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The Good Question Podcast
Preventing Heart Disease Early: Dr. John Osborne On Hidden Cardiac Risk & AI Diagnostics
00:32:45
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- [00:01]
A
You're listening to the Good Question podcast with Richard Jacobs. Our goal is to make each of our guests exclaim, hmm, that's a good question. I don't know the answer. Because when that happens, it means you, the listener, may be inspired to learn more beyond the interview and to ask great questions yourself that lead to new insights. In this podcast, we cover historical and current anthropology, comparative religion and history. Welcome. And let's get started.
- [00:36]
B
Hello, this is Richard Jacobs with the Good Question podcast. My guest today is Dr. John Osborne. He's a Harvard trained, triple board certified cardiologist, co founder of Clear Cardio, and we're gonna talk about plaque. And I was known as a silent killer. So welcome John, thanks for coming.
- [00:52]
C
Oh, my pleasure. Thanks so much for having me, Richard. It is a pleasure and an honor to, to join you. Thank you.
- [00:58]
B
Yeah. So tell me a little bit about, about your background. So you were, I guess you were a clinician for a while, surgeon, and now you've changed.
- [01:05]
C
Sure. No, I, I mean, honestly, I've been doing really the same thing for, for 30 years. This is my 29th year in practice in 2026, but so I'm a, a, I like to call myself a preventative cardiologist. My goal, detect problems early, take care of them, and we don't end up with, you know, what we think of as heart disease, which is stents and balloons and bypass surgeries and strokes and people keeling over dead. So that's really been my passion for the last almost 30 years. And really during that time, doing a very, very long deep dive in preventive cardiology and getting all kinds of silly board certifications and as I call it, expensive pieces of paper on my wall, that's really been the passion. And then identifying technology that allows us to identify heart disease literally decades before we have trouble, have symptoms, angina, whatever, and then coupling that early detection with proven ways to stop reverse what is really the ultimate cause of the vast majority of heart attacks and strokes, which is plaque. So crude. Cardio is just an organization that we put together, but it really is what I've always been doing. I'm a, I like to call myself a medical cardiologist. So no heart surgery. I don't do stents or balloons or those kind of things. In fact, pretty much everything I'm doing is to help people avoid manifesting heart disease, which needs stents and balloons and surgery, or worse yet, having strokes or heart attacks or killing over dead. So really I started my training over 30 years ago and have been really had a Monomaniacal passion for prevention and early detection. And that's really what clear cardio is all about.
- [02:41]
B
One thing I've interviewed a few cardiologists. One big thing that I focused on is, I may be wrong, but how much of the blood supply to the heart is for the microvasculature around it, not the macro vessels?
- [02:53]
C
Yeah. So it's a great question. And for a long time, we've been looking at the microvascular system because it really is also as important as the larger vessels. Right. The larger vessels would be what we call the epicardial vessels. Those are the vessels we think about that get plaque in them and get blockages, and we do stents and bypass surgery and mechanical things to fix that. The microvasculature plays a very big role. Kind of takes a separate kind of technology to look at that. It's always been trickier to really understand and measure that in a. A quick, easy, reproducible way. And it is very, very important. The challenge is on the microvascular this, because these are not vessels you can mechanically fix. Right. They're really super small. These are almost essentially microscopic vessels. There's really nothing we can do mechanically. And a lot of our emphasis around cardiology is stuff we can balloon and statin, all that. So just plain old plumbing. Whereas the microvasculature is really the domain of diet and exercise and lifestyle and in certain people, perhaps even medication. Well, but it's a great area. It's been recognized as being important. But the challenge has really been able to really measure the. And look at the microvasculature. We still have substantial barriers as far as being able to reproducibly look at it, measure it, detect it, and treat it.
- [04:17]
B
Yeah, understood. But if you were to just bluntly assign a percentage of the total perfusion of blood to the heart, you know, microvasculature versus epi, you know, the epicardium larger. What would that percentage be? Approximately.
- [04:30]
C
Yeah. So I'll tell you. And this is true.
- [04:32]
B
True.
