can really take to reduce it. So there's not a lot of emphasis on studying what we could do about that.

[00:33:33.220] – Dr. Kendrick

No. Well, yeah, I mean, it's part of it almost a twelve angry man approach, is that you say, oh, look, there's cholesterol crystals inside atherosclerotic plaques, then there are cholesterol crystals inside atherosclerotic plaques. And the argument goes, well, cholesterol is carried around in LDL, low density lipoproteins, and therefore the cholesterol we see as these crystals must have come from the LDL. Where else could it have come from? Of course, the answer to that is that cholesterol is carrying around in proteins as our fats, and some of the things that the cholesterol is all carrying around in what's called a cholesterol Ester, which is one cholesterol molecule attached to a fatty acid that's just, Esther is acid plus up. But don't worry, the chemical is relatively straightforward, but one thing you cannot do is turn the cholesterol Ester into phosphorus Crystal, because you need pure cholesterol in order to do this. So the one place it could not have come from a cholesterol Crystal is the LDL. That's not a possible source for it. Then you ask the question, where could it have come from? And the answer is, the only tissue in the body that contains sufficient free cholesterol is the membranes of red blood cells.

[00:34:49.590] – Dr. Kendrick

And neurons have quite a few, but they don't float around in the bloodstream. In fact, cholesterol is essential to the function of red blood cells because it modulates the what they call the lipid layer, if you like, and allows the oxygen to get in and the oxide to get out. Without this intercollation, which is the thing within the blood cell membrane, it couldn't work. So it's very high in cholesterol, and that is the only potential source of enough free cholesterol to form a Crystal. And in fact, there are several papers, if you go and look, and if you decide to look, people have looked at it and said, basically, yes, the cholesterol crystals are found not in all plaques, but in a lot of them, and that this cholesterol cannot have come from cholesterol esters within LDL, therefore, they must have another source. The only possible source is red blood cells. I mean, this is written down in ten papers that I read. These people have just come to this conclusion, but the next conclusion is therefore, well, if it didn't come from LDL and it came from red blood cells, this changes our entire thinking about what's inside plaque, doesn't it?

[00:36:01.480] – Dr. Kendrick

Well, apparently it doesn't, because there is no evidence you can present that interferes with people saying, well, it doesn't matter anyway. The other thing I need touching on it is, of course, you can find the remnants of lipoproteins, low density lipoproteins in plaques. We can find the remnants of anything if you decide to look, I don't know. And then people have said, well, that they must have been LDL. And you go, well, yes, you can find these things. But of course, if you went past 100 primary care physicians or 100 doctors patients and said, what is LPA? Lipoprotein, what is it? They don't know. They have no idea what it is. And when you say to them what LPA is, is an LDL molecule with an extra protein attached to it. And that protein is April Hypocritein. A. That's why it's called LPA. So this extra protein is stuck to the side of an LDL. It's quite a big protein. And you get asked, well, what the hell is it doing there? Why have, say, 20% of your LDL molecules floating around in your blood got this additional protein stuck to the side of it?

[00:37:10.890] – Dr. Kendrick

It can't be there by accident. It has to have a purpose. What is the purpose? Well, the interesting, the fascinating thing is that is that if you look at all blood clots when they form contain a protein called plasminogen. And plasminogen is incorporated into all blood clots. And it doesn't do anything, except if it is activated, it turns into plasma, which is an enzyme which splits apart blood clots. The plasma is a blood clot destroyer. And you turn plasminogen into plasma with a substance called tissue plasminogen activator. Some people may have heard of this because when you have a stroke or heart attack, you can be given this enzyme as an injection. And it finds a blood clot and it strips it apart and gets rid of the clot. So the circulation opens up again. Now, TPA turns plasminogen into plasma. Lpa, the Apollife protein, a protein that is attached to LPA, is almost identical to plasminogen. In fact, it is chemically identical, except it's folded differently at one end. That's important because enzymes, if they come across a protein that's differently folded, can't do anything with them. So TPA comes across LPA and bounces off it.

