Most people think heart disease starts with a bad cholesterol number. But the truth is, the damage often starts decades earlier—before you feel it, before you see it, and before your doctor catches it. Endothelial is the first layer in the arteries that gets injured. It's like the canary in the coal mine for your arteries. It's a protective gel coat. And once that early damage begins, it's silent, but it's not inevitable. You just need to know where to look and what to do next.

Your mitochondria are what keep your heart beating. Most cardiologists don't talk about nitric oxide. They don't measure V2 max. They don't ask about grip strength or muscle mass, but they should because muscle is one of the most powerful protectors of your heart and mitochondrial health; that might be the key to your entire cardiovascular future. We test endothelial function, arterial stiffness, nitric oxide, and inflammatory markers, not just cholesterol.

In today's episode, you'll learn why standard cholesterol labs are incomplete, how the loss of skeletal muscle speeds up heart disease, what biomarkers matter more than LDL, and why diagnostics, not guesswork, are the future of prevention. Sarcopenia accelerates cardiovascular aging, but strength training can reverse that trend. This is the medicine of what's possible, and my guest today is one of the few cardiologists practicing it: Dr. Michael Twimman, expert in mitochondrial optimization, arterial imaging, and a bioindividual muscle-centric prevention approach.

Voteax is one of the most predictive markers of longevity and it's trainable. So, if you could prevent a heart attack before it starts, wouldn't you want to know how? You can't manage what you don't measure, and you can't prevent disease if you're not looking in the right places. Let's talk about what it really takes to become heart attack proof with Dr. Michael Twimman.

Dr. Mike Twimman, welcome to the show.

Thank you for having me back.

Has it been 40 seconds yet?

Not yet.

Okay. Well, as soon as it reaches 40 seconds, someone in the US had a heart attack, and every 33 seconds, someone dies of cardiovascular disease. It's a horrible stat. You know, it makes me think, how have we not gotten better at treating that?

I think we're getting there, but it's still the number one killer. You know, we did this episode three years ago. Stats haven't changed that much since then. And I think we're going to dive into a lot of the topics today that I think might be beneficial to really help people become more heart attack proof.

Can someone actually die of a broken heart?

Absolutely. It's known as Takotsubo syndrome, or broken heart syndrome. Um, Takotsubo is a—a Japanese kind of fishing vessel—I should say fishing pot that they catch octopus in. And that's what the left ventricle looks like when people have this broken heart syndrome. So, they present after an emotional event—you know, somebody in their family dies, they're in a car accident, they smoke cocaine, something happens where their sympathetic drive is very high. Uh, and they present to the hospital like if they're having a heart attack, and we would rush them off to the cath lab, find out that they didn't have any significant blockage in the arteries. And then when we did the left ventricular, their heart wasn't pumping very well. Um, and so kind of supportive care after a couple days, usually the heart function returns to normal. But it's a high risk of sudden cardiac death when you have that.

Mhm.

Is it mostly women or men?

Generally women, older women particularly.

We hear the term heart disease all the time, but what is heart disease?

That's the umbrella term. I mean, there's coronary heart disease, there's heart failure, there's valvular heart disease. Um, so you really have to define terms, but you know, vascular disease—you know, 60,000 miles of blood vessels. You got to go looking where the disease is at.

H—you know, as I was preparing for this episode, cardiovascular disease, as you had mentioned, is still so prevalent and it's not getting better, which is surprising, and it makes me think, okay, what do we know that drives heart disease, and again, it is an umbrella term, so perhaps we start with—I don't know—take your pick—stroke.

So stroke can be either ischemic or thrombotic. So ischemic means there's not blood flow coming to the tissue, and without oxygen and nutrients coming to the tissue, that tissue starts to die. An embolic event is where more of a blood clot forms. Many times in heart patients, it's due to fibrillation—a clot forms in their left atria. That clot breaks free, gets lodged in the brain, and you know, steals blood flow from the territory downstream, and that tissue will die unless it's revascularized. Um, so stroke, honestly, is probably more scary to many people because heart attacks, if you survive to get to the cath lab, you usually do pretty well, but a stroke can be debilitating for the rest of your life. But the same risk factors for heart disease are the same things that contribute to stroke in most people.

And what are those things?

I mean, it's the common ones. It's smoking, it's high blood pressure, it's diabetes, high lipids, physical inactivity. Those are probably the top five, but there may be 395 other things that can really damage your arteries.

Do we know if we take smoking out of it, do we know what would be the biggest contributor of heart disease?

It's probably pretty close between um, dyslipidemia and high blood pressure. Um, you know, lipids get a lot of the headlines. Um, you know, because there's a lot of dietary interventions some people can do that make their lipids change, but blood pressure is really that silent killer. You don't feel it often. You know, if you're starting to feel your blood pressure, it's pretty bad. You know, you're usually pretty close to having a stroke or going blind. So, it's really called the silent killer for a reason. Your organs are getting pounded with this high pressure for years and just starting to age faster than they should.

How would someone know that?

Do you feel heart disease?

Generally, no. I mean, the unfortunate fact is that when people have heart attacks, that's often their first symptom that they had heart disease. Um, if you're having chest pain, tightness in your chest with exercise, severe shortness of breath, or exercise intolerance, those are often signs that you're developing severe atherosclerosis in your coronary arteries, uh, the arteries that provide the nutrients to the heart. But typically, you're not going to have that sensation until your arteries are blocked 70 to 80% with uh, plaque. Um, so most people have no symptoms until they're pretty late to the game.

M—you know, Matt, uh, my producer and uh, wingman over there, we were talking about exercise and then we were talking about obesity and heart disease, and Matt was saying, you know, if someone is struggling with obesity, they have a much bigger body mass, and the heart has to work so much harder when you add in exercise. Is that safe? How do we begin to think about introducing exercise without overloading the heart?

That's a great question. And if somebody has truly been sedentary for many years, oftentimes they probably should consider a cardiac evaluation to make sure that they're going to be safe enough to really push it hard with exercise. You know, if they're, you know, doing body weight exercises or walking, I'm not really concerned for those people. But if they're saying, "Hey, I really want to get into HIT training. I really want to get into heavy lifting," okay, show me that your heart and cardiovascular system can tolerate that. And then maybe simple as just, you know, getting an evaluation where, okay, what is this person's blood pressure, maybe they do a, you know, CT coronary calcium score—like, do they have heart plaque in their arteries already—um, and then for some people, you would actually consider doing a stress test, and stress tests are good tests if people are having symptoms—as said before, somebody has a 70% blockage in their arteries, you're usually going to be able to pick that up with a stress test—but stress tests are no guarantee that you're at risk for a heart attack. If you pass a stress test, you can still have a heart attack later that day. But they can give somebody an idea of their exercise capacity. Um, so put them on a treadmill. It's often—it's going to be the Bruce protocol where every three minutes the treadmill goes a little bit higher and a little bit faster, and you push them until they say, "I can't do this anymore," or you see some EKG change to say, "Hey, stop." But if they can't go seven minutes on that stress test machine, they have pretty low functional capacity, and they're gonna have to work up from there. But you're just making sure you're not seeing some high-risk findings while they exercise.

M—what would be a safe way to incorporate exercise? Someone is listening to this, maybe they have seen a cardiologist, maybe they haven't. Is it safe to start with cardiovascular activity? Is it really based on the pace or the um, heart rate? Or would it be better to lift weights? Is there some kind of standard?

I would say it's probably a combination of kind of perceived exertion. You know, there's the Borg exertion scale. You know, 10 out of 10, like you're only be able to do this for a few more seconds. You know, the tiger's chasing you. Um, or is this a pace you could do it all day long if you had to, but when you start kind of losing your breath, that's when you start getting probably, you know, 70% or so of your maximum heart rate when you really can't, you know, maintain it much longer if you kept going higher and higher than that. Um, so if you get to the point where you have a little bit mild breathlessness, probably okay. But if it's severe or you're getting tight in the chest, you got to really back it off and get that worked up first.

And when would someone think to go to the emergency room? Right? Because if heart disease and heart attacks are really as robust and prevalent as we believe that they are, it seems as if they can be fatal. How many heart attacks are fatal?

Um, I mean, it used to be about 50% of people had heart attacks. You know, that was their first sign and they didn't make it to the cath lab. So, you know, a higher percentage than should be. Um, when should someone go see a doctor? But your question about the ER, I mean, there's like over 8 million presentations at the ER a year for chest pain. And you got to rule out the bad actors. Is it a heart attack? Is it a blood clot in your lungs, a pulmonary embolism? Is it an aortic aneurysm where your arteries are tearing? Um, you know, is it pneumothorax? You know, but you know, three times out of four, it's not a heart attack when people have chest pain coming to the ER. And there's a lot of dollars spent working these people up. Um, but if you're having, you know, severe symptoms where, you know, you feel like you have impending doom, you feel that there's an elephant on your chest, you absolutely can't breathe, you know, if that doesn't go away in, you know, a few seconds, you got to go in and get it checked out. Make sure it's not, you know, ST elevation MI where you've ruptured a plaque in a coronary artery. And those can often be fatal unless you're revascularized. But if you've not having symptoms, that's probably the better question is who needs to be screened?

And who would you say who needs to be screened?

Essentially everybody. Everybody has a heart.

It just—what? I don't know. That's questionable. Just what age and what test should you be really considering for those people?

You know, people with very strong family histories. My family included. You know, my grandmother on my mom's side started having cardiac events in her 40s. Uh, had ultimately bypass surgeries, strokes, had peripheral artery disease, revascularization. You know, she died at 63 from a stroke—way too young. Um, you know, my mom, she has a very high-risk calcium score, but no symptoms, well managed at this point. So, people have strong family histories really should get checked out earlier, probably under 40. Um, I used to think 40 is kind of the starting point for many people, but I've seen more and more people in their 30s have very high-risk calcium scores the past few years.

And can you explain what a calcium score is and what does that mean to be high risk?

So, you have 60,000 miles of arteries. The coronary arteries provide the nutrients to the heart tissue themselves. There's a test called a CT coronary calcium score. It's a low-dose radiation scan that looks at the coronary arteries and if there's calcium in the walls of the arteries. Calcium is supposed to be in your bones and teeth. If you have calcium in your artery walls, then that indicates that there's hard plaque in your arteries. The higher the calcium score, the higher the risk. So, as you live your life, you know, you can have a calcium score of zero. And I've seen people in their 80s with scores of zero, but I've seen a gentleman who was 36 years old who had a score of over 1400. That's extremely high for somebody at any age. But the journal cutoffs are, you know, over 400 on a calcium score is high risk. Over a thousand is very high risk. And I always get asked, "What's the highest score I've ever seen?" 7,770 was the highest score I've ever seen.

