Understanding Women's Cardiac Health In Menopause

So menopause is a cardiovascular transition. It's not just a symptoms transition, and women are still being assessed and treated based on a male playbook. So today I'm actually joined with Dr. Peter Osborne, and Peter Osborne is one of very few boarded in 7 different boards, including interventional cardiology, internal medicine, interventional hypertension, and many other board certifications. And he's one of the most experienced at running a clear cardio— clearly cardio angiogram. All right. So, Dr. Osborne, I want to— I want to talk a little bit about women's health. And sort of the first things to think about is the fact that women think that cardiovascular disease is a men's disease. You know, in the United States, the last stat I read, 60 million women, which are about 44%, are living with some form of cardiovascular disease, heart disease, stroke risk. And there's a whole bunch of things that are going on here. We've been largely underrepresented in cardiovascular-related research. And I think a big part of what also gets missed, we often have more fatal cardiovascular events, whether stroke and heart attack, because we don't even present like men. And, and so we often get told, oh, it's, you know, it's your anxiety or you're just fatigued. And so women just assume that it's not happening. So we get misdiagnosed. And so I want to go in today and help women understand how much cardiovascular disease is of importance and that it's a midlife thing that we need to work on so we can have a better lifespan and healthspan, you know. As a sidebar, Dr. Osborne and I were talking right before this call, and this is so personal to me. My mom is actually in the middle of the last few days of her life on the planet after having a fatal heart attack that brought on a watershed stroke. And, you know, my dad had his first heart attack when I was 6 years old. And so this is super personal to me. And when I hear women say, oh, you know, I really worry about my husband, I'm like, whoo-hoo-hoo, hold on a minute, I worry about you. And so I'm so glad we're talking today because you are one of very few people on the planet that understands cardiovascular disease at the level you do. So I'm excited.

Well, that, that's very, very kind, Betty. Thank, thank you very much. And I'm, I'm incredibly excited and honored and, uh, such a pleasure to be here today. And, uh, so we can share and talk with, uh, what is the cutting edge? What is the, the, the state of the heart? I like to call it, uh, as far as diagnosis, figuring this thing out. And because a lot of this, as you mentioned, gets back to not just lifespan but healthspan, right? And my point is, in fact, I was at a longevity conference earlier this year, and it was all about healthspan, right? And I gave a talk on cardiac CT and early detection of heart disease because I just made this a very simple point. If you do not have lifespan, your healthspan really doesn't matter. So you can definitely have lifespan without healthspan, but you can't have healthspan without lifespan. And, you know, given the fact that cardiovascular disease has been the leading cause of death in the US for both men and women for 120 years, I think it's relevant that we talk about that today.

Yeah, you know, I was reading a stat in 2023, like 380,000 men died of a cardiovascular event and 310,000 women. Like, there's not a lot of distance between that. And you're right. And so, so, you know, there's— so obviously women get missed. So let's start with the big things. So how do women present differently in that emerging sort of emergent situation, whether they're having a heart attack or stroke? Because a lot of times we do get dismissed as whiny women, or it's anxiety. You know, let's talk about that. Like, what's different?

Yeah, no, that, that's a great, great point. And I think, too, one thing is that women do present differently than men as far as the symptoms, right? Men, the classic Hollywood heart attack, heaviness, tightness, pressure, ache, burning, you know, as we like to say, anywhere between the earlobes to the belly button, right? So it can be, right, very heterogeneous presentations. But, you know, heaviness, tightness, pressure, ache, burning, radiation down the arms, shortness of breath, nausea, thrown up, that kind of stuff, right? That's the Hollywood heart attack. Uh, which by the way will only have those kind of symptoms about half the time before the heart attack hits. And it gets worse about half the time in men and about one-third of the time in women. So in half of the men, two-thirds of women, the first symptom of a heart attack specifically is you have no symptoms until the potentially fatal event occurs, uh, which is problematic. And I think another, another thing that's layered into this is that women, as opposed to the Hollywood heart attack that I mentioned, tend to have more shortness of breath. I'm tired, I'm fatigued. I can't do physically what I could do last week, last month, 3 months ago, a year ago, or just even things like nausea, throwing up. I mean, kind of infectious disease or GI type symptoms as well. So it's very easy with their more nonspecific symptoms to either ignore them or to diagnose them with other things that they don't have, or that that's not really what, what's causing the problem. I think another factor is, you know, God bless women, uh, guys who are married live longer than guys who are not married, right? Because our women look out for us, right? Because the guys are going, yeah, I got, you know, crushing substernal chest pain, feels like an elephant in my chest going down my arms. I can't breathe. I'm throwing up. But you know what? It's probably nothing. I'll just keep going, go to work today, right? And the women say, wait a minute, something's terribly wrong, and, and save our lives. And so who's going to save the life of the women, of your wife or your spouse, or, you know, what, you know? And so I think they take on a major, major aspect of healthcare for the men in their life or the people in their life. And they also conversely tend to downplay their own symptoms, which are already nonspecific. and then they go, well, you know, it's probably nothing. I Googled it. It says it's okay. So I think all of those things contribute to the fact that after, particularly after menopause, that the rates of cardiovascular events, and when I say that, I'm really lumping strokes and heart attacks together, really rapidly catch up, particularly over the next 10 years after menopause, to basically within 10 years to equally match men as far as cardiovascular events. And if you look at strokes and heart attacks lumped together, cardiovascular disease or cardiovascular causes of death, that women have a little bit more strokes, men have a few more heart attacks. But if you sort of lump those two cardiovascular events together, strokes and heart attacks together, neither of which we want, although people tend to be more worried about strokes than heart attacks because, you know, Joe or Jane had a heart attack last week, got a stent, they're out mowing the lawn or doing whatever they do. Whereas Joe or Jane had a stroke. Yeah, they're sitting out front on the front porch and can't move or can't talk. And so that is probably in most people more of a feared outcome than even a heart attack. But I'm just pretty much against any kind of cardiovascular event as a preventative cardiologist, to state the obvious.

You know, I think, you know, I think what's, what's, you, you hit on some very true points. Women, there's nobody there to do the safety net for the women in their lives, you know, the women in your life, right? And, and the symptoms you described, again, no symptoms are kind of vague, uh, you know, fatigue and maybe a little upset stomach. I can tell you as a woman, that is a consistent thing that we deal with all the time, and we will be really dismissive of, right? You know, and, and so it is kind of scary. Uh, you know, I think the other thing that you sort of pointed out too is like looking at, you know, we think of, we think of everybody's going to have that crushing pain, which often is your bigger vessels. But women also suffer from more microvascular disease, where we may not see that in a standard stress test, or obviously a lipid panel, which is so very limited.

Oh, I, you know, 100% agree. Yeah. Yeah. No, it, you're absolutely correct. So if you look at the pathophysiology, what's happening that causes these cardiac events, men and women, yeah, it's definitely different, right? If you talk about, you know, one of the key critical events, which is plaque rupture, not to get too technical, where basically we have a plaque, it's not causing a blockage, we have no symptoms, no chest pain, normal stress test. By the way, never trust the stress test. By the way, it's just, I will say for the record, stress testing And there's different flavors of stress testing, nuclear stress testing and stress echo and blah, blah, blah. But regardless of what other kind of stress tests we do, they are 20th century technologies useful back in the old days before we had 21st century technology. Now that we're into the 26th year of the new millennium. But stress tests are really truly 20th century technology. I haven't done them for decades. They're very inaccurate. They're very insensitive. Lots of false positives, meaning we send people to the cath lab, find out they're fine, particularly women, or they look fine and there are severe blockages. So just a very, very poor, inaccurate test. Here's the bad news. We do 10 million nuclear stress tests a year in the US in 2025, right? Which is about 10 million more than we should be doing. Yeah, but, but I was just saying, do you think that's—

oh, I'm sorry, go ahead.