[00:38:43.830] – Dr. Kendrick

So LPA inhibits the function of TPA. So if you have a blood clot with lots of LPA in it, TPA can't turn plasminogen into plasma. And the clot cannot be got rid of, at least not so easily. And what's interesting is that if you have damage to an artery, almost the first thing that's attracted to it is LPA. It sticks to the surface area, forms bonds there, and you've got like a super glue or whatever you call it, layer, which is absolutely rammed in there. So the more LPA you have in your blood, if you get arterial damage, then you get harder to remove blood clot forming there. It's a tough thing to remove. So the TPA comes along, tries to activate the plasminogen to turn the plasminogen into plasma. Lpa is there. It says no, you ain't touring anything to anything else. And so therefore you have a blood flow. So the LPA doesn't cause the damage to the artery wall. But when there is damage, it accelerates or accentuates the damage considerably. It's more difficult to get rid of this clot. So instead of a blood clot size A, you have a blood clot size two A.

[00:39:56.990] – Dr. Kendrick

So that point of damage with people who have high LPA levels is going to become more of a rapid focus for the development of heart disease. Now of course, the other thing that happens is that the LPA becomes incorporated into the plaque and the LPA, if you look at it and you don't look for the apolypoprotein a protein looks exactly like LDL because it is LDL. So if you just look for LDL, you find LDL. But if you look for LPA, you find it's actually LPA. It's just a complete idiotic guide to grabbing the wrong end of the stick. By the way, this is not controversial. I'm saying these things, putting the whole story together. This way people don't tend to do it, but nothing I am telling you about the structure of plasminogen, TPA, apolypoprotein A, blah, blah, blah. This is all just factual. You can go and look it up and you will find I'm just saying things that are absolute scientific facts. So you're right, LPA is more of a risk factor than Ldl. Ldl isn't that risk factor. It is a risk factor for heart disease. But if you don't have any of the other underlying problems that cause endothelial damage, it doesn't matter.

[00:41:14.980] – Dr. Kendrick

Nothing's going to happen. And the reason why we have LPA in the first place is because humans can't produce vitamin C. And vitamin C, if you don't have enough vitamin C, we can't make it ourselves. We have to eat it. If you have enough vitamin C, one of the first things that happens is your blood vessels start to crack because vitamin C is required to produce collagen and collagen strengthens your arteries. And when your arteries start to weaken, your blood vessels start to weaken. Which is why the first sign of scurvy is bleeding guns and then bleeding everything else. And then you bleed to death. So LPA comes along, finds these cracks and sticks to it. Now that's great if you don't have enough vitamin C. But if you have too much LPA and you've got cracks forming and you don't want to form, then you're at more risk of dying of heart disease. This is just a fact. Again, in fact, everything if you turn it around, if you decide LDL causes heart disease, you look at plaques, you see they've got LDL, then you see they've got cholesterol in them and then you go.

[00:42:12.530] – Dr. Kendrick

If it's all. There you go. Yeah, but cholesterol can't have come from LDL. It could only have come from a blood cell. And the LDL particles you're seeing are actually LPA, which is a completely different thing. It's actually a blood clotting factor. It's got nothing to do with raised lipid levels in your blood. So it's just again, as you said, the planet circle the Earth, circle the planet as a sun. You can almost create and in fact, people did a model where you have the Earth at the center of the solar system and the sun going around and the moon going around, and people did. They had complicated models. 600 BC, the antiquthera mechanism produced by the Greeks, where you cranked it round and round and then the planets moved in order and the sun moved in the moon, and you could work out where you were. It was completely the wrong way around, but it very nearly worked. Ldl hypothesis, it's the wrong way round, but it very nearly worked. So, in other words, that's why it continues, because you can look at an individual thing and say, oh, that's proof. And you go, Actually, that's contradiction, not proof.

