133. Dr. Abid Husain: The Hidden Drivers of Heart Disease

Welcome to Extend with me, Dr. Darshan Shah, a podcast dedicated to cutting-edge science, research, tools, and protocols designed to help you extend your health span. Having become one of the youngest doctors in the country at the age of 21 and trained in board certified to the Mayo Clinic, I've accumulated three decades of practice as a board certified surgeon and longevity expert. Over that time, I've discovered that a mere 20% of health knowledge yields 80% of the results when it comes to your health span. We are living in a new era where we are creating a new healthcare system, no longer focused on disease management but achieving optimal health and vitality. Join me as an interview world-renowned experts offering you a step-by-step guide to proactively avoid disease and most importantly, extend your health span. Today on Extend, we're going to be talking about the number one killer in the world, heart disease, and the way we approach cardiovascular health and how it needs a shift in mind set. Our guest today is Dr. Hussein. He's one of the foremost leading voices redefining Martin cardiology today. After years working inside the traditional system, he recognized the biggest flaw of cardiology. We're only treating heart attacks after they happen, not preventing or reversing the diseases that lead to them. Now, as a triple board certified cardiologist trained in functional medicine, hormone therapy, peptides, and regenerative care, he blends the full spectrum of medicine to deliver truly individualized cardiovascular and longevity treatments. In this episode, Dr. Hussein explains why most heart issues start in the micro-vascular chair long before plaques or blockages show up on scans. On nitric oxide, hormones, and lifestyle repair, vascular health, and why mental stress contributes up to 30% of heart disease. He also breaks down what's called the glycocalix. This is the body's protective endothelial shield, and why protecting it is a game changer for preventing heart attacks. If you care about living longer and keeping your heart strong, this conversation is essential. Dr. Hussein, this is a pleasure for me too. Thank you. I met you at a conference for longevity doctors, and I was incredibly, I don't see surprise, but I was just incredibly just in disbelief that there was a cardiologist there at this conference. Because as you and I was talking earlier, I feel like I have family members and friends and other cardiologists in my circle all the time. I'm always referring to cardiologists. I'm just so surprised at how the knowledge of cardiology has not been really changed in my mind in the traditional medical establishment since the 80s. Cardiologists have been stuck in the 80s for decades now. That's right. The training we get is focused on procedures. Most cardiologists are very good with their hands or the very good visual interpretation. That's why we do a lot of imaging. We do echoes, new clears, and we interpret cats and now CTs. Then we have a lot of hand-eye coordination. That doesn't lend to a lot of thinking about prevention. Everything that is an emergency in cardiology is at the end of the spectrum in the hospital. We're trained to take care of that. It's understandable. I don't think it's at a detriment or a deficiency in cardiologists, but it's just a lack of curiosity. It's the number one killer in the world, and we don't have enough cardiologists. The cardiologists that exist are get a day loose of people that have structural heart disease, coronary artery disease, and they're fixing people. In their defense, it's important that they think that way so that they can get the best outcomes, but it's also lacking in serious funds of knowledge because then they just become plumbers. They become carpenters because they're replacing valves, putting in tubes in other tubes and just pushing things out of the way for temporary outcomes. It's so well said. That's exactly what's happening. Cardiologists, there are not enough cardiologists out there because there's so many people having heart attacks. There's so many people having valve disease. They're constantly just trying to patch up these problems. The fire's here in LA. There were not enough fire people to go around because everyone's doing something and trying to put out the fire. No one worked on preventing these in the first place. That's why we got into that situation. Populations getting older, people getting disease younger. There's a crunch. There's a mismatch and a crunch and what's going on. There's so many aspects of this conversation that we can go into. I love that you went into longevity medicine, which in my mind is really increasing health span and reducing carpenters disease. You really spend a lot of time thinking about how do we prevent all these disasters from happening in the first place? Yeah, I try. That's where the term regenerative cardiologist comes in because it's not only about returning the things that we had when we were younger that could allow us to recover from things like plaque deposition or hypertension or deficiencies that cause a fib or hypertension. We have these abilities when we're young to regenerate and recover. We lose these as we get older. Hence the idea of regenerative cardiology. Start replacing those things that we can replace and that we start to understand that there are pathways involved with that. Maybe peptides can do that. We replace those things to bring back the body's ability to regenerate its own function or to reverse some of the things that damage that has been done. To be completely frank, this is a completely novel approach to cardiology. It really is. It's not just about good prevention. It's about trying to reverse. A lot of it is looking at mechanistic studies. A lot of it is looking at experimental studies and trying to extrapolate what we see in those experiments versus what outcomes are happening with similar studies or similar agents or even anecdotal cases and trying to bridge the gap. Yeah, it makes total sense. I think a lot of the way we think about, let's talk about heart attacks. Most people don't even find out about they have heart disease until their first heart attack. 50% of those are fatal to be able to. If you're lucky enough to find a great cardiologist like you, many great cardiologists exist in hospitals, they will save your life. They will save your life. A lot of damage has been done not just over years but also in that one moment where you had the cardiac event. We're saying now there's tools and techniques that we have that I can regenerate your cardiac function. Sure. We can amplify what's existing and then there's experimental data that looks at recruiting cardiac stem cells. Now this is still extremely preliminary and we're looking at animal studies. But we're looking at the ability to recruit stem cells to go to the areas that had death, heart cells that had death and then be able to deposit and regenerate muscle. Now we've tried this in the past with stem cell infusions, even interventional procedures where they inject stem cells directly into those areas of the heart. Those are old studies that didn't do that great. This was pre-peptide era and I think that when you're looking at regenerative therapies, you have to layer all of the therapies. There is no one thing that does it. It's