- [04:32]
C
It's a hundred percent and 100%. So 100% of the vessels of the blood flow going to the microvasculature comes from the larger vessels, the coronary arteries, the epicardial vessels. So it's 100% of the flow into microvasculature is provided by the larger epicardial vessels of the heart that historically are the ones we stent. Blue bypass, vertridium developed plaque. But the larger vessels are only delivering to the microvasculature 100% of that blood flow. So the answer is truly, it's 100% and 100%. So 100% of your blood flow is going to pass through the epicardial vessels, and 100% of the blood flow is also going to pass through the microvasculature, too.
- [05:11]
B
You know, the reason I'm harping on this, because, you know, I'm an engineering background, so I look at it from that standpoint. So if there's any plaque buildup and you have these tiny vessels, it doesn't take much, I would think, to fill them and occlude them, and then they die. And now that shunts more of the blood flow to the larger and larger vessels. So therefore, like, I would expect blood pressure to go up in the remaining vessels, you know, blood volume up to a certain point, probably the acceleration of plaques in the larger vessels, all that. But the cascade, I think, would start from the smallest to the largest. That's why I asked.
- [05:42]
C
Yeah, no, great question and a great engineering, logical way, but. But here's something you may not know. Atherosclerosis, plaque that we can treat, of course, we've treated mechanically for a long time, as it turns out the best way to treat it, take care of it, reverse it, as medically as it turns out, diet, exercise, whatever. Here's the thing. Atherosclerosis only forms larger vessels, right? We're looking at vessels basically 1 millimeter, a millimeter and a half or larger. It. It does not form. We do not form plaque or atherosclerosis in the smaller vessels that are smaller than one to one and a half millimeters.
- [06:16]
B
Well, really? Why?
- [06:17]
C
Yeah, a great question. Hopefully I'll have a great answer for you one of these days. All I can tell you is that at a historical basis, an observational basis, and scientific basis, that is the fact. So atherosclerosis is a disease that really is confined to the larger vessels. It does not in small vessels. Now, that's not to say you can have microvascular dysfunction and vasoconstriction, et cetera, but that process is not via plaque or, you know, the stuff that builds up in the larger vessel, maybe the
- [06:46]
B
precursors, the building blocks of plaque are so large they wouldn't even fit into smaller vessels. But. But then I would think you would see the entrance to the next, you know, more narrow vessel. You would see a. A big buildup there. It's very strange. Do you see that?
- [07:00]
C
Yeah, and I. I can't tell you. I. I think sort of analogous to this, to kind of get in the weeds, I think Is that, you know, people think about heart disease and blockages and stents and surgery and all that stuff, but also too remember, plaque atherosclerosis can be in any artery or blood in your. In your body. Right. We find it in the neck, in the carotid arteries, causing strokes. You can have it in your legs. You can have it literally in any vessel in your body. Right. But interestingly, there it is. Can be very different from person to person. One person can have severe plaque build up in the neck and cause strokes or that kind of stuff and have nothing in the heart. Or someone can have severe heart disease and need stents or balloons or surgery because of the significance of the plaque and the burden and the burden of plaque in the heart and have nothing in the carotids or in the legs. So we really don't have an explanation except those vascular territories. There's something different and unique about them. So that, you know, you could have plaque build up in one place and have nothing in another place. And that's just, you know, how plaque behaves. I think down the road we'll find molecularly looking at adhesion molecules, you know, if you will, sticky vessels, that kind of things. I think we'll find that based on the blood vessel and which blood vessel that is. I think they. We will really find that they are more different than. Than we think. But we. We don't really have a good handle on why someone builds up a lot of plaque in one place and no plaque in another place. So I think those two questions are probably somewhat linked to. To what you mentioned.
- [08:26]
B
Yeah. Because I was thinking of pressure differences. Like how much of a pressure variation is there in the legs where plaque would accumulate versus in the neck, you know, or the center. Center body. But then I thought, okay, so maybe what if there's niche construction going on? I don't know, there's this exosomes or whatever material going out, and when it finds an amenable spot in the circulatory system, it starts again. Like instead of a pre metastatic site, a pre plaque site where it builds some scaffolding that then attracts more plaque for the. To that region. I don't know why, it's just a wild guess. But what's your thought there?