No, I was going to say I got, uh, misdirected for a little bit, or digressed. But for, uh, that plaque that is the ultimate cause of the heart attack in most people— not everybody, in fact, more women have non-plaque-related heart attacks— so women have plaque erosion Men have more plaque rupture. So just how we form a blood clot on that spot in the vessel, uh, it's actually quite different, and there's no question about that. Women have more microvascular disease. That is, you have your heart cath, you do your stress test, and here's what's interesting: women have a lot higher risk of having an abnormal stress test than guys. And in the old days, right, no question, right? We all know this. We then would take them to the cath lab, spend $20,000, do invasive tests, put catheters in your heart, risk of kidney damage, heart attack, strokes, blood vessel problems, bleeding, infection, all that stuff, right? We do an invasive test. We'd squirt dye into your blood vessels or your heart and find out they look fine. Here's the problem. When women have that negative that positive stress test. The stress test shows that there is, to use the technical term, ischemia. That is, there's just not enough blood flow to the heart muscle. We go, hey, there's a problem, there's a blockage, right? We take the cath lab, we don't see the blockage. Well, which was correct? Was it the heart cath, the direct visualization of the channel, the lumen we call it, the blood vessels, the vessels themselves are really the channel, the lumen, or was the stress test? Well, as it turns out, and this is fairly new data, that in those women that have a positive stress test, there is reduction in blood flow. Many times it's not because of a blockage that we can stent, balloon, or bypass. It's because the microvasculature— this is, these are the very small vessels that come off the larger vessels. They are literally small enough that we cannot see them with our eyes, right? There's problems in those vessels, right? Much more common in women than men. So what would happen is they'd flunk a stress test, they'd have symptoms, they'd have chest pain, they'd flunk a stress test. We get worried that they have a blockage. We take them to cath lab, they don't have a blockage. And then we'd say, there, it stops, you're fine, all is good. And that's not true. So microvascular disease is a big deal. It is present. It's more common in women than men. Another related issue is something called Takotsubo disease. Or this is from the Japanese word that describes the, the octopus traps that kind of look like a big bulbous kind of device. And what happens in women much more than men is under stress, usually physiologic stress or psychological stress or mental stress, right. That I know, you know, no one has, and particularly not women, as they're worried about other guys in their life. Right. And there are people around them. But you can have a stress-induced heart attack with completely normal vessels, right? You literally can go into rapid heart failure. The, the heart stops squeezing, pumping. We take 'em to the cath lab, there's no blockage. We go, wait, what's going on? That is another very severe manifestation of microvascular disease, just illustrating, and that takotsubo or the quote broken heart, as we call it scenario, which is true, right? Huge. You know, some— and the classical scenario, some very emotional scenario occurs or some tragedy or something terrible happens to you that really amps up your sympathetic nervous system. You'll cause vasoconstriction in the microvascular that we cannot see with direct visualization, even in the cath lab, which then can cause a heart attack. Can cause heart failure. And interestingly, in the old days, I think we're smarter, we're knowledgeable now, we go, ah, your heart's fine. And it absolutely is not. So we really have to be very, very appreciative of the differences in how this disease presents in women than in men. Another thing, another factor that again, a lot more common in women than men is something called SCAD, S-C-A-D. that's a coronary artery dissection, a sudden coronary artery dissection. Literally, the vessel rips open, breaks open, and can cause a heart attack. And that again is much more common in women than in men. And in fact, even younger women— in fact, we see it not uncommonly in pregnant women as well. There's something about pregnancy that makes our vessels a little more delicate, and those vessels can rip and tear open. It could be aorta, it could be coronary arteries, it could be any artery, but those are probably two most common. Uh, not that this does not occur in men, but it really is predominantly seen in women. And again, not picked up on a heart cath or stress test or anything like that. So, so women are, are, uh, uh, I, I'm going to say this to be funny, and, uh, I, I'll, I'll except the slings and arrows of outrageous fortune. But women are a different species than men as far as how they present with heart disease, how they present with their symptoms, and literally what's happening with their blood vessels, which is— can be— there obviously is overlap between men and women as far as how all this presents and the underlying conditions. But the vascular issues that women have can be quite different than guys. So, I apologize for saying we're different species, but just, just—

Yeah, we are. Yeah. I mean, you know, we were left out of studies until 1993. So, you know, largely a lot of the kind of old cardiovascular recommendations are antiquated to begin with, but absolutely never involved women. You know, I think the thing that's so abundantly clear, you know, coming out of an emerging really out of the research in the last decade is we know that estrogen has a protective effect on vascular function, including endothelial lining and the glycocalyx, the little hair-like structure that helps produce nitric oxide and protects the arteries, the tone. And we also know that the loss of estrogen in menopause drives insulin resistance, body fat, visceral adiposity, so increasing kind of belly fat, inflammation. And then we have that sort of cortisol, you know, stress response that is largely there because of the hormone change and also life. And, you know, I think what's really frightening to me is if we look at the menopausal woman today, you know, of the 100% that are going through menopause, statistically less than 7% are actually being treated appropriately with hormone replacement through this transition. And that's where we start to see this age matching to men. We're protected until menopause.

Right.

And, and I think that's the big challenge is, is we, we see that and even like the lipid changes, the LDL changes that occur occur that are absolutely tied to perimenopause, menopause. I mean, for me, that was very, very clear, right? Mine—

estrogen reduces LDL, right? Uh, and another thing is, you well, well know, this is your domain, not mine, but obviously good news in the last month, right? This is very topical. We've seen big changes, uh, from the FDA relevant to the role of, uh, hormone replacement therapy in women, which is about 20 years overdue, but finally sense has prevailed. And so that's, that's fantastic news. And I think that number that you quoted, 7% or 5%, that range, but very, very low, will actually go up. In fact, what's interesting, I've seen at least here locally, I'm from Texas, that getting estrogen for women right now at this moment, it's on back order. So, right. So essentially we're seeing is all these women, now that the label has changed, the the boxed warning has been removed from estrogen and, and those different products, uh, that women, and now fortunately doctors, are going, wait a minute, we, we got to catch up. So it lit— we were actually seeing that at the pharmacies, that, uh, estrogen and those products are actually backordered, uh, because of the, the huge demand that's suddenly there.

Yeah, and I think, you know, one of the important things that I've seen too in the research is, you know, oral estrogens in the form of conjugated equine estrogen, or especially that with synthetic progestins, particularly in older women, do have increased clotting risk. But we're starting to see, particularly in large observational studies, you know, where we've got large amounts of data, that the topical forms don't carry that. So the earlier we—