a battery of therapies that can eventually lead to something that can regrow or maybe there's, we're looking at ways to turn on gene function too. There's just so much being done and it's in the longevity space because we're looking at ways to try and reverse aging and reverse the small insults. But that can extrapolate to the big insults and really help people at the end of the line too. When you see small insults, what are you referring to there? Because we have a microvascular disease that goes unnoticed and this can be from nutritional deficiencies. It can be from lifestyle issues. It can be from smoking. It can be from environmental toxins like the fires. These will impact our vascular health and it will impact inflammation in those arteries and we know that inflammation itself causes ischemia. There are diagnosed conditions that look at clean arteries, completely clean arteries when they're imaged but people still have, they still have lab evidence, biomarker evidence of decreased blood flow and cell death. So what we're saying here, which is extremely important for people to realize, heart attacks and are basically how a big vessel, one of the major vessels in the heart could block. And then you have cell death or the muscle of the heart actually dies. That's the biggest problem with heart attacks and that causes sudden death and causes sudden death. Exactly. But up till that point, there's also micro damages occurring that weaken your cardiac muscle. There lead to conditions like heart failure that can lead to poor heart function and that's occurring all the time and that might not be picked up in even a scan of those major blood vessels. So scans can be clean but you still have damage heart tissue. That's right. And so we see this in other organs. Yeah, look, think about the brain. When we see white matter loss and we call it normal changes with age, this is micro vascular disease that's steadily, slowly over the years, killed off cell tissue, brain tissue and then they just have less brain volume. When they get scanned, oftentimes their carotid artery is open, clean, clean and they don't see much in the arteries that are visualized but it's still a micro vascular problem. So that happens in the heart too. Absolutely. That's such a great analogy. Like you don't have to have a stroke, a cellular death in the brain. We know that people are suffering from neurocognitive neurodegenerative diseases all the time. That's right. The same analogy applies to the heart muscle and the heart tissue. So it's not enough just to make sure that you don't have plaque in your blood vessel. That's right. There's a lot more work that needs to be done. So much. Specifically, you mentioned inflammation, micro vascular, your metabolic health is part of the story. Definitely. Tonsic exposure is part of this story. Wow. So lead us through kind of how do you assess your micro vascular health? It's difficult right now. I think the best way to do it right now is to consider some, there's some lab markers that we'll look at. And they will look at nitric oxide function. A lot of those are, they're not, they're not necessarily available in regular lab testing but you can actually, you can get them in, in most conventionally available labs. The vibrant has a cardio zoomer that's coming out that has multiple of these lab tests. Yes. Cleveland heart labs also has it has a few of those. So one of the labs I look at is called ADMA, SDMA. These are compounds that our arteries make that counteract nitric oxide. And so when those are elevated, it means that nitric oxide is low. Nitric oxide is a foundational compound that helps with vascular health and reduces inflammation. So if that is, if that's low, then we know that we have to amplify or at least we know that there is something inhibiting their nitric oxide and we have to do something to help it because inflammation may be high. It's tied into C reactor protein and it's been assessed as an independent risk factor. So that's one thing, ADMA and STMA. They're also indicators of methylation. So the body's ability to detoxify, connected with almost cysteine. So they're connected to multiple different processes. The other things we can look at are, there are ceramides. And ceramides are a new category of their phospholipids. And when we look at phospholipids, and these are the lipids, the phosphate lipa cholesterol compounds that are in the membranes. They make the membranes fluid and resilient, but they also are susceptible to inflammation. And these are early indicators of inflammation occurring in the membrane. What leads to ceramide oxidation is low nitric oxide. So this goes back to looking at some, so when we identify that, then there are ways to tease apart if it's from low precursors. And so you can just give somebody citrulline, arginine, make sure they get the right things like a certain amount of bejuice for instance or extract like that. Or you can see if the enzyme function is actually low. And if the enzyme function is low, then you stimulate it with hormones, with supplements. Not forbid a statin. Statins have a place. I use them a lot in really low doses, especially if the cholesterol is or LDLs are okay. But it's a use case. It's not a blanket on everybody. But every medication has a positive and a negative. So you got to use it specifically for the individual. So you're saying statins have an effect beyond just cholesterol lowering the energy help with the inflammatory pathways of nitric oxide. Yes, yes, that's one of their most powerful functions. I don't think anyone knows this. Yeah, that's more. So when we look at the, so the LDL, LDL decrease is what's been talked about. But the pleatrophic functions, the other anti-inflammatory functions that happen with statins occur primarily through nitric oxide stimulation. Okay. So it amplifies enos that enzyme to create nitric oxide. And it does that so much so that that outweighs all of the negative effects of statins. So if you look at high dose statins, what ends up happening is people still get anti-inflammatory benefit, but they have a lot of side effects associated with it. So the balance is still in favor of inflammation being reduced. So if we reduce the dose, reduce the incident of side effect, then we can potentially get and still get that anti-inflammatory amplifying enos effect. So and what that tells us is how important nitric oxide is the vascular system. Wow. So because if that's the major driver of what statins do and it outweighs all of the negative side effects that can happen with a high dose statin, that's a really powerful lever to pull. That's a massive lever. And you still get that effect with the low dose of statin? Yes. Are you drinking like five milligrams of rosy-san or like lower than that? Yeah. Five or even two and a half. Two and a half, okay. Something to stimulate enos. So the message there is that if you're put in a statin and maybe you have clear, cornering blood vessels, right? Yeah. And you decide I'm going to get off my statin because I think statins are the devil. Yeah. You should at least consider staying on a low dose because it can help with the nitric oxide production. Yeah. Any enos enzymes? Mm-hmm. Interesting. What are some of the other ways people can increase nitric oxide, increasing enos? Stosterone. Really? Yes. One of the powerful effects of testosterone and