You don't say.

Yeah, that is uh—um, really, really high.

The calcium, where does the—the calcium come from? Is it dietary calcium that then gets deposited or is it damage that then creates a cascade where calcium is then deposited in these arteries?

It's kind of an endgame where the body's trying to repair the damage to the artery. So on the top layer of the artery, there's something called the glycocalyx. It's a protective gel coating. Think of a fish coming out of water that's slimy. That's kind of what your arteries are covered in. It's a carbohydrate gel coat. Underneath that's the endothelium—one cell thick. If you took out all your endothelium, which would be very hard to do, it'd be about the surface area of six tennis courts. And those are kind of like the protective barriers to the lining underneath called the intima. Once things start getting deposited in the intima, then you're off to the races, developing plaque in the arteries. And the body's repair mechanisms will include depositing smooth muscle into the arteries and eventually calcium. Think of it like just forming a bone to kind of solidify that plaque to prevent it from rupturing.

Hm. You know, it makes me think the vasculature of the heart has a mechanism if there's damage, and that's calcification. I don't know what that mechanism would look like in skeletal muscle, you know? I mean, because it seems like the body has these very interesting processes to protect itself, and the calcium deposit isn't—it's not the cause. It's—it's the response to whatever is happening, right?

It's the scar essentially.

Yeah. You know, um, and in the brain, there's tau proteins. I—it just makes me think what is that like in skeletal muscle. I—again, I don't know, but it's—it's just—it's something to think about.

How long have you been a practicing cardiologist?

I finished my fellowship in 2012.

Okay. So, that's a while. And you did your fellowship in preventive cardiology.

The fellowship was in general cardiology. I graduated and was an invasive cardiologist for many years. So I was doing heart procedures in the cath lab, you know, doing angiograms to determine how much blockage people had in their arteries. Um, but eventually got more interested in the preventive side of things in the last few years.

Now, by the way, you are wearing uh, blue—would those be uh, blue light-blocking glasses?

They are.

Now this is a very different version. If you guys do not know Dr. Dr. Michael Twimman, who again is my cardiologist, and it is—he is the guy that we send everybody to since I've known you, which—how long have I known you now?

I think it was around 2019.

Okay. I have never seen you without those orange lens glasses.

Unless I'm outside. I usually have them on.

Why?

Helps with my circadian rhythms. Helps with my sleep. So, sleep's very important. Uh, no, don't know about that. Hard pass on that one. But do you wear it for circadian biology or does it affect—do you think it affects cardiovascular disease?

I think it does. I think it helps mainly by optimizing your circadian rhythms so that you're able to sleep better, and when you sleep is when you repair your mitochondria. Um, and I've had a, you know, sleep tracker for at least nine years, and I just noticed my data would always be better when I would do this. And the main thing is, you know, you're evolved to be under full-spectrum light. So, we evolved to be outside in sunlight. We weren't ever evolved to be in front of artificial light that tells our body it's different times a day than it is. Um, so I'm always just trying to let my body know, okay, it's daytime versus it's about to be evening, it's evening time. And these daylight glasses just help my body stay in that kind of a rhythm.

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Talk to me about red light therapy and photobiomodulation.

So photobiomodulation is using light therapy to change your biology. The target of red light therapy is the mitochondria. And there's various devices. Um, but skin contact is better because the major issue with light therapy is the acronym RATS: light reflects, bounces off the skin. So, we're—like 60% of it just bounces off. The light's absorbed. The light's transmitted, which with red light therapy, it's not going all the way through. It's not an X-ray. Or the light scattered. The light comes in, bounces around, and maybe gets in the mitochondria, or maybe it bounces and goes back out. So you want to try to maximize how much light's coming in. So ideally, the device is on the skin or as close as possible, as recommended by the manufacturer. But once the light comes into the tissues, the main location where it's working is the mitochondria. The mitochondria absorb the red and infrared light—cytochrome oxidase for the geeks out there. And that does a couple things. It releases nitric oxide from the mitochondria. It increases ATP, which is an energy currency in the mitochondria. And it decreases reactive oxygen species, and has, you know, multiple thousands of studies—most of it's going to be based off of, you know, musculoskeletal injuries and repair, but it helps lower pain, inflammation, decreases swelling, helps tissue regrow—so I—it helps tissue regrow—so hold on—we got to—we got to—we got to rewind on this photobiomodulation, red light therapy, but it has to be on the skin like those masks because I sit in front of panels all the time.

So most of the trials are using laser technology and then later LED. But that's the challenge is how do you know what dose you're actually delivering? Um, and that's what's challenging with—I call it the Wild West of the red light companies right now—is because there's a lot of claims out there of what their devices can do. But you need to know a few things. You need to know the wavelengths. What color of light is coming off of the device? It should probably be some form of red and infrared. What are the wavelengths that you look for? There's many, but like 660 generally in the red, 810, 850 in the infrared spectrum. Um, then you got to look at what's known as the power density or the irradiance. That's how many photons of light are coming out of the device uh, divided by the beam area. So, are you using like a pinpoint type of thing on the skin or using a big panel? I've been to your office, and you have the world's largest panel. How—how big is that panel?

8 ft tall by 4 ft wide.

Okay. Number one, that looked very expensive. And number two, did you test the irradiance?

I don't have a laser power meter, and that's what you would have to—

Have to actually accurately accurately measure it. But, you know, when they say that everything has to be at least 100 millatts per centime squared to get a benefit, that's not true. You know, most the trials, at least in the cardiovascular world, you know, they're using like 10 mills per centimeter squared. So, you don't need these high radiances to get the benefit. So you have to know the power density. So like how many photons of light are coming out and then the time, how long are you using that device for, and then that equals basically the dose, and the dose is different for the tissue types.

Um, so there was a cardiac trial, more kind of limited in scope but very interesting, was it was an Israeli trial where they took patients who were having ST elevation or having the worst kind of heart attack. They got rushed off to the Kath lab. I believe there's 12 people in each group. Each group got standard of care. They all got stances, but half the group got photobiomodulation during the procedure, a day later, and three days later. It was a device that was utilizing 10 ms per centime squared. They used it for 100 seconds, one jewel. This is what's interesting. It was not over the heart. It was over the tibia. So, their leg bones. Why would you do that? There are stem cells in those tissues. What they had studied is that they gave the dose during the case, a day later, 3 days later. The people who got treated had troponin levels that were approximately half those that weren't treated. So troponin is a protein inside of the heart that gets released when the heart cells die. So when the heart cells die, it's like popping a balloon. All the contents spill out. If you measure troponin in the blood, heart tissues getting damaged, and high enough levels can indicate a heart attack. So the people had half the size of heart attacks when they got treated. Everybody got the same treatment otherwise.

How would that work? Well, when the stem cells are activated, potentially that's helping lower inflammation in the heart. You're also putting energy into the system while the heart is starving of energy because there's no blood flow going downstream. Proof of concept study only at this point. Safe to, you know, use it, but very interesting to think about like they weren't even treating the heart. These people had quote smaller heart attacks. So, this is why photobiomodulation was really fascinating for me. It's like, you know, I'm a cardiologist, but where can most people use it? It's musculoskeletal injuries. That's where most of the data is at. So, if you get injured and you can't train, one, that sucks, but two, then you're not going to be able to get the cardiovascular benefits long term if you keep getting hurt. So, this potentially helps you recover faster and get back into the game.

You mentioned um that it has to be on the skin. Can the red light penetrate through the skin? It's preferable to be on the skin if possible. So, but can it penetrate to muscle? So infrared light at best probably penetrates 3 cm. Um, most data shows that like maybe five millimeters is kind of a red and then infrared start to hit but maybe up to through to three. But think of this like a lot of photons at the top of the skin and then only a few getting down deep. So that's why it's kind of the recipe. So again the time is important because you could use a higher radiance for one minute, you could use a lower radiance for a longer period of time and get the same dose. So, it's kind of the analogy of like cooking a turkey. Do you go low and slow or do you drop the thing in a boiling pot of water or and fry the thing? But is it the effect on the skeletal muscle or is it the effect on other areas that then generate the help of the tissue? It's decreasing pain receptors, it's decreasing inflammation. It's decreasing swelling in the tissue. And it's potentially that swelling in the tissue, particularly around the nerves, that causes some of that delayed onset muscle soreness. And so this is why you potentially want to use it, you know, after training.

Now there is some debate on like what is the perfect time after training because if you immediately run to the red light panel after you do, you know, strength training exercise, you know, you might blunt that inflammatory adaptation. You might not be as sore but you might not get as much hypertrophy if you use it immediately afterwards. Same story like why you wouldn't do a cold plunge immediately after doing a strength training episode. You know, I've thought a lot about that and I would say to be fair, the influence might be really small, you know, like I don't know if if someone if you're going to use red light, I would, from my perspective, go ahead and do it. I I don't think it's going to affect their I don't think it's big enough for most people to make a big deal. Like, you know, if you're an Olympic athlete, maybe you need to time it down to the minute. But I also get asked like what time of day? Think of these devices almost as a joke as as a sun. Like sun up to sunfl up to sundown is when you ideally would like to use the thing. You know, if you use it in the evening time, you just gotta be mindful that in some people, it's not the wavelengths of light, it's the intensity, the lux that affects their sleep. So, if you blast yourself, particularly in the face with these panels 20 minutes before you want to go to bed, it might affect your sleep in some individuals. Other people, it has no effect. Some people they sleep better with it. You just have to be kind of a biohacker and see what time of day works best for you.

You know, I was looking at some data. It seems that there's a potential for certain red light to improve eyesight. Is that true? It is true. I don't know which um irradiances they were using in those trials, but it's a very short period. I believe that the treatment session is only like 3 minutes long.