[00:43:18.970] – Allan

But like I said. Once you find your keys, you quit looking. So let's talk about that, because the if is a really important thing. If there's damage, if there's significant damage, then we have a problem, particularly if we have these other risk factors. I want to go through a few of these because these are really important because you're probably going to hear the alignment with a lot of things your doctor will tell you. And this is kind of the lynch pin. If you address these things, you lower your risk considerably. So the first one is blood sugar. And before we jump in, I wanted to say one thing real quickly. I really appreciate that you took the time to discuss diabetes and prediabetes and really kind of just came to the whole conclusion. Let's just call them the same thing, because just because you haven't diagnosed it doesn't mean it doesn't exist. We're already long down that road before it happens, but the core of it is what's happening with our blood sugar and then the insulin response of our body. Can you get into why blood sugar, high blood sugar, particularly, is a problem for our endothelial. Endothelium.

[00:44:44.050] – Dr. Kendrick


[00:44:45.260] – Allan


[00:44:52.330] – Dr. Kendrick

Well, as I said, the Endothelium has this lining called glycocalics, which is like strands of sugar and protein all stitched together again. We'll call it 1 mm thick. It isn't 1 mm thick, it's about zero or whatever. It is 1 mm thick. And you want it to be checked because it acts as a protective layer. It starts by crossing, blah, blah, blah. So when you look at and it's possible to look at the glycocalics layer under a microscope. Now, there's a glycol check monitoring, where you can stick it under the tongue and you can see the thickness of the glycocalics and you can do certain things to it. You can make people's blood sugar go up and if their blood sugar goes up, you can see the glycocalics' shrinking and people who have high blood sugar levels have got damaged clumpy, not very healthy glycocalics. This is, again, just you can go and look up like a check or something, but you want to go and look at it. It looks like a good glycocalics anyway. So obviously this makes the entire underlying endothelium is now exposed to the blood. Things come along and stick to the endothelium. Things damage, the endothelium. Endothelium gets stripped off.

[00:46:04.220] – Dr. Kendrick

Blood plots form. It's just the same process really going on. Double trouble with diabetes is because not just your blood vessels that have got glycogenics lining them, the small blood vessels, your capillaries, your arterials, these are tiny, tiny sizes, big enough to allow one red blood cell to squeeze through some size. They have, like, glycocalics on them and obviously they don't have room for atherosclerotic plaque to develop inside them. That would be like a small snake, swallowing an elephant. We're talking, whether that's the correct size or not, a blue whale maybe. You can't get atherosclerotic plaques in tiny blood vessels, but what you can do is you can destroy it. So if the glycocalics is damaged and then the capillary is exposed to things going through it and then it's damaged and ripped off, what happens is the capillary just breaks down or bursts and they're no longer there and you can see the damage that you get in diabetes is not just big blood vessel damage. Small blood vessels, the key areas of your body where you need these small blood vessels really is the back of the eyes. Tiny little blood vessels

[00:47:19.500] – Dr. Kendrick

There are nourishing your macula and your retina. And you can see if you look at the back of the eyes with diabetes, you can see little hemorrhages and bursts and white bits where things and exudates have come out. This is because the small blood vessels are being destroyed by the diabetes, which is the shy sugar levels damage any glycocalics and allowing the damage to occur. So diabetic blindness is a real problem. Same thing happens in your kidneys, because in your kidneys, at the very smallest level in your nephrons, you have a really small blood vessels going into these nephrons and capsule, blah, blah, blah. Now, if these small capillaries doing all the work, all the waste products going out and it's really complicated, but if they start to break down and the nephron dies and it stops working, so you get kidney failure as the nephron starts to die due to, again, small blood vessels damage. And then you get very small blood vessels that are supplying around the nerves at the end of your fingers and things like this, these start to block off and break off. So you start to kill your neurons at the end of your fingers so you get peripheral neuropathy, you lose sensation.

[00:48:29.970] – Dr. Kendrick

And of course, the problem with losing sensation is you bash them and then you get ulcers, and of course, then the skin itself, these are where the smallest blood vessels are going. So the blood vessel supplying your legs and your periphery are starting to die off as well. And so if you damage the skin, it doesn't prepare and you get ulcers. And in fact, it's ulcer and gangrene problem and you lose toes and you lose limbs. The commonest reason for amputation, below knee and the other form of amputation nowadays used to be smoking. There's no diabetes because you lose circulation to the skin, to the nerves, to the eye, to the kidneys, blah, blah, blah. And this is what's going on. It's just the same process. So people say a small vessel disease and atherosclerosis are different things. No, they're not. They're just different manifestations of exactly the same process. The problem is, of course, if you start to break down small blood vessels, then the total, what they call the peripheral resistance, the blood is going to go out of big blood vessels. The arteries go through the capillaries, back into the veins and back up.