hold on—

the earlier we start it and the—

and the hepatic first pass kinetics and all of those factors, uh, the, the topicals are definitely, definitely the way to go. I completely agree. Another thing too, I do want to mention it as we talk about estrogen and cardiovascular risk, endothelium, all those things you beautifully mentioned and eloquently mentioned. But another thing too, and you know this as well, but I'll just leap into this because I love it because I'm the lipidologist, is Lp(a), right? Lp(a), estrogen lowers Lp(a). In fact, we saw that from a study a number of years ago, must be 20 years ago almost from the ERA study that Lp(a), which by the way, for those who do not know this, it's also called lipoprotein little a and in parentheses little a, big A is different, that Lp(a) is a really nasty form of cholesterol. It is very sticky. It is very inflammatory to your vessels, makes the vessels very sticky, and it is, it makes them very clotty, much more likely to clot. 80% will be normal. 20% of us, although it does depend upon ethnicity, so African Americans, South Asians, etc., will have higher rates of elevated Lp(a). So it does depend upon ethnicity somewhat as well. But roughly 20% of us will have high levels of Lp(a). It is essentially nearly 100% genetically determined. Either have it or you don't. Recommendations from the National Lipid Association Dr. Betty Murray, uh, that I've been part of for over 20 years and one of their fellows and on the board, uh, says everybody should have their Lp(a) checked once in their life. 80%, it'll be normal, it's done, never have to worry about it, rule it out. 20% will be high. And the reason that it needs to be checked is that it is not picked up on a standard cholesterol or lipid profile. It is completely invisible. So you have to check it. It's a simple, inexpensive blood test. Check the box. Everybody should have this once in their life. 80%, fortunately, will be normal. Forget about it, it's not a big deal. But 20% will be elevated. And I will say it has been challenging because our current tools we have available as of 2026 are modestly effective. These are PCSK9 drugs. Okay, that's a, a mouthful, uh, But these drugs have been around now for over 10 years. They do lower it 20 to 25 to 30%. Statins actually, ezetimibe that we use and other drugs actually raise it a little bit. However, don't worry about it if it's raised, it's fine. We need to lower it. If you're getting those drugs, you probably need them to lower Lp(a). But the drugs like Repatha, Praluent, Inclisiran, Leqvio, and some others actually lower Lp(a) modestly by 25-30%. Yahoo! Aspirin also is very effective. Aspirin is a great drug for secondary prevention. People had balloon stents, bypass surgery. However, aspirin lowers cardiovascular events by about 50%. So it's uniquely effective in patients with elevated Lp(a) because their vessels tend to be much more prone to clot, much more inflamed and sticky. And the best news is coming up here, so keep an eye out that we're all incredibly excited in the world of lipids and cholesterol, is that the first half to '26, we've been doing a study called Horizon, is the name of the trial, with a drug called Pelacarsan that lowers Lp(a) by 85%. Not 20, 30%, by 85%. We started that trial in 2019. 8,000 people globally, worldwide, with cardiovascular disease, with elevated Lp(a). Half get the drug, half don't. That trial will report out the first of the, uh, RNA, uh, targeted tools to lower Lp(a) by 85%. That trial will report out in the first half of '26. If that trial is positive, suddenly we'll have a new novel highly effective tool to treat something where our interventions were pretty— medical interventions were pretty modest. And again, getting the fact that this is a 100%, essentially 100% genetically determined form of cholesterol, it does not respond to diet, exercise, not smoking, all the good stuff that we promulgate, right? It, it just doesn't respond because it is genetic. It is hair color. So we're right on the verge of a major, we hope, We're all crossing our fingers. The people in Vegas are voting that are betting that this would be positive, as I like to say. But we're right on the verge of a major, major lipid breakthrough, we hope. And then behind that drug will be drugs that lower it by almost 100%. And then we also have oral drugs in development. These are— these drug initial drugs will be given by injections every month or every 3 or 6 months. Uh, but after that will be oral drugs to target Lp(a). So it's an incredibly exciting world in the world of lipids. Uh, and I think again, uh, if there's one message from everything I've talked about, next time you get blood drawn, particularly if you have a family history of heart disease, early onset heart disease, uh, those kind of things, make sure your doc is checking your Lp(a), your lipoprotein little a is the top, is the the, the real name, if you will, but we call it Lp(a). Make sure they're checking that Lp(a). Check it once, just once. If it's normal, you're normal. It'll never become abnormal. You're done. But if it is abnormal— and in fact, the other interesting thing that's come out of the literature is that it can be normal in the premenopausal women. When you lose estrogen, it can become elevated. So right now we say everybody should have it checked once. However, if you are postmenopausal and say it was checked and it was okay before, maybe borderline, It may be even worthwhile to have it checked again if you're menopausal, postmenopausal, to see if it did bump up in, in the absence of estrogen. And I'll shut up on that.

Oh, no, absolutely. So what— while we're talking about the lipoproteins, you know, everybody knows, you know, we look at cholesterol and cholesterol, just a regular cholesterol with LDL, HDL isn't very determinant of cardiovascular risk.

Very, very poor. Very poor.

And, you know, so let's talk a little bit about the other lipoproteins, particularly like, you know, apolipoprotein B, because because that's another thing that we see shift quite a bit in menopause. I know, I know mine did. You know, I was like, whoa, okay, that's starting to move.

It absolutely does.

Yeah. Let's talk a little bit about that because your traditional cardiologist is not doing this. No, your primary care does not do this.

We should. So, so let me just explain that this thing called Apolipoprotein B, as you pointed out, Betty Murray, yes, shift does happen.

Yes. Yes, it does.

ApoB, as we call it— Apolipoprotein B is the real name, but we call it ApoB. Uh, it's Apo, big B, and A is, is what we call it, or if you see it, ApoB. So ApoB is actually the single best cholesterol tool to understand the total amount of bad cholesterol that I'd like to say acts as fertilizer for your plaque. Okay, historically we've used other tools like LDL. It's okay. It's not great. It's okay. We've used tools like non-HDL, which is total cholesterol minus HDL, a little bit better. But the best tool out there to really understand the total amount of plaque, total amount of fertilizer that's available to fertilize that plaque, which we do not want to fertilize, is actually measuring ApoB. So every time I check someone's cholesterol profile, lipid profile, to get total HDL, triglycerides, and LDL, I also check ApoB. And ApoB is not only a better target, it's also better prognostically to indicate who's at higher risk than LDL. It also is a better prognostic target for who is going to have events down the road, or someone that has had events. ApoB really should be the target that we're using. By the way, we have different numbers for LDL and ApoB, but for ApoB, we really want— if we want to reverse plaque, which yes, we can reverse plaque, that's a myth I love busting every day, that if we want to reverse plaque— and I'm just talking about the effects of cholesterol, there's lots and lots of things we can do to stop reverse plaque, which is great— but particularly for cholesterol, we want to get that, that ApoB— here's the number— at least below 60, probably below 50, is really the targeted approach to be able to— where we can get the vast majority of people to actually reverse plaque ApoB of at least 60, probably close to 50. So have your doc check your Lp(a) once. If it's normal, you're done. But also, when they're checking your cholesterol, make sure that they're checking your ApoB. Everybody should be doing this. The National Lipid Association, the Europeans, European Atherosclerosis Association, the National Atherosclerosis Society, all of those organizations have recognized this. The Canadians, going back a long, long time, by the way, Dr. Alan Snyderman has really led this charge, have really recognized that ApoB is the better, superior way of really understanding the total amount of bad cholesterol. LDL is old school. Sometimes people get particle numbers. That's a little bit old school. ApoB, cheaper, easier, better, doesn't, is not impacted by fasting or non-fasting, et cetera. So you don't even need to be fasting to check an ApoB. It's still accurate whether we're fasting or not. So Lp(a), please, and an ApoB. And that, that is really the state of the art as far as sort of better understanding our lipid or cholesterol profile. But having said that, I can show you people with high LDL, again ApoB, and no plaque. I can also show you people with great-looking ApoB or LDL, average or even well below average, that have extensive plaque. So to your point, looking at cholesterol does not tell us whether that cholesterol is sticking or not. In order to do that, that is where imaging is absolutely mandatory.

Absolutely. You know, I'm glad you said that. So I'm going to share a little bit about my history from a cardiovascular event. I said my dad had his first heart attack when I was 6 years old. Now, I'm adopted. I'm not his genetics, but heart disease has been a big part of my life. Like, he had two quadruple bypass, 11 stents. He was a human pincushion, quite literally.

Right.

And then my mom had a heart attack, you know, that brought on a stroke. So I've always been hyper-aware of, of these markers. And I've followed my ApoB since it's been able to be kind of tested. And what's really interesting is even in the very early part of menopause, it didn't really jump wildly until the last year and a half. And it went from, you know, probably about 75 when I was, you know, in my early 40s to like 80-something, and then all of a sudden, it jumped to 155 in like a year and a half time.

Yeah.