hormone replacement therapy is amplifying enos, amplifying nitric oxide. So that's what, and testosterone and estradiol. So that's another reason why I use it, I use it therapeutically. You know, if testosterone is low on my cardiac patients, I have a hesitation about adding it on board. Amazing. And anti-hypertensive medications, a lot of them, ACE inhibitors, those can sometimes do it. And then lifestyle. Yeah. Exercise is one of the most powerful ways that we do it. Shear stress. So improving the, so increasing blood flow over the arteries, you know, the shear stress is the stress of two surfaces going against each other. So if you have a stable, fixed arterial surface and blood flowing across it, there is a stress that happens in that interface. So as shear stress goes up, it stimulates nitric oxide. So that's a mechanical way of doing it. Got it. Exercise does that. Our blood pressure goes up, our blood flowing increases, and it doesn't matter if it's aerobic activity or if it's anaerobic activity like weightlifting. Okay. In fact, the two do it differently. So this is why aerobic activity and anaerobic activity are important together. So interesting. And that also increases the inus. It does. Okay. What about EECP therapy? The, yeah. Yeah. That's another, just on the same topic, a really powerful way to increase, definitely, shear stress in the, exactly. You're absolutely correct. That's one of the ways that was used for heart failure patients, when they couldn't engage in activity. So it was a mechanical way of putting blood pressure cuffs on the legs and arms, and they would time it with the cardiac cycle with the heart rate so that it wouldn't squeeze at a specific time that would challenge the heart. And so that would cause blood pressure to kind of, it would increase a little bit of what's called afterload and sort of the back pressure, and that would increase some of that shear stress. So we're looking at bringing EECP into every one of our next health locations. Because I think it's one of those most powerful therapies around that really is very difficult to find. You know, it's only, you can't find it anywhere. But for cardiovascular health, I think it could be a potential game changer for people. I think so. Yeah. It was, it was used for heart failure patients many years ago and sort of as falling out of favor just because it's, I mean, it's a large device and I don't know that insurers companies were paying that much for it. And that's usually when things die out. Until someone's willing to pay, pay out of the pocket for understand, and understand that it provides benefit, maybe outside of that population. Exactly. And preventive benefit too. That's right. Very, very much so. So, okay, so we're looking at the microvascular. I'm so glad we're diving into this because so many episodes have already been done on macrovascular problems like LDL and plaque and APOB. We've talked about that extensively, but the microvascular problem I think is, it's just as important, if not even more important. Oh, yeah. We don't talk about it. Well, we don't. And this is, I mean, this is what, it, I mean, look at women's health and women's cardio and women's health. It is. I mean, easily, we call it, you know, there's a, a, a, a, a, a, a, a lack of blood flow or a heart attack that happens in women that that is specifically about microvascular disease. They have microvascular angina or chest discomfort. And in decades ago it used to be just ignored, you know, and it, or they would get cast and wouldn't find an answer and they would say it was anxiety. I mean, bullshit. All right. We know now that this is bullshit. So if anybody tells a woman that they have anxiety, that, you know, because of chest pain, they've got to look into the biomarkers, look into the inflammatory markers and see if there's something that's really causing it. Right. You know, we've got to take people seriously for their symptoms. Right. Another, another issue with microvascular disease and women, spontaneous coronary artery dissection. Yes. And so, it's a man usually and this is when the artery splits, you know, and it causes a blockage in the artery. This is very particular to women. And, and I think underdiagnosed. So there's a lot of a lot, you know, when we look at microvascular disease, there's a lot to be learned from women because they suffer from it a lot more than I do. Absolutely. Yeah. And I think what the important thing to highlight there too is women's symptoms are so different than the men's symptoms, right? Because microvascular heart disease symptoms can lead to heart attacks. Absolutely. And these microins, also these micro heart attacks, they don't present like the left traditional left-sided arpeggine and crushing chest pressure. It can be misdiagnosis anxiety, right? And so back pain sometimes, shoulder pain. Sure. There's all different ways that it manifests itself that's very different than what we think about as a traditional heart attack symptoms. Absolutely. And especially important in women because women also suffer from heart disease and they get catheterized, they get their LDL managed with stans, but really we're barking up the wrong tree. Yeah. Yeah, we have to look at them in a much more diverse manner. Right. I mean, it's there. They have multiple, it's a hormones play a role in this tutorial, right? Because they have a protection, microvascular protection, getting up into menopause once they lose their estradiol and progesterone and even testosterone, they start getting these microvascular disease. And it gets ignored. Right. Just so we are complete here, microvascular disease doesn't just affect your heart. No, it does. It's every organ of your body, your kidneys, your liver, it's your brain, it's your eye. This is a problem. And it's just now thanks to people like you, we're just now talking about it. And so I'm really excited to have this podcast with you because I really want to bring this to the forefront of people's attention. Yeah. So let's talk a little bit more about some of the biomarkers here. So you mentioned two biomarkers, say those again, ADMA and SDMA. Those are, it's asymmetric dimethyl arginine and then symmetric dimethyl arginine. These are blood tests, right? And then blood tests or urine tests? Blood or urine tests. Okay, great. Now there are some nitric oxide test strips that you can do under your tongue. Are there useful at all or valuable at all? You know, those are, those have some value, but when we're looking at serum levels, I don't think they're as useful. Okay. Because what happens is, so when we, when we take something like a beet juice extract, or we take nitric oxide precursors from our diet, they interact with our saliva, get into our, our stomach, absorbed and then recirculate into our system. Okay. All right. That nitric oxide or those, those nitrates make their way back up into our saliva. And it's a different, it's, it's a, it's, it's, those are precursors and they're also more of the nitric oxide, arginine reservoir instead of the actual activity of the enzyme. Okay. And what's on the actual, what's in the, in the lining of the artery? Okay. So when we look at the enzyme and the, the enos enzyme, it sits on the lining of the artery and inside what's called the glyco-calix. And the glyco-calix is a gel-like layer that sits in around the artery, sits between