008 - High LDL (209) on a Carnivore Diet: What My Heart Scan Showed About Heart Disease Risk

Think of this as like the really bad hot lava. You don't want that.

Is that a dangerous amount of— like, that looks dangerous to me.

Please don't try this at home. I guess in summary, what I'm telling you is the good news is—

Hi, and welcome to Clear Cardio's Prevention is Power podcast, where we expose the truths behind heart disease and show you how to take control of your health before it's too late. I'm J.D. Enright with Clear Cardio, and today we're bringing you a story with Dr. Osborne and one of his patients. And you're going to see a live discussion about the actual results of one of our Clear Cardio patients with Dr. John Osborne. So sit back, enjoy, grab some popcorn, and enjoy the podcast.

Thank you for that stellar introduction, JD. You're always the best. I am so excited. We're going to do something really, really exciting today. We are going to do a live read. This is Dr. John Osborne, chief Medical officer of Clear Cardio. I'm here with Jamie Gruber, who flew in all the way from—

Punta Cana, Dominican Republic.

All the way from Dominican Republic to get his scan. He does not know the results.

No clue.

I know the results. We have the ambulance crew next door. No, I've been kidding him all day about that. But we're going to actually go through the whole process, look at all the pictures. He got scanned this morning. So what was your experience this morning? It was great.

I'm not a big hospital guy, but I mean, it was 10, 15 minutes. I was shocked at how quickly I was done. I didn't know what to do with the rest of my day. So yeah, so came here and excited to see—

We try to under-promise and over-deliver.

Very simple, very easy. It was great, honestly.

Fantastic. So glad you had a great experience. And so in the background, we did the scan, we get this incredible Multi-gigabyte dataset. It's a massive dataset. It actually takes a DVD to store all the data on it. All that, and all that data obtained from your heart is obtained in about 1 second. Everything else is putting in the IV, position you, putting you in the CT scanner.

Sure.

Another thing I'll ask you about, because this is a common question, right? So we use a CAT scanner, A CT scanner, right? So I always describe it as a donut, right? I call it the donut of destiny, right? Or the magic donut. But I think sometimes people can confuse easily a CAT scanner versus an MRI. Have you ever had an MRI?

Never.

Okay, well, good. Well, let's keep that up. Yeah. So an MRI is a whole different imaging device. If you've ever— more typical with that, it's— I call it the coffin, right? So they put you in this long tube, it's enclosed, it's pretty tight. And you're going to be there for half an hour, an hour, it could be even 2 hours depending upon the scan we're doing. With a CT scanner, CAT scanner, whole different technology. It's a donut, but it's open. You got plenty of room. In fact, our particular machine, I'm very proud of, the first install of this particular machine called an Atlas was the first install in North America of this particular CAT scanner.

Okay.

Very, very sophisticated, Cool machine. It has another advantage of it beyond the speed and the resolution of this machine for our purposes. It also has the biggest bore, that is the biggest hole. So just less— more room for you and less issues with claustrophobia. So I'm glad you did well with that.

No issues. Yeah, I appreciate it. Perfect.

That's great. So we had talked, I guess, last week or so, just kind of get a little background and you know, family history and medical problems and all that. And as you can tell, look at him. He's a guy in great health, which is awesome. But, you know, it is interesting that even people who are in great health can have terrible heart disease, which you don't have.

Okay. That's a good reveal.

I'll take that. But also, too, and here's the magical, incredible breakthrough of adding AI to cardiac CT. So I've been doing cardiac CT for 25 years. And in the last few years, we now can layer on top of that incredible high-resolution dataset, which is this 3-dimensional high-resolution data which comes out of the CAT scanner. We now upload that, which we've already done, we did that this morning, to the cloud. It will then analyze every single one of the millions of pixels out of the study. And if you're familiar at all, ever seen an X-ray or a CAT scan or MRI, whatever, those images are what we call grayscale, right? So they're anywhere from black to white and gray in the middle, right? Everybody's seen these, right? The important thing is when we look at a CAT scan as an example, MRI, chest X-ray, whatever, we can image or see or delineate about 50 to 100 shades of gray from black to white.

Makes sense.

That's, that's as much as our eyes can, can see. Encoded in every one of those millions of pixels coming out of the machine electronically is encoded over 2,000 shades of gray.

Oh, wow.

So when we do the AI, there's several advantages. One, it's analyzing every single pixel. It's analyzing it across 2,000 shades of gray, not 50 to 100 that we can see with our eye. So we literally can use AI to see things that would otherwise be invisible.