And, I'm watching it, I'm like, "Okay." So, I did, in full disclosure, I'm not a huge fan, I don't love, but I did all the things. I'm like, "Okay, let's try lowering it with a statin." Well, I got liver enzymes increased, but you know what was even crazier, Dr. Osborne, is it didn't really touch my ApoB very much at all, right? It came down a little bit, but nowhere close to those reference ranges. I tried ezetimbe. And it raised my liver enzymes and didn't really do much to it either. And so, I've had other scanning. I'm getting my CLEARLY done, but I already know that I have some small— Yes, yes. I was going to do it last year, but I was on flights. I was like, I can't get it in. But, the reality is I already know I've had a Prenuvo done. And then, in my brain, I had some small microvascular ischemic area, which is that small microvascular activity that you talked about. And, I have a little bit of plaquing already in my arteries. And so, You know, if I was just going on 2 years ago, I probably wouldn't even pay attention to it. So if my doctor checked it at 50 and my ApoB was normal, I wouldn't have any idea. The fact that I was educated and watching it allowed me to start looking, right? And so what we're going to talk about now is, is really the state of the art in imaging. And we've already expressed why just looking at cardiovascular lipids like cholesterol is inadequate. Looking at ApoB and Lp(a) is going to help a little bit, and getting a stress test in women might be a little more meaningful. But if you don't actually look at these arteries, you may not know. And I, and I want to make sure we also cover the difference between a calcium score and the Cleerly, because people get those, you know, Lifeline, and they're like, my calcium score was low, and I'm like, absolutely zero capacity to tell you your risk at this point.

Right, right.

Yes, let's talk about—

yeah, let's unpack that. You mentioned a lot of stuff here, so let's start unpacking that. So, I, I, I will say the, in no particular order, blood tests that we do, right? And, and we talk about ApoB, we talked about LDL. I'll also mention other things that, in fact, the ACC, the American College of Cardiology, just issued a big paper and guideline on the use of markers of inflammation. HSCRP is probably the one that has the most data behind it now saying that, that is no longer a maybe, could be, possibly. It, it is something that should be routinely used, right? So it gives us an idea of how sticky your vessels are, which gets back a little bit to that point I made a moment ago. I said before, I've seen people with high cholesterol numbers, however we measure it, LDLs, ApoBs, ApoB better, versus people that have no plaque versus people that have what looks like great numbers or great LDLs or ApoBs or average or below average that can have extensive plaque. So here's what's happening. There are two variables that are working together. Cholesterol is, at the end of the day, the factor, the stuff that is literally getting into our blood vessels, right? So if you look at any plaque in any vessel, whether it's your carotid artery going to your brain, your coronary arteries to your heart, vessels in the legs, any artery, and, and, and look at that plaque, that plaque is full of cholesterol. So plaque does not occur in the absence of cholesterol. However, here's why cholesterol levels are not a great marker of understanding if you have risk. That is, is that cholesterol sticking or not? So remember, when we measure cholesterol, we're only measuring how much cholesterol is floating around your bloodstream. It tells us nothing about is it sticking. The other big variable, though cholesterol is mandatory, necessary, maybe not be sufficient, but it is the critical central factor. It is the stuff that gets into our blood vessels, right? However, that's not the whole story. The other side of the story is basically, as I like to say, how sticky your vessels are. To be, to be scientific, we'll say inflammation, right? So you can have, imagine a vessel like Teflon, or as one of my partners says, a slip and slide. So even despite having lots of cholesterol floating by, that vessel is so slick it doesn't penetrate into the vessel and start building up. So that's how you can have high cholesterol and have no plaque whatsoever. And we see this, and there are lots of people on drugs, taking drugs to treat their cholesterol, where they've never done imaging to see if they have plaque, and they're taking a drug to lower a number, but they will not benefit from that lower number because they do not have the disease. It's like saying to somebody, you look like you have cancer, I'm going to recommend chemotherapy for 6 months because you look like you have cancer. Well, that's insane. Yeah, we do that all the time in the world of lipids. Conversely, so that's bad enough. You're taking a drug, you may get side effects, paying for it to no, to no benefit to you. So that's bad enough. The worst thing is there's lots of people whose cholesterol numbers look great many times they haven't checked ApoB, by the way, or— and certainly not Lp(a). Only about 1 or 2% of the US has had their Lp(a) checked. So we have lots of opportunities there. Okay, so make sure ApoB and Lp(a) get checked. But you can have vessels that are incredibly sticky. So the opposite of Velcro— of the opposite of Teflon and slip inside would be you have vessels like Velcro, right? Sometimes that's genetic, sometimes it's due to diabetes or prediabetes, sometimes it's due to tobacco, high blood pressure. So there's a lot of factors that can give you sticky vessels. So in the setting of sticky vessels, even if your cholesterol, even if your ApoB looks okay, you can have extensive buildup of plaque because that plaque, that, that cholesterol is sticking. So that is why imaging of the blood vessels themselves is absolutely critical, which I'm going to go into stress testing. Okay, now I'm going to say, as a preventative cardiologist, I've been doing this now— this is 29 years now in preventive cardiology— let me say this for the record. If you go to a cardiologist and the first thing they do is say, they say, let's start with a stress test. Now, there can be some value if you interpret the data correctly with a stress test in women, because it may look abnormal and they don't have plaque or blockages because of the microvascular disease. However, Having admitted that, just appreciate that with a stress test, we're only looking at blood flow down the blood vessels. Our vessels are much bigger than they need to be. We have massive reserve in our blood vessels, right? They're much bigger than they need to be. We will not restrict blood flow going down the blood vessels till there's already a 70% blockage.

Oh, wow.

So anything less than 70% So completely normal, 10, 20, 30, 40, 50, 60, 69%. As far as blockages go, your stress test will appear normal. Doesn't mean your vessels are normal, but it will appear normal. And because when we do stress tests, and there's all kinds of different stress tests, there's stress echo, there's cardiac stress, there's nuclear stress tests, PET stress. Bottom line is any kind of stress test out there is looking at blood flow. Some are a little bit better, a little more accurate, a little more sensitive, specific, but they're just looking at blood flow, which is the problem. Their threshold of detecting a problem doesn't start till 70%. And furthermore, because we're not looking or visualizing the vessels themselves, we're looking at blood flow. About 25 to 40% of your nuclear stress tests, which are very expensive, lots of radiation, 25 to 40% will yield a false negative. There is a severe blockage, the stress test looks fine. And I can't tell you how many people said, hey, I had a stress test, doc patted me on the back, said I have the heart of an 18-year-old, and then something bad happens the next week, next month, the next year, right?

Oh yeah. So you get lost to friends.

Yeah, all the time, right? And we've known this for— for— this is not new news. We know it in cardiology, um, Now, when we only had stress tests 20, 25 years ago, that's what we got. But that was the last millennium. So 20 to 25%, at least false negative rate. And what makes that— I'll tell you, I'll dive a little deeper into the weeds. 20 to 25%, 25 to 40% false negative rate. There is a severe blockage, it looks fine. However, the more blockage you have and the more blood vessels that have blockages, the sensitivity, the ability to detect that blockage goes down. So the worse the disease, the sensitivity doesn't get better, it actually gets worse. The flip side of that are false positives. So the stress test looks funky. Now, again, women, they can have microvascular disease. We panic, they panic. We cart them off to the, to the cath lab, spend $20,000, put catheters in their heart only to find out they look fine. In fact, 70% of our heart cath today— we do 2.5 million a year in the US, which is about 2.5 million too many— 70% of our heart cath will be normal. That is, there is no obstructive disease, right? So if you flunk your stress test or you have symptoms or somebody's worrying, right? I'm talking about elective patients, not having a heart attack, not, you know, in the midst of a heart attack like your poor mom, but people that go, well, I'm worried, let's do a heart cath. Guess what, 70% chance they won't find a blockage. Doesn't mean there's not a problem, but they won't see a blockage, right? So we have a 25 to 40% false positive rate, which then buys you an invasive $20,000 heart cath. Yeah, to find out. Yeah, you look fine.

To find out it's nothing there.

Yeah.

Oh my goodness, right?

