Eat Your Heart Out

Dr. Loren Cordain:
I’m Loren Cordain, founder of the Paleo Diet movement.
Shelley Schlender:
I’m Shelley Schlender. This is the Paleo Diet podcast for February 2015.
Dr. Loren Cordain:
The Paleo Diet tends to be an anti-inflammatory diet because it removes many of these substances which tend to promote inflammation. In my books, I’ve talked about there are other dietary compounds that we consume regularly that also increase intestinal permeability.
One, if you like to have a margarita with your Mexican food, bingo; ethanol increases intestinal permeability. It’s a concentration gradient-driven phenomenon meaning that if you drink a lot of it regularly, you’re going to have problems.
Shelley Schlender:
Oh, darn it. Alcohol makes a leaky gut.
Dr. Loren Cordain:
The point I’ve already made is that if you eat one slice of whole wheat bread once in a blue moon, it’s not going to be a problem for most people unless you got celiac disease. Same thing is true. If you want to have a cocktail, or a glass of wine occasionally, it’s not going to be a problem because it’s concentration gradient-driven. Unless you drink the entire bottle, and you do that day in and day out, you’re probably not going to have chronic problems with a leaky gut.
Same thing is true. We talked about the margarita with the Mexican dinner. Mexican food is spicy. We all like a good spicy salsa. We like all those jalapeño peppers thrown in. There are compounds in peppers, particularly the really hot, spicy ones like habanero. The spicier and the hotter it is, the more the concentrations of what are called capsaicins. Capsaicins also are potent elements that increase intestinal permeability.
Shelley Schlender:
Lots of ways to increase intestinal permeability. What’s left …?
Dr. Loren Cordain:
Yes, ibuprofen.
Shelley Schlender:
Wait a second here. You just said ibuprofen?
[00:02:00]
Dr. Loren Cordain:
they’re called NSAIDs, non-steroidal anti-, N-S-A-I drugs, non-steroidal anti-inflammatory drugs, they’ve been known for decades to increase intestinal permeability. They’re horrible. Because they do that, people taking other drugs through the GI tract, in many cases that’s why you can’t take NSAIDs on top of these. They increase the plasma concentration of these other pharmaceuticals.
Shelley Schlender:
Because they make the gut leak more, whatever else you’re taking in leaks more too.
Dr. Loren Cordain:
That’s right. Non-steroidal anti-inflammatories, we’re in America. You get an injury, or an ache, or you got a little bit of rheumatoid arthritis, what do you do? You take an NSAID and you take it for 20 years. The epidemiologic literature shows that people that take NSAIDs regularly are at increased risk for these pro-inflammatory diseases like cardiovascular disease.
Some NSAIDs like aspirin and so forth, they tend to prevent the final event, the clotting event. They tend to cause low-level inflammation, but they tend to prevent the final even that kills you, which is the rupturing of the fibrous cap.
Shelley Schlender:
The rupture of the fibrous cap meaning inside the arteries, if there’s a blister that formed on the ….
Dr. Loren Cordain:
The plaque that forms.
Shelley Schlender:
It’s like a really rough bandage that’s the best way that the body has to cover up a scratch in your arteries. Those can be unstable. If they’re unstable, that’s a ruptured cap. It bursts and that makes a blood clot.
Dr. Loren Cordain:
That’s right. The compounds in our bodies that tend to dissolve the fibrous cap, that’s what the body does. It’s got this injury on the inside of the artery. It walls it off. It does this over the course of the lifetime. That tends to narrow the arteries. It’s not the narrowing of the arteries that seems to cause the fatalities. The arteries seem to respond to that narrowing by enlarging a little bit. What happens is finally one of the fibrous caps breaks. Then it goes downstream because the arteries are larger upstream and smaller downstream. It goes downstream and it forms a clot. That clot then is what causes a heart attack or a stroke.
[00:04:00]
Shelley Schlender:
It’s the scab basically that pops off. The scab travels through the bloodstream. It gets stuck or else it gets other blood to clot around it.