Yeah.

So telescope to microscope.

Yeah.

In addition, we can get very, very precise numbers because really, as it turns out, and here's another sit down for a moment for the audience and everybody, probably tell you something you don't know. We in cardiology have, for literally decades, I like to say, worshiped at the altar of blockages, right?

Mm-hmm.

And you think of it intuitively, right? A blockage is a bad thing. That's what causes heart attacks, and that's what kills people, right? Yeah, it's wrong. It's absolutely wrong. And we have, for the last Rough, since the 1990s, right? So 30-plus years. Every 10 years, we have done studies where we compare optimal medical therapy, which of course has changed and evolved and gotten better and better over the last 30 years, but optimal medical therapy for the treatment of plaque versus optimal medical therapy. And when I say that, I'm talking about treating your cholesterol, being on an aspirin, if you have diabetes, taking care of that, blood pressure, taking care of that. So that's optimal medical therapy versus optimal medical therapy with what we call technically revascularization. So what is revascularization? I call that the mechanical stuff. That's your balloons, the stents, the bypasses, right? And the belief was that, and we thought we'd prove this easily back in the '90s, that optimal medical therapy with balloon stents and bypass surgery would be and offer a superior outcome. if you look at heart attacks and cardiovascular death, death from heart attacks, would be better than just drugs, just optimal medical therapy. And optimal medical therapy is obviously healthy diet, exercise, not smoking, all those things too. We'll talk about diet too, because that's going to be, I think, very intriguing.

Agreed.

So we got a little interesting— that's a hook to hold on for that. But we did that back in the '90s, and guess what? We found out there was no advantage of optical medical therapy with balloon stents or bypass surgery. There was no advantage. So we all shook our heads, scratched our heads, and went, that can't be right.

Yeah.

10 years later, we did the same study. Now, stents had evolved, drugs had evolved, science moved on. That's great. So we knew that if you mechanically treat blockages with drugs to treat plaque, it's got to be better. So 10 years later, we did that study again, basically duplicated, but with more state-of-the-art tools, drugs, stents, came up with exactly the same answer.

Hmm.

And within cardiology, there's always been a little bit of a divide, right? You have what I call the interventionalists. The interventionalists are the guys, the women, That do stents and things like that. And not terribly surprisingly, if you're given a hammer, the world looks like a nail. So if you put in stents, you go, well, this has got to be the way to go. So I understand that. Well, I've been on the other camp. I'm the very, very small minority of preventative cardiologists who says, as it turns out, and I was clued in back in the '90s, that what really treats plaque and really prevents heart attacks and also strokes, but cardiovascular events and balloons and stents and bypass surgery, and works to put my interventional colleagues out of business, I like to kid them, is not the mechanical things, it's the medical things. It's diet, exercise, medications, et cetera. So that's been a long-term, ongoing, decades-long debate within cardiology. So 2008, we did this trial called COURAGE, optical medical therapy, or optical medical therapy added to that balloon stents, et cetera. Still no difference. Well, there's got to be something wrong. So let's do the study again. By the way, these studies were all paid for by the NIH. So we all paid for them as taxpayers, right?

Yeah.

So I'd like to say that. So there's no pharmaceutical company shenanigans thrown into the mix. Okay? So we did the trial again. Optimal medical therapy, you hear a theme here, optimal medical therapy versus optimal medical therapy and stents or bypass surgery. Okay? Yeah, 2019, the trial was called ISCHEMIA, NIH-sponsored, we all paid for it, exactly the same results. No difference in heart attacks, no difference in cardiovascular death.

So just extra hardware.

Yeah. Or as I like to say, you know, stents, right? These little mesh things we put in the blood vessels to open up and all that are about roughly— MSRP is about $3,000, right? So I like to say $3,000 installation extra, right? And that's just one stent.

Yep.

Sometimes people get lots of stents, right? So that is a great theme to understand. So as it turns out, it is not the blockages That we have been looking for and fixing mechanically for decades, that is not what predicts heart attacks or mortality. What actually does predict mortality, cardiovascular mortality, deaths from strokes and heart attacks, and heart attacks is actually, ready for this, total whole heart plaque volume.

Mm-hmm. Okay?

That's what we're gonna look at in you in just a moment. So, but I think it's so important to set that stage because I think a lot of people intuitively go, oh, I got a bad blockage. Thank God, thank goodness it was found. We put a stent in it. Whew.