Where else would you use various lights? When I we were upstairs, all of us, and you pulled out this device again, I feel like it's Christmas when you come over because there's all kinds of gadgets. Although, you should leave some here. Yes, I did. And uh you said, "Oh, this is cool. You put it on because it's blue light." So blue light doesn't penetrate the skin very deep. So it's for topical use only. So the dermatologist will know about its benefits. So it can help treat acne, but on skin contact, it may help liberate nitric oxide. And that's obviously one of my areas of expertise and interest is that anything that can improve nitric oxide maybe helps arterial elasticity or blood pressure. So I bought these wearable patches a couple years ago and played around with them. I haven't done enough data with them to say that they absolutely release nitric oxide yet, but theoretically, but I thought it was pretty interesting when I was reading up on them is how they kind of showed that they did work is that they got some recruits, probably some college students, paid them 20 bucks and they made them stand in front of a tennis serving machine and they blast them 80 miles an hour in their quads. Um, and so I was like, I don't know if I'd do that for 20 bucks or whatever they paid them, but half the kids got the light patch, the other kids didn't. They got, you know, you know, here's some ibuprofen, some cold packs. But the people got light therapy, they had like 40% smaller bruises the next day because it helps break up the hematoma. So, it just helps speed up that wound recovery.

People talk about red light for wrinkles, all those red light masks, which by the way, I think I have three or four. Does blue light help with wrinkles or skin integrity? It would actually probably make it worse. Yeah, blue light is oxidizing to the skin. This is probably why people who have Okay, so don't put that patch on your face. Yeah, do not put the patch on your face. And this is probably the reason why when people have a lot of screen time, they tend to get a lot of fine wrinkles is that blue light is dehydrating their skin and it's oxidizing. I didn't know that. Hey team, did you know that? Absolutely not. So, do you put a flux on your screen? I usually have different software on my computers that pull it out and then if you've been to my office, I always always have in the corner, I have a red light panel that's on at that distance. It's not really for photobiomodulation, but it's trying to balance out the spectrum of light that's in my office. So that red and infrared light's kind of bouncing off my computer monitor back into my eyes. Could you protect your skin and eyes with some kind of panel over your screen? It's hard because it penetrates the screen. But if if someone were to come to you and say, "Hey, I want to protect my eyesight. I want to protect my skin. What do we do?" So I don't know the companies that make it anymore. The one I used, I think, went out of business, but there used to make these like orange acrylic plates and then you would just physically put them in front of your monitor for the people who don't want to wear the glasses for any reason or birth control over here. Yeah. Like it's like the Marine Recruits with the birth control glasses. Um, no, it was, you know, the case where, you know, I got some of them because, you know, I have nieces and nephews and they're not wearing these glasses. So, I was like, would they put these in front of their, you know, like an old school screen protector? Some would, some wouldn't. Um, but you know, there's always options, but the physical blockers, they work well. Um, and then, you know, it just being mindful that try to use some red light therapy when you're using a lot of blue-lit devices.

Does it have to be red light therapy or could it just be a red light lamp? The lamp is just helping more kind of balance out the the spectrum of light in the room, but if you have the red light mask or you have a panel, it doesn't have to be skin contact for the the face mask, but that helps stimulate collagen production, which is decreasing the wrinkles. That's why it works. But I mean, so for example, like last night, I'm working on this book. Um, turn I have to turn in my edits and I put the nighttime screen situation on. You know, you can you can switch it uh on your Mac, but I also use a little lamp. It's not red light uh per se with the uh infrared and and you know, all of that massive intense red light. It's just a little lamp. Is that helping to balance out the blue light or um is it just something? Yeah. How does that work? I would say that that it's helping balance out the blue light and it's just helping maintain your circadian rhythms. So, you want to dial down the intensity post sunset. So, yes.

Are there things that you've now introduced into your practice, say over the last two years? Um, I know that you're talking a lot more about nitric oxide. You're talking a lot more about this endothelial glycocalyx, which nobody can spell. What is new on the horizon that you've really landed on? I think the endothelial glycocalyx is the biggest thing over the past couple years. um, is that you know when I kind of transitioned out of traditional cardiovascular care where you're more reactive and now I'm a little bit more proactive is you kind of go down that pathway where you find functional medicine and you realize that like nutrition and exercise are extremely important and there maybe some supplements and instances that are helpful but eventually you realize that that's not the whole story and so then you find maybe the biohackers and the circadian biologists and you start doing some of those things but once I was found that pathway I came upon you know Dr. Mark Houston, Dr. Nathan Bryan, and they really taught me a lot about how nitric oxide was important to the vascular system that is released mainly from the endothelial lining. But in the past few years, it's been noted that there's another layer called the endothelial glycocalyx. It was first visualized in the 1960s, but only the past few years is getting a lot more attention as people have potentially treatment options for it. And some of the diagnostic testing that I offer in my office or potentially you can do at home that can tell you the health of that glycocalyx and underlying endothelial layer. I think that's where really it starts is that if you have a healthy layer of glycocalyx and endothelium, it's not that your arteries are completely, you know, bulletproof, but it's much less likely you're going to develop severe atherosclerosis. And I think cardiology doing a great job treating people when they have the end-stage disease, but sometimes it gets a little bit too lipid focused. And lipids are important. I'm sure we're going to talk about them today, but if you keep the glycocalyx and the healthy, you don't have to worry so much about the downstream effects.

Does what I'm hearing you say is that this endothelial glycocalyx is really at the root. For example, I believe muscle is the root and the health of skeletal muscle is the root. You believe and correct me where I'm wrong that the endothelial glycocalyx is in part really the root and if you can address the health of that then things like lipids, LDL cholesterol, apo are important but not necessarily at the root of heart disease is that is that what you're saying? Correct? I think it's too myopic to focus on one risk factor, you know, focus on the layer that is the first line of defense, you know, it's your force field. If your force field is healthy, you're not likely to develop plaque in the first place. Or if you've already developed plaque and you've picked that up on a calcium score or a CT angiogram, if you repair the glycocalyx in the underlying endothelium, you stop laying down plaque and then you have the potential for plaque regression, which I know that's going to be a question, you know, can plaque be shrunk or regressed? The answer is yes, but you have to stop doing the damage first. And in part that's improving the nitric oxide pathways that help support that endothelial glycocalyx.

How can someone who is at home listening, going gosh my mom had a heart attack and she had a heart attack really early. I am just entering menopause and menopause seems there seems to be major changes in LDL cholesterol, apo all kinds of things. And they're thinking, well, how can I measure if my endothelial glycocalyx, not that I can spell it, but how can I measure it? Sure, we can just call it the EGX going forward if you like better. EGX. Yes. So, there's not a direct way you can actually measure the EGX at this point. There are some more research uh uh options where they're using certain type of intravital microscopes typically in the sublingual space where they're looking at the um how well the red blood cells are basically repelled from the glycocalyx in the blood vessels under your tongue and that correlates with what's potentially going on in the rest of your 60,000 miles of blood vessels. So they they've done that for sepsis. Um, and there are some tests that are still research where they look at the um, glycosaminoglycans, the GAGs that come off of the glycocalyx when it's damaged. So, you can pick that up in blood and urine, but at this time there's not a commercial lab that does those tests.

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Um, so you have to kind of look down to where the endothelium is. And again that's one cell thick layer that lines your entire artery layer. It's kind of like the air traffic controller which determines what stays in your blood and what gets into the walls of the arteries. And testing. They can look at that is um, you know, one you could do blood pressure. If your blood pressure is normal. What would you define normal? Normal is under 115 over 75. 115 over 75. That should be optimal. 120 radius quote normal. Oh my gosh. So I've got uh uh Julia here. She's on my team. Julia, what's your blood pressure? I think it's 112 over like 68. Yeah. 112 over 68. That'd be awesome. Um, well one so what is what is it? 115/75 is where once it starts getting above that the risk of atherosclerosis increases but do some people have a higher vascular tone cuz I'm going to measure my blood pressure you're going to measure it actually with your very fancy machine that you you always come I love it when you come to visit because you have about 15 obscure items that could probably save my life on a plane. That's the plan. Yeah. um that number, this 115 over 75. So if someone is at home and they're thinking, well, how do I measure their how do I measure my own blood pressure? They need to sit down for 15 minutes. At least five minutes. Gosh. Five minutes. No caffeine, right? No caffeine, no nicotine. Yeah. Sounds like Yeah. Feet on the ground, back supported, arm at heart level, and on the bicep. Stick away from the ones that are on the wrist because they're generally highly inaccurate. So on the bicep, take a measurement, record the number, and look at trends. One number is not the problem. It's the blood pressure load. And so if you're consistently, you know, over 140 over 90, you need to talk to your doctor. Potentially going to need to be on pharmaceuticals while you're working up the root cause why your blood pressure is so high. But that is just one sign that potentially have low nitric oxide availability is your blood pressure starts to rise. There's test strips, these salivary nitrate test strips. They look like litmus paper. You put them in your saliva. The brighter red they are, the more nitrates you're potentially getting in your diet. So, think beets, green leafy vegetables. Those compounds conventionally become nitric oxide in your stomach. Um, and then there's pulse wave velocity, which is essentially a marker of how stiff the arteries are. So, the Oura ring can measure it. I have a device over here called the iHeart that can measure it. Um, so the arteries when the blood comes into them, it's kind of like an accordion. The blood expands them and then they snap back. And these tests can measure are the arteries really elastic or are they really stiff? Are they like a lead pipe? If your arteries are getting stiff, your arteries are aging faster than you are on the outside. 115 over 75. And is that across all age groups? That's the cut off where you start going above that the risk of disease starts to increase. But what about So I did my fellow, you know, you're from St. Louis. I did my fellowship in geriatrics and we kept the geriatric population closer to 130 over 90 maybe even higher for cerebral perfusion for someone listening or watching that's uh blood flow to the brain correct and those trials like the SHEP trials in the past that was what was thought is that you know let the older population run a little bit higher but more recent studies the SPRINT trial had shown that irrespective of age 120 rating is really the goal for treatment. Dang.

Um, speaking of treatment, what is nitric oxide? Nitric oxide is a gas. It has a very short life. You know, it's around for about a second, but it's a signaling molecule and a hormone. Um, from a vascular standpoint, it was so important for its discovery in the vascular system that it won the Nobel Prize for medicine in 1998 for the three um, researchers.

Who discovered that? Um, from a heart standpoint, nitric oxide helps with arterial dilation. So, it helps keep blood pressure normal. It acts somewhat like Teflon, preventing the cholesterol particles, the white blood cells from sticking to the artery in the first place.

And I'm sure the question is going to be how do you improve nitric oxide? Well, in part, it's exercise. As blood's flowing across your artery lining, that glycoalix, it stimulates underlying indothelium to release nitric oxide. The arteries dilate. You know, sunlight, particularly the wavelength of UVA, when that hits your skin, the nitrates are liberated from the surface of the skin, releasing nitric oxide.