Dr. Loren Cordain:
The $64,000 question is two things. One, what causes the fibrous cap to rupture? Two, what causes the clot to increase? I hate to say it, but everybody eats wheat in this country, except for Paleo people and gluten-containing grains. Wheat contains WGA. We’ve talked about this lectin.
What WGA does is once it’s in the circulation, once it’s bound to red blood cells and white blood cells, it up-regulates meaning that it causes increased secretion of an enzyme called metalloproteinases. There are a number of metalloproteinases, MMP2, MMP9, in particular. MMP2 and MMP9 are what cause the dissolution of the fibrous cap.
We don’t have that in vivo, meaning we don’t have experiments to show that in either animals or in humans, but we have tissue studies that show that frequently if you take a fibrous cap and you infiltrate this with WGA, or other lectins, then it tends to up-regulate these metalloproteinases, which cause the cap to rupture. Secondly, the cap and that whole mess goes downstream and it forms a clot.
[00:06:00]
Shelley Schlender:
Just so I can picture this, here’s this scratch on the artery. The body goes and puts a fibrous cap on it to mend it. If that cap is allowed to be there and just settle in, it will become a scar that is stable. It doesn’t mean that it’s going to rupture. It will just settle down and it won’t be a problem. You’re saying that the WGA and some of these other anti-nutrients, if they get into the picture, then we’ve all had scabs on our legs, or on our arms where if they get bumped at the wrong time, they break off and we’ve got a big bleedy spot there. That can happen in our arteries?
Dr. Loren Cordain:
Exactly, Shelley, that’s precisely the point I made. Here’s an interesting little side story on that. In the far north, above 60 degrees north latitude, 70 degrees north latitude, in places in Greenland and Alaska, Inuit living 400 years ago, 1,700 years ago, were actually trapped in mud and snow slides. They became perfectly preserved and frozen for four or five, 1,500 years.
In the late 1970s, early 1080s, some of these bodies became unearthed. They were found. Fortunately, a couple of pathologists from Texas did autopsies on these frozen Inuit bodies. It turns out that they had extensive atherosclerosis in their coronary arteries. These are people that lived before sugar, before wheat, and they ate basically only animal foods in the far north.
Shelley Schlender:
Meaning that they had a lot places where there was evidence of basically scratches and blisters in their arteries and places where there’d been a plaque bandage that the body had put on there to protect it. They had a lot of places that in modern humans could have ruptured and caused a heart attack.
Dr. Loren Cordain:
Right, and so if we fast forward and we see this in many non-westernized people is that they have atherosclerosis, but they don’t die of atherosclerosis. They don’t die of heart attacks or strokes.
Shelley Schlender:
Just a second here. You’re saying that here are these people that would panic a modern western doctor because they have so much scabs and bandages …
Dr. Loren Cordain:
Plaque buildup.
Shelley Schlender:
… plaque buildup in their arteries, but they don’t have heart attacks and strokes in these Paleolithic-style people.
[00:08:00]
Dr. Loren Cordain:
That’s pretty much how our research group interprets it. Atherosclerosis seems to be almost a universal condition of humankind. It seems that we get it, but it normally doesn’t kill us from heart attacks and strokes; whereas in the western world, it does. We go back to the fibrous cap.
Shelley Schlender:
That’s the bandage again.
Dr. Loren Cordain:
That’s the bandage. What are we doing differently that the Inuit and the Eskimo; they’re not eating any junk or processed foods, or sugars. They’re eating all animal products, lots of fat, lots of saturated fats. The historical studies, when I say historical, when we can actually go in in the 1900s, and ’20s, and ’30s, we don’t see mortality from heart attacks. It basically doesn’t exist.
Shelley Schlender:
In the 1920s, modern scientists could look at people who were still eating in a Paleolithic way, such as the Inuit, because they weren’t eating a lot of junk food yet. There were a few other places where there were more ancient styles of eating and life where modern scientists could go and look. They saw this plaquing, but they did see heart attacks in these people.
Dr. Loren Cordain:
They didn’t have the sophisticated instrumentation and the ability to do the measurements in 1920 as we do now. They didn’t have all the assays. Our grandfathers, and great-grandfathers, and great-great-grandfathers that went up to the far north to help these people with modern medicine, what they found, and they reported in the medical literature; I’ve recorded it in many of my articles, what they found is that heart attacks were essentially unknown.