[00:49:34.020] – Dr. Kendrick

You start to lose capillaries. What they call peripheral resistance starts to increase. So as a peripheral resistance increases, the blood pressure has to go up the first the blood through less filleries that are there. And you see this happening as well in later stage. And then the kidneys start to fail and then you get chronic kidney disease and blah, blah, blah, the whole thing starts to multiply in effect around itself. So is diabetes from a perspective of a population wide problem, high blood sugar levels. As I said, just because no one said you've got diabetes doesn't mean you're not high blood sugar levels. It's just not high enough that anyone says it's diabetes yet, and sometimes it's hiding when you look for it. So it's ridiculous to say we have diabetes and we've got prediabetes and we've got medical, all these stupid terms that we've got. What you've got is there's resistance to the impact of insulin. Your blood sugar levels up, your insulin level goes up and insulin itself is damaging to blood vessels. And to feel yourself when the concentration is too high, fantastic self insulin, but you don't want it up here, which is obviously one of the things that happens currently.

[00:50:42.830] – Dr. Kendrick

The treatments are to force the sugar level down by driving into the level up. It's like, okay, fine. That's why lifting up the edge of the go up and sweeping everything underneath, dump it up and down it and going, well, we've sorted that out.

[00:50:57.510] – Allan

Yes. Now, a related thing is cortisol. It's a hormone. Most of us know of it as a stress hormone. And in our current environment, anyone that says they're not stressed out at some point or another, it's not being Truthful. Stress is a thing it's out there. And I think for a lot of us, it's adversely affected our health because our Cortisol levels are not where they should be. Normal stress of I see a bear, the bear is dangerous. I know this. I run away. I've burned off a lot of energy doing that, and the bear is no longer an emergency and I move on with my life. Whereas if my boss is always yelling at me and I'm always feeling stressed about my work situation or my finance situation or anything else, I'm under a constant state of elevated Cortisol that's also very damaging to our heart, right?

[00:51:52.470] – Dr. Kendrick

Absolutely. I mean, I started my world of looking at other causes for heart disease with stress. I don't like calling it stress. I think of it strain. But anyway, we use the word stress. Everyone uses it because everyone kind of knows what they mean. But yes, if you look at the impact of chronic negative stress and people react very differently to stressors, some people cope with it, some people don't. Is that, yes, it triggers. Whether it's just Cortisol, probably isn't. When you trigger the fight or flight system, which a lot of people have heard of, and you have operating at a chronic level, you cause damage to the whole system. There's a neurohol system, there's nerves throughout your whole body called autonomic nerves that most people have never heard of. They go to your heart, they go to your liver, they go to your blood vessels, they go to your eyes everywhere. Sympathetic parasympathetic system starts in your brain stem. It's really complicated. Operates alongside a whole bunch of hormones, like adrenaline, noradrenaline, cortisol definitely collect mistakes. Cortisol, blah, blah, blah. So this whole system is all fight up system. Cortisol is easy to measure, and Cortisol has distinct metabolic problems.

[00:53:04.390] – Dr. Kendrick

It's a direct antagonist to insulin, for example, at many sites. So if you're stressed in your insulin, if you're stressing, your Cortisol level goes up in order to fight this, your insulin level goes up, but it sometimes doesn't go up enough. Glucose goes up enough. I'm a firm believer that chronic negative stress is one of the primary triggers for raised blood sugar levels leading to diabetes. In fact, in the book, I mentioned a study in the First World War, people had soldiers who had what they called ShellShot, which we now call PTSD. They call it kind of acute neurosis. They actually you could measure blood sugar, you can measure sugar in the urine. The impact of stress on their system was such that they became the sugar levels were so high that sugar started to escape from the kidneys, which is very late stage in diabetes that we would recognize now. And this was entirely due to psychological stress. And you can see with various serious mental conditions like schizophrenia, bipolar disorder, et cetera, that many of these people end up with what's diagnosed as type two diabetes. And this is really what kills if schizophrenia, for example?