When we visualize the blood vessels, and there's two main, uh, tools we use nowadays, the 21st century technologies. One is called a calcium score, okay? Broadly available. We started doing these— I wish they— I could say they were new. We started doing these in the '80s, right? Yeah, this goes back 40 years ago. Uh, a calcium score, we put you in a CAT scanner, not an MRI. This is the donut, not the coffin or the, the tube. It's just the big open donut. Uh, very quick, takes a few minutes, no prep, no IV, no contrast. You don't have to fast. You literally— we put you in the donut of destiny, as we call it, and look to see if there's any calcification associated with blood vessels in the heart. Okay? And here's the important take-home: the only normal calcium score is 0. Anything that's not 0 means you have plaque. And I don't care whether it's 1 or 10 or 100 or 1,000. Now, those do mean different things based on how much burden of plaque you have, roughly. But it's zero versus not zero, pregnant versus not pregnant, okay? If you have a non-zero score, my friend, you have plaque. End of story, full stop, okay? Which, by the way, the plaque that we're gonna detect with the calcium score is generally gonna be seen years before you ever get a blockage. So we're not looking for blockages. We're really looking for, do you have— and this is where I love using this term, uh, These tools are, are the cardiac colonoscopy. They are the ability to allow us to find the polyp so we can take care of the polyp, stop the polyp, reverse the polyp, by the way, so that you don't get the cancer, right? The equivalent of cancer or heart disease. So a calcium score will, will pick up these calcified plaques. However, here's the caveat. When plaque builds up in the blood vessels, the first plaque that's laid down is the lipid soft or cholesterol-rich plaque that is invisible on a calcium score. As that plaque matures, as we mature, right, there is a genetic process, a cascade of genetic activation and transcription that occurs that turns that lipid, which is invisible on a calcium score because it's a calcium score. By the way, this— I'll mention this as well because this comes up all the time. A calcium score, a coronary artery calcium score, or a CAC, is not a blood test. It has nothing to do with calcium floating around your blood vessel, floating around your bloodstream. It's looking to see, are there calcifications developing in the blood vessels of the heart specifically? So you need a scan to see this. About 10% to 50% of people with a zero calcium score will have significant lipid-rich soft plaque in the blood vessels that the calcium score cannot see. 'cause the calcium score only sees the hard plaque. Here's the other issue. The plaque, the calcified plaque is generally plaque that is older. We can kind of carbon date plaque. If it's calcified, it's older plaque, generally inactive, generally not gonna rupture, break off, flake off, cause heart attacks or strokes if it happens to be in the neck. Um, tends to be more passive plaque, right? It's end-stage plaque. It's no longer active. The plaque that is active, what I call the lava. So the calcium is the cinder cone, the extinct volcano. The lava, which is the lipid-rich plaque, the soft cholesterol-rich plaque, which is invisible on a calcium score, that is the active plaque. That is the growing plaque, the active plaque, the plaque that could rupture. That cannot be seen with a calcium score. The only way it can be seen is with what's called a cardiac CT. Calcium score No contrast, low resolution. We take about 60 or 70 slices through the heart, so it's fairly low resolution. When we do cardiac CT, much more sophisticated CT scanners, it's a still a donut. It— the hardware is a lot more sophisticated, a lot higher resolution. There we're going to take about 2,000 slices through your heart, very high resolution, three-dimensional imaging. And we're going to put an IV in your arm, give you some contrast, the same contrast we use in the cath lab, by the way, contains iodine, but a lot less contrast with cardiac CT. That will allow us to see all of the plaques. We can see hard plaques, the calcified plaques. We can see the soft or the cholesterol lava plaques. We can, uh, see if there's blockages, which we can't see on the calcium score. With the calcium score, I can't tell if you're block— if you have blockages, and I can't see the lipid-rich plaque. When we do cardiac CT, a more sophisticated test, we can see lipid-rich plaque, hard plaque, soft plaque, blockages, or as I call it, the whole cardiac enchilada, right? To use a— and I think this analogy is very relevant to this show— the way I think of a calcium score, it's like a mammogram, right? So mammogram has false negatives. You can have breast cancer and have a normal mammogram, right, as you well know. And if you have a mammogram that looks abnormal, we say it looks abnormal. We do not diagnose breast cancer on a mammogram. We say we need a biopsy. So the way I think of it is the mammogram is sort of the calcium score. It's pretty good, not perfect. I will say, unlike a mammogram, we do not have false positives with a calcium score. If you see calcium, you have plaque, and store— end of story, right? Doesn't say you have blockages, uh, but you have plaque, and it demands further evaluation. So just like a calcium score, if the calcium score is positive, we should get a cardiac CT. That is the biopsy— that's the biopsy equivalent with mammograms and biopsy, calcium scoring and cardiac CT. The latest, greatest, biggest breakthrough— I call it cardiac CT 2.0. I've been doing this for 25 years now, but we've done about 25,000 cardiac CTs. I have, uh, is now the ability, just like everything in life, We're adding on AI to the cardiac CT. When we take that high-resolution 3-dimensional imaging, add on AI, now we can literally see plaque that I could, that we cannot see with our eyes. There literally is plaque there that we cannot see with our eyes. The AI can see it. And then furthermore, we can quantify that plaque, hard plaque, soft plaque, the calcified plaque, the lipid-rich plaque, quantify it down to a 10th of a cubic millimeter. To understand what a tenth of a cubic millimeter is, think of a period at the end of a sentence. If that were a sphere, that would be about 1 cubic millimeter. We can see a tenth of that sphere, and we can resolve plaque to a tenth of that volume. And then now, because we can now detect plaque that we could not see before, quantify plaque extremely accurately, break it up into soft and hard plaque, we can now— and this is the first time ever we could do this clinically— we can now track plaque. So not only can we say your cholesterol is better, your Lp(a) is better, your blood pressure is better, your blood sugar is better, you've lost weight, you quit smoking, we're exercising, we're doing all the great stuff, we're taking Repatha, but we can literally say over time, is the plaque better? That was impossible for cardiologists to do until we had abilities to detect and quantify plaque, which is new just over the last few years. And that's what we do at Clear Cardio. With the, the CLEARLY AI exams with cardiac CT and the AI. Anyway, I went way, way too long with that response.

No, you know what I, what I'd like to do is just give a visual to everybody. So you were talking about the hard calcifications, right? So it's hard and crusty and it makes it less flexible, but it doesn't break loose.

Correct.

I visualize like my way of explaining this because we run all those advanced lipids and we refer out to CLEAR Cardio. And, and so when you think of those soft plaques, they are the equivalent of a sunny-side-up egg.

Got it. Exactly.

And the hard plaque is a nice hard-boiled egg. If something goes by like a fork and nicks that soft plaque, what happens is it busts open, spews its contents, and rips the edge of the, of the vessel apart. So it blows a hole in the artery. Yeah, that's it. So you cannot see those if you don't have it clearly.

Right.

And, and, and And I can't remember what the statistics are, but like, that's how— from a heart attack kind of zone, what percentage?

85%.

Yeah, 85% are non-visible, non-calcified plaques.

Right. 85%.

That's like, we just need to hit that home, ladies. 85% of heart attacks are brought on by plaques you cannot see in a calcium score, identify with an LDL, even an ApoB, or a stress test.

Well, and I'm going to say big picture. Historically, we'd look at numbers, right? We would look at ApoB and Lp(a). We're sophisticated. We look at those things, right? Again, doesn't tell me if you have the disease or not, right?

Right.