Avoided.

Crisis avoided.

Right.

No, I will tell you what stents are good for. And when I say stents, when I say mechanical things or revascularization, the fancy 50-cent word, is, we'll lump together balloons, which we don't really use anymore. I won't bother with that. But more realistically, it's stents. We put in stents, which open up the vessel, and the stent stays behind to keep that vessel open. Kind of like snowplowing, pushing it off to the side and something to hold the snow back, right? And then bypass surgery, which I think everybody probably has a pretty good idea what that's talking about.

Yeah.

So as it turns out, the mechanical things are useful for one reason. They're useful if you have really bad symptoms. We call it angina or angina. So in other words, the pipes supplying the blood flow to the heart are relatively small. As the load or the demand of the heart as a pump goes up, if the pipes are too small, you get chest pain, angina, breathing problems, shortness of breath. Could be a lot of different symptoms across different people. But as it turns out, the mechanical things— The stents and bypass surgery are very good at restoring blood flow. Here's the problem. They do not treat the disease. The disease is the plaque. If the plaque grows to an extent where it causes a blockage, you start getting symptoms.

Yeah.

But we will not have symptoms, chest pain, angina, flunk a stress test, until you have at least a 70% blockage. So waiting for symptoms, We're trying to detect the disease with tools like stress tests, which we've done for decades, are only detecting late, late disease. It does not detect early disease. It can't detect early disease, which is why 25 years ago, when the very, very early, very crude cardiac CT scanners became available, knowing that they could see that plaque, they could detect it Long before we ever had a blockage, obviously that was an epiphany. That was, you know, holy moly. Obviously, I had to wait till the technology got better and sharper and easier to use, but I knew that this was going to be how we deal with this disease and detect it. So that's what we did with you today.

I can't wait to see.

So a little background. Okay, so with no further ado, unless you have any questions, comments, quips.

No, none yet.

Okay, criticisms and complaints go to JD.

But quips potentially are coming. They're incoming.

Perfect. Okay. So we're going to show you your Cleer Cardio exam live. So what we have done here is, and I'll ask for a little mind experiment. So we've taken your heart, we've taken these very high-resolution pictures of the heart, we've now deconstructed your heart, we've taken it apart. So what I've done here is we've taken the heart, pulled out just the blood vessels alone. I call this CAD/CAM of the heart, right? Once it's digital, we can manipulate it all kinds of ways. We've done that CAD/CAM of the heart, and I've taken your right coronary artery, which is this vessel here, and we now can straighten that vessel out. This vessel is not straight, but with the magic of computers, we've now straightened that vessel out.

Interesting.

So this is your right coronary artery. This is the channel, the lumen, and we can actually— these aren't live pictures. If it were, with these degrees, We can sit here, press that little arrow, and literally spin that vessel around, right? So one of the things about plaque is it tends to be, we use the term eccentric. That's not your weird uncle. Eccentric means it's not like rust in a pipe where it's kind of equally coating.

That's how I think of it.

It could be like 3 o'clock or 12 o'clock or 6 o'clock, right?

Gotcha, yeah.

So you really have to spin the vessel around to be able to see that plaque. Another important thing about plaque, plaque always forms in the wall of the vessel. Okay? So think of a donut, right? Historically, we've been worried about the donut hole.

Yeah.

But that's the last thing to go bad. Plaque begins in the donut. And early on, that cholesterol literally gets deposited in the donut. And the donut will expand outwards. The hole is the same. There is no change here. There is no blockage.

So when we're looking into the—

whether there's a blockage or not, it's great. Down the barrel of it, right?

Yeah. You're not looking up and down.

It's perfect. But we couldn't see what's happening in the donut. And the whole vessel can literally expand to about twofold before it starts growing in. And remember, historically, waiting for symptoms or flunking a stress test, we're already at a 70% blockage. So that plaque has literally been there For decades.

Yep.

Right? And we did nothing because we didn't know we had an issue.

Yeah, makes sense.

So what the AI does, right, it can see plaque that we can't even see with our eyes. And in addition, it will then tell us exactly how much plaque we have in each vessel. And we also get a summary of the whole, how much plaque in the entire heart. Okay? So I'll show you in a moment kind of what this number means. But in the right coronary artery, we did detect a little tiny bit of plaque. Again, this is the degree of plaque that historically, before we had CT, before we had AI, was undetectable.

I know what we've seen. Yeah.