[00:54:25.520] – Dr. Kendrick

Yes, a lot of people commit suicide, but the vast majority of the others die Heartisans do, in my opinion, and the opinion of other people, to chronic stress, leading to the chronic activation, stress, fight and flight system, leading to the metabolic disorders that lead to diabetes that lead to heart disease. You can see this pattern again, if you look at PTSD, you can see the same pattern. If you look at people who have I don't know if it States they use fibromyalgia, which is very unspecific term, but it basically means lots of pain and difficulty and blah, blah, blah. People with PTSD and fibromyalgia is a big crossover. And there's like a five or 600% increase in the risk of diabetes and five or 600% increase in the risk of dying of heart disease. So the interrelationship between your brain and your body and how this all works together and creates problems with stress. Now, whether this is all modulated to cortisol, I don't know. But if the cortisol level is upward arranged or is malfunctioning, that's a very good sign that your what they call stress fight or flight, hypertrophinolaxis, give it or whatever term you want is not working properly.

[00:55:36.100] – Dr. Kendrick

And it's really important for people to try and get this as normalized and as healthy as possible.

[00:55:43.570] – Allan

Yeah. Now, one thing and I want to jump ahead because we know I think anyone knows it's like there's some conversations about if you have bad dental health, if you're taking certain drugs, those are obviously going to cause some problems. If you have you smoke or you're subject to air pollution, if you have high blood pressure, all of those are major risk factors because they're doing damage to your system and eventually that is causing the heart attack. But what I wanted to jump forward in because I haven't talked about it here. But it was one thing that my doctor and I started talking about when I was really looking at, well, care versus health care. Health care, because normal health care is, oh, you have a disease, let's fix it or let's cover it. Mostly, let's cover it. But he and I would have these conversations about health markers on how to improve my wellness. And one of the things we would talk about would be my homocysteine level. Can you talk about homocysteine and how that's also a factor here for the damage and the factors and things we're looking at?

[00:56:47.120] – Dr. Kendrick

Well, it was a guy called Kilmer McCully, who is part of a group that I'm also a member, was the first man, I think, to say that homocysteine, which is a protein in your blood, it shouldn't really be there. It's a breakdown product. It's an intermediate breakdown product. And if it's in too high concentrations, it damages the glycocalic and endothelium. This is just a fact. And there are certain drugs like lanzoprazol, which is a direct name. I don't know what they actually call them in the States with regard to their common name. I think it's called Loosec here and something else. Anyway, these drugs which are commonly used for indigestion and whatever, they block part of the pathway that stops homocysteine from being broken down so the hormone cysteine can go up. Also there are other things, diabetes actually in itself. If you have a high blood sugar level and a high insulin level, this interferes with the breakdown of homocysteine in your blood. And some people have a high level and some people are mostly blissfully unaware that they've got such a thing in their bloodstream. And therefore if it is high, one of the other things that you can do with the noncysteine is certain B vitamins can reduce because they help with a process that gets rid of the homocysteine.

[00:58:15.540] – Dr. Kendrick

So certain B vitamins off the top of my head I just forgot which ones they are. But I think it's B. Yeah.

[00:58:22.470] – Allan

It was definitely Folate B6 and I think B12 is what you mean.

[00:58:26.250] – Dr. Kendrick

Yeah. If you have these hormones at a good level, then they assist in cleansing the homocysteine from your system. And there has been research and looking at this with vitamin B, but it's been really weirdly manipulated by, in my opinion, primarily by the pharmaceutical industry. I just don't want this to be seen as a thing that people can do. But there is very interesting research on this and I think the other thing I did touch on in my book is if you have a high homocysteine level, you are more likely to get Alzheimer's disease. And if there has been evidence group in Cambridge who gave people the vitamins. And again I just forgot which ones they are. But they demonstrated almost complete stopping of the neuronal damage as well, which I think is when you're talking about well being hypocrites, people don't want to get Alzheimer's. So get these B vitamins in. If you have a high home assisting level and you will not only reduce the risk of heart disease due to endothelial damage, you also assist yourself in brain shrinkage and neuronal damage. Whether it's the same process going on, I don't know. I don't think anyone really knows Alzheimer's disease.