- [08:58]
C
Yeah, and it's. It is interesting. I mean, there's a whole science of rheology, which is all blood flow and, and a lot of that focuses on shear stress. Right? What is that she. Shear stress that you're familiar as an engineer with, and that varies very differently. From vessel to vessel based on the size of the vessel, also based on the anatomy, based on curvature of the vessel, based on branch points. Right. All of those factors, those rheological factors can change the shear stress. And we do know that shear stress is very, very important to the formation of plaque. And interestingly, it's not high shear stress areas that form plaque. It's the low shear stress areas that are more predisposed to plaque as well. So it's an ongoing area of interest in research. And I suspect down the road we'll have more and more detailed, better answers to this. But right now, we're still at the observational phase for this. But we do. I mean, there's a lot of science in the world of rheology, but not much is sort of migrated practically clinically into the, into the clinical world.
- [09:54]
B
What about, you know, the edge number of cadavers, all the age, sex, blah, blah, blah. And then you scrape some plaque from the neck, from the leg, leg, from different body parts and compare the composition of it and the structure. As I'm sure that's been done. I mean, is there.
- [10:10]
C
So. So once atherosclerosis has kind of created a. A beachhead, basically, it's very similar regardless of the vessel. Right. Whether it's a coronary arteries, the carotid arteries, the peripheral arterial vessels, et cetera. So once it's started, and also then therefore, the ways that we can diagnose it, the ways that we treat it are frankly, fairly similar. Right. We don't treat carotid arteries really much than we do coronary arteries in reality, as far as diagnostics, the medical mechanical approaches and the medical approaches. So it's the. I would say the plaque is quite similar. But why does it form in one particular vessel in one location and not elsewhere? Again, rheology, the science of that world and wall stress gives us some insight, but we're not completely there, I have to admit.
- [10:59]
B
Well, what about the condition of the endothelium? So someone that's had high blood pressure for many years, again, I would strain certain vessels, I would guess than others strains everything. Maybe the ones that are now stretched and weakened are more preferential sites for plaque buildup. Like, has anyone found any correlation anywhere?
- [11:17]
C
Oh, oh, sure. I mean, so I actually did my PhD in endothelial dysfunction and nitric oxide a long time ago back in the 80s. But it's. It's an area of tremendous research. And we know the endothelium, which, for those that aren't familiar with that word, that's the, the single cell lining of the blood vessel that plays an absolutely critical role in whether we form plaque or not, regulates blood pressure, produces nitric oxide. Should be more like, as I like to think of it, more like Teflon, nice and slick or slip and slide, as my partner says, versus Velcro. And we do know that inflammation, sticky vessels, if you want, but inflammation, to keep it scientific, plays a very, very large role. In fact, some argue that inflammation is more important than the stuff that gets deposited in the vessels, which is cholesterol. And that inflammation, the endothelium, when it's under stress, the big modifiable things that cause the endothelium to get sticky to go from Teflon to Velcro, the big. And again, there's a lot of factors, but I'll, I'll kind of hit the top. The big factors that turn that endothelium from Teflon to Velcro would be tobacco of any form, by the way, whether you vape it or otherwise consume it, would be high blood pressure. And the harm from high blood pressure probably starts at a lower blood pressure than you. You'd probably be aware of, from, from quite good epidemiologic data. And then the other big thing is insulin resistance and diabetes. There are many other factors, even inflammatory conditions like rheumatoid arthritis and lupus and psoriasis and psoriatic arthritis and on and on. So kidney disease, by the way, also causes the endothelium to become dysfunctional, as an example. So a lot of times I'll say I'm really the pipes, pumps and filters guy. But yeah, so the inflammation, the changes in the endothelium, reduction in the production of nitric oxide, the expression of a whole variety of adhesion molecules that are expressed under, in, in states of inflammation, which then again makes the vessel sticky, more likely develop and plaque and for cholesterol to get deposited is an absolutely critical role. In fact, interestingly, in the, in the, in the cardiology literature, just the last couple months, there's a very important paper that kind of a white paper that really said inflammation is a critical aspect to, to forming atherosclerosis. In fact, some studies published last year show if we looked at hscrp, which is typically how we measure inflammation, there are lots of other ways, but HSCRP is sort of the canonical way of measuring it. And LDL and apo little lp, which is another form of cholesterol. If you looked at those 30 years ago, and we have large prospective cohorts doing that, that understanding and measuring those levels 30 years ago very much predicted the instance of cardiovascular disease 30 years later, which as, again, as a preventative guy is very exc. Because now we can begin to identify these factors literally decades before you get in trouble. So, no, I think it's a great question. And the bottom line is the endothelium is absolutely critical and plays a critical mandatory may not be sufficient, but mandatory and necessary role in the genesis of atherosclerosis.