that endothelium and the blood. It's like a, a Kevlar coating and it protects the artery. It will shrink and expand depending on inflammation. It's very dynamic. It'll, it'll be different sizes and different arteries. It's in the entire system. It's in our arteries and our veins. And this is where the enzyme sits. So it's, it's variable. Enos will have different expression and different tissue. So what we try and measure in the saliva and in a test strip does, it doesn't give us an idea of what's going on in the coronary arteries, of course, say in the muscles or in other arteries that need, you know, they have different expression. Got it, got it. Okay. Because you know, one of the things that, that I've been given before, some of our conferences are these test strips. Yeah. And I've always wondered like, is that a true representation of what's really going on with my nitric oxide levels and you're saying probably not. Probably not. I think it gives you an idea of how much reservoir you have, what your Arginine reservoirs are, your citrulline type of thing. And because the precursors that they're giving you are to replace that, they're Arginine based. Citrulline based. They come usually as a beet juice extract or something like that. And if it's dosed enough, it fills your system with it. But then it's got to make its way into the cells. And then the cells got to, and then it's a right cell. And then the cells got to convert it into usable compounds. And that's where the measurements like A, D, M, A, and S, D, A, M, A come in. There's other ones. There's homoarginine. There, you know, it's look at precursors. So this, this test from, from vibrant is extensive. And it looks at all of these compounds, the precursors of, of Arginine and citrulline, the ratios of what you have in precursors and cellular stores versus what's in the serum. So it may not measure directly what the activity is, but it looks at ratios that give you an idea of what the activity is. Yeah. And that's better than anything we've had so far. Much, I mean, this is all brand new. It's just, I just sent mine in a few days ago. So I can't wait to see what my numbers are. But this is a whole new kind of unlock with cardiology, I feel that we've never had before. And it can potentially really explain a lot. Like why are so many people having heart disease and, you know, for all intents and purposes, we had people on statins now for two decades, right? And we still have a massive amount of heart disease out there, right? Yeah, I think that, I mean, it's my humble opinion that anybody that focuses on LDL's alone is being myopic. We know from decades of data how complex cardiovascular disease is. And to think that all we have to do is lower APOB is the solution. And now that the most complex disease we have that kills more people on the planet is solved. It's a little simplistic. It's simplistic. Yeah. You know, I mean, there's easily, you know, there's easily five, four or five different systems that interact to cause this disease. And this is what we know, there could be more. Right. Absolutely. Can we dive? Okay. So there's four or five different systems. And I'd love to touch on all of them, actually. So they both be kind of system with the more macrobaster disease and the act formation. We've covered that a lot. And we can talk about that more if there's anything new you want to add to that topic. Not really. Okay. Great. I love it. You're like, I'm done with that topic. I just want to add to. And now we're talking about the microvascular disease system, which I think is incredibly important. Nitric oxide, some of these neuro biomarkers, the enus enzyme. It's so important. And I do want to dive a little bit more into exactly for the listeners that are first now hearing the term nitric oxide. That's a gas that lives inside of our blood vessels that causes the ability for the vessels to be able to die late. Yeah. Open up. Yeah. So we're talking about what is nitric oxide? Why is it important and what happens as we age and why does the levels decrease and how do we keep our levels that are good? You talk a little bit about some lifestyle factors. You mentioned beetroot extractor. Yeah. So I'm sure people like, wait, why do you talk about beetroot extract for? Can you tell us a little bit more about that old system of nitric oxide? Yeah. So when we talk about some nitric oxide, there are three different enzymes that make nitric oxide. There's enus, inus, and then there's one for your brain also. Okay. All right. So the two that make anti-inflammatory nitric oxide are the two areas where it's used as an anti-inflammatory compound, come from your arteries and in your brain. All right. And that is actually the minority of what is made. The majority of what is made is an inducible nitric oxide. And that's what your immune cells use. So it's a multitasking gas. And what happens is your immune cells use it to create compounds that actually destroy foreign objects and quell information. All right. It's one of the powerful things that macrophages and other immune cells use to try and attack invaders. It'll control inflammation. But if it gets out of control, it will create too much inflammation. Enus and inducible, the enus endothelial nitric oxide is used in a different manner. So it has anti-inflammatory properties when balanced, but it also dilates the blood vessel. So it interacts with that muscular portion of the artery and allows that muscular portion to relax. And that opens up the artery. So it has much more function in the arterial system than it does in the venous system because venous system doesn't have as much, it doesn't have really any muscle when it goes down to the capillary level. But even in the larger scale level. But so it functions more as an anti-inflammatory in the whole system, but as a dilatory or relaxation compound in the arterial system. Got it. Got it. And to improve nitric oxide levels, beat juice extract is a sub-unit. One of the ways. One of the ways. And this is available in pill forms, in all over the place. And a lot of companies. A lot of companies. Yeah. And if you're going to take it, you've got to have, it's a short acting compound. So you've got to take it twice a day and you'll need at least about 400 milligrams. This is what weightlifters used for years to get a pump. They use arginine or citrulline. And it improves the vascular system, makes the veins look bigger. And it also improves blood flow in general. So that's why you want to do that. You want to increase the size of the arteries, improve the blood flow to the muscles, at least the weightlifters, that's what they're doing it for, improve their the amount of activity they could engage in and then the speed of their recovery. So that's 400 milligrams is really the minimum dose to get to that point. So I love weightlifters because they experiment on themselves to a detriment and we get to learn from them. The second podcast that we've talked about weightlifters, we talked about them with Androlone and some of the other growth peptides. And we've learned a lot from weightlifters. Which is great. They definitely like push it to the end levels so we know kind of where to moderate. But absolutely, that's that's great data to have. And so do you think this is something, this is a compound that everyone should consider as part of their like foundational