They asked the people, “Did somebody do this? Did they ever keel over? Did they ever put their hand on the left side of their chest? Do you know of anybody that spontaneously died from a stroke, or did anybody ever lose the ability to speak and have the facial …?”
Shelley Schlender:
A droopy face.
[00:10:00]
Dr. Loren Cordain:
A droopy face. That stuff really didn’t exist. Finally, in the late ’30s and ’40s, when we had the ability to draw blood and measure blood cholesterol, and measure some of the indices in these people, it was suggestive that they didn’t have the risk factor for cardiovascular disease. This goes up into the 1950s, when we really started getting more sophisticated. Even an isolated group in the ’50s, they still didn’t have these risk factors.
Starting in the early ’60s, when everything changed and they got junk food, and white bread, and sugar, and the entrapments of western society, tobacco, and all of this, then what we see is we start to see increased rates of all of the western diseases, the cancers, heart disease, and so forth.
Shelley Schlender:
This is in the Eskimo and the Inuit communities?
Dr. Loren Cordain:
Yeah. I want to finish up one final point. Maybe you can make it come back to where it was. When we talk about wheat, and we talk about wheat up-regulating the metalloproteinases, which destroy the fibrous cap, wheat also causes compounds in platelets.
Platelets are these formed elements in the blood stream that cause blood clots. If you nick yourself with a razor, you’ll notice that the blood bleeds at first. Eventually it clots. What causes the clotting to occur are platelets. There’s a certain compound in platelets that causes the platelets to start clotting. Guess what? WGA is a potent up-regulator of that compound in platelets that causes clotting.
If you’ve got platelets in the presence of WGA, like I told you before, we think WGA binds to red blood cells. Is, “Holy mackerel, now we got a perfect storm.” We’ve got the WGA that causes the breaking of the fibrous cap. We’ve got the WGA that up-regulates the clotting.
Shelley Schlender:
Clotting on our skin is one thing. We want blood to clot when it’s on our skin. We don’t want it to keep bleeding. If the clotting happens in an artery, there’s an awful lot of blood there to clot.
[00:12:00]
Dr. Loren Cordain:
That’s right.
Shelley Schlender:
It can stop the heart. It can just make everything turn into sludge.
Dr. Loren Cordain:
Right, but the alternative is if you are in an accident and you have a small artery; if we have a large artery that is severed, we bleed to death. We have small arteries. If we don’t get clotting in small arteries, we’re dead. We’ll bleed to death too. Evolution through natural selection has allowed that process to occur.
Clotting is a good thing in tiny to medium-sized arteries. Chronic clotting is a very bad thing. It depends on where it occurs. The myocardium in the coronary arteries, clotting is fatal. In your arm, or your foot, or your leg, or what-have-you, in small to medium-sized arteries, clotting is a very good thing. It promotes survival. You won’t bleed out to death.
That’s actually a very good thing. That’s why atherosclerosis occurs. The body’s doing what it’s supposed to be doing. When it forms these plaques, we’ve got inflammation. How do we get inflammation?
We have shedding of the glycocalyx. The glycocalyx lines all endothelial cells. I won’t say all, but most, like the gut. We talked about the glycocalyx in the gut. The glycocalyx also lines the arteries, of all arteries.
Shelley Schlender:
I’m picturing it like the Saran wrap before the actual stuff.
Dr. Loren Cordain:
Do you want to see what it actually looks like?
Shelley Schlender:
Yes, I’d like to see this thing called the glycocalyx. It’s such a beautiful name. You’re looking at your computer to show this thing called the glycocalyx that lines our arteries and lines our gut.
Dr. Loren Cordain:
Yeah, I’ll show you exactly what it looks like so you can get a real good visual on this. Maybe you can describe to the viewers what it looks like. Let’s see here. Where am I?
Shelley Schlender:
That’s a lot of presentations.
[00:14:00]
Dr. Loren Cordain:
Yeah, I’ve been all over the world. It’s been a lot of fun. All right, let’s magnify this. Let’s get out to a little bit where you can see it. I’ll show you a glycocalyx. I’ll show you a gut glycocalyx; and then I’ll show you an arterial glycocalyx.