- [14:22]
B
And one more question. One is vain, I guess pun intended. Good one. I've heard stents don't work. And it seems crazy. Like, how could a blocked vessel that gets stented or mostly blocked against stente now open? I mean, what do. What do papers mean or clinical outcomes mean when it quote, unquote, doesn't work? And why.
- [14:40]
C
Yeah, so. So it's a great question. And let me just kind of refine. Refine the response. So. And I'm going to lump stents and I'll say balloons. We don't really do balloons in coronary arteries really much anymore. But I'll say that for historical purposes. So we have balloons and stents and bypass surgery. These are the mechanical ways that we've played around with lots of other ways to open vessels. Many of them don't work, but those are those kind of the standard things we do mechanically to open vessels. So here's the issue. The blockages that we use the stents and balloons and bypass surgery on, they do work for, for one, and they are quite effective. For one thing, they improve blood flow. The problem is that atherosclerosis, which is a very slow glacial process that literally takes decades to evolve to a blockage, but can be detected literally years before then, can ultimately translate to a blockage. And we have restricted blood flow. And then therefore, we have symptoms in that organ where that restricted blood flow is in the heart, we call it chest pain or angina in the neck would be mini strokes, et cetera. In the legs could be what we call claudication, which is really just angina of the muscles of the legs. So stents do work, but they only improve blood flow. Importantly, they do not treat. Treat the disease, they do not treat the plaque, which is the genesis of these blockages to begin with. So the reason that you might hear they don't work is this. We have done multiple studies over the last 30 years and come up with exactly the same finding every time we do the study that putting stents in, even in people have critical blockages who have Symptoms, who even had positive stress tests. That is, we have objective evidence they have restricted blood flow down the vessel by putting in stents or even bypass surgery. It improves symptoms, we improve blood flow. And by the way, a stent does not fix the disease or plaque. It really just pushes that plaque off the side so we have better blood flow so that the issues due to restricted blood flow causing symptoms are resolved. But by putting in a stent, it improves symptoms, just like doing knee replacement improves symptoms. But we would never say putting in a knee replacement will make you live longer. Right. It improves symptoms. You're less disabled if you're willing to put up with the small mortality and morbidity of having a knee replacement improves your quality of life, but it does not make you live longer. The same thing is analogously true with stents. Stents improve blood flow, they improve worse. And again, surgery. They improve blood flow, they improve symptoms, they do not treat the disease, the underlying disease of plaque. Therefore, they do not impact hard endpoints such as do you die of a heart attack? No. Do you live longer with a stead? No. They improve blood flow, they improve symptoms. They are the knee replacement, I like to say, of cardiology, but they do not treat. If you want to think about knee knee replacement and arthritis and degenerative joint disease and. And DJD osteoarthritis, we're just putting in a new knee. But we did nothing to affect or improve your cartilage, which is worn out because variety of factors, genetic and other factors. So that's why if you hear scents don't work. They do work for symptoms, they're quite effective. But they do not treat the disease and they do not prevent the disease and they do not make you live longer. They don't prevent heart attacks.
- [17:47]
B
Okay, that makes sense. Well, actually, you know, I see you said no, why wouldn't. Well, they're not going to prevent heart attacks. I mean, in that vessel at the skins and point at least probably not. But there's so many other places where it could happen happen. I guess it just.
- [17:59]
C
Absolutely.
- [17:59]
B
Access to the next most clotted point.
- [18:01]
C
Right. Well, and here's another thing that again, we've known since the 1980s that the plaques that cause heart attacks, as far as blockages, right, just stenosis blockage are not the 70, 80, 90% blockages. Right. They can cause symptoms, they make you flunk a stress test, they can cause angina. Those are not the plaques that cause heart attacks. The vast majority, 86% of the plaques that are causing the heart attacks are not 70, 80, 90%, they are 20%, 30%, 50%, 40%. They are sub restricted. They would not cause symptoms, they would not show up in a stress test, which is why stress tests are useless, frankly. And it is those non obstructed plaques that are there. They are present, they generally are full of lipid or soft or cholesterol rich or lipid rich plaques. And what happens is they undergo plaque plaque rupture. They break off, like off pop, like a pimple, whatever analogy you want to use. And they then rapidly expose the underlying cholesterol and all this stuff in there that's very thrombogenic, very clot forming to the blood. And within seconds to minutes when that plaque ruptures, which again would cause no symptoms, would never show up on a stress test. That is what within seconds to minutes your body responds, forms a blood clot, which is why we give aspirin by the way. And, and then we go from a 20% to 100% blockage within seconds to minutes that deprives that organ, whether it's brain or heart.