[00:59:44.460] – Dr. Kendrick

Anybody who claims to do so is probably not telling the truth currently. That's my take on it.

[00:59:51.630] – Allan

Yeah. Okay. Well, Dr. Kendrick, I define wellness as being the healthiest, fittest and happiest you can be. What are three strategies or tactics to get and stay well?

[01:00:02.410] – Dr. Kendrick

Well, I think going back to the stuff I was talking about about mental health and stress and whatever, there's very good evidence that people who look after their mental well being so they have good social interactions with other people. If you have a rubbish job, a bullying job or a stressful job that you hate, get out of it. The population with the highest rate of heart disease in the world are the Aboriginal Australians and young Aboriginal women have a rate of heart disease, which is 3000% higher than the surrounding population. And this population is really almost identifiable by the very high levels of what you call psychosocial stress. Aboriginal young male Aboriginals have a complete lack of the early morning cortisol rise in their bodies, showing that their neural homeowner system is seriously damaged. So I think looking after your mental health, looking after your mental wellbeing, having friends, having good relationships, these are having a sense of purpose, doing what you do, having interests. This is really important. I think I see health as being three things. It's psychological, social and they're all interconnected. And you can't get proper physical health without having your social health in good state as well.

[01:01:27.170] – Dr. Kendrick

The social health must be in good condition and I think this is hugely important. Certainly for stressed populations is really important. Then, of course, there is the obvious things to do with them. Don't smoke. But I think everybody knows that from a physical perspective. There is exercising. Yes. And if you have got to raise blood sugar level and you have to look at trying to pre whatever condition you want to call it, this is happening to you, then you need to look at in my opinion, the way that you do with this is to reduce carbohydrate intake simply is one thing to do. Absolutely. The trouble is you then end up in this huge battleground of dietary stuff. Another thing is I say to people, don't see food as the enemy, which we've kind of come to see it as people don't enjoy eating any water or you can't eat, that all that's terribly bad for you. It's very nuclear, blah, blah, blah. But in general, normal natural food stuff that you would recognize as food stuffs are usually healthy for you, good for you, and enjoyable and stuff that you have to read the label and it's got 56 ingredients.

[01:02:38.530] – Dr. Kendrick

Probably trying to look at avoiding that, I would think, and getting outside in the Sunshine and exercising all three together. Absolutely critically important. We're not designed to be inside as animals. I don't think we're designed to be outside most of the time. Sunshine is good for us. The exercise when we're outside is good for us. Just being outside in the countryside is good for us. And you can see populations that live longer than any others. This is kind of how they live their lives as well. So it's getting back to kind of looking at how people maybe were designed to live and getting back to as close to that as you can manage, which sounds a bit kind of generic, but it also happens to be true.

[01:03:25.270] – Allan

Dr. Kendrick, thank you so much for that. If someone wanted to learn more about you or learn more about the book, The Clot Thickens, where would you like for me to send them?

[01:03:35.290] – Dr. Kendrick

Well, there's a large river in Brazil, that sells the book.

[01:03:45.890] – Allan

It doesn't damage the..

[01:03:49.550] – Dr. Kendrick

Speaking as an author, where they take 70% of the straight off the price of that, something like that. I do have a website called drmalcomkendrick.org where you can read my great thoughts on everything. And the book is available there from the publishers apparently just run out of copies. But is getting some more printed.

[01:04:11.090] – Allan

Yeah, that's not a bad news.

[01:04:16.170] – Dr. Kendrick

And obviously, I have written other books and stuff like that as well. But if you go to my blog, you can find that out. The book is available on the Amazonian rainforest. You can make Mr. Bozos even richer if you want. But I suppose just say to people, the people that I admire as well, that you should go and have a look at as well. People like David Diamonds, fantastic researcher. And if you have Musculf and the work of Nina T. Shults and those groups over there looking at them and trying to give you a healthy diet to eat the work of Gary Taubes, these people are working hard. They need all the support. We need, all the support we can get.