So I'm going to tell you, to put this into perspective with analogy, I think most people get, if this were a colonoscopy and we're looking for polyps, yeah, you got a little polyp.

Okay?

Not a big polyp.

Yeah.

Not a worrisome polyp, but you got a little tiny polyp.

Got it.

Which, how young are you now, Jamie?

46.

46. Okay. Which took you 46 years to get to this point.

Got it.

Okay. So, important, but historically undetectable until we had this technology. So that's how sensitive this is. So we can measure in that particular vessel, in the right coronary artery, we have 3 major vessels. If you look at that diagram here, it's sort of illustrating that diagram of that vessel, the right coronary artery. And then you'll see, Shadows. We'll look at the others in a moment. The other 2 major blood vessels. So in that particular vessel, 2.8 cubic millimeters of plaque. Note, we can measure this down to a 10th of a cubic millimeter. So if you look at a period at the end of a sentence, slice the end if it were a sphere, cut that sphere into 10 pieces, that is a 10th of a cubic millimeter.

Got it.

So that is the resolution that we can see.

What is a worrisome number or a number that makes you— is there a number that kind of like, ah, you're above this, we get a little nervous?

It's a continuum. I'm going to say the only normal is zero.

Okay.

Right?

Yeah.

I mean, that's normal. Everything else is not. If you had a colonoscopy, you don't have any polyps or else we saw some polyps, right?

Got it.

So yeah, but it is a continuum. I will show you towards— after we look at this, I'll show you some data that sort of puts this with respect to— because people always want to know that question, and how much, what does this number mean, how do I compare to everybody else? Hold that question, we will come back to that.

Got it.

Okay, so in this particular vessel, 2.8 millimeters. Next slide, if you could, JD. And again, you can see a nice, beautiful vessel there, right? Fantastic, right? And by the way, and here's another tragedy, in my humble but accurate opinion. So we do about 10 million stress tests a year in the US.

Yeah.

Right? That vary in cost. And there's lots of different flavors of stress testing, but they vary from $500 to $5,000. Right? And I just told you, they only detect severe disease. They only detect severe blockages. They can't detect early disease. And on top of that, when we do a stress test, and I think this is so important for everybody in the audience, When we do a stress test, again, the sensitivity to detect the disease only detects severe disease. Imagine we did colonoscopies and the GI doc says, all I can detect on a colonoscopy is metastatic colon cancer. Anything less than that, it'll be normal. And you go, you know what? If that's all you can detect, I probably won't do this. Because if I have metastatic disease, I'm just going to live in ignorance for the short period of time I have and we're good.

Right.

But that's not the case, right? When we do stress testing, and again, any kind of different kinds of stress testing, very insensitive. Plus, we're not visualizing, as we are here, the actual vessels.

Yeah.

Right? So all the detail that I was telling you about, we can't see on a stress test. Furthermore, with stress tests, depending upon the kind, you have anywhere between a 25 to 40%, what we call a false positive rate. Your stress test looks funky when in fact you're actually fine. Well, that's no fun.

Yeah.

Right? That's bad because in the old days, we would then take that person with the funky looking stress test and then they'd go on for a $20,000 invasive heart catheterization. Right, right, right. Of which we do a couple million a year at about $20,000.

Right?

By the way, that diagnostic test is a diagnostic test, invasive. We put catheters, tubes, silly straws up in your heart. Takes a day of your life, basically. Risks of strokes, heart attacks, vascular events, bleeding, infection. And it is purely a diagnostic test. Doesn't fix anything.

Just gets at what it is.

And all I can see on a heart cath is the donut hole.

The donut, right.

Right?

Yep.

Nothing but the donuts.

Yeah.

Okay. That's why I stopped doing that 20 years ago.

I don't blame you.

Silly, expensive, ridiculous. So the next vessel, the one going down the front here, total plaque volume is 26.4. Okay, so we got a little bit more. Okay, but again, a nice big vessel, nothing that would ever show up on a stress test or even a heart cath. And I think the next slide shows where you have a little bit of plaque. So what we can do now, we can take that data, we're flying up and down that vessel. Please don't try this at home. And we're cutting through that vessel. This is the cross-section of that vessel right there. And if you look out here, you see that little— looks like a little pimple there?

Yeah.

That's your plaque. And it's in the wall of the vessel.

Is that a dangerous amount of plaque? That looks dangerous to me.

Well, so again, on a heart cath, completely invisible.

Sure. Okay.