supplement routine? If you're not, if your diet isn't balanced, then it's something to use. You can get most of your nitric oxide if you just have enough green leafy vegetables, vegetables in general. And there are multiple different foods that have enough arginine. In them that your body can use to convert into the precursors that you need. So it's not something that we need to supplement. I mean, I think that if you're getting your greens, which sounds silly, but I have to emphasize that to all my patients. For sure. And for so many different reasons. And this is just one of them. If you're getting a balanced diet, you don't need to take arginine supplement. Unless you're a bodybuilder and you want to get a pump and you want something to get a little more amplification of your pump or your workout. So that's fine. It's a use case situation. For the average person, you don't need more beet juice. You need more ability for your body to create nitric oxide. And that's where a good exercise routine comes in. That's where you know, even controlling inflammation, you know, controlling the things that consume nitric oxide and maybe even do what's called un coupling of nitric oxide. So there's three ways, three places or enzymes that create nitric oxide. Your body controls it. It knows how to do that. It knows where blood flow needs to be increased and where it needs to create more to kill off bad guys. But what happens is if there's too much inflammation for too long, then it does what's called un coupling. And it forgets where it needs to send all the nitric oxide or how to distribute it. And those enzymes don't function as well. And all the sudden, all the nitric oxide goes to making inflammation. Oh, okay. Got it. So this is why we need to control the risks that create inflammation and then control inflammation itself because if one of the things that happens is because we get a stack of multiple things that happen with sustained inflammation, nitric oxide is just one of them. There's one of the problems. There's another way, chronic inflammation will be detrimental as it uses up all the nitric oxide. Yeah. And then you don't have enough. Or you're making too much. Yeah, from I know you're making too much for my nose exactly. Hi, Dr. Shah here. I want to take a minute to talk to you about cellular health. So in my clinics, I've actually seen 30 year old people with cells that look like they're pushing retirement. And I've also seen 60 year olds with cells that look like they're 40 years old. So what's the difference? It's really about how fast their telomeres are breaking down. Your cells, you see are like phones and they have limited cell phone battery. Poor sleep, stress, processed foods, all of these things can drain that battery way faster than it should. So this is the reason why it partnered with IMA. IMA powers that cellular battery. It's not just another multivitamin. 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If you go to drshaw.com slash IMA or go to IMA health.com slash discount slash drshaw and you can get 20% off with my discount code drshaw. You can also find the link below. You mentioned the glyco-calix a couple of times. Yeah. Can you talk a little bit more about what that is? You said it's a it's a layer like above your endothelium. Yeah. And I remember I used to do like carotid end-order actamines and when I'm my surgical residency. And there was kind of like this almost like a slippery layer. Whenever you opened up someone's carotid artery that you would find that's the glyco-calix. That's the glyco-calix. Got it. OK. And you know, it's what it is is it's a it's a gel layer. Yeah. And it's what's fascinating about this layer is that it's composed of the same things that we find in our joints. Interesting. It's got how you're on a acid. How you're on eight. It's got condroitin in it. And then it's got something. It's got an anti-coagulant. It's got a heparin in it. And so though and then it's got albumin. It's one of the largest reservoirs of albumin. Wow. OK. So it houses so many different vital compounds. It will open. It will it'll it'll thicken and and shorten depending on need. OK. Depending on inflammatory exposure. Got it. And it serves as a bulletproof layering. All right. So an additional layer of protection for endothelium. Yeah. And this is one of the things that that are integral to controlling the effect of LDLs and even things like L.P. Little A. Sure. So when we have higher amounts of inflammation, it wears away at this layer. We liberate compounds that are trying to control inflammation. And then we end up losing the that slickness of the artery. It can be any I mean obvious things that reduce it. Smoking and then standard American diet. Right. Anything that causes a lot of inflammation in activity. And then on control glucose. You know, any of those metabolic derangements can. You know, it's it's a and then one of the big things that we've seen over the past few years is COVID attacks the glycochloric. Really? OK. And this is one of the reasons why we see a lot more cardiovascular disease in acute COVID and then in the aftermath of COVID. Yeah. Now, that's a very important piece of the puzzle for COVID and cardiovascular disease, for sure, is the glycochylics. Yeah. Yeah, it is. It's our it's our body's own bulletproof light layering for the end of the ethelium because the endothelium is only a cell layer thick. Yeah. And it can't really manage everything that it needs to protect itself. Right. It's got these it's got these adhesion molecules on the receptors. And this is what the immune system activates and sticks to and is the beginning of plaque formation. So when the glycochylics is healthy, it's thick. It covers those up and doesn't allow the immune system to bind on to the endothelial layer. So when we do things to compromise that gel layer, the immune system is more likely to connect to those receptors and then getting underneath the lining of the artery, same thing with the LDLs, same thing with, you know, with macrophages or any other inflammatory compounds. Yes. So that's the like the it's the gatekeeper. It's the gatekeeper that protects the endothelium from plaque development. That's right. How would one thicken and create a healthy glycochylics? Obviously you want to avoid smoking. Make sure your metabolic health is under good control. Is there anything else you can do for glycochylic self? This is like a hot topic right now and cardiology, I think, right? I don't know that it's to be honest with you. I don't know that it's a hot topic. Really? I keep hearing about it in longevity. Yes. We're hearing about it in longevity, but in cardiology, I mean, there's there's 30 years of worth of data, maybe more. And this is not something that was ever taught in fellowship. This is something that I'm learning now on my own. Oh my gosh. And, you know, it's crazy that as 20 years into my practice is when I'm finally getting an education in this, when it's such a vital component of our microvascular health. Anyway, that's it on the side. Even macrovascular health, right? Yes, right. Yeah, yeah. Any other techniques to improving glycochylics? I exercise, I've mentioned a couple of times that's one of my favorite ways. There are some supplements. There are some compounds. One of the things that is really important about the glycochylics, take a