Shelley Schlender:
I’m looking at a picture that looks like it’s the small intestine. It has this shag carpet stuff called the microvilli. It almost looks like a little crop of cornstalks growing on the soil. That’s what the small intestine looks like. There’s this fuzzy fog above it that you have labeled as the glycocalyx, above the shaggy stuff.
Dr. Loren Cordain:
That’s right. The glycocalyx are actually composed of glycoconjugates, meaning that they’re sugar molecules that are actually bound to this brush border, or these microvilli. Microvilli are these cells in certain parts of the intestine where the absorption occurs.
Shelley Schlender:
This is where food on the outside of the world gets absorbed by the intestines to go into the circulatory system. It’s where the outside world we eat joins into our inside world.
Dr. Loren Cordain:
Right, the glycocalyx; think about it as a sieve. It’s like the baleen on a whale that filters water to get the small elements out. The glycocalyx in the gut tends to prevent large macro-molecules like proteins and viruses, and even big protein molecules and peptides to get past.
Remember, we only absorb amino acids. We have to break down these large molecules into their constituent amino acids. Above this is the mucus layer. The glycocalyx and mucus layer are all influenced by the food we eat. This is a glycocalyx in a gut. Let me show you a glycocalyx in an artery. It looks slightly different.
Shelley Schlender:
It’s different than mucus. That surprises me. Mucus is a glyco product also.
Dr. Loren Cordain:
Mucus is a liquid. Glycocalyx is a solid.
Shelley Schlender:
Oh.
Dr. Loren Cordain:
It’s actually ….
Shelley Schlender:
It’s like cheesecloth or, like you say, a sieve. It’s something that’s a …
[00:16:00]
Dr. Loren Cordain:
It’s this structure. It’s a solid structure that is bound to the cells. It actually contains more mass than the endothelial cells themselves. Let me show you this.
Shelley Schlender:
In that picture, it just looked like fog.
Dr. Loren Cordain:
This is …
Shelley Schlender:
It didn’t show up as much.
Dr. Loren Cordain:
It’s very difficult to stain this thing. As a matter of fact, it’s so difficult to stain it wasn’t even studied much ’til the early ’90s. The stains couldn’t stain it. The reason it couldn’t stain it is let me show you what it looks like in the arteries. Now you get a much better picture. See how big it is right here?
Shelley Schlender:
We’re looking at the whole of an artery.
Dr. Loren Cordain:
This is an artery in a cross section. These are the cells that line the artery. These are called the endothelial cells. Shelley, you interview many, many scientists. I’d be willing to bet that half of them that study cardiovascular disease aren’t even aware that there’s a glycocalyx.
Shelley Schlender:
It’s invisible. Here, it looks like little feathers, like downy little feathers.
Dr. Loren Cordain:
If you look at the mass, the weight of these cells that lie underneath it, there is more mass in the glycocalyx than what you find in these cells.
I want to tell you why it was so difficult for scientists to find and study. That’s why I mentioned when I was a PhD. student, when I was taught arterial anatomy, we weren’t taught this. It hadn’t really been demonstrated. It had been predicted because of the flux in flow.
In other words, when you put liquid through the inside of this, mathematically, we can predict that there’s some kind of resistance that’s going on that we can’t see.
Shelley Schlender:
I’m starting to picture this glycocalyx like the chain link fence. It’s something that’s meant to be a barrier.
Dr. Loren Cordain:
I view it more like I said, it’s like the baleen. Do you know those big, structures on whales that filter the water?
Shelley Schlender:
A chain link fence is designed to keep pretty much everything out. You think this is a filter to only allow what is safe to come through.
[00:18:00]
Dr. Loren Cordain:
To come in, that’s exactly what it is. It’s not a fence at all. It’s filter that prevents large molecules from getting through it. Red blood cells are tiny cells. They can’t get through here.
For atherosclerosis to occur, you have to have monocytes, these white blood cells. They have to get in here and get into the sub-endothelial space. Without that, you can’t have atherosclerosis. The glycocalyx has to be shed in order for any cells to make it into here.