Because it's in the donut, not the donut hole. Now also too, and this is again what AI does, there's 2 kinds of plaque basically, right? And I'm going to use my favorite analogy. The first kind of plaque, the plaque that's always initially deposited, right? The starting plaque, which is also the dangerous plaque, the active plaque, the growing plaque. Okay? I'm going to call that— we call it soft plaque or lipid-rich plaque. I'm going to call it lava, right? Because I'm going to tell you the volcano analogy. All plaque starts out as lava, right? All volcanoes start out as— even extinct ones start out as lava. Over time, after that gets deposited, that lava will cool down and it'll become—

Rock, solidified.

Yeah, solidified. A cinder cone, an extinct volcano. So what AI also does is it tells me exactly how much plaque you have. Then we'll break it down into how much soft plaque you have, the lava, and how much hard plaque.

Ah, okay.

Okay. I don't care about the hard plaque.

Yeah.

Okay. Extinct, inactive, no longer progressing. Who cares? It's evidence that there was an eruption there at some point.

Yeah.

But it's no longer active.

So what is that?

That is a calcified plaque.

So that's hard plaque.

Exactly.

26, whatever it was, that's all hard plaque, no soft plaque?

Well, there is a tiny little bit of soft plaque. So if you look at these numbers here, the hard plaque measured in cubic millimeters is 5.5 cubic millimeters, and there's about 20.9 non-calcified lava.

Okay?

However, this calcified plaque is easy to see. It's generally calcified, easy to see. The soft plaque is dark.

Hmm.

That's where the AI comes into play. This is the stuff that is enorm— can be very hard to see. I mean, I've done over 20,000 of these.

Yeah.

Thank God for AI, because it gives me a whole— it's like putting on glasses.

Extra eyes. Yeah.

So, but, you know, it is what it is. I would say if I were to compare you to the average 46-year young guy, you got much less plaque than the average bear. Okay. But also appreciate this is an extremely sensitive tool.

No, understood.

So that's That's that vessel. And again, you can see out in the donut hole. And again, unless we had AI, I'd be able to see that visually. I could see there was a plaque, but I really couldn't do this kind of quantification or see some of the lava plaque there.

That makes sense.

More active plaque. Okay.

Last one.

And then this is the last vessel called the left circumflex.

Zero?

And this was a zero.

Look at me, I'm a boss.

So I always like to say, if you're a zero, you're my hero, okay? I'm my own hero right now. Thank you for working to put me out of business, okay? That's what I like to do. That's my ultimate goal, right, is preventive cardiologists put me out of business.

This may be a dumb question. No dumb questions. Of these 3—

There's only dumb answers.

What is the widowmaker? Or is that none of this?

Yes, comes up all the time. So the widowmaker, go back to the last slide, is, it's a really bad term. Not used in a very consistent scientific way. If there is a widowmaker, and here's my objection, some would say it's a blockage anywhere along that vessel. That's really not true. If you look way at the top there, there's something that says LM. That stands for left main. That is the largest of the coronary arteries, right?

Mm-hmm.

And it's usually only about a centimeter or 2 long. It then rapidly divides up into the vessel going down the front and then shoots off the vessel to the left. So that's a really critical vessel. That's your 31-inch water main, right? If you get a blockage there or rupture a plaque or whatever, that's going to be pretty disastrous because it supplies so much of the heart muscle.

Got it.

Some of my colleagues would say anything in the LAD, which is the vessel that starts just after that, right there, Would be the widowmaker.

Any of this? The whole thing?

That's the whole LAD.

That's what they would say.

Okay, got you. I disagree with that. I think it's a bit of hyperbole. They say it to get you excited, worried, and then when they put a stent in it, even though you have no symptoms and you feel fine, and they show you the picture of the narrowing and then the stent afterwards, and they say it's the widowmaker, you go, my God, my life was saved. And we have no data that supports that.

Where is the plaque in this artery specifically?

So that plaque is in that— we break it down into 3 sections, right? Proximal, we call it proximal, mid, and distal, right? The front, the middle, and the latter part. So it's in the— it'd be—

Proximal.

In that section.

And it actually gives you a little bit of color there.

Gotcha. Okay.

By the way, I don't have this slide, but the other cool thing that the AI does is it will give me a very precise analysis of any blockage, and it will color code that. The computer said in that little tiny baby plaque, they call that a 4% narrowing, which honestly, again, if I did a heart cath on you—

You wouldn't see it.