Where we start from now, the very first thing we do— now, we'll get all those fancy lipid numbers, right? hs-CRP, inflammatory markers, all those things. The very first thing we do, though, is let's start with the imaging. Let's start with the ground truth. Do you have plaque or not? The only way to know that is, and if you really want to know it, cardiac CT with AI. We start with that ground truth, then we figure out what your numbers need to be. Because we will find people whose numbers look bad, they don't have plaque. Yahoo! God bless you. Don't really know why. It's okay. You should, but you don't. Conversely, again, we'll find people with great looking numbers with extensive plaque, and you do not know until you start with imaging. So in 2025, 2026 now, right? Start with imaging, then we'll figure out where your numbers need to be. Historically, we just looked at numbers and guessed. So there is no more maybes, could-bes, possibly should-bes, right? Got plaque, don't have plaque. Look under the hood, right? And if you want to look under the hood for heart disease, you get in the donut of destiny. We add the AI, then we're start talking about 100%. We're talking about binaries, right? That's why I also call this the virtual autopsy, right? It's there, it's not there. If it's there, we will see it, quantify it, track it, etc. And if it's not there, it's not there, right? There is no more maybe, could be, possibly, I'm worried about this, or whatever. No, it's just it is or not. And I will say, I will argue, and I'll stick my neck way out, but I'm going to argue this, being a preventive cardiologist, the vast majority of cardiovascular events— strokes, heart attacks, and there's other vascular events, but atherosclerotic plaque events, the vast majority with early detection and all of the incredible tools we have to check and monitor lipids and how we're doing and all the tools we have to drop it. And again, non-pharmacologic as far as pharmacologic, lots and lots of tools. We have a very big, highly effective, highly proven toolbox. Our major problem in cardiology is we have incredibly effective tools that we use so late in the game, after the stent, the balloon, the bypass surgery, the heart attacks, stroke. Our biggest problem in cardiology, cardiovascular medicine, is the fact that we've not done your cardiac colonoscopy. We've not looked for the polyps. We wait until you have a cancer, and that is never going to cure heart disease.

Yeah, no, you're exactly right. And, and like I said, I think women need to understand that menopause is a cardiovascular event and the risk factors that go along with not treating it, right? The sleep issues, they increase cortisol, the inflammation.

Sure.

All of those things are going to increase our risk for that. And, and that we do present differently. And we have to be— I think because of that, we have to be much more aggressive about upfront screening before there's a problem.

Yeah.

Because we're more likely to even die in the hospital, in the ER, from the event. Than a man.

Yep, absolutely. Mortality rates are striking, and it is not favorable to women at all.

No.

And even in the hospitals, you point out, right? Or even after bypass surgery or stents. Again, which means that we had 20 to 30 years to find the problem, take care of the problem. We didn't. The disease basically showed up analogous to cancer as stage 4, widely metastatic, advanced disease. Then we have to use mechanical approaches And women do less well and have worse outcomes with those mechanical approaches— stents and balloons and surgery— than do the guys. And they're also that much older, which is not helpful too.

Yeah, exactly. Now, if you could, if you could wave a magic wand and, and, and sort of say, okay, if I could make one change in primary care, or in a lot of cases women's care, which tends to be the gynecologist that sort of gets relegated to it, What are the things that you're like, absolutely, if your primary care physician is not doing this, you need to probably shop for a new one because I'm a strong believer in, you know, medicine is a customer service industry. The patient is the customer. You know, what things would you love to do that? Yeah. What would you like?

Pure everybody, right? Because here again, the picture, 40, roughly 40, 45%, again, men and women lumped together, balloon stents, heart attacks, strokes. Vascular events, cardiovascular death. 40% to 45% of us will die at this moment in time, unfortunately, of a cardiovascular event, generally plaque-driven. So it's not 100%, but that's nearly 50%. So that is our major limitation, our number one major limitation to lifespan in the US, which is cardiovascular disease. Unquestionably the case. In fact, Cardiovascular disease, strokes, and heart attacks kill more people, men and women, than the next 7 causes of death, including cancer. Now, for cancer, we do pap smears, mammograms, colonoscopies, right? Guys get their PSA. What do we do to detect early when it's incredibly effectively treated and stopped and reversed? What do we do to identify the number 1 leading cause of death in the US early? We don't. We just wait till the fecal material hits the rotary impeller.

Yeah, and that's exactly right, right?

No, we get it for cancer. Why don't we do it for heart disease with simple, easy, non-invasive techniques that— particularly given cardiac colonoscopy that I brought up before, right? I mean, it's expensive, it's tedious, general anesthesia, 0.1% chance they perforate colon. And yes, everybody should have them, to be able to find the polyps or the cancers that cause the 2 to 3% of mortality that colon cancer causes. And yet for heart disease that kills 20 times more people, what do we do to find it early? Or even— and I'll say this again, I'm just stating the facts— that even women who are diagnosed with breast cancer, with diagnosed breast cancer, more women with breast cancer will die of heart disease than the breast cancer itself. So, you know, I think we just have to recognize the facts. So to my magic wand, I would at least start with a calcium score for everybody at age 40. And kind of like colonoscopy, where if you have a bad family history of colon polyps or whatever, we start earlier, maybe even earlier, depending on family history, cholesterol, blood pressure, diabetes, those factors, smoking, etc. But I would say calcium score in everybody starting at 40. And if you really want, want to know, now again, a zero is generally good. However, be careful because you could have lots of lipid-rich plaque, particularly if you have a bad family history. Diabetes, smoking are the big things. Also, another factor which we did not bring up here, but I think is very important to mention, are, and, and these conditions are more common in women, are the inflammatory conditions. We're talking rheumatoid arthritis, lupus, psoriasis, psoriatic arthritis. Literally a whole bunch of other inflammatory autoimmune conditions. They not only can take a toll on your joints and all kinds of other different areas and tissues, but they also cause inflammation. They cause your vessels to be sticky. And so having those inflammatory conditions— and there's a long, long list of them, beautiful articles written about this a couple of years ago in Lancet, 19 different, you know, I just mentioned a handful of those— Crohn's, ulcerative colitis, and that lots and lots of these inflammatory conditions, again, more common in women. Than in men generally. All of these cause sticky vessels, which then start that cascade of atherosclerosis. So, so I would say everybody start with the calcium score at age 40 if you really, really want to know. No question, no false negatives. That is, again, you could have lipid-rich plaque not showing up and a zero calcium score. Get a cardiac CT, particularly if you have more risk factors, family history, et cetera, or if you just simply absolutely want to know. And by the way, cardiac CT really was the phenomenal tool. It still is. But I will say cardiac CT is now only part of the word. The word now is cardiac CT with AI, or in our case, we use a tool called Clearly, which is AI. There's several out there. We like Clearly. But, and I don't wanna be brand specific here, but that's what we use. But it's now cardiac CT with AI. That's, that's the binary test. It's black, black and white. It's zeros and ones. It's there, it's not there, end of story. Uh, and I will say, when we now use the microscope of AI, I call it— cardiac CT is amazing. I've not cathed anybody, done a heart cath, an angiogram, like we were talking before, since 2005.

That's awesome.

21 years ago, right? It's all done with cardiac CT, and that was, that was before AI. but even back then, 25 years ago, with using what I call the iPhone 1 version of cardiac CT, the machine we now have is the iPhone 17. But even with those earlier versions of cardiac CT, it was so good that I could no longer justify an invasive $20,000 test with lots of potential risk complications with a tool that gave me better information, more accurate information. I could see hard plaque, soft plaque, none of which you can see on a, on a, on a heart cath. I can see into the wall of the vessel, right? So we didn't talk about the donut, the donut hole. I think many times we think about blockages, think of that as the donut hole, but where plaque always, always starts is in the donut, in the wall. And literally for years to decades, that plaque, cholesterol-rich plaque, calcium plaque, will literally grow outwards, right? The donut hole is fine. All the action is occurring in the donut, impossible to see. Certainly with stress tests, and absolutely even impossible on the quote gold standard heart cath, which again, I gave up angiography, heart cath, whatever term we use, uh, 21 years ago, uh, and have never looked back. Tenth of the cost, better data, more accurate data. And now with AI, it really is the microscope. And where it's leading to this is now hundreds of thousands of AI exams later, here's the big, the big data dump, 1% of us, using the microscope of AI, will have no plaque. 1%. Wow. 99% of us have plaque that we can see, detect, and quantify. And we now, just like cancer, we now have staging. So 0 is 0, stage 1, 2, and 3, mild, moderate, severe, uh, increasing amounts of plaque. So on one extreme, only 1% of us have no detectable plaque, right? Yahoo, eat right, exercise, that's great, you know, we're done, right? Nothing, your heart's probably going to be fine. 99% of us have plaque. And if you look at the, the opposite extreme, stage 3 severe plaque, that in a third of our patients getting the machine for the first time, I feel fine, no symptoms, no chest pain, I like to say normal stress test last week, a third of our patients will have stage 3 disease the first time they get in the machine. So the penetration, the prevalence of heart disease is ungodly high, to be honest, right? As we have more birthdays, I like to say, right? As we go through life, as, you know, men go through andropause and women go through menopause and, and, and basically just, you know, the wear and tear of years, right? So that's why cardiovascular disease continues to be and has been for 120 years the leading cause of death in the US. And the great news is— so that's the bad news. The great news is we have technology both on the therapeutic side to stop it, treat it, reverse it, but most importantly, but dramatically underused, are tools to detect disease. As I like to call it, the cardiac colonoscopy with cardiac CT and AI, at least a calcium score to start with. Not perfect, but that's better than any stress test we've ever done. And I always like to say, using my cardiac colonoscopy analogy, so cardiac colonoscopy is cardiac CT. Cardiac colonoscopy or cardiac CT with AI is not just the cardiac colonoscopy to see the polyps, detect the polyps, but with— we use AI, it is cardiac colonoscopy with histopathology, with histology, right? Just like we do a colonoscopy. We see a polyp, snag a polyp, look at it, not cancerous, okay. But that really is the— probably the best analogy to cardiac CT with AI. It is not just a cardiac colonoscopy to find the polyps, but now allows us to analyze those polyps. Are they high risk, low risk, calcified, non-calcified, etc.?

