A (3:02)

Yes.

B (3:03)

Most cardiologists are very good with their hands or they're very good at visual interpretation. So that's why we do a lot of imaging. We do echoes, nuclears, and we interpret caths and, and now cts. And then we have a lot of hand eye coordination. So that doesn't lend to a lot of thinking about prevention. And everything that is an emergency in cardiology is at the ends of the spectrum in the hospital. So we're trained to take care of that. So it's understandable. And I don't think it's at a detriment or a deficiency in cardiologists, but it's just a lack of curiosity because look at, it's the number one killer in the world and we don't have enough cardiologists. So the cardiologists that exist are get a deluge of people that have structural heart disease, coronary artery disease, and they're fixing people.

A (3:51)

Right.

B (3:52)

So, you know, to their. 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.

A (4:02)

Right.

B (4:03)

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, you know, temporary outcomes.

A (4:16)

It's so well said. I mean, that's exactly what's happening is, you know, cardiologists, there are not enough cardiologists out there because there's so many people having heart attacks, there's so many people having bowel disease and they're constantly just trying to patch up these problems. You know, it's like the fires here in la. There were not enough fire people to go around because everyone's, you know, doing something and trying to put out the fire.

B (4:39)

Yeah.

A (4:40)

Like no one worked on preventing these in the first place. That's why we got in that situation.

B (4:44)

And population's getting older, people are getting disease younger.

A (4:48)

So there's a crunch, there's a mismatch and a crunch in what's going on. So, you know, there's so many aspects of this conversation that we can go into. And I love that you went into longevity medicine, which in my mind is really increasing health span and reducing chronic disease.

B (5:02)

Right.

A (5:02)

And so you really spend a lot of time thinking about how do we prevent all these disasters from happening in the first place.

B (5:09)

Yeah, I try. And that's where the term regenerative cardiology comes in. Because it's not only about. It's 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 afib or hypertension. So we have these abilities when we're young to regenerate and recover. We lose these as we get older. So hence the idea of regenerative cardiology. Start replacing those things that we can replace and that we've started to understand that there are pathways involved with that, maybe peptides can do that. And so we replace those things to bring back the body's ability to regenerate its own function or to reverse some of the things, the damage that has been done.

A (6:02)

Yeah.

B (6:03)

I mean, to be completely frank, this is a completely novel approach to cardiology.

A (6:08)

It really is.

B (6:09)

And so, you know, it's not just about good prevention. It's about trying to reverse. So a lot of it is looking at mechanistic studies, a lot of it is looking at experimental studies and trying to extrapolate what we've seen in those experiments versus what outcomes are happening with similar, you know, similar studies or similar. Similar agents or even anecdotal cases. And so trying to bridge the gap.

A (6:32)

Mm. Yeah. It makes total sense. And so, you know, I think a lot of the way we think about. Let's talk about heart attacks, right? We. Most people don't even find out about they have heart disease until their first heart attack of 50% of those are fatal to begin with. Right. And it's. It's. If you're lucky enough to find a great cardiologist like you, many great cardiologists exist in hospitals. They will save your life.

B (6:53)

Right.

A (6:54)

They will save your life. But a lot of damage has been done, not just over years, but also in that one moment when you had the cardiac event. And you're saying, now there's tools and techniques that we have that I can actually regenerate your cardiac function?

B (7:08)

Sure, yeah, we can. We can amplify what's existing. And then there's experimental data that looks at recruiting cardiac stem cells. Right 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, the areas of 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. And 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. So 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. So 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.

A (8:23)

When you say small insults, what are you referring to there?

B (8:25)

Well, there's, there's, you know, we have microvascular disease. We have. That goes unnoticed, you know, and this can be from nutritional deficiencies. Deficiencies. It can be from lifestyle issues, it can be from smoking, it can be from environmental toxins like. Like the fires. You know, these will impact our vascular health and it'll impact inflammation in those arteries. And we know that inflammation itself causes ischemia. You know, there. There are diagnosed conditions that look at clean arteries, you know, completely clean arteries when they're imaged. But people still have. They still have lab evidence, you know, biomarker evidence of decreased blood flow and cell cell death.

A (9:09)

Yeah. 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 get blocked, and then you have cell death or the muscle of the heart, actually. And that's the biggest problem with heart attacks. But.

B (9:29)

And that causes sudden death and causes kill people.

A (9:32)

Right, Exactly. But up till that point, there's also micro damages occurring.

B (9:37)

Yes.

A (9:37)

That weaken your cardiac muscle, that 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. Those blood vessel scans can be cleaned.

B (9:51)

Yeah.

A (9:51)

But you still have damaged heart tissue.

B (9:53)

That's right.

A (9:55)

And so, I mean, we see this in other organs. Yeah.

B (9:58)

You know, look, think about the brain. You know, we see white matter, white matter loss, and we call it normal changes with age.

A (10:07)

Right.