Invisible. But we do get that. We do get the narrowings. I can't say they're not— they're useful if you had bad angina, we're going, do you need a stent? Is it going to help your quality of life?

Right?

Doesn't save your life, but does it improve your quality of life? You don't want to be taking 3 nitros every time you go to the bathroom. You get the idea. Then stents are fine. So stents are really, in my world versus orthopedics, are really like knee replacements. No one says if you don't replace that knee, you're going to die. You may be disabled, you can't get around, but— and some people can be bone on bone and feel fine, and other people doesn't look that bad and yet be in terrible pain. And if the pain is bad enough, then you say, I elect to get that replaced.

Yeah.

That's really how stents work, right? They're really quality of life tools. Nothing more, nothing less. But no, great question. So, the left main is really the widowmaker, just because it's such a critical vessel. You got nothing there. Itty-bitty tiny bit in what we call the proximal, or the beginning part of that LAD. And again, in that vessel here, the third of the vessels, nothing whatsoever.

Plaque-free?

Plaque-free and loving it.

I'll take it.

Exactly. Okay. And I'll show you now, I think we have some other slides here. It's just another picture of that. By the way, this is the— you will get a copy of all this. We're going to send you a report. This is just the front page. The report's about 20 pages long. The first 15 pages basically tell you what is plaque, how it behaves, donut holes, lava, calcified plaque, all that stuff. So all the stuff that we covered. So I just saved you 15 pages of reading. But it is a cool report. It's very well written, very scientifically accurate. It has cool visuals. So it's a great take-home if you ever want to look at all this stuff. So get that. But I'm going to go back to your actual report. So again, we've taken the vessels. Before, we showed them horizontal. Now they're vertical, same data. And so you can see, this is the right coronary artery. There's a little itty-bitty plaque there. You can see the channel, the donut hole is perfect. And you can see right there, make sure to lose the mic there. See that? It looks like a little pimple.

Yep. That's my plaque.

That's a little bit of plaque, right?

Gotcha.

So in that particular vessel, which is a branch of the right coronary artery, so it's a pretty small vessel, there's 2.8 cubic millimeters of plaque in that vessel. It is all lava. There's no calcified plaque, and all the others are basically zero.

Okay.

Right, for the rest of that vessel. Okay, next slide. And then there's that LAD. This is the one that had a total of 26 cubic millimeters of plaque. We break that down into 5.5 millimeters of calcified plaque, that is blue, and then about 20.9 cubic millimeters of the LAVA, the lipid-rich plaque. Again, channel wide open, Heart cath, the quote used— they still call it the gold standard, which I laugh at— would be completely normal. And again, you can see they almost look like pimples. I hate to use that term, but they're kind of stuck on the outside. But we have a very precise quantification here, a little branch there, all zeros through there, and then that last vessel, the left circumflex, which I think we have here as well, which is the next slide.

Next slide. Yep.

Was, again, zeros all the way through.

Okay.

Yeah.

So, not dying.

No.

So far.

And then I've got, I think, one more slide I just wanted to show you that just shows the zeros. This is the— we're going to send you both these reports. You have the patient report. This is the provider report. Basically gives us the same data I just walked you through, but one additional thing that I'll show you as well. So, here we have on the left-hand side, you can see the total plaque volume, all plaque, lumped together across the 3 different vessels, 2.8 in the right coronary artery, 26.4 in the left main LAD, 0 in the left circumflex. Then it breaks it down into the 3 kinds of plaque. There is a 3rd kind of plaque that if you have it, tends to be quite low. It's called low-density non-calcified plaque. That if we talked about lava, think of this as like the really bad hot lava.

Got it.

You don't want this. You don't have any of that. A little bit, and we'll look at that, normalize that here in a second, of the non-calcified, a little bit of calcified plaque. And also too, a lot of times, and more and more people are hearing it and using it, and it's a good tool, but I think this is a beautiful illustration. Another imaging tool that, again, really goes back to the '80s, we've been doing this a long time, is called a calcium score.

Yeah.

So this is not a blood test. It's also done with a CAT scanner. Kind of a very, very crude version of what we're doing here. There's no contrast. It's easy to do. It just takes a few minutes. Huge amounts of literature behind it. The limitations of a calcium score is because we're not giving contrast, I can't see any blockages. And number 2, I can't see the lava. So if you had a calcium score, and really that's a very low calcium score.

Where does the calcium score start?

So the calcium score is that 5.5 number. So there's that, remember that little speck of plaque in that one vessel that was white?