step back and talk about it, it's got that compound called heprenin in it. Yes. That's our natural ability to control thrombosis. So it's also this, this layer is a vital layer in controlling clotting in our system. If it's, when that gets worn down, we start getting microscopic clots. And those clots can also be, they will sit on the layer of the artery and that will also make it vulnerable to plaque formation. And there's some, there's books out there that talk about how some people think that some physicians think that it's the fiber, that's the fiber and the microscopic clots that are the drivers of atherosclerosis more than say LDLs in cholesterol. Oh, so interesting. So when that layer wears down, it's that compound called heprenin in it, is in it. That's what regulates the nice slickness and anticoagulant ability of it. And then when it wears down, we lose that. So we want to maintain the ability of that heprenin to stay in the ar end that vascular area too. Another reason it's super important. Yeah. So then this is where things like, so there's, so there's supplements that can help support that anticoagulant function. And that one goes is nato kinase. Yes. That's one. And the other one is lumbar kinase. Yeah. Nato kinase is from is from a nato, nato plants, you know, it's like a soy, a soy plant, right? Yeah. Yeah. It's a soy that's got like some sort of, I think it's a fungal growth on top of it. Yes. I might be wrong. I don't know if it's fungal, but anyway. Yeah. I know. As fermented fermented, that's fermented. Yeah. As fermented nato. Yeah. And that's what nato kinase is. And it helps to maintain the heparin. It will in the glyco-calix. So it doesn't cause anticoagulation, but helps your body regulate it. Because it either keeps it in the glyco-calix or releases it when it needs it. So and that's one aspect of controlling, of maintaining the length of the glyco-calix. And there's a recent study on nato kinase that said, you know, most people have been taking too low of a dose. Yeah. 10,800 I think. Exactly. So we're trying to get the true anti-plac effect. And it could actually reverse plaque, right? Yeah. Is what the studies show as well. That's what we, that's what some, yeah, in animal models, we're seeing it can reverse plaque. That's what it's incredible. Particularly for kinds of plaque. It's a soft plaque. Yeah, soft plaque. We're not seeing it in calcified. That's still the hard one. Which is, you know, where there's some, there's some potential for other therapies with nato kinase that may be able to help loosen up hard plaque. I don't know, it's still sort of something we're thinking about. You know, you look back at all the Ornish studies and, you know, the plant-based diets and reversal of plaque. And it just makes me think that it was the green leafy vegetables the whole time. Yeah, yeah. And the nitric oxide and the enos. And that's what's helping with the plaque reversal. I'm sure there's a million other mechanisms with that one direct biochemical mechanism. Yeah, definitely. And so, so other things to help strengthen the glyco-calix. This goes back to what I was saying that there are multiple, there's multiple things in the glyco-calix that are the same as what's in our joints. So taking something like condritan sulfate. Condritan sulfate, right? You know, that helps your glyco-calix. Taking howeronic acid or howeronate, that helps potentially collagen peptides. So there's taking some of those supplements and their studies that look at glucosamine and condritan sulfate and showed that there was a cardiovascular benefit, not talked about much. And there was a study that looked at condritan sulfate and condritan sulfate and there was an arm that showed significant cardiovascular benefits. Oh, that's incredible. So these joint health supplements can actually help with your cardiovascular health because of the glyco-calix. Will this new cardio-zimmer, is there a test for glyco-calix health or thickness? There are some tests that look at, there's some visual tests. Like radiology or... It's not radiology, they're ultrasound-based. Ultra-sum-based, okay. They look at it underneath tongue. Oh, okay. So it looks at an isolated spot for your glyco-calix. Arguably it's a reasonable area to look at it because it's so well-vascularized, but it does change. It changes on a moment-to-moment basis. It doesn't give us quite a long-term idea of what the thickness is and I think it's going to be user-dependent on who's measuring it. If you look at images of what the glyco-calix, they're like little hairy projections. Each projection is a different length. So it's like a shag carpet. That's a different length. I think that it would be difficult to really quantify where it starts and sometimes where it ends, too. I think direct visualization is limited and there is a serum test that we can use. It's not widely available. It looks at something called syndicine. I think it's syndicine one. They'll have to off-to-check that. But anyway, it's looking at breakdown products of the glyco-calix. So every time when we see degradation of the glyco-calix, this compound is one of the proteins that sits inside of it and it gets released. In fact, when we were doing studies on the glyco-calix and COVID, this is how they determined that COVID was breaking down the glyco-calix. Really? The syndicine levels were elevated during acute COVID and then in long COVID patients. So interesting. I hope that test becomes more available. Is that going to be in the cardio-zoomer, you think? I don't see it in the cardio-zoomer. Okay. But you're going to call them up. We've got to call them out. That's really important. I think having an indicator of glyco-calix could be another dimension that we look at. Okay. So we talked about naturopathcy. We talked about the glyco-calix, microvascular damage. What are some of the other not too often talked about mechanisms around cardiovascular disease? Well, we touched on it looking at the thrombotic-efficient effects. The thrombotic effects, right? Exactly. And that can be looked at in a couple different aspects. I mean, you can look at Fiberinogen directly and that'll give us an indication. There's a test from Cleveland Heart Labs. It's called aspirin works. Okay. It is looking at 11-DH thromboxane and looking at if those are, that's what aspirin inhibits. Okay. It looks at thromboxane and it gives you a Fiberinogen antigen. That's useful in more than just assessing aspirin because if thromboxane is elevated, your clotting mechanisms are going to be a little bit more active. And then if you have a high Fiberinogen antigen, that's another indicator that you have a high clotting state. Okay. So, it's a test to determine if you need or would benefit from aspirin, but it'll, you could use natal kinase on these kinds of patients, too. Yes. Absolutely. So, that brings up a really important question. The aspirin recommendation, baby aspirin recommendation is kind of common gone and come and gone and come and gone. And so, what are your thoughts around that? And I mean, it sounds like this test could potentially be a great way to know if you could benefit from aspirin. But also, natal kinase can also solve the issue. It could. Natal kinase is widely available as a supplement, but you got to get the right amount and that can be an issue because a lot of the supplements have a very