And then dietary wise, it's mostly the green leafy vegetables: spinach, kale, arugula, and beets. As those nitrates come into your uh oral pathways, you know, you chew them; if you have the right oral microbiome—the oral microbiome—the nitrate-reducing bacteria break down the nitrates. Um, eventually, it becomes nitrates, and if you have stomach acid, it becomes nitric oxide.

So, those are the three big lifestyle things that can boost nitric oxide. And then there's various neutrauticals and pharmaceuticals that can also help.

And the way that someone would be able to tell if their nitric oxide is where it should be is test strips. Test strips are a starting point, but there is a caveat: if you have an oral infection, they'll be falsely positively high. So, you can't rely on just one data point. But if your test strips are low and white, sometimes it's the person; maybe they're carnivore and they don't eat any vegetables, so they're not putting any nitrates in. Maybe they're a vampire and they never go out in the sun. Maybe they don't exercise. Okay, you have all these redundant pathways, but if they all start breaking, you're probably going to start developing vascular disease. And that gets picked up by your arteries getting stiffer on these pulse wave velocity testing, or you can start seeing people's blood pressure start to rise. And it can start rising, you know, just very mildly at the beginning. But you know, if they go get tested, yeah, they may have low nitric oxide. Support them; those things can be reversed.

What is the most effective way? So if someone is coming in and their blood pressure is over, let's say it's 125 over 85 or something. So it's not grossly high. It's not emergent. And you give them a nitric oxide precursor. What kind of dose are we looking at? Because what I'm hearing you say is that one reason blood pressure—potentially one reason that blood pressure gets high—is that people are nitric oxide deficient. Is that a right, a correct word? How would we dose in behavior? Um, again, I understand that that's probably a very specific question, and some people, you know, are more sensitive to the diet and they might produce more. How do we go about dosing and course correcting blood pressure using nitric oxide?

So I would start first with, you know, a good lifestyle, you know, history, like, you know, are they exercising? Are they eating the green leafy vegetables? You know, what is their stress load? Stress isn't bad, you know, that's how we, you know, are resilient, but are you chronically stressed and not recovering from that stress? Do you sleep poorly? You know, are you not allowing your body to repair at night? So figure out, okay, is there some obvious lifestyle intervention you can utilize? If you've done all those things and don't see it, then that's where blood work can come in. You know, some people have high homocysteine. You know, it's an amino acid that when it's high, it affects some of these nitric oxide pathways. If you have high uric acid for numerous reasons—you know, you drink too much alcohol, you, you know, ingest too much fructose and have high uric acid—that uric acid can damage the glycoalix, affecting the nitric oxide pathway. So sometimes it's getting the root cause of what's causing the nitric oxide and removing that, and the nitric oxide gets back into uh homeostasis.

That is very helpful. Um, I suggest everyone get nitric oxide strips just because it's fun. Uh, you'll be very disappointed at your nitric oxide levels, most of us. Uh, I know that I was.

Tell me about—There's a lot of talk in the cardiology space about a few things. Number one, testosterone and cardiovascular disease and also GLP1s and cardiovascular disease. You choose what you would like to talk about first, but again, this is very relevant. And then finally, there was that study—um, that was the keto CTA trial. So cardiologist choice. Let's go for the low T. Okay. Oh, I love that. All right. Talk to me about that.

So something that when I was in training wasn't much discussed. Um, I trained at St. English university for my internal medicine, and we did have a, you know, world-famous geriatrician there, John Mley. Um, he's the one that actually came up with the ADAM questionnaire—the Androgen Deficiency in the Aging Male questionnaire—which is still often used for people to figure out like, are the symptoms due to low testosterone or not. Um, he was a big proponent of it for people who were sarcopenic, which was a term that I only learned because I still had geriatrics at Slooh. Um, but that was something that, you know, I just put in the back burner for a while. Did my cardiology training and then started taking care of people who were more on the high-performance end, and they're, you know, kind of super physiologic testosterone. Like, well, we know that that can be a problem, but what about people who are on the low side? Okay, what is the risk?

Well, if you don't have a lot of muscle mass, you're probably going to be more insulin resistant. You may have more inflammation. Um, so those are not good things, you know. So, you know, always look at, you know, is low testosterone, you know, something that first has an easy reversible cause, like the person sleeping four hours a night and abusing alcohol. Can you get them to stop those things? And testosterone is kind of a biomarker of like, are they doing the lifestyle things that could support a quote healthy testosterone level? But if they're doing all the right lifestyle things and their testosterone is 250 on a couple of occasions and they have horrible symptoms, then it's reasonable to replace those people. But in the past, it was thought that testosterone was going to be cardiotoxic and actually had a black box warning from that day for many years until the the recent TRAVERSE trial came out. Um, the TRAVERSE trial was done in men who were hypogonadism, middle-aged and above, and they were using topical gel preparation, which still is used but probably is not the most common way that most people replace testosterone. Uh, and it at least showed that people did not have more cardiac events when they're on testosterone. Didn't show benefit, but didn't show harm, which was a good thing.

But some of the caveats for the the TRAVERSE trial is that, you know, over 60% of the men who started testosterone stopped it before the trial was done. Either because they felt better and they just want to come off and see what happened, or the gel wasn't working well enough for them, and maybe they went to something else. Don't know. And the issue was that the doses that they put them on didn't really put them into really quote optimal levels. And there's might be a real range of where people say it's optimal, but you know, 500 to 1,000 is generally what I see kind of thrown around is that most people feel best around that. They barely got these people up to like 350, 400 on gel. So did they get, you know, benefit? No. But they didn't have harm at the doses that they replaced them to.

It's a really important point, and basically, the TRAVERSE trial uh really addressed the risk-benefit use of testosterone, and there has been this long-standing belief, like you said, that—and especially cardiologists—they at least before I met you—for the majority of the cardiologists that I have known, they were very anti-testosterone and anti-hormones, and that seems like that's a bit outdated. And it always again takes um evidence to kind of change people's minds over time. But what they found at the TRAVERSE trial is that there was no increased risk of heart disease with the utilization of testosterone. And I think that there is evidence that low testosterone is a risk for heart disease.

Absolutely. And they have higher calcium scores, they have higher risk of diabetes, you know, all-cause mortality. So it's one of those things, right? Is it a chicken-egg? Is the low testosterone causing those things, or is it just that the person has so many comorbidities that their testosterone is so low? So one thing I sometimes explain to patients is that think about your heart and brain being very energy-dense. You know, they're going to take the lion's share of energy. If the body is kind of starting to fail, it's going to take away energy from the sex hormone cascades and say like, we don't need to think about reproduction right now. We need to think about keeping your heart and brain alive. So your testosterone levels are going to be low for now.

Do you think—do you happen to know why they thought that testosterone utilization was contributing to heart disease? My understanding is that it was some poorly designed trials uh that had shown some potential increased risk. But when they actually went back and looked at the data, it probably was neutral at best. But because of those trials, the testosterone got a black box warning. And many cardiologists, you know, they're busy. You know, they're taking care of, you know, whatever their 40, 50, 60 patients a day. And if someone says it's a black box, they're like, "Don't use that stuff." And they move on. Um, but the more interesting thing is like, why is low testosterone a problem from a cardiovascular standpoint? Most likely, it's because when you have low testosterone, you don't have the ability to aromatize it into estrogen. And it's the estrogen for men that's probably more cardioprotective. When estrogen is in more optimal ranges, it helps support healthy nitric oxide levels that help support lipoproteins being more optimal. Um, you need the estrogen for brain function. You need it for libido and bone health. So, it's the estrogen that's probably the benefit in many of these guys.

That's fascinating. And is there a range where you like to see estrogen? We have a range. I don't know. Is there a range that at least 30? Yeah. So, we like 30 to 70, or is it 70? Um, it depends on the lab, but I would say at least 30. Um, I I think that that's a a good range. You know, there was a period of time when everyone was on an estrazol and uh so that is in a a somewhat of an estrogen blocker, decreases estrogen. Um, and people really felt terrible. So uh things are changing.

What about GLP1 and heart health? It's very interesting. Yeah. When the drugs came out, you know, they were first approved for diabetes. And at that point, you know, I was already, you know, full-fledged cardiologist, and so I wasn't—I had many patients who were diabetic, but they had endocrinologists or internists or family practice doctors who were managing it. And most of the time the cardiologists were kind of hands-off with their blood sugars at that point. Um, and so I didn't really pay much attention when they first hit the market. You know, I had a very wise attending, you know, when I was at Slooh who said like, don't be the first doctor to use a drug and don't be the last one. So, let's see how this plays out. So great data on people who are diabetic. But yeah, I got my current practice launched up in 2019, busy taking care of people who are more proactive, and I honestly probably on one hand can count how many diabetics I have in my practice. It's so few. So I see a lot of patients with insulin-resistant pre-diabetes, but those aren't necessarily the patients who are going to be on GLP1. So I didn't think much about it for a while. But I went to the American College of Cardiology conference back in 2024, and the SELECT trial had recently come out, and the SELECT trial was looking at GLP1s—uh, particularly semaglutide—in patients who were not diabetic. They were just overweight and, you know, be what it is, you know, a BMI, you know, above 27 or 30, and these patients, you know, had known vascular disease, coronary disease, had prior events but not recent events, and I believe it was like 17,000 plus patients were evaluated on the trial, and at the end of the—I believe it's 40 months—the people who were on treatment had about a 20% uh decrease in MACE—major adverse cardiovascular events—so it was the first trial in non-diabetics that showed people had less cardiac events, and so that was really a game-changer, and so the push is really to be more aggressive potentially with these medications in the right population. I don't think it needs to be in the, you know, the water or, you know, everybody being using this up, but it should be more liberally used in patients, particularly who have known coronary disease.

Known coronary disease—is there a range, and does someone not have coronary—is there a spectrum, I guess, is a better—is a better question? That's a great question, and that's one of the challenges that trying to apply, you know, clinical trials to the person who's sitting in front of you. You know, the classic terms are you primary prevention and secondary prevention. Most cardiologists are living in the secondary prevention world. So, the person's already had a heart attack. You're just trying to help them not have another one. And very clear evidence, you know, use your statins, your beta blockers, your GLP1s. You know, there's a lot of new tools out there that can help those people not have another event. The real question really is the primary prevention people, the people who've never had a heart attack, stroke, stents, or bypass. How aggressive should you be treating those people? And there's a window: is that if you don't look and you just plug people's numbers into a risk calculator, which can give some idea of, you know, risk, but I'm more the size of like, look at the arteries themselves. You know, it's—if you look at the arteries and this plaque, that person's high risk irrespective of what some little calculator says. Start treating that person more aggressively, particularly if they have a strong family history. You know, your grandma started having heart attacks in her 40s, maybe the family should be screened a little bit earlier and treat it more aggressively for their blood pressure or their lipids, and so treat the person who's in front of you to the best of your ability, but base it off, you know, data. You know, if that person has plaque in their arteries, they're at higher risk of having events down the road, and maybe they're not necessarily primary prevention anymore and they're not secondary. They're maybe like 1.5.