That's it. That's the 5.5.

It was 5.5.

So, but if I had a regular calcium score without contrast, it probably would be lower than 5.5.

Yeah. You probably wouldn't even see that.

Probably be a 0.

Exactly.

Okay. Got it.

So you couldn't see it, nor could you see what is actually a more relevant plaque and a more important plaque, which you have more of, which is the lipid-rich plaque. Gotcha.

Yep.

Which again, here was 24 cubic millimeters roughly of non-calcified plaque at about 5.5. But if you did a calcium score, it'd be normal. You probably wouldn't even see this.

So this is heart.

Yep.

I think of a calcium score, there would also be an ultrasound done of the carotid.

Yeah.

So plaque can form in any artery of the body. The 2 big ones, there's really 3, the 2 big ones, heart, Right? We call that heart attacks and balloon stent bypass surgery. Plaque can form here, causing strokes.

Yep.

And certainly plaque can be spotty, right? You could have a lot here, none here, or vice versa.

Yeah.

So if you want to know what's in the heart, you got to do this.

Yeah.

We did not image the carotid arteries. However, I will tell you, with a relatively small amount of plaque here, I'm really I'm not worried that there's anything of significance going on here.

Got it.

If you wanted to do that, we could do that with ultrasound. We can also do, as we did with the heart, we can do these beautiful images of all the carotid vessels. One of the limitations of ultrasound is we can't do quantification as we've done here. We can't really divide it up into the soft plaque, hard plaque, as we've done here. And then the other problem is, With ultrasound, I can only see from roughly here above your collarbones to your jaw.

Can't see underneath. I can't. Right, right, right.

So anything above the jaw is invisible because the ultrasound doesn't go through bone. And so when we do carotid CTs, same concept here, contrast, same scanner, we can see the entire carotid artery everywhere from where it comes off the aorta, that main vessel coming out of the heart, all the way up into the brain. So we see the entire vessel.

Gotcha.

So it depends. Practically, if you had a prior history of stroke or mini stroke, we're going to do that.

Sure.

Obviously, if you, on examination, I always listen with my stethoscope over the carotid arteries. If I hear what is called a bruit, it's a French term for murmur, basically, that might indicate a narrowing and say, we need to look at this further.

Okay.

But again, with this pretty low score, I'm really not worried about anything going on here.

Good.

And also too, when we treat plaque, it is and can be a systemic disease, right? The other major places, although plaque can build up in any artery vessel supplying any organ, the third area is in the legs, right? You can get in the arms too, but you can get in the legs. We call that peripheral arterial disease or PAD. And the symptoms of that would be you start walking, and because demand load goes up, the vessel's too small, your muscles start cramping and you can't walk. And what happens is an interesting phenomenon where you walk, they cramp up, you can't walk because of insufficient blood flow. And then you rest for a bit, blood flow catches up, and then you could walk, and then it happens again. So that's called claudication. So claudication is sort of angina of the legs.

Got it. Got it. Got it.

Okay.

Generally, the biggest burden of PAD though are for patients that either smoke or have diabetes or both, right? Not to say it doesn't occur in those 2 people, but rare. But anyway, the last thing I wanted to show you, and then there's a couple little trivial narrowings that the AI detected. And then that little box there to the right, we can now, with the ability to quantify AI, We can now put people in stages. Okay? So of course, 0 would be 0. Stage 1, which we call mild, ranges from not 0 to 250. And your total score was 29.2. Okay?

Yeah.

Moderate, or stage 2, would be 250 to 750. And stage 3 is above 750. By the way, about a third of the people that we do CLEAR cardio on, are actually stage 3. And these are people who have no symptoms, feel fine, whatever. So I guess in summary, what I'm telling you is the good news is that no blockages. We did detect a little bit of plaque, join the crowd.

Yep.

When you begin to use the incredibly sensitive tools that we now have access to, cardiac CT combined with the Cleer Cardio AI analysis, we will find Upwards of about 92% of asymptomatic people, when you use this microscope, have detectable plaque.

That makes sense. That makes sense.

Right? Yeah. Which is why 40% of us die of plaque, right? So early detection is the key. I would say you have a very small amount of plaque. It's a very slow, glacial process. So what if you're— and we've already worked out looking at those stages. If you are stage 1, that the stages help dictate what we should do to stop and reverse plaque. And yes, we can stop and reverse plaque. We have multiple tools that can do that, but it also dictates when we should take another look. So if you're stage 1, 3 years.