- [19:26]
B
A newly, is a newly formed clot and maturity tart.
- [19:31]
C
Right.
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B
It starts out with a plaque material that broke, it is broken off and gets lodged downstream.
- [19:36]
C
Yeah, it certainly does that. But at that site of plaque rupture, your body responds to it in a way that it's thinking about, I like say 30,000 years ago, I just got, you know, my, my, my leg torn off by a saber tooth tiger, right. It's going to form a blood clot. Right. The plaque rupture is interpreted as this blood vessel just ripped open, tore open, and I need to respond and form a blood clot. Not the right response, as it turns out. Again, useful when you know, we only made it to our 40s 140, 50 years ago, atherosclerosis was generally not seen. It is a disease that takes time to develop. In the last hundred years, since we've roughly doubled the lifespan in developed countries, now it is for the last 120 years the leading cause of death in not just in the US now, but globally. It is atherosclerosis. Because we as human beings, as Homo sapiens, have never lived as long. Now we get. We overcame infectious disease and trauma and all of those things and cured by sanitation and all those things. We live long enough to develop high blood pressure, we live long enough to develop atherosclerosis, and of course, you know, we live long enough to develop cancers that again, 100 years ago, not, I mean, all those things did occur, but really at fairly small levels because we're dying of infectious disease and, and various traumas and, you know, all of those things that people just don't die from anymore.
- [20:55]
B
Very interesting. I didn't know that. That's okay. So what does your organization do? What is its focus and methodology?
- [21:00]
C
Yeah, so clear cardio. We really focus on early detection of atherosclerosis of plaque long before we get symptoms. And what's fascinating is, and the tools we use, the key critical tools to that, we do not use stress tests, we don't use heart gas. That's really 20th century technology. Believe it or not. You're hearing this from a preventive cardiologist who's been doing this for a long. Those tools will never detect disease early. They will never detect those 20, 30, 40% plaques that would cause no flow disruption, no restriction, no symptoms. Your stress test is normal. And even on a HER cath, those levels of blockage or plaque are really difficult to see at all, if you can see them at all. So you can have an absolutely normal heart cath, which many of my colleagues, not me, would say that's the gold standard. It was back in the 20th century. It no longer is. Instead we use cardiac CT. High resolution cardiac CT. We put you in the donut of destiny, I like to call it. The scan takes less than a second with the right cutting edge iPhone 17 like I call it technology. We then take that raw CT data and then use AI on top of that. That allows us to actually see plaque that we can't see with our eyes and then also quantify it. That is the tool that will allow us to eliminate heart disease. Early detection and then in a personalized way. Once we detect someone has plaque, we can then determine a personalized and this is where it becomes very personalized to the person. Depending upon what are the factors in that that are contributing to that plaque formation. Then we come up with a strategy to stop and reverse that plaque. That is how we're going to overcome the horrible burden that's been there for the last 120 years of cardiovascular disease. We do a great job of on treating end stage heart disease, ballooning, stenting, bypassing. We have incredibly effective tools, diet, exercise, lifestyle and medications that can stop and reverse plaque. Our problem is we're using that late, late into the game. It's like only identifying and treating stage four cancer and it's not going to be a good outcome. Let's instead identify the stage three, two and one that we cannot do with stress test or her casts, which we can readily do with cardiac CT and AI, which is what we do at clearly find that problem early, take care of it early, and we're really honestly copying our oncology colleagues who understood early detection is a great thing, hence colonoscopies, pap smears, low dose CAT scans for lung cancer, people at risk for lung cancer, mammograms. Right. So they completely get early detection. We in the world of cardiology, where cardiovascular disease only kills 45% of it, percent of us, I say facetiously, we have never understood early detection. I can't tell you why the technology exists. It's really existed for a long, long time. It's gotten better and better, of course, over the last 25 years. But this is what I have been doing in my preventative cardiology practice for 25 years. But we went from the iPhone one 20 years ago, we now have the iPhone 17. And of course, like everything else in the world, we now add AI on, on top to make it even better, more accurate, more sensitive and be able now, for the first time ever, be able to identify plaque early, treat the plaque. And for the first time ever with AI, the ability to very accurately quantify plaque and the various kinds of plaque, now track plaque over time to make sure that not only are we doing the right things to street to stop and reverse the plaque, but we can literally track that over time. All of that was impossible until we had Cardiac CT and AI and that's really our foundational technology. And then my 30 years of preventative cardiology, board certification, location in lipids, hypertension, all those other things, and expensive pieces of paper on the wall that allow us to come up with the approaches, I will use the term cocktail, if you will, that allow us to treat that plaque, stop it, reverse it, and that's really going to be the ultimate solution to how we're going to eliminate the massive burden of cardiovascular disease in our population and really ultimately globally too.