One of the reasons why it’s so difficult to shed, view this as thick, hairy-like substances that have such a narrow space between them that nothing can really get through. Have you ever gotten your hair all fluffed up, and you got it shampooed, and it sticks out nicely? You got it just as you want it. If you go under the shower, have you ever noticed how all that fluff just folds down on itself? It’s the same thing with the glycocalyx. When there’s liquid flowing through the artery, it doesn’t stick out like this.
Shelley Schlender:
It isn’t fluffy. Instead it bends over.
Dr. Loren Cordain:
It’s like when you wash your dog and the hair is standing up. Then you wash the dog, the hair flattens out.
How about your grass? If you haven’t cut your grass in your lawn for a while, it sticks up. If you put too much water on it, it flattens out. This is why it was so difficult to see this glycocalyx. Under normal conditions, when blood is flowing in our arteries, it’s not sticking up as you see it here. It’s flattened like this.
When it’s flattened, these tiny little thread-like substances are flattened down. It’s very, very difficult to stain and to view even with an electron microscope. Special staining techniques that came out in the late ’80s and early ’90s allowed us to get a real good view on the glycocalyx.
[00:20:00]
This is how a blood clot forms in arteries. As I mentioned, you can see. Here’s the artery. It’s wide out here. As it gets narrower and narrower, this is what happens. The clot forms. There’s a compound called P-chemone that is found in leukocyte and endothelial adhesion molecules. WGA up-regulates p chem and causes platelet aggregation. If you’ve got WGA in your bloodstream, this is something that is really, really bad.
I want to show you a visualization of the fibrous cap. This is a picture of the fibrous cap. You can see right here ….
Shelley Schlender:
Again, this is basically the Band Aid that’s put on the artery lining, or blood vessel lining to keep it from rupturing if it’s got a blister on it.
Dr. Loren Cordain:
That’s right. This actually is the plaque that forms underneath it. What causes this fibrous plaque to ultimately rupture and form the thrombus, or the clot are MMPs. These are metalloproteinases. We have practitioners that are acupressurists that tell us that we should be eating lectins.
These people aren’t scientists. These people are lay people that are really unfamiliar with the literature. If you see right here, here’s two studies showing that PHA, a lectin, that is universally found in phaseolus vulgaris, which is basically all kidney, black beans, and what-have-you. It up-regulates MP9. WGA up-regulates MMP2.
If these things are in our bloodstream, on a chronic basis, and you’ve got atherosclerosis, tissue studies tend to show that this is what they do to the fibrous cap.
[00:22:00]
Shelley Schlender:
Meaning that some of the compounds in grains and beans will take that special bandage that is in most people, this plaquing to keep the arteries from rupturing, and it will dig into those and the bandages get disrupted and the scab falls off too soon, and there’s a lot of bleeding in your artery all of a sudden.
Dr. Loren Cordain:
Yeah, and this is even actually a better slide, too. It shows you this is the inside of an artery. This is the lumen of an artery. This is our LDL cholesterol. These are T-cells and these are monocytes.
Atherosclerosis and these plaques can’t form unless monocytes and T-cells, which are in the bloodstream itself, they have to breach this arterial barrier. Meaning they’ve got to get past the glycocalyx. They’ve got to get past these endothelial cell linings. They do this by binding onto these little substances here. Then they have to get into the cell. The monocytes become macrophages. They eventually become foam cells. They eventually produce this plaque.
The $64,000 question is is the monocytes and the T-cells, and the macrophages need to get past arterial blood, past this membrane and get into this endothelial space. That can’t happen unless the glycocalyx is disrupted.
Shelley Schlender:
Protect your glycocalyx. That’s one of the ideas here. There’s this invisible filter that makes a huge difference. What foods we eat can make a difference in how stable that glycocalyx is so that it can do its job.
Dr. Loren Cordain:
That’s right. There’s one final clue. I hope I’m not getting too complicated science. There’s one other factor that the readers might be interested in. That is where atherosclerosis occurs.
In arteries where there’s laminar flow, in other words where the artery is straight, and it doesn’t bifurcate, atherosclerosis never occurs.