Got it.

Stage 2, 2 years. Stage 3, which means you got lots of plaque that stuff could happen soon. We got to make sure that, again, we're very, very aggressive with that. And also, we look within a year to make sure that not only are the numbers better and cholesterol's better and we're doing all the right stuff, but is the plaque better? And we could never do that before in the practice of cardiology. That's incredible.

That's good to know. So I have a 3-year stay of execution.

You do.

Amazing. Right?

Now, I will tell you one thing. So I got your labs. They look perfect, right? You're the Specimen of health. Your LDL is about 209.

209. Yeah, that makes sense. Yep.

Okay. And we were talking earlier, you do basically all keto, 4 eggs in the morning, ribeye for breakfast and lunch. And it's interesting, there's a massive debate going on right now. It's in no way settled, right? I will tell you, as a cardiologist, when I see high LDL cholesterol, I get nervous. On the other hand, your HDLs are great, which by the way, Keto will raise your HDLs.

Sure.

Triglycerides.

And triglycerides really get suppressed. And those are— HDL is a very messy number, but triglycerides are bad, right? So it definitely suppresses the triglycerides. So I think it'll be an interesting experiment to do. Here's our N-of-1 experiment. We know where we stand in a very, very precise way as of 2025. Let's reconvene in about 3 years, see what we look like.

Yeah. So diet-wise, am I sustainable as a carnivore?

Whether it's sustainable for you is up to you.

Sure.

Right? I mean, some people just go, I can't eat any more protein fat, whatever.

I could eat meat all the time.

Right. Other people, yeah. So I think sustainability's up to you. Whether that LDL is feeding the plaque or not is still, In people who do carnivore is still a very interesting but unanswered question.

Yeah.

There is no way that you're going to rapidly progress that plaque. Let's say that 209 is bad, right? There's no way in the span of 3 years with the ability to detect and quantify plaque that that's going to progress on to something that's going to need stents, balloons, surgery, or whatever, right? So I am very comfortable saying, Eat right, exercise, don't start smoking. No, tell people I did smoke my first cigar recently, but I don't—I didn't like it.

That's all right. I'll look the other way. I'm out. Yeah, good.

That's good.

That's good.

And you know, stay active. Keep an eye on your blood pressure. Very, very important. The silent killer. I would do that, and then let's relook three years and see how we look. You know, there are certainly members. I'm also a board-certified lipidologist that would say, "Oh my God! We need to get you on probably at least two drugs to get that cholesterol down." Statins. Yeah, but. I think our mistake has really been we've always looked at the number and assumed that's what your vessels look like. Here we have a number, LDL, that's high, but when we actually look at the vessel and look at the disease and look at the plaque, it's minimal.

Right.

Right? And it is a very slow glacial process. So I would say, let's do our N-of-1 experiment. We will have other science coming out about this specific question. The high-fat carnivore keto diet, whatever you want to call it, and what happens with plaque in that setting, even though in many patients the LDL goes up.

Yeah.

But the HDL goes up, whatever that means. I'll admit, who knows? I don't really trust that. But more importantly, the triglycerides do come down, and that is a bad fat. So I say we do our N-of-1 experiment, and we'll reconvene and schedule for your next scan in 3 years.

He's going to keep eating meat. Let's see what happens.

You know, at this point, because we can now look under the hood and see you just don't have that much plaque at this point, we can very easily quantify it. We'll bring you back in 3 years and let's see how things look.

I love it. Well, this is great. Thank you so much for, for going through that. That was really fascinating, actually. So yeah, good stuff.

I, I love doing people's virtual autopsies.

Yeah, emphasis on the virtual. Yeah, I love it.

Thank you so much, Jamie. It's Really been a pleasure. And thank you for being willing to go through the process, letting us look under the hood and share it with the rest of the world.

Of course. Glad to do it. Glad to do it. I appreciate you. Thank you.

All right. Tune in 3 years from now.

I'll be back.

Okay. Wow, Dr. Osborne, that was fantastic. And again, Jamie, thank you for coming on and sharing that with our viewers here on the Clear Cardio Podcast. Prevention is power. Podcast. So tune in again. And for those of you who are really interested in finding out, like, like Jamie was, what was going on under the hood, as Dr. Osborne would say, please reach out to Clear Cardio at clearcardio.com and come on in and find out what's under your hood. Until next time, this is J.D. Enright with Clear Cardio. Have a great day.