Yeah, I think, you know, it's— we've covered so much ground, and I think, um, you know, everybody that's listening, whether it's you or you're thinking like so many women are like, I worry about this for my husband, the reality is 99% of us are going to have an issue. And, you know, maybe you get it done and there's not a lot going on, that helps you decide how often or how frequent you need to look, right?

I love saying, no matter what we find on the exam, frankly, you're breathing and have a pulse. Right? We— if you find stage 3 disease, no problem, we can take care of it. It's not a big deal.

Yeah, right.

We have incredibly effective and proven tools. Not just— not only do they lower numbers, like Repatha and lots of other drugs we have, but more importantly, they are proven to make you live longer. In fact, the trial that just came out early November called Vesalius, 12,000 people, high risk, had not had a heart attack yet, but high risk for heart attack. 12,000 people Half got Repatha, half not. Everybody was on background statins. We dropped their LDL from 90 to 45. 4.5 years later, 36% reduction in major cardiac events— or sorry, 28% reduction, 36% reduction in heart attacks. Most importantly for me, a 20% statistically significant reduction in all-cause mortality. Literally, if you are at high risk, you took Repatha versus not taking Repatha, these people are already on statins. Mm-hmm. You've dropped your LDL to 45. We further lowered your risk of dying from any cause by another 20%. You literally lived longer on Repatha even despite being on a statin than not. So that is tremendously exciting. New data that has just come out in the last 2 months, uh, called Vesalius. Check it out. Really a big, big deal, uh, which just shows We have really, really effective tools to treat and stop and reverse plaque. Our problem is we're not looking for it early. So imaging, just like we do with colonoscopy, with mammograms, with, you know, all, all those imaging tools we now do in people high risk for smoking, former smokers or current smokers. We do low dose, uh, CTs to detect lung cancer. Mm-hmm. 20% reduction in lung cancer mortality, right? So we need to think like oncologists with respect to heart disease, right? So, uh, that, that's going to be what's really going to be able to allow us to break through that glass ceiling of the tremendous burden, both mortality, morbidity, strokes and heart attacks, even if they don't kill you, uh, of cardiovascular disease that we still see. It's imaging, imaging, imaging, and early imaging. So we have to do the cardiac colonoscopies.

Yeah, I'm glad you, you know, so the big take-home message on that one, ladies, is even if you have advanced activity, we actually have the toolkit between diet, lifestyle, medications, and other things to actually, actually reverse some of that plaquing. And I want to bring up— you brought this up, and I know I'm going to get questions about this because there's a lot in sort of the wellness world. Sure. Let's talk about cholesterol. Right. We have a lot of people out there in the wellness world, and I had to do a deep dive into the research to get this straight in my head. Is there too low of a cholesterol level? Because you have a lot of people going, oh, it's in the brain, and we're worried about taking it out of the brain.

Great question.

I want to talk about it.

Uh, no, no, no. I mean, interestingly, if you use ApoB— here's another, another promotion for ApoB versus LDL. Now remember, when we see LDL, that is a calculated number. It's not measuring something real. It's a calculated number in general. Now there are other tools, but we can now direct order direct LDLs. However, LDL, again, not a very good tool, particularly if we're on drugs and dropping that number low. I have people, because it's a calculated number, that literally have negative LDLs. My record thus far is -22. Well, that's not reflected— that, that's not real. That doesn't reflect reality. That is a calculated number with certain assumptions. When we use ApoB, that is a directly measured number. Okay, now there are very, very— to get in the weeds a little bit— there are very, very, very rare conditions where we don't make ApoB. This is called A-beta lipoproteinemia. It's a bad disease. You don't want it. Okay, their ApoBs, if you measure them, will be 4 to 5, extremely low. Okay. When we talk about targeting plaque to reverse plaque, we're talking about below 60, below 50. If I'm really throwing all of the kitchen sink at you, we'll say statins, ezetimibe. I mean, we got lots of great cholesterol drugs and the pipeline is unbelievable of what will be here in the future. But we have lots of different cholesterol-lowering drugs. Unlike 10 years ago, we had pretty much statins. Even if I throw several of those drugs at you, and some of my patients, that's what it takes. If I get your ApoB to 25 or 30, that's pretty much as far as I can get it with any approach we have. The full, the full-court press, throwing the kitchen sink at you, right? So that whole thing about, yes, it is true, lots and lots of cholesterol in your brain, lots of fat in your brain. Lipid metabolism in the brain is 100% completely different than lipid metabolism in the rest of our body, right? To give you an idea, the half-life of LDL measured in the, in the, in the, in when we check cholesterol levels in the body, right? Or ApoB, doesn't matter. LDL or ApoB, the half-life, if you think like a drug, that the time it circulates in the blood is in the range of 3 to 5 days. Okay. The half-life of cholesterol in the brain is 5 years. Lipid metabolism, 100% different, right? We traffic cholesterol in our blood vessels. I won't get too deep in that. That, that'd be a whole nother discussion. Uh, but the tra— the metabolism, the synthesis, the metabolism, what happens to cholesterol in the brain, 100% different. Right? And the drugs that we take really do not affect cholesterol in the brain. They do not affect cholesterol-dependent steroids and hormones, rather, like vitamin D, estrogen, progesterone, testosterone. They do not affect that. We have all of the cells in our body have all of the molecular machinery to make as much cholesterol as they need, right? They do not depend upon cholesterol floating around our bloodstream. It's there for a whole different reason, which I'm not going to go into. But we have all the molecular machinery to make as much cholesterol as any cells need, whether to support their cell membrane or to make steroidal-dependent hormones, etc. We have as much cholesterol as you need, or cortisol or things. In fact, HDL cholesterol is actually what fuels in stress conditions because we, again, we have lots of cholesterol synthesis available in stress conditions. Where we need extra cortisol during significant, you know, physical stress or whatever, that cholesterol that's turned into cortisol doesn't come from LDL, it comes from HDL, by the way.

Oh, I did not know that.

Exactly. So that whole thing about lipids, you know, statins in particular or any other cholesterol-lowering drug affecting cognition, affecting the brain, we've done those studies. We have done more studies with statins. Not that it was— I mean, they're a tool.

Right?