[01:04:58.600] – Allan

Thank you, Dr. Kendrick, thank you so much for being a part of 40+ Fitness.

[01:05:03.270] – Dr. Kendrick

My pleasure. Thank you very much.

Post Show/Recap

[01:05:11.890] – Allan

Welcome back, Ras.

[01:05:13.690] – Rachel

Hey, Allan. That was a really interesting conversation you had with Dr. Kendrick, and it's kind of refreshing to see a scientist taking a look at a problem in a new light. And personally, I'm kind of glad to hear a little bit more talk about blood sugar being a problem. More so than the actual cholesterol.

[01:05:32.240] – Allan

Yes. And this is really hard because most doctors are going to go through school, they're going to get very little nutrition education. But they're going to be told one thing about heart attacks, and it's cholesterol causes heart attacks. Your client has high cholesterol. You got to get them on statins. You got to lower that cholesterol. That's the math. And the standard of care is the obligation that the doctor has. And you can try to have that conversation. Most doctors are not going to have that conversation with you. They're just going to tell you you've got to manage your cholesterol, you've got to manage your blood pressure. And if you manage those two things, you're good to go. But I want to put forward this quote that was on my timeline from years and years ago, and I want to make that okay. Mines are like parachutes. They only function when open. And that's Thomas Dawar was the one who said that. So the reality of it is, it's not that science changes. And we've heard that over and over lately with regards to things that we learn that we didn't know before. And the reality is nothing really changed, just our knowledge of it changed.

[01:06:47.620] – Allan

So at one point, people thought the Earth was flat, and then they learned maybe it's not. And then at some point, everybody thought that everything circulated around the Earth. The sun went around the Earth, all the stars and planets went around the Earth and the Earth was the center of the universe. We now know that's probably not true. So it's not that the science changed, it's our awareness of the world around us. And that changes as we learn new things. So having an open mind and basically saying, okay, this is what I thought. And now that there's new information, I have to rethink it. I have to open myself up to the fact that what I've been told my whole life could actually be wrong. There's nothing wrong with that. That's what you were told, but it comes down. And like you said, I think this is the key takeaway. The last part of this book of What Can I Do About It? Because all these books, regardless of what they say, it's What Can I Do About It? And What Can I Do about It is not new. We all know we should keep our sugar lower.

[01:07:59.410] – Allan

I talked in history. At one point we were eating 2 pounds of sugar a year. Now we're eating closer to 150 pounds of sugar per year. Could that be a problem?

[01:08:11.410] – Allan

Yeah, maybe.

[01:08:13.290] – Allan

Okay, smoking is on a decline, as is heart disease. Correlation cause effect? I don't know. But the base point of what he's saying is and this is true, if we're damaging our body, our body has mechanisms to fix itself. But if you just keep damaging your body, at some point, even that repair system doesn't work well. And we see this across the board. Autoimmune disease is a perfect example where something's going on that shouldn't. So maybe we have a gut leaky gut and as a result of leaky gut and our immune system constantly having to do these attacks, it finally just flips out and then it starts attacking other things. Hazimoto's disease, something's gone wrong and your immune system is attacking your thyroid. And so there's these things that happen. And if we keep doing what we're doing that caused what we were doing, then we're going to have those problems. So the fix is the same fix you've heard in every other book. Cut your sugar, cut your processed foods, don't smoke, manage your stress, keep your blood pressure down, exercise, get some sun. There was so much in the book that I wanted to cover, but we already went, I think, an hour on an interview and I could have talked to Dr Kendrick for a year.

[01:09:44.340] – Allan

There was so much in that book. And so it's a book worth reading. If heart disease is something that goes in your family or something that you're generally concerned about, it's worth reading the book to just get the idea. And you don't have to agree with the theory that it's a blood clot. And then the reason that the cholesterol is in there is because of the LPA versus the actual lipoprotein, low density lipoprotein. You don't have to get into all that. You can read all that. It's cool, it's information. But the reality of it, the biochemical, the stuff that's happening underneath, isn't really anything you can control. You can control the inputs, the sugar, the stress, the pollution, those things. And so that's the only thing I like to say is keep your mind open and just realize that it doesn't matter. It doesn't matter if it's cholesterol, it doesn't matter if it's blood clots. No medication is going to save you if you're not doing the right things otherwise.