small amount in it. So, you got to really look at the labels. You know, I feel like aspirins have the same problem the statins have had. You know, the recommendations are based on wide populations. And this is something that you've got to use in particular people. You've got to know if the person is going to benefit from it or if they're at high risk for complications happening. So, an elderly patient or a patient that's got gastrointestinal issues, sensitive stomach, I mean, you got to take all this into account. Absolutely. Which they didn't do in these older studies. No. When you look at what aspirin does mechanistically, it improves our ability to make what are called SPMs and PRMs, which are anti-inflammatory metabolites of omega-3 fatty acids. And these are sold as anti-inflammatory supplements. So, you could increase your body's ability to make it just by taking more fish oil, more omega-3s and maybe taking an aspirin. Maybe aspirin, right? Yeah. And then in my patients that have heart disease that don't have contraindications to using aspirin, I will use it whenever I can. Okay. So, you know, and of course that's taken knowing their history. If they have issues that they can't tolerate it, a lot of bruising, then I'll cut it back. I'll do it maybe every two, three times a week. Or something like that. Okay. Got it. And using a baby aspirin dose like 81 milligrams. Okay. Great. Yeah. I think it's really important to talk to your doctor about baby aspirin. If you are to high risk for like stomach ulcers or bruising or any other things and probably, you know, risks that way, the benefits, but big picture. Like don't just completely cut out the option because of what you heard in the media, which is what I've seen. You know, the minute that story came out a few years ago of aspirin might be doing more harm than good. Everyone just stopped their ass. Yeah, that's right. Yeah. It's never as binary as that. You know, there's a reason why these things have gained such a purchase in our therapeutic option. And so we just, and if there's a, if there's a study that contradicts it, we've got to look at the weight of it. It's not just the one study. Exactly. And it's very end of one. That's why it's so important to see a practitioner to help guide you through all of this and have, and make sure the practitioners are with the latest date and the latest knowledge. Which it sounds like in cardiology, it's hard to find that. It is. Yeah. And then, I mean, going back to the things that affect our heart disease, I mean, the big one is metabolic disease. Let's talk about that. You know, and that's not just your blood glucose. It's hepatic health. It's liver inflammation, things like that. And this is where I really appreciate what GLP ones have done for the industry for the world, really. Because they've put a lot of attention on, and given so many, given everybody an incredible tool to help change metabolic health. Right. And it's even, it's even trickled its way into cardiology. So this is the, the gateway that is going to make cardiologists become more sort of cardiometabolic doctors. Right. I love that. Yeah. And, but when we're looking at, you know, the root of a lot of the problems, a lot of it is going to, the most common problem, the root of the, the most common root of cardiovascular disease is metabolic issues. It's glucose dysregulation. It's inflammation that may be coming from glucose dysregulation and how it affects the liver. Because then the liver is where we make our cholesterol. And if we're, if we have an inflamed liver, we're going to make small, dense LDL, which will be more damaging. They're like bullets instead of big beach balls. Those bullets are going to penetrate the glyco-calix. They're going to wear down the glyco-calix and get under the lining of the artery. So you know, it all sort of comes back full circle. You've got to do multiple things to control the risks of your arteries. And, and definitely cardiometabolic disease is one of those things that are even, we just call glucose dysregulation. It will wear down that lining of the arteries. It'll increase production of enzymes, proteases that wear down the lining, that glyco-calix and expose the artery and then have plaque form. I see. I never knew the mechanism of why the liver formed small, dense LDL particles. Like why? Why does it choose one or the other? Yeah. And it's metabolic disease is the reason. Yes. So, G-O-P1s can be an incredible part of the treatment algorithm for cardiovascular diseases. Yeah. Yeah. I agree. Like, you know, people need to stop thinking about G-O-P1s to just weight loss drug. It's really about metabolic health and metabolic control. We, we started doing the fibroscan liver scan on our patients and it's mind blowing the number of people that have fibrodic liver disease and their enzymes are not elevated. So, you're not seeing it on the blood test. Yeah. It's really a lot of people that have advanced liver disease that we're not catching even with standard blood tests. Absolutely. I think it's really important for people to get their metabolic health right. Definitely. And reduce alcohol intake as well, all those things. What else have we noticed? We're not on pernuvo scans. Yeah. Yeah, that's true on a full body MRI. That's where it's showing up as well. We're seeing, surprisingly, you know, where we're seeing a lot of these, a lot of people who are, who are thinking about, who have good lifestyles, who are thinking about prevention and getting scanned because they want to, they want to know what's going on and we see fatty liver where it's unexpected. Yeah. And they're like, wait, I have no idea that fatty liver. Why? What happened? Yeah. And then, you know, the hemoglobin A1C might even be an acceptable range. Sometimes, and you just don't know how bad about disease is going to manifest itself. Yeah. Are we missing? Sounds like, you know, we've covered a lot of ground there. Are there any other missing topics that people need to think about, or they're thinking about their heart health? Yeah. There's, this is something I'm going to be focusing on this year. Okay. And this is mental health. Oh, talk about that. Yeah. It is underrepresented in how significant mental health involved engages and adversely affects the heart and the cold cardiovascular system. Really? You know, if you look back at studies pre-COVID, even, the inter-heart study is one of those. There's a finished study, Scandinavian studies that look at large populations, you know, double digit thousands. Like I think the inter-heart study might have been 27,000 people. And it came up with a conclusion that mental health has about a 30% contribution to heart disease. Yes. What's the mechanism? The mechanism is multiple mechanisms. Okay. This is what I'm seeing happening in a lot of my patients right now. It is activation of a sympathetic nervous system. All right. We know that that increases your risk for hypertension, increases your risk for heart failure, increases your risk for atherosclerosis, dementia, you know, sleep disorder. You name it. High sympathetic drive has, we're not designed to be in fight or flight mode all the time. And that's what we are in this world. So that's one thing. That leads to cortisol and hypothalamic pituitary adrenal dyspurgis regulation. That means that we either have too much cortisol flowing around