Not the old tool. They're a tool. It's great. They're proven. They're cheap. They work, work well in most people, but not the only tool around. It doesn't matter. I mean, if it happens, we have a discussion. Do we use them or not or whatever? But in fact, I always tell people they get, oh, I'm not going to take a statin because for whatever reason, it's fine. I got lots of tools. It's fine. Right? Sometimes you need a Phillips head. Sometimes you need a flathead. Right? I got lots and lots of tools in my toolbox. And that toolbox is only getting bigger and bigger quite dramatically. So statins are a tool, but that whole mythology of all that stuff about the brain and cognitive function, all that, we have looked at that extensively now for decades, even strokes and stuff like that, intracranial hemorrhage, all that stuff. It, it doesn't— it's not there. The data is not there. The science is not there. And having appreciate, we have done more studies with statins specifically than any other drug in the history of humanity. Period, full stop. Right? We understand them. We understand where they can have problems, harm. We understand where the benefits are. So again, they're tools. But specifically, more broadly, if you look at cholesterol, that whole cholesterol brain issue, the brain makes as much cholesterol as it needs. That's just not an issue. Period, full stop.

Thank you. Thank you for clarifying that because I knew I was going to get a bunch of feedback on that.

Oh, absolutely.

So Yeah. And so, you know, I want to say, Dr. Osborne, you're uniquely poised to have this conversation. You're an interventional cardiologist. You're also boarded as a lipidologist and a cardiovascular physiologist as well. You're like one of 55, I think, worldwide, or at least in the United States with all of those boards.

Well, actually, as it turns out, I have 7 boards now.

No, I didn't even know about the other ones.

And the reason I say that, right, I just call it fancy, expensive wallpaper is when I started out 30, almost 30 years ago, right, at Harvard, right? There was no such thing as preventive cardiology. In fact, I didn't even know what it was till about 15, 20 years ago. And we came up with the term preventative cardiology and go, oh, that's what I do. Because my interest was, we knew the plaque always started decades before you had trouble, but decades before it had symptoms, decades before it shows up on a stress test or a heart cath. and I was always going like, let's focus on the polyps, not the cancer. So what tools do we have to detect polyps? What tools do we— the, the cardiovascular polyps, if you will, the plaques, and what tools do we have to treat and prevent and stop the plaques? So that journey for me started 30 years ago. We did not have a specific training program for preventive cardiology, right? We were focused on blockages. Let's fix the blockages. You're fine, which is not the case at all. And so I basically did my own on-the-job self-training saying, hey, I need to learn this. So I got boarded in lipids and all that. I got boarded in hypertension. I got boarded in cardiac CT, echocardiography, nuclear cardiology, as well as cardiology and internal medicine. So I didn't do that purposely just to get pieces, expensive pieces of paper on the wall, but that was the training that I needed to be able to really fully and encompass and envelop the totality of cardiovascular prevention. It just happened to do that. Nowadays we actually do have, although it's still in its infancy alas, we still have, uh, we, we now do have training programs in preventive cardiology. Uh, they're still in their infancy, uh, but those 7 boards that I have and that training and all that, uh, yeah, I'm the only one that was stupid enough to do all that paperwork and tests and put myself through that. But that's— I mean, I've never worked a day in my life. I just get paid to do my hobby, and hopefully I make a difference and save some lives along the way.

Yeah, you and me both. I'm a little bit of the same, like acquisition of, of very expensive plaques on the wall. But it's because I'm a scientist, I love to learn, right?

Yeah, exactly right. I mean, all that stuff, I, I do it again in a heartbeat, no pun intended, because it's just— I love to learn. And if I then can change, turn that learning into I can give advice for my patients that's going to make a difference for them. I mean, that's what life is about.

Yeah, absolutely. And so for everybody listening, if you're thinking, oh my gosh, I need to have access to Clear Cardio. So Clear Cardio is your organization. You have an entire program. I, we, you know, in disclosure, we've had clients that, that from both our telemedicine company and our, our clinic go through because at the end of the day, This is not highly accessible everywhere, but you have a very wonderful kind of white glove service for people that really can come in and get some preventative services. Ideally, get it done before you're at the critical step, you know.

But again, I recommend if you're breathing, have a pulse, we'll be fine, right? I mean, the real thing in cardiology, unlike many other specialties, pretty much whatever we find, I can take care of, right? We have the tools. Even if you're stage 3, right? No problem. I, I can take care of you. And we can prove over time that we're actually shrinking and stopping plaque, which again is remarkable, something we could never ever do until the last few years with AI.

Yeah, I think that's really important because I, I think the message of reversibility is not really out there in the marketplace. That is sort of this—

I just ran into somebody, it happens all just this week, someone went through the process and a couple stress tests and heart casts and blah blah, and they said, we can't reverse plaque. And this is coming from an interventional cardiologist. I'm going, crack a book, go to a meeting, read some papers, my friend. We've known this for 20 years. So yes, there's tremendous hope, right? But the first step is let's just look under the hood, right? We just got to start there.

Absolutely. Well, Dr. Osborne, this has been fabulous. I could talk to you for hours. Like, we didn't even dive into, like, we didn't even dive into, like, hypertension and all those other things.

Oh gosh, I know.

I mean, Fix that, fix that, fix that, fix that. You can't feel it.

Well, maybe, maybe, maybe we can— that's something we can circle back to later if there's interest on your part. Uh, but yeah, high blood pressure, I gotta say, let me put this in the parking lot. Wow. I mean, high blood pressure, so poorly diagnosed, treated, huge burden of strokes, heart attacks, kidney failure, kidney disease, uh, very much intimately related, as I like to say, When people say what I do, I just say, if I'm snarky, I'm just a general contractor. I do some plumbing, I do some electrical, right? But if you think about plumbing, pipes, and filters, right? Blood vessels, heart, and kidneys, all intimately related. Throw on hormonal issues and all those things. But yeah, I'd love to just chat. We could spend easily an hour, a really useful deep hour just talking about high blood pressure itself. So we'll put that in the parking lot, but, uh, thank you.

Yeah, we'll definitely come back to that. Yeah, because obviously that's a big, that's a big, uh, narrow focus of mine because of my mom's experience, because she was mistaking her medications and being mismanaged, quite honestly. Honestly. And she kept telling me, I'm going to feel it, and we— you're not going to feel it.

The big W, capital W, do a horrible, pretty much horrible job of diagnosing, treating, and taking care of and controlling high blood pressure in the U.S. It's terrible. There is no excuse.

Yeah, it's— I agree with you.

So we will, we'll have you back in August, so maybe that might be fun to chat about next time.

So yes, absolutely. Well, Dr. Osborne, thank you so much for being on Menopause Mastery.

It is an absolute pleasure, really. Thank you so much, uh, Dr. Murray, for having me on, and thank you for allowing me to talk about how we are going to ultimately eliminate heart disease, because my ultimate goal as a preventive cardiologist is to eliminate heart disease. Okay. And thank you for having me on. Thank you for this discussion. Thank you for getting the word out. And in fact, at the end of my discussions with all my patients, I always say, hey, my primary goal is to eliminate heart disease. Along the way, I want to save your life and prevent strokes and heart attacks, but I really want to eliminate heart disease. That's my major professional goal. And if you follow that logic far enough down the road, really what I'm asking you and all your listeners to do is something very straightforward and simple. Okay? Take into account what we said. Think about it, cogitate about it, take it to heart— pun intended. And really, what I'm asking you and all your listeners to do is put me out of business.

Yeah, you're right. Exactly.

Yes, right? When we have cured heart disease and there's no reason for me to do what I do anymore, I will be very, very happy. Okay? Yes. Please. Okay.

We'll take that on.

Okay. So if you are interested, clearcardio.com, C-L-E-A-R-C-A-R-D-I-O, clearcardio.com. Also, we do have a great YouTube channel, clearcardio.com powers prevention. Lots of cool videos, educational videos, great patient stories, all that kind of stuff. So if you're interested in doing some deeper dive on video and all that, check all that stuff out. Lots of other great places to learn about how we are going to help to eliminate heart disease and again work to put me out of business.

Absolutely. Well, thank you so much, and we'll have all of that in our show notes, so you can go directly to our show notes and get connected with Dr. Osborne's company and, you know, start, start the process. And so thank you so much, and thank you everybody who happens to be listening in your favorite podcast platform or on YouTube, and we'll be back next week.

Fantastic.