B (10:07)

This is microvascular disease that steadily, slowly, over the years, killed off cell tissue.

A (10:13)

You know, brain tissue.

B (10:14)

And then they just have less brain volume.

A (10:16)

Right.

B (10:16)

So. And 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 microvascular problem. That happens in the heart, too.

A (10:33)

Absolutely. And that's such a great analogy. You don't have to have a stroke to have cellular death in the brain. We know that people are suffering from neurocognitive, neurodegenerative diseases all the time.

B (10:43)

That's right.

A (10:43)

And so 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 vessels.

B (10:51)

That's right. That's right.

A (10:52)

There's a lot more work that needs to be done.

B (10:54)

So much.

A (10:55)

Specifically, you mentioned inflammation. Microvasculature metabolic health is part of the story.

B (11:01)

Definitely.

A (11:02)

Right. Toxic exposure is all part of this story. Wow. So lead us through kind of how do you assess your microvascular health?

B (11:11)

It's difficult right now. I think the best way to do it right now is to consider 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 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.

A (11:37)

Yes.

B (11:38)

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'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 and it's tied into C reactive 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 homocysteine. So they're connected to multiple different processes. The other things we can look at are ceramides. And ceramides are a new category of. They're phospholipids. And when we look at phospholipids, and these are the lipids, the phosphate lipid 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, you know, 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. Like, and so you can just give somebody citrulline, arginine, make sure they get the right things, like a certain amount of beet juice, 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. God forbid a statin. You know, statins have a place. You know, I use them a lot in really low doses, especially if the cholesterol is. Or LDLs are okay. But it's a use case. You know, it's not a blanket on everybody. But, you know, every medication has a positive and a negative, so you got to use it specifically for the individual.

A (13:55)

Yeah. So you're saying statins have an effect beyond just cholesterol lowering. They can actually help with the inflammatory pathways. Nitric oxide?

B (14:02)

Yes. Yes. That's one of their most powerful functions.

A (14:05)

I don't think anyone knows this.

B (14:06)

Yeah, that's.

A (14:07)

Tell us more.

B (14:07)

So it's when we look at. So the ldl, LDL decrease is what's been talked about. But the pleiotrophic functions, the other anti inflammatory functions that happen with statins occur primarily through nitric oxide stimulation.

A (14:25)

Okay.

B (14:25)

So it amplifies Enos, that enzyme that creates 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 still get that anti inflammatory amplifying Enos effect. And what that tells us is how important nitric oxide is to the vascular system.

A (15:08)

Wow.

B (15:09)

So because if that's the major driver of what statins do and it, it outweighs all of the negative side effects that can happen with a high dose statin. That's a really powerful lever to pull.

A (15:20)

That's a massive lever. And you still get that effect with a low dose of statin.

B (15:24)

Yes.

A (15:24)

Are you drinking like five milligrams of Rosa sand or, like, lower than that?

B (15:27)

Yeah. Five or even two and a half.

A (15:29)

Two and a half. Okay.

B (15:30)

Something to stimulate Enos.

A (15:32)

So the message there is that if you're put on a statin and you maybe you have clear coronary blood vessels, right?

B (15:39)

Yeah.

A (15:39)

And you decide, I'm going to get off my statin, because I think statins are the devil. You should at least consider staying on a low dose, because it can help with the nitric oxide production and Enos enzymes. Interesting. What are some of the other ways people can increase nitric oxide? Increase Enos.

B (15:56)

Testosterone. Really? Yes, testosterone. 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. If testosterone is low on my cardiac patients, I have no hesitation about adding it on board.

A (16:20)

Amazing.

B (16:21)

And the antihypertensive medications, a lot of them, ACE inhibitors, those can sometimes do it, you know, and then lifestyle exercise is one of the most powerful ways that we do it.

A (16:33)

Right.

B (16:33)

Sheer 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.

A (17:02)

Got it.

B (17:03)

Exercise does that. Our blood pressure goes up, our blood flow increases, and it doesn't matter if it's aerobic activity or if it's anaerobic activity, like weightlifting. In fact, the two do it differently. So this is why aerobic activity and anaerobic activity are important together.

A (17:19)

So interesting. And that also increases Enos.

B (17:22)

It does.

A (17:22)

Okay, what about EECP therapy? Yeah, that's another. Just on the same topic, a really powerful way to increase sheer stress.

B (17:33)

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 the. It would increase a little bit of what's called afterload and sort of the back pressure, and that would increase some of that sheer stress.

A (18:04)

So. 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 can't find it anywhere. But for cardiovascular health, I think it's. Could be a potential game changer.

B (18:19)

I think so, yeah. It was used for heart failure patients many years ago and sort of has fallen out of favor just because it's. I mean, it's a large device, and I don't know that the insurance companies were paying that much for it. And that's usually when things die out until someone's willing to pay out of the pocket and understand that it provides benefit maybe outside of that population.

A (18:