[01:10:47.500] – Rachel

Yeah, absolutely. Eat better and exercise more. And I'm just really thrilled to see that blood sugar is being looked at for other diseases as not just diabetes and all of those terrible side effects of that disease. But there's something to having and keeping an eye on your blood sugar. And I was happy to hear that.

[01:11:08.900] – Speaker 1

Yeah, well, I'm using this continuous glucose monitor and just check your mind. But I mean, okay, I'm keto, there's no sugar. So, yes, my blood sugar follows a pretty common path throughout the day. I'm fasting or I'm moving. And so the exercise affects it with the foods I eat affect it just kind of looking at it like my blood sugar is pretty darn steady and not a problem. But it's just the function of saying, okay, what you put in your mouth is going to affect your biochemistry. It's going to affect your body. And it's so funny that people will think, oh, well, this pill is going to do these amazing things for me. And then they're not thinking food right would have any impact whatsoever. And so just realize that diabetes and heart disease are interrelated. We've known that. He actually shows why? Because the damage we're doing to the arterial load lining of our arteries, that we're cheering it off, we're causing all kinds of problems. And then it's clotting when it's in a big artery over time, that creates that plaque we're talking about when it happens in smaller arteries, which it will if you're diabetic prediabetic is doing that damage.

[01:12:33.740] – Allan

Now you're losing a toe. Now your kidney stops functioning. Now you can't see all the things we say, well, what's happening with diabetic? They lose their eyesight, their kidneys fail, and they lose feet and toes. Why? Well, those arteries are getting messed up and they're clotting and they're plugging up, and the blood is not getting where it needs to go. And that tissue is dying, and that tissue dies. And then that organ or the skin or the foot, it's no longer and it's gone. So you lose your eyes, you lose your kidney, you lose your feet. It's the same disease. When you really break it down, you think about it in those terms. It's the same disease, the same cause, and the same solution.

[01:13:22.190] – Rachel

Yeah. Something that's really worth taking a look at and monitoring what you're eating If you don't already do that.

[01:13:30.770] – Allan

It's just cut the sugar, the processed foods and the sugars. If you're eating whole foods, just real whole foods and, yes, even fruit. I eat beets almost every night. I'm in ketosis. It's like I, oh, you can't eat beets every night and never go out of ketosis, but I do a lot of work during the day. I move a lot during the day, and then as a result, I have some needs and the muscles and the liver say, “Hey, thank you ror that glucose. I appreciate it. I'm going to split it over here. We might use that tomorrow.

But we don't need the sugar if you haven't used glycogen. You don't need the beet sugar, right? Where most of our sugar comes from is beets. But just realize, give your body the nutrition it needs, and it will protect you, it will heal, it will get healthy, and we just don't give that enough thought. We want the Magic Pill, we want the science to save us. And what's going to save you is your next meal. If you make sure your next meal and the meal after that and the meal after that are mostly whole food, you're going to be 1000 fold better off than if you're throwing down Little Debbie's and doing that stuff.

[01:14:54.850] – Allan

So just realize you have control of this. And if you don't think you do, you have a food addiction or some kind of problem like that, then get help, get help for that. because, yes, that's a problem for a lot of people, but the reality of it is food is nourishment. Food can be delicious. But if you're eating just for the sake of something emotional, something bored, those types of things, you've got to get away from that because that's the killer. That's the one that's coming after you. There's no other plot. There's no other twist. The murder mystery Is solved. We've just got to catch the criminal. And the criminal is the sugar and the processed foods and the stress and the pollution and smoking and those things. We know that. We know who did it. It's time to catch them and stop them.

[01:15:48.470] – Rachel

Yes, time to make some changes.

[01:15:51.390] – Allan

All right. Well, Rachel, I'll talk to you next week.

[01:15:54.410] – Rachel

Sounds good. Take care.

[01:15:56.050] – Allan

You too.

[01:15:56.860] – Rachel

Thank you.


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