- [24:50]
B
But as you're saying, plaques can occur anywhere. I understand the heart CT is great, but what about the rest of the body? Like, oh yeah, my doctor's like, oh, we got to do this cimt, you know, I'm like, the other is that they miss an extra picture.
- [25:02]
C
Yeah, people do cmt. I don't have to tell you, I don't have the time to tell you why it's not very useful. But we, we're talking about using cardiac ct, basically aiming our imaging on the heart. But we can take that same exact tool, same exact imaging, and now Actually AI, and use it to look at your neck and the carotids. Right. Far better, more accurate, more, much more quantitative than cimts. Or we can use it to look at any other vessels in your body, body, literally from the top of your head to the bottom of your toes, depending upon the person, what the question is in that person. But because most people, the number one way to check out and to check out from atherosclerosis is cardiac. Obviously, we focus on the heart, but we use that same technology literally depending upon the patient, literally to look at any vessel we want, just by turning our camera on whatever vessel we're interested in. Again, top of the head, you know, from the top of your head to the bottom of your toes, including obviously key, key vascular beds, such as, you know, the heart, of course, but carotid arteries, now aorta, legs, wherever it might be relevant for that individual person.
- [26:02]
B
Okay, nice. I see. That makes sense. So what, what unusual things are you seeing that you hadn't seen before now that you're able to look, you know, over the whole body?
- [26:12]
C
Right. So with, I like to call AI, the microscope and cardiac CT is amazing, right? It's incredibly sensitive. But adding on the AI, which we've only had for about five years now, really takes cardiac CT to a whole nother level. Being able to see plaque that literally we cannot see with our eyes, and then being able to quantify it and quantify plaque and break it down into the various kinds of plaque, hard plaque, soft plaque, and measure it down to a tenth of a cubic millimeter. As an engineer, you understand that's almost an infinitesimal volume. And then being able to track that, because we can now measure it very precisely. Here's a stat that I think is fascinating. Now, hundreds of thousands of AI exams later, here's what the population looks like. 1% of us using the microscope of AI will have no detectable plaque. 1%. It's like getting a perfect score in the SAT. The other 99% of us humble humans have detectable plaque using this tool. Now, only half of those people, 45%, will die from it. But we can detect plaque in 99% of the population and then measure it, quantify it, stop it, reverse it, and prove that we did. And so it's amazing when you think of it, a very small number of us will be free of this plaque plaque. 99% of us have various amounts of plaque. And now with the ability to quantify plaque, we can put people in stages just like cancer. So we have stage one Two and three that are based on the burden of plaque measured in cubic millimeters, which also relate to the instance of heart attacks over the next 10 years. That's why you have stage one, two, and three. But what's amazing is on the opposite extreme, our stage three patients, which for the record is more than 750 cubic millimeters of plaque in your whole heart, that's your plaque burden. That would be stage three. With the tools we have now to quantify plaque, that a third of our patients getting into our CT machine for the first time feel fine. No symptoms. I like to say normal stress test last week, which are really crappy tests that should been restart, retired two to three decades ago. Now that we have cardiac ct, that a third of our patients, no symptoms, normal stress tests, I like to say getting in a machine actually have stage three disease the first time we look. So massive burden of plaque out there. The problem is we do not develop symptoms or awareness of it or flung stress tests or start having symptoms until we have real, really very, very considerable amounts of plaque. And another stat half of men, 2/3 of women, the first symptom of heart disease is either a heart attack or sudden cardiac death. That's the first symptom. So by the time you have symptoms, you don't have a little bit of disease. That's never stage one. If you want to think of cancer, it is always advanced, extensive disease. Which is why we've invested, unfortunately not medically the best over the last decades in massive programs to balloon and statin bypass, which again, doesn't treat the disease, doesn't treat plaque, doesn't reverse pl, it improves blood flow. Our real emphasis should be early detection, just like oncology, and then using all of the medical therapies, again, diet, exercise, lifestyle, not smoking. We have a very large toolbox of highly effective and proven medical therapies as well. Individuals and individualized and personalized to the person that literally, particularly coupled with early detection, can stop and reverse plaque. So I think we are on the verge of a major tipping point point in eliminating not just heart disease, but also equally strokes. If we began to kind of frankly do what we're doing at clear Cardio.