[00:24:00]
Shelley Schlender:
Here’s s straight tube; a straight blood vessel just flowing along. There’s a lot of blood vessels where they branch. One blood vessel becomes two different blood vessels. It’s more turbulent where that happens.
Dr. Loren Cordain:
That’s right. You can think about it as squirting something down with a hose. If you create a lot of turbulence, then if there’s an underlying structure, then you tend to wash it out. That’s the idea that atherosclerosis only occurs in these turbulent areas where we have bifurcation or splitting of the arteries.
Shelley Schlender:
There’s a fair amount of plaquing that occurs near peoples’ hearts. We’ve all seen those pictures that show the arteries and the blood vessels going in and bending into the heart.
Dr. Loren Cordain:
The coronary arteries, that’s exactly why they’re call coronary arteries. Coron means crown. They sit on top of the heart like a crown. They branch down as they supply arterial blood to the working heart muscle. Where they branch, this is where we see atherosclerosis. Why is that?
It’s because there’s a mechanical transducer here which changes flow to a biologic phenomenon. The biological phenomenon is the shedding of the glycocalyx. Somehow here’s flow, laminar flow is sensed. There’s nothing going on. What is the mechanism? What is the thermostat here that senses that there’s no problem here? It’s the glycocalyx.
Here, what happens is because of this turbulent flow, if you have compounds and red blood cells, i.e. WGA, that tend to cause pro-inflammatory cytokines to be secreted and to shed the glycocalyx, we probably could have spent the last two hours just on this slide itself.
Most cardiologists, they deal with symptoms. They’re very good body mechanics. Somebody comes with symptoms; they know the tests to order. They know to see what problems they have and they can do that. The theoretical part of how this whole thing happens and the steps involved and how the steps are related is ….
[00:26:00]
Shelley Schlender:
Why do people get plaquing in the first place? You’re mentioning that the plaquing happens wherever there’s a bend, where there’s a branching and that it also happens more if somebody’s body’s a little irritated.
Dr. Loren Cordain:
Normally, where there’s a bend and a branching, is if the glycocalyx tends to be removed, or taken out, then it’s healed. That’s a normal process. Where it tends to stay, we continually have this chronic process of turbulence, plus something else, plus inflammation; then we form these plaques.
Normally, everything is healed up and is okay. When we have pro-inflammatory cytokines that are in our bloodstreams, for instance, I mentioned the Inuit. One of the things that the Inuit did that were studied four and 500 years ago, is they burned seal oil.
To stay warm in their snow caves in the winter time, they had this enormous carbon vapor matrix that they were breathing in constantly. It’s just like cigarette smoking is, that it tends to be pro-inflammatory. When you get all this crap in your lungs, the response is that pro-inflammatory response. That pro-inflammatory response in the lungs is translated virtually throughout the body.
Shelley Schlender:
Loren Cordain, I’m curious about the Inuit, the people that many people know as the Eskimo. Given that they were eating a diet that wasn’t the kind that you would expect to have plaquing in their arteries, but you’ve mentioned that one thing that the Inuit were doing that wasn’t so good for their health, didn’t kill them, but it wasn’t so good for their health, is that they used a very smoky oil inside their igloos.
[00:28:00]
Dr. Loren Cordain:
That’s right. As I mentioned, we talked about elements that promote inflammation. There’s all kinds of things that promote inflammation that don’t necessarily kill you on the short haul. What is interesting is that what we have here in the western world is that we have people dying from Type II diabetes, stroke, and heart disease in their 40’s, 50’s, and 60’s. That is what is unusual. That’s really the environmental factors that we need to identify.
That’s all for this edition of the Paleo Diet Podcast.
Shelley Schlender:
Our theme music is by Chapman Stick soloist, Bob Culbertson.
Dr. Loren Cordain:
Visit my Web site, thepaleodiet.com for past episodes, and for hot links to my research studies, books, and latest writings. For questions, or comments, the place to go is thepaleodiet.com.
Shelley Schlender:
For the Paleo Diet podcast, I’m Shelley Schlender.
Dr. Loren Cordain:
I’m Loren Cordain.

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