You know, there's a lot of backlash against statins. Could someone reverse heart disease with diet and exercise alone? Let's say that they have plaque and they have a greater than 400 calcium score. Could they do it with diet and exercise alone?

Depends on where their their lipoproteins are starting with. Um, and that's why I say it's one risk factor. You know, if you have a 90th percentile APOB, for example, you know, your APOB is 150. Is diet and, you know, exercise going to get you down to an APOB of 70? There's no way. It's just not going to happen.

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There's so much genetic control for you having those levels that high most of the time. I know we'll get into the ketoca trial in a second. So those people, you can do whatever lifestyle interventions, but most people—unless they're on kind of like extreme dietary kind of platforms, you know, they're keto or they're extremely um like high, you know, carb—making dietary changes doesn't have the biggest driver to affecting their lipoproteins. Yeah. Um, I was reading some data, and it's really—it's interesting because we make these dietary guideline recommendations, for example, cholesterol uh recommendations, which dietary cholesterol is taken out of the guidelines in 2015, but the saturated fat percentage—when you think about those dietary influences—it's really 20% of people that seem to be really affected by dietary fat. Um, and just nutrition, it seems as if there's a genetic predisposition. Remember Bob Harper? Yes. Uh, for those of you listening, for my Gen Zers, Bob Harper was uh the trainer on *The Biggest Loser*. He was super fit, very healthy, and he was running on a treadmill and he had a heart attack. And he again ate quote very healthy. And it was—he had genetic hypercholesterolemia. He actually had lipoprotein(a).

Oh, how high do we know? Don't know. Um, and lipoprotein(a), Mike Dr. Twimman can talk about that. Those are—it's a genetic marker. Again, there's a series of markers that we look for: Lp(a), apo B, yes, LDL cholesterol, which will then bring us into this keto trial. Are there other markers? Are those—would those be your top, and what are they?

So I usually kind of break it down into three big buckets. So I look at tests that affect your nitric oxide pathways: so uric acid, homocysteine, um, look at urine microbiome and creatinine—old-school test to look to see if you have kidney disease. But if you have protein in your urine, you're damaging the glycoalix to the kidneys. So if you're damaging that, potentially you're damaging the heart artery ones. Um, so that's kind of one bucket. There's a few others, you know, like the salivary nitric oxide strips and blood pressure. Second big bucket is the oxidative stress and inflammatory markers: so hsCRP, LPL2 activity, which is a marker of inflammation in the artery; myeloperoxidase, which is a marker of white blood cell activation, which is potentially going to be damaging your HDL and the top layers of the arteries; interleukin-6 is an inflammatory marker. And then there's a bunch of oxidative stress markers. So often start with GGT—gamma-glutamyl transferase. It's a test, simple. It's on a complete metabolic panel. But if the person has high GGT, they have low glutathione. If they have low glutathione, they have a lot of oxidative stress potentially. And then you can look at the oxidized LDL, oxidized phospholipids, apo. If you look at those things, those people are at higher risk. And then you get into the lipids. So I usually start like that. It's like, okay, we heard the nitric oxide, where's ocular choice, inflammation? Now we'll take a look at the lipids. So yes, I will always look at the traditional lipid panel. It's free. Included. So if the person's total cholesterol is over 300 and their LDL cholesterol is over 190, they potentially have familial hyperlipidemia, but the keto trial—we'll talk about the least responders in a second—but I will look at their HDL cholesterol, but it's not really that predictive for most people. You know, there's people with low HDL that have heart attacks or people with high HDL that have heart attacks, but sometimes it's an insight into their metabolic health. Um, and then their triglycerides, which generally I like to see less than 80. You know, if there's some genes, 80, that's—that's pretty low. That's pretty aggressive. Yeah. But if it's not below 80, then you guys are looking like, is this person likely insulin resistant or, you know, what is their kind of carbohydrate tolerance? Um, and then looking at the lipoproteins themselves. It's the lipoproteins that actually predict risk. The—or particles predict risk. Another way to say it, the cholesterol is just being transported in these lipoproteins. The lipoproteins can be measured directly. You can get an LDL particle number, but you can also look at apo B or apolipoprotein B. So the example I use for patients is that the lipoprotein is a tennis ball. The cholesterol goes inside. The triglycerides go inside. Vitamins like A, D, E, and K and different phospholipids, which are building blocks for cells, all go inside these little tennis balls. But on the outside of the tennis ball, that white stripe, that's essentially apo B. It's a structural protein. It holds that thing together.

A sphere and then acts like a little key to bind into different LBL receptors. There's NAPO B on the outside of every LDL particle. There's an APO B on that side of LPLA, VLDLDL, ILDL. So LPA is very similar to LDL. It has an apo B, but it has an extra protein, apo lipoprotein A on it, and it's like a little corkscrew protein, and that protein allows it to kind of dig into that glycoalix a little bit easier to damage it.

What number would you want to see LP little A and when would you get concerned? So it's generally better to measure this, and that this is the one challenge is that it's measured in animals or it's measured in milligrams, and you want to go for the milligrams per deciliter variant and generally want to see it less than 75. Everybody has LPLA, but there's a genetic control with it where up about 20% of the population has higher levels than that. And it's almost linear. The higher LPLA, the more vascular risk. And it can double your risk of having a heart attack or stroke compared to having normal levels.

Do you think there's any way to predict who's going to have a heart attack? Yes, but it's mostly based off plaque and vascular inflammation and low nitric oxide. You can just almost see the people who are going to be the train wrecks.

Oh gosh, you know, um, we are going to talk about the the keto trial. I have a couple questions prior to that. Alcohol and heart health. Can people drink alcohol and have healthy hearts? The short answer is yes. But the question is always going to be what dose? You know, alcohol is a poison. You know, I tell people I'm definitely not a tea totler. I have a very nice bourbon tea totler. Person who doesn't drink alcohol. Okay, I'm not, you know, I have a very nice bourbon collection. I have a very nice wine collection, but it's measured at this point. You know, I have to have a very good reason, good family, good friends. Got to be a good celebration. You I just had my 25th wedding anniversary. I enjoyed the wine pairings at dinner. It was great.

But congratulations.

Well, thank you.

But is it hard healthy? That's a little bit more debatable. You know, nobody who's not drinking should take up drinking for some perceived benefit for their vascular the reratrol of wine. Correct. They should not pick up drinking red wine just because they think it's gonna be good for their heart. That being said, is what is it doing to the person's sleep? That's probably the biggest concern is that alcohol for many people once they get over like one glass it's going to start impacting their quality of sleep. And while you're unconscious with alcohol on board, you're not getting that reparative sleep. And that's the challenge. You know, you're in a very low HRV the next day likely with alcohol on board the night before. You know, does it impair your decision to go train the next day? Like, you know, that's the things I'm concerned about when people have a routine alcohol habit.

How come alcohol then, you know, really heavy alcohol use, this is what we are taught in uh training, causes cardiomyopathy, a bigger heart, it's basically it's an alcohol cardiammyopathy, and I definitely saw a few cases of that in my career earlier um it I don't know what the exact dose is, but it's you know someone probably neighborhood to like you know a 12-pack of alcohol every single day for weeks on end makes your heart bigger. Well, the alcohol directly poisons the cardiammyioytes and then the heart becomes weak and doesn't pump well.

Oh gosh. What about caffeine and heart? I'm just asking for a friend that doesn't drink enough um energy drinks to kill a draft horse. But uh yeah, asking for a friend.

Yeah. I mean, everybody has a different tolerance to caffeine. Generally, if people stay under 400 milligrams a day, probably going to be pretty neutral from a vascular standpoint. So, a cup of coffee has about 100 milligrams for

Not my coffee.

Yeah.

Yeah. The super strong coffees. Um, but not everybody who drinks coffee or caffeine from any source nec has any heart issues. But those that have palpitations, they feel their heart fluttering, you know, they're measuring their blood pressure and they see their blood pressure going up or they have some of these fancy toys that look at arterial stiffness at a certain threshold, everybody's already started to have some kind of impact. Um, and then the other issue is sleep. You know, it blocks the denosine receptor. So, it affects how easily some people can fall asleep. So ballpark six out of 10 people are slower metabolizer of caffeine. So those people they need a bit more careful with that particularly on their timing. They should keep caffeine to earlier in the day so has a better chance to start washing out of their system before they're going to bed.

You know, I recognize that I didn't finish the question on statins. You know because I was so excited about alcohol and caffeine. The if an individual shows calcifications and again we share many patients together um in our medical practices if they are given a statin can you reverse that hard and soft plaque? It generally will not reverse the hard plaque, though I have seen some calcium scores go down on statins. Typically you actually see the calcium score going up on statins, and the thought is that it's taking the soft plaque which is more prone to rupturing and causing it to become more firm. And so the calcium scores will go up. If you do a calcium score test and then don't make any changes, the calcium score test will generally go up about 20% a year.

If you make

That's really high.

Yeah. 20% a year. So, no wonder everyone's dying of her. So, that's why you got to look for it as early as possible and start intervening.

Yeah. Yeah. Like I said, I saw a third six-year-old with a calcium score nearly 1400.

A six-year-old?

36y old. 36y old. Yeah. And so that person, it didn't happen in from 35 to 36. It been happening since about his 20s. So the sooner you can find it, the sooner you can start intervening. But if you do an intervention and you see a calcium score stay about, you know, no more than 5% increasing, you probably got ahead of the game and you've stalled that plaque buildup. And there's a chance that the salt plaque will shrink. But you're not going to see that on a calcium score dash. You'd have to do the CT androgram to see that part.

How do people then, you know, when we talk about regression, what are we talking about? Generally, you're talking about the the lipid ridge cores of the plaque shrinking down. So, you can think of the plaque as almost like a pimple and it has a thick cap over it hopefully. The ones that have thinner caps over it, they're more prone to kind of opening up. All that damaged cholesterol, white blood cells, the smooth muscles, all that stuff spills out into the blood and now the blood clots and you go from having a 50% blockage to immediate 100% blockage is the platelets are sticking in that area and that's what essentially most heart attacks are. Um, the statin is helping that lipid rich core shrink and also putting a thicker cap over that plaque so it seals it off.

Does heart disease cause erectile dysfunction? Absolutely can. So the analogy is ED equals ED. So erectile dysfunction equals endthelial dysfunction and vice versa. So if guys are starting to have issues with erections, often times it's a vascular cause. They're not getting enough blood flow into the sexual organs to allow an erection to happen and it's due to low nitric oxide.

When you see patients, how early does this seem to start? Uh, ED can happen under 40, but it tends to happen more when people over 50, 60 years old. And do you treat with phasodilators or do you use agents like Seialis as a cardiologist? I do on occasion. Um it's kind of the canary in the coal mine question is that if guys are having ED and they're asking for you know the low blue pill or you know sedenaphil or tedalapil. It's not that it's a problem that they need to use those things, but it's a marker that they don't have good nitric oxide to begin with. And that's some of the myth is that these are not nitric oxide promoting medications. They just keep nitric oxide around longer. You have to get the nitric oxide I call like into the funnel. You have to be eating the greens. You got to be exercising. You got to be in the sun. You got to be taking the nitric oxide promoters into the system and then the tadalaphils and the Viagra, they just keep the nitric oxide around longer so that it has more effect on the vascular system.

That's fascinating. I didn't I didn't actually know that and in my mind that seems like there could be a great combination of you know we use seialis in our practice and tadalapil if you use that in conjunction with a I don't know beetroot juice or something like that seems that seems like that would be very helpful and just a real nerd note arginine increases nitric oxide. That is True. And I'll hit that one in a second, but that is a good point is that, you know, those medications, they work, but I'm sure you've seen some non-responders. You know, you keep ramping it up and they said, "This stuff doesn't work." Or by the time you get to the highest doses, they're having headaches or back pain, like I can't take this stuff. Well, maybe if you got the nitric oxide boosted up, you could use a lower dose and they get the effect. But the the question about arginine is that the greatest majority of people are not deficient in arginine. So what happens with arginine which is an amino acid in the presence of oxygen you need this enzyme called enos endthelial nitric oxide synthes. The enos enzyme converts the arginine into citrine and nitric oxide. So you can shove all the arginine you want into the system but if the enos enzyme doesn't work you're not getting nitric oxide on the backside. And a lot of supplements that's all they are is arginine. So if it doesn't work for the person it's kind of a de facto that enos enzyme isn't working. And after the age of 40, that enzyme is significantly reduced in its capacity to kind of crank arginine into citrine. So that's why you have to kind of back up with the oral pathway or sunlight or doing something else to support people. That's why vascular disease gets more prevalent as people's age because that enos enzyme becomes less and less functional.

How do you know that? Lots of training and learning. And Dr. Nathan Bryan taught me that many years ago. And would someone supplement with the enzyme? You don't not the enzyme directly. You would supplement with things that could support the enos enzyme recoupling turning back on or some of the product technologies when they are lozenes they dissolve. They release nitric oxide gas and that just gives it nitric oxide directly without having to have that arginine pathway working.

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That's really fascinating.

I Can you do me a favor?

Sure.

I hear a lot about nascin and HDL. Someone very close to me came home uh and I found a bottle of nascin ordered off of Amazon. I'm not gonna say who ordered it.

Shane, my husband.

And I said, "Honey, why are you taking that?" And he said to me, "Well, um, the flushing and it improves my HDL." Both are correct. The flushing definitely is going to happen. Um, that means it's actually working for those people. So, for the people who are going to take nasin under the direction of their doctor, if you have the no flush nascin, it is not going to give you any type of cardiovascular benefit. You have to get the flushing because that means that the prostaglandins are being released. But the theory that using some type of supplement or medication to raise your HDL is going to have a positive cardiovascular benefit has not been proven. Um, you know, all the old CEP trials show that when they use drugs to raise HDL, the people who got those drugs, they died faster than the placebo group. So, we should throw out that nasin. Not necessarily. It's just that maybe it's neutral, but what dose are you going to use? I mean, most people aren't going to tolerate going up to like 2,000 milligrams of niacin where, you know, most people need to if they're going to have that significant effect on their lipids. So, I use it on occasion. It still does work for some people who are statin intolerant or just prefer not to be on a stand for any reason. But, it's sometimes a harder drug or supplement to use because to get to the doses that work. Most people have significant enough flushing that they're like, I can't tolerate this stuff. But to be clear, does nascin affect health outcomes with HDL? I mean, I I when I was looking at the data, I wasn't convinced. I I felt like it might change HDL, but it's doesn't seem to affect any significant health outcomes. That's the best way to probably explain is that like the HDL numbers will go up, but is that mean that the person has less heart attacks, stances, strokes, the things patients care about? Probably not. And I don't think any of the trials today have actually shown that nin does that.

Do you think that there's anything that people are really missing that seems to be really toxic for heart health? Poor sleep.

Don't say that. I have two little kids. I slept two and a half hours last night.

But season of life.

Season of life. Well, yeah, except my daughter is going on six. Um, and my husband's in residency, right? I mean, you remember residency like the worst time of your life for sleep. I mean, you don't sleep in your own bed, you know, except for every like third night. And when you're working, you're working working 36 hour shifts without sleep. You do it because you have to do it. But in hindsight, you're like, that's like the worst thing you possibly ever could do from, you know, a health standpoint long term. And so, you do it when you're young, but once you realize that like, hey, this is going to kill me if I kept trying to do this, you have to do something different.

Okay. Aside from sleep.

Yes. Besides, would it be for example, people are really into CBD gummies or CBD? Um, there's just a whole host of things that there's always these evolving or, you know, the biocharger that's up in um our bedroom. Thanks, Kim. Uh, are there any items whether supplement, substance, drug, and or activity that someone would not necessarily think about being very damaging. I mean, the the CBD1 is interesting. I don't proclaim to be an expert. I have some patients that have utilized it. And I say that the biggest challenge is that like it's not regulated in a way where there's a standardized dose that you know, okay, like this dose from this dispensary is comparable to this dose from this dispensary. I'm least relatively neutral for CBD from an anti-inflammatory standpoint or if it can help the person sleep. But where the challenge comes in, but more is when there's more THC in the product. Now, in certain instances, it's beneficial. You have epilepsy. I'm not talking about that. Or if you have cancer, it's just like the general kind of use case for it. There's definitely some increased risk of increasing your triglycerides with it. There's increased risk of atroofibrillation, which is a heart rhythm issue that potentially increases the risk of stroke. So, something you probably don't want to play around with unless you have a strong medical reason to be on it.

THC. I see. Um, let's talk about the epic lipid inflammation and controversy of the keto CTA trial. So, I am going to let you kick this off because I am certain that you've gotten a ton of questions.

Yes. And I've seen many of these lean mass hyperresponders over the years. And what is that? It's a phenotype where the person is lean. I believe that the BMI has to be less than 25. Um, they have no evidence of insulin resistance or pre-diabetes. And then on their labs they have this panel where you know before they went on to a low carbohydrate diet the LDL cholesterol had to be less than 160 milligrams desellier. And they didn't have to have any genetic abnormalities with their lipids. They start a ketogenic diet their LDL cholesterol goes north of you know generally 190. I've seen them as high as 500 in my practice.

LDLC of 500.

Um, but we're not before. Just to not before to understand this for the listener or the viewer, a lean mass hyperresponder is someone who changes their diet, goes to a lower carbohydrate diet, and is it a higher fat diet or just low carb? It's low carb, but generally it's higher fat.

High fat.

And instead of um improvements technically, they shoot their their cholesterol changes drastically.

Correct. Their lipids look like they have familial hyper lipidmia and you know their other parts of their traditional lipid panel their triglycerides are low their HDL high and you know they will often say like well I'm you know metabolically healthy so this cholesterol doesn't matter.

Maybe maybe not, and this is what they're trying to look at in this observational trial um I applaud him for at least looking at the arteries because in the past it used to be that like well I don't have diabetes resistance so I'm pretty protected from vascular disease and it's like I believe yes that you know there are other things that drive plaque in arteries other than just LDL cholesterol. But that is one variable that is like blinking red like the check engine lights on. You got to go looking like is it causing damage to the arteries? Because I used to get a lot of patients who would have this kind of phenotype. They go get just a calcium score and might say my calcium score is zero so I don't have to worry about this. You don't have to worry about it right now. It may be in a year, but if you left your labs like this for the next 10 years unknown. You're likely to have more plaque in your arteries. You know, it's based off of mandelian randomization trials in the past that say that if your LDL cholesterol is here, you're more likely to have plaque. Doesn't mean it that you're guaranteed, but you know, it's risk. So, it's like you drive your car, you don't expect to crash your car, but you wear a seat belt. This is sort of like if your LDL cholesterol is 500 and it's causing plaque in your arteries, maybe you want to do something about that LDL cholesterol. So, at least in this keto trial, they're actually looking at the arteries with more invasive or say non-invasive technology. They're using a CT andogiogram and then they're using the Clearly AI overlay on top of it. So Clearly is a company that uses AI software to analyze the the images and can quantify the type of plaque that's in the arteries. So I believe there's like 100 patients were in the trial. It's an observational trial. I think it was um you know volunteers from kind of like a social media outreach. So it's a highly selected population of people who are you know motivated to see what's going on with their vascular system. And the interesting is that these people had been on this type of diet for a couple years and they've had these high lipids for many years and were untreated. So either they've gone to a doctor and the doctor said like, "Hey, I recommend you stop this diet and start meds." Or they just said like, "I'm not going to go to a doctor because the doctors can yell at me because my numbers are so high." So they get a CTO at baseline. They stay on the keto diet. They confirm it by using the Keto Mojo strips and such. Um, and confirm that, you know, they stayed on that diet for the full year. And then they repeated a CT angio at the end of the year. And

The primary outcome in the initial UM study was supposed to be how much change in non-calcified plaque was present. So, non-calcified plaque is soft plaque. Plaque that's more potentially vulnerable to rupture and causing heart attacks. It's not the hard calcified plaque that's usually kind of a scar in the artery. So that was their initial primary outcome.

But in the actual uh paper, they really kind of gloss over that and they focus more on that like, well, these people had high APOB and they didn't seem to have more plaque because APOB. But when you actually look at the actual um graphs, the non-calcified plaque increased in almost every person in the study, and it increased like 18 millimeters um cubed of plaque in that time frame, which would be more than what a kind of general healthy population would.

So it's still kind of early. Let's say it's observational. It's kind of, you know, uh, hypothesis generating. Doesn't prove that this diet is healthy. It doesn't prove that this diet is going to cause you to have a heart attack next year. But it does mean that you have to look a little bit deeper.

So that's why I always kind of go back to what we talked about earlier. It's like it's the root cause, like what's going on with the glycocalyx and the endothelium. If that layer is healthy, maybe you can get away with having these LDL cholesterols of 500 for years. But the second you see that the glycocalyx is damaged and the dysfunction's happening and your arteries are stiff and your nitric oxide's low, that person's the time bomb ready to go off in a few years. And you don't want to reduce the risk of a heart attack in one year. You want to reduce the heart attack risk for the next 30, 40 years.

You know, you had said something earlier that there's a 20% increase in plaque year-over-year, the calcium score, the calcium score. Um, was that the same as those in this uh keto CTA trial? It's kind of apples and oranges because mostly people did not have calcified plaque at the beginning because they're too they're young and and relatively quote healthy.

You know, again, you and I have been friends for quite some time. I want to talk about muscle. Excellent. I want to talk muscle and heart health. I believe that skeletal muscle is the most important muscle, and you believe cardiac muscle is the most important muscle. We will probably have to come to some understanding. Yes. And I am very curious as to the muscle heart connection from your perspective.

Let's just say that they're synergistic. I don't think one is better than the other. You need both. Um, and that's something that, you know, I obviously other than my geriatric training, I didn't learn about a lot in my cardiovascular training. The only people that would talk about it would be the heart failure doctors because those patients, you know, who were ending up on heart transplant lists, they usually were sarcopenic. They're cachexic because their heart is failing. Their body is demanding all the energy resources being sent to this weakening heart. Their skeletal muscles are getting eaten up by all the inflammatory compounds that are coming from a failing heart. Um, so those are the guys that really worried about muscle health.

Do you think it's important to measure V02 max and grip strength? I think both are important. You know, grip strength is very easy. I check it almost every single patient that comes to my office. Do you check your own? I do. I'm pretty Shane's like, "Oh, so Shane's my husband if you're a first-time listener." And he is a third-year urology resident, which is pretty funny. Um, his I won't say the joke, but anyway, he's always checking his grip strength. Where is he at now? Uh, I don't know. Probably superhuman. Okay. I mean, he's way more muscular than me, but um I'm pretty happy. Like, I'm 130 lbs on the right side, 120s on the left side, so I'm top 1% for my age. Okay. Looking great for 25, friend. Looking great for 25.

Do you routinely, you know, in our clinic, uh, we don't, even though our clinic is, uh, largely remote except for my private patients, we don't measure V02 max. We just a lot of patients, they don't want to. Um, they can, but, you know, we we have people that will measure it for us. I am curious from a cardiovascular muscle connection standpoint, do you think it's necessary to measure V02 max? Necessary, probably not; beneficial, yes, if you're willing to do it. I've done at least two on myself. Um, yeah, and they're not fun. I mean, you know, you go to you absolutely feel like you're about to die. And then like, okay, you can stop now. Um, and then, you know, at that point, yeah, when I did it, they're like, you're average for age. I'm like, great. I'm not trying to be an Olympian. Like, I I want to live well. I don't want to be at peak, you know, aerobic capacity all my life. Like, I don't have that much time to train to be an Olympic athlete. Um, I don't know. You could probably do it. I could probably do it if I wanted to. I'll tell you a funny story about when I did a stress test when I was in the fellowship in a minute. But the V02 max, it's a good metric of, you know, your aerobic capacity. You know, how well can your mitochondria engines actually work for you? So, you know, it's very similar to, you know, doing a regular stress test on a treadmill, but you have a mask on that's capturing your expired gases. And they can figure out like, well, where is your capacity to continually utilize that oxygen? And then where do you hit that threshold? Ballpark, you know, you know, 20 to 40 is kind of like where most people are going to fall. If you're above 40, you're doing something right. If you're under 15, and the cut off was 14 when I was uh still doing kind of like hospital work. If your V02 max is under 14 and you had a bad heart, that was kind of a cut off saying like, "Yeah, we should list you to get you a heart transplant."

Oh, and you don't routinely, just to to kind of close this out, you don't routinely measure V02 max. If patients are very interested, I will send it for it. You know, I have the uh the Frontier X2 chest strap, which is probably the most sensitive heart strap you can use for exercising. It can measure uh a EKG while you're exercising, and they claim to be able to kind of relatively accurately measure estimated V02 max off of that. So, I think it's good enough for most people, but if you're really hardcore, got to go do the real thing.

Why don't you think more cardiologists focus on skeletal muscle health because they're focusing on cardiac muscle? Yeah. The the analogy is time is muscle in the cath lab. You know, when your arteries aren't, you know, open, they're rushing to open those arteries up because the muscle cells in the heart are dying until they get the restored blood flow. So at least they use analogy time is muscle, but they're thinking about cardiac muscle.

If you you know, you've covered a lot on how to protect your heart and really if we were to sum this up, it was lifestyle, be active, sleep well. I'm going to fight you on that one. Listen, a lot of parents don't have an option. Get outside. Wear um blue-black glasses. Maybe eat a diet that augments nitric oxide. Keep your blood pressure low. Keep your stress under control. Don't drink alcohol. Uh, caffeine. Okay. Drink alcohol in moderation. Yeah. Um, figure out if you are a high or low metabolizer of caffeine. And if you are high, 400 or more is just fine. Just kidding. Check with your doctor. Did I miss anything? No, that's an excellent review. And it's the the basis of, you know, test don't guess. Like everybody's has their own individual, you know, story, their individual genetics, and then they go out in the world and do the things they need to do. But some people are at higher risk of ASCVD than others. If you do the right testing, you figure out who those people are and which levers you can pull back on to reduce that risk.

If you could pick three tests, you covered the blood tests. The blood tests that we talked about were Lp(a), apo B, LDL cholesterol, hsCRP. Yes. And then also you talked about myeloperoxidase. I will say that in our clinic almost every woman seems to have higher levels of myeloperoxidase. Is there a reason? It's associated with autoimmune conditions, and women are at higher risk for autoimmune conditions. Um, highly myeloperoxidase can be a marker of HDL dysfunction. So just having high HDL doesn't mean that it's necessarily doing anything beneficial to your vascular system. You know, one of the roles of HDL is to go into the arteries, pull out the cholesterol, and take it back to recycle it. But if you have high myeloperoxidase, it keeps damaging the HDL, and the liver has to keep replacing it. So your HDL numbers are going up in your blood, but they're not actually working. But if you have high myeloperoxidase, you got to look and see. Do they have some type of autoimmune condition or some other chronic infection that's driving that? And if they don't, how do you fix that? Pomegranate potentially helps. Okay. You know, um I wonder if it's pomegranate or I wonder if it's urolithin. It's probably that. So for those of you listening, we work a lot with Timeline, and MitoPure is this clinically tested urolithin. Are you taking it? Not yet. Okay. Well, I have some. I'll give you some. But I I think it's probably maybe it's not the pomegranate, but it is the I don't know. I mean, we should probably combination. Yeah, look into that.

The other tests and you know, I'm curious as to what home tests are accurate for looking at heart health. It's a great thing to to kind of look into that because the contents of your blood, it's easy to obtain for most people, but it doesn't tell the whole story. It doesn't tell you what's going on in the arteries. And so, you know, yes, I have a whole fancy, you know, lab of equipment in my office at Apollo Cardiology, which you've been to a few times, and we put you through the battery of testing. I'm due, by the way, aren't I? Or in another year, whenever you want to come, I'm happy to have you back, you know, but in the office, you know, the the biggest test that we probably do is the EndoPAT test, which we didn't talk about here today. And that's probably the gold standard way to really test what is your nitric oxide um availability and, you know, ability for the arteries to dilate.

So, for those that haven't heard of the test, which most people haven't, um, the EndoPAT test is a non-invasive test. Takes about 15 minutes. You're laying down comfortably. Your fingers have probes on them and they're measuring the flow in your fingers. They do a five-minute warm-up, and there's a five-minute period where we have a blood pressure cuff on your arm. Pump it up higher than your systolic blood pressure, and the flow cuts off. Your hand goes numb. Generally, not dangerous. And after 5 minutes, you open up the stopcock. The blood rushes back down into the arm. This simulates exercise. Is as the blood rushes back down into the arm. It stimulates the glycocalyx. The glycocalyx says, "Oh, here comes a bunch of blood. The underlying endothelium releases nitric oxide. The smooth muscle in the artery opens up." And the blood rushes back down to your hand. Your hand wakes up. And then the test can measure, well, how much do the arteries dilate with that response? And your arteries should at least double in size, but optimally triple or quadruple in size. If it's less than 1.68, 68. So your arteries only dilating 68%. You have what's known as endothelial dysfunction. The arteries can't release nitric oxide on demand. It's kind of like the force field is down. You're more prone that whatever is floating through your blood, the cholesterol particles, the white blood cells, they're more likely to stick to the artery, and you're going to develop plaque in your arteries unless you do something about it. So it's the stress test for the arteries that we do in the office. Now, you can't do that at home yet, but there are tests that you can do that can give you an idea. Is this a problem? And so we talked about it and we got some of the Oh, here comes the toys. other toys that All right. So, for those of you who are listening, not watching, I'll describe them. So, let me let me try though. So, I just drank um stuff. You're not supposed to drink anything. You're supposed to wait at least, you know, 15-20 minutes, but center of the earth is kind of cool. All right. You talk about this. I'm going to She's going to play around with the I'm going to play around with it. It's okay. This is not going to be accurate because I just have been drinking. So, they look like little lipus paper strips. There's a little pad on it that you put saliva. You then bend the tab over. There's a little developer pad on the other side. And if you have nitrites in your salivary pathway, the thing will light up red. If it does, that means you're generally getting a lot of nitrates into your diet and you potentially have good bacteria in your mouth. You have the nitrate-reducing bacteria in your mouth to be able to break that stuff down. That ultimately becomes nitrites and nitric oxide. Not everybody has high nitrates in their diet because they're not eating green leafy vegetables or they have dysbiosis of the oral microbiome because they're using mouthwash. They're using things with fluoride, and her numbers are really not red. So, she's getting good nitric oxide through that pathway. So, that's step one. I talked about pulse wave velocity. So, I'm wearing an Oura ring. The reason I got the Gen 3 was because they did add a feature last year, the cardio age, which is measuring pulse wave velocity. So, as the blood rushes past the ring sensors, it's looking at how fast the arteries expand and contract. And you can look at the waveforms and determine how stiff the arteries are. So, you want your cardio age to be close to your biological age. Mine is aligned, which is normal. And this is a pulse ox. It's not a This is basically a pulse ox. Let's see. Turn that sucker on. So, this one's called the iHeart. So, this is a little black box that looks like a pulse ox that I have in my emergency travel kit. Correct. So, it's going to give you your heart rate and oxygen sats, but I'm not going to pull out my phone right now. But, if you had the app running, you do like a 2 and a half minute uh run for it and it will measure the arterial stiffness and we'll give you a vascular age reading, which can change throughout the day. But generally, when I do this, it's usually at my biological age or much younger. If it's higher than biological age, don't freak out. Like, look at your life. won't do anything. You can feel free to do that. Yeah. Figure out why it might be high. It's like, oh, you know, slept 2 hours last night. I, you know, just did a bunch of nicotine before I jumped on this podcast or something. Whatever. That's probably going to happen.

How bad is nicotine? We have a lot of people that Let me Let me see. Wait, let me see a toy. So, we have a a lot of friends um and people that we know, Matt, the producer, who uses a lot of nicotine. What does that do? It's a vasoconstrictor. Um and so similar to caffeine, you know, it can cause people to have higher blood pressure, can cause palpitations. Um and so it's once again like test don't guess like a certain amount of nicotine maybe it doesn't affect your blood pressure cause you to have you know issues with palpitations but you know if you're going at a person level a level where it is got to dial it back you know and I understand you know it's a nootropic for some people you know that is a cognitive booster but you know but can also be a vasoconstrictor. So uh so for people have coronary disease sometimes it may contribute to them having chest pain with activities. So everyone is throwing their uh zins out the window. Matt he is six six six milligrams. I tried to just try it. I almost threw up like immediately. Yeah. And if you're not sens if you're not sensitive to or I should say if you're sensitive to it like you know less than a milligram would make most people pretty nauseous. It was a terrible idea. Uh, and of course I tried it again. Yeah. What else you have in there? Next toy. So, this is a a new one that I'm pretty interested in. This is the Connect QT Pulse. It's a little box uh that, you know, measures blood pressure. So, it has a brachial blood pressure cuff. So, you'll get your traditional number. You know, it's going to say whatever, you know, 120 over 80, which is a good starting point, but that's the blood pressure just going down to your hand. The thing that this box does that no other one to the market yet does is it measures central blood pressure. So when I was still an invasive cardiologist, we would feed a catheter into your radial artery or femoral artery and put a pigtail catheter in your aorta and we can measure blood pressure in your aorta and then measure the blood pressure in your left ventricle. Why would someone want that? Well, when you're doing a procedure, it's a good idea to know kind of like how well their heart is working. You know, how hard is the pressure coming out of their heart? Because the higher the pressure in the aorta, the higher the pressure in the coronary arteries and the more likely that high shear stress could damage the coronary arteries. So, nobody wants me putting catheters in them just to measure that pressure. But this device can assess what that pressure would be. So, the cuff is on your arm and after it takes the regular measurement, you'll feel it kind of pulsating a little bit. It's basically assessing how stiff the arteries are because, for example, if your heart's beating 60 beats a minute, the left ventricle pumps, the blood comes out of the heart, goes down to your legs, and it's going to hit those arteries in your legs, the uh the iliac arteries, and it's going to be a reflection wave. So, it's kind of like splashing water at a wall, the water comes back. You can measure how fast that blood is coming back and that estimates what is the blood pressure as it's coming out of your heart because that central blood pressure is what the blood pressure that your brain when you talk about the patients you're geriatric and you know you don't want to infect their central perfusion it's that central pressure that you want to focus on that's the pressure that the coronary arteries the heart arteries and then also your kidney arteries that's what they sense so if your central blood pressure is normal less than 120 or 80 but the arm is 150 leave them alone their perfusion in the brain is Perfect. Don't mess with them. So, you want to treat their central blood pressure. You don't want to treat just brachial.

If we were to kind of pause and think about that blood pressure medication, beta blockers, what else? What is first line that you're using? Generally, ACE inhibitors, and angiotensin receptor blockers, or calcium channel blockers are first line. Beta blockers. Interesting. Yeah. Particularly the older ones, they lower brachial blood pressure, but they have no effect on that central blood pressure. So you're not really getting the benefits, but the ACE inhibitors, the angiotensin receptor blockers, calcium channel blockers, they lower both brachial and central. And what are the main side effects of those drugs? It depends which class, but ACE inhibitors generally it's cough. Angiotensin receptor blockers, not a lot. Um, sometimes, you know, if you get your blood pressure too low, they can just get back up in the dose. Calcium channel blockers generally peripheral swelling in their feet. Um, sometimes cause some constipation at higher doses. Um, and the beta blocker is classically pretty hard to use particularly in younger people, particularly people who are very active. You know, they're going to block catecholamines, so they're blocking adrenaline being secreted. So, it can be useful for people who have a lot of palpitations or, you know, performance anxiety. But for blood pressure, they really weren't that potent. And then the person's probably going to have exercise intolerance. Their extremities might be cold. They might have sexual dysfunction in guys. So, hard to use. But the newer class of beta blockers like Nebivolol, trade named Bystolic, it does have an effect on blood pressure because it affects the nitric oxide pathways. So it's pretty much the only blood pressure medicine in the beta blocker class that I'll use if we're going to be using it. But it's going to be probably third or fourth line after they've exhausted the angiotensin blockers and calcium channel blockers. The reason I asked you that question is if someone is

Just getting a brachial artery blood pressure, which is what would be standard, and one an individual is treated off of that, is it true that they might not need it because it's not actually measuring the central blood pressure?

Correct. And that's sometimes the case, is where the person says like, "I'm taking the medicines, you know, I'm getting really lightheaded and dizzy at home. I don't feel good." And you check their blood pressure in their arm in the office and they're like 125. You're like, "Well, your pressure is a little bit high." Their central pressure is probably like 100 over 60, and their brain is like, "Hey, I need a little bit higher profusion pressure." So, maybe need to back off. Let the breaker run a little bit higher.

So, that's why this device is going to probably be a, you know, a game changer for many people who are at high risk or just very interested in their vascular health because this is kind of like the check engine light going on. When your central pressure starts to rise, you have a problem. This device also can measure things that will look at the stiffness of the arteries as well. And you know, this is a good kind of add-on to somebody who has a calcium score of zero. Great, you have a calcium score of zero. But a calcium score of zero, it means that you haven't developed hard plaque in arteries yet. But this is going to tell you like if your arteries are getting stiff and your central pressures are high, you're more at risk for that. So for those people in that keto trial, this might be an interesting device for them to have.

If you're—because I know that going into the trial, they had to have normal blood pressures, which if you see a cardiologist in the real world, everybody has kind of the triumphirate. You know, they got high blood pressure, they got diabetes or pre-diabetes, and they got high lipid issues. Nobody just has just lipid issues in a real cardiology practice. But if you have stiff arteries with this type of device, maybe you want to start backing off on that kind of keto diet because maybe you're making a ton of oxidized LDL that's affecting your arteries.

That's really fascinating. And that's called the connect connect QT.

Well, we—Hey guys, we are all trying that immediately.

Yeah. What? I was going to say we'll link it.

Oh, okay. We'll put links for all these devices.

Yeah. Okay. Um, uh, Julia said we'll put links to all these devices.

Just to close out, are there a handful of supplements that are evidence-based, not anecdotal, but that have randomized control trials and evidence in humans that you think are valuable for heart health?

The short answer is yes. But it's not a blanket statement where like everybody should take all of these things. You know, you have to look for deficiencies and you got to look for tolerances of certain ones. But start again with, you know, the glycoalix and the endothelium. If you can't make nitric oxide, there are products out there that can help with that. There's products that can support the glycoallex. If the glycoalix is getting damaged, there's supplements that can help regenerate the glycoalix. Then there's that be like a beetroot juice and Neo. You sent me like a Neo40 is a little tab.

Yeah, the little tabs.

Yeah, Neo40. That was initially uh the product that Dr. Nathan Bryan developed. He now has a um a competitor that is in his own company called M101, which I often utilize. There's another product called Baskinox from a company to Calroy. Full disclosure, I speak for them sometimes, but that's it. Throw them off the podcast. Doesn't it doesn't affect my ability to like talk about because I often I'm taking that product myself because I've looked at their research and it works well for me and I do this testing. My numbers look good. So, I'm a pretty good biohacker. I try almost everything on myself first and make sure it works and then I talk about with my patients.

Um, and then, you know, there's things, you know, like CoQ10. CoQ10, you know, may help with people who have like muscle symptoms when they're on statins. You know, omega-3s. I prefer people eat their seafood than supplement. But if they're gonna supplement, you know, generally two grams a day on fish oil. But it's also really hard to get enough omega-3s. It's generally very hard. Um, the um CoQ10 is there a dose and is there a form? So generally you want to just target blood levels over three. You know, you can either do ubiquinol or ubiquinone. You know, the the nubicquinol should be absorbed a little bit better, but it's more expensive. So I just tell people like, okay, you know, pick a good brand that your doctor you know works with but check blood levels and then whatever dose it takes. So ballpark, you know, if you are deficient you're going to probably need between 100 and 300 milligrams a day. If you're on a statin or beta blocker add 100 milligrams per drug that you're on that depletes uh CoQ10. Magnesium—for three to four different rations of the body. So anybody has blood pressure issues, palpitations, coronary disease, sleep issues or 75% of Americans who are deficient in consider and you know what forms basically not oxide because oxide isn't absorbed from the gut if you're constipated take oxide you but if you're not but if you have a big event do not take magnesium oxide or if you are going on a plane or any kind of long trip, correct, because it will work not ideal.

Yes, those probably are the big ones that I would say.

Well, thank you so much, Dr. Michael Twimman. You are just an wonderful human, a wonderful doctor. I am so grateful that you are willing to take care of me and our patients, and just you do such a fantastic job. Thank you so much for coming on.

Thank you.

By listening to this episode, you're already doing what most people never do, thinking about prevention before the problem starts. Most heart attacks are preventable, but only if we look deeper than LDL, only if we challenge outdated norms, and only if we value data diagnostics. If this episode shifted your mindset, send it to someone you care about because heart disease doesn't wait and neither should we. If you haven't already subscribed to the show, thanks for being here. See you next time. [Music]

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Preventing Silent Heart Attacks: The Tests & Tools Your Doctor Isn’t Using | Dr. Michael Twyman

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