- [29:28]
B
Yeah, no, that's fantastic. Last question on this approximate age of stage three people. Is it all over the place or
- [29:35]
C
is it all over the map? Right. And I will say, historically, what we've done to assess risk is not see if they have plaque. We would say, do you have high blood pressure, cholesterol, what's your age? Right. We didn't even ask about family history because that wasn't included, which is crazy critical. But that wasn't part of the tools we use to assess risk. We'd measure blood sugar if you have diabetes or smoking. Right. Those tools have continued to evolve, they've gotten better. But the problem is that those are population based tools. Pretty good at saying in a population of 10,000, 100,000, 10 million, what percent of people over 10 years will have an event where they fail is they do not identify the individuals very well. Right. So that's risk. We don't deal with risk anymore. We don't deal with probabilities, maybes, could bes. We put you in the machine, we look under the hood, as I say, and you either have have it or you don't. So it's gone to maybe possibilities and probabilities to zeros and ones. It's binary. And I think that's really where we're going to be going in cardiology and obviously preventive cardiology. But in reality all cardiologists should be preventative cardiologists. But many of them are just really looking at the very, very end stage of a disease that's been there for decades and going, you need stents, you need bypass surgeries, you need balloons. All those things which started out for me kind of frustrating when early on, 30 years ago. Now it's got to be almost inferior.
- [30:51]
B
Amazing. So how can people find cardio testing?
- [30:55]
C
Absolutely. If you want more information, again, you know, we, we love educating people. Lots of, of information, videos, all that stuff on our website it's clear cardio C L E A R cardio C A R d I o clearcardio.com and also to get educated, educational, great patient stories. All those things on our YouTube channel, which again is clear cardio on YouTube powers prevention. Lots and lots of cool stuff. Highly recommended. Obviously I'm biased, but again, lots educational stuff. If you want to dive deeper into any of these topics.
- [31:25]
B
Thanks and well, thanks so much for coming on the podcast. They're very, very important at the topics and I'm glad you came. Thanks for the time.
- [31:31]
C
Entirely my pleasure, My pleasure. Richard. Thanks so much for having me on. And again all I want to do as a, as a preventive cardiologist, my single monomaniacal goal is to eliminate heart disease. Now along the way, if we prevent heart attacks and strokes and people do better. Right. That's all fantastic, that's a byproduct, but really my ultimate goal, professional goal is to eliminate heart disease. And thank you for, for really helping to educate the people listening this podcast. There is a better, newer way it's out there. I encourage you to become educated in this space and I never tell anyone to do anything, but I will educate them.
- [32:04]
B
Excellent. Thank you so much Dr. Osborne. I appreciate it.
- [32:06]
C
Pleasure. Richard thank you so much for having me.
- [32:08]
B
If you like this podcast, please click
- [32:10]
C
the link in the description to subscribe and review us on itunes.
- [32:15]
A
Thank you for listening to the Good Question podcast. Please email support@thegoodquestionpodcast.com if you have any referrals to great guests for us to interview. Visit thegoodquestionpodcast.com to hear more interviews. And please help us spread the word by rating and reviewing us on Apple podcasts, iTunes, Spotify, YouTube, or wherever you listen to this podcast.