or even worse we have not enough. And we get into a state where our mind says, I can't take as much cortisol as you're giving me. I need to take control and stop making it. And then we get fatigued, we get, you know, we get prone to illness and then our whole system sort of shuts down to protect itself, to go into a low functioning state. Yeah. So that's just two systems that kind of engage. So mental health, especially looking at the studies, they've all been done pre-COVID show an incredible contribution that is under recognized because it's so hard to treat. You know, how are you going to tell a CEO of a multi-million or billion dollar company that he has got to slow down? Even though he's doing everything that he's supposed to be doing. And this is what's really interesting about this time right now. CEOs of the past, we have reasons for why they showed up with heart attacks, why they have poor health. The new CEOs, these are sharp, well-minded individuals that are focusing on health. And they're still showing up with early heart disease. That's true. They're still showing up with plaque where it shouldn't be too early. And what's the X factor here? For me, it's the stress burden. And even though they think that they don't have stress, when you look at the load that people are bearing, it's exceptional and it is so high that they've just lost perception of what stress it is. They become numb to it. They become numb to it. And our system is supposed to be cyclical. We're supposed to have stress and then have relaxation. So this is how we gain resilience. If you're always in the top of that stress category, that just leads to system breakdown. And that's what you're lecturing me right now. Because this is me totally. I'm always up here. And you're absolutely right. This is not sustainable. You cannot be in a high sympathetic state all the time. It needs to cycle. It's not bad to be in there every once in a while, but you got to cycle it for sure. And even like daily stress control mechanisms such as meditation, breath, work, that helps as well. Definitely. That helps. I mean, this is why fitness is so important because it's an outlet. Yeah, it's absolutely. Breathing techniques. You know, you need to have social outlets. Yeah. All right. You've got to be time to reflect. Time is such a commodity for all of us. And you've got to just put down the phone, be present with who you are, reflect. And it doesn't have to be a lot of time. But there's got to be something dialed in to do that. Of course, sleep is really important to it because you got to recuperate. But this is me too. I mean, anybody that is trying to perform at their peak level, this comes to a point. To a philosophical question, are humans meant to survive at peak level for longevity? I don't know. I don't know. We're trying to figure this out right now. Is there a hack to be able to be at our peak for 100 years? Nature has said no. Probably not. You know, nature has made warriors die young, but they have the warrior gene that makes them live exceptionally. Sure. You know, these are just stupid thoughts that come through my head. The philosophical questions that really do get down to, you know, as we continue to improve our understanding of the science and aging, I do feel that we may hit a brick wall here in like what is nature really programmed for us? Yeah. For once we get everything else right, we reversed all chronic disease. There is going to be a wall there, you know, and it's going to come somewhere in the philosophy of what you're talking about is we're just not built as humans to always live at a peak state. Yeah. You know, if I am a student of Carl Jung and I read a lot of philosophical books, you know, humans have this secret desire to be gods. We have this drive to be superhuman. This is why comic book movies are so popular and they've been for comic books themselves. We want to touch something exceptional. We want to touch the divine, whatever you want to call it. That comes at a cost. Humans burn out when we do that. Is there a way that we can do that without burning out? I don't know if that goes contradictory to what it means to be human, but we're going to find out. Yeah, absolutely. You know, there's so many Greek and mythologies around humans trying to be gods and exactly what happens. So history has one answer. Yes. We're trying to figure out if there's a different one. So that's the exciting part of I think what longevity and performance medicine is doing. Really? It's so true. Well, this was incredible. So much from you today. And I feel like we have to have you on again and again and again because this is definitely an ongoing evolving conversation in cardiology. I really appreciate you updating my audience on what they really need to be thinking about. And moving beyond, you know, LDL and plaque and all that stuff, there's more to the story. And I think all of our listeners will really benefit from hearing from you today. So thank you so much. Thank you for having me. It's been a pleasure, Dr. Sean. Can't wait to see you again soon. Thank you. Dr. Hussein is a massive wealth of information. Here are my five takeaways from this episode with them. Number one, heart disease starts in the micro vessels long before a heart attack. Most people don't know they have heart disease until their first heart attack event. And 50% of those are fatal. Micro vascular dysfunction from stress, air quality, poor nutrition or inflammation can build for years without showing up on any standard scan. Number two, nitric oxide is one of the most important molecules for cardiovascular longevity. It keeps vessels open, supports blood flow and improves recovery. Exercise hormones like testosterone and estradial, leafy greens and beetroot extract all help restore nitric oxide function. Number three, the glyco-calix is a heart's bulletproof vest. This gel-like endothelial layer protects all your blood vessels from plaque, clots and inflammation. It can break down due to stress, smoking, metabolic dysfunction or even the COVID virus. Support comes from exercise, nato kinase, condrugin sulfate, hyaluronic acid and collagen. Number four, LDL alone is not the full story. Cardiovascular disease involves multiple systems, inflammation, micro vascular function, nitric oxide pathways, hormones, stress and endothelial health. Focusing only on LDL is dangerously incomplete. Number five, mental health is a major driver of heart disease. Chronic sympathetic activation and cortisol disregulation contribute up to 30% of cardiovascular risk. Even healthy high performers may be silently damaging their heart if they live in constant stress. Thank you so much for listening to the podcast today. Please remember to subscribe if you liked this episode and give us a good review and share a link with your friends. It really helps to support all of our efforts. I also want to remind you that the information shared on this podcast is for educational purposes only and is not intended to replace professional medical advice, diagnosis or treatment. Please consult with your healthcare provider or physician before making any decisions or taking any action based on what you hear today, especially if you have any underlying health conditions or on any medications. Your doctor knows your personal health situation the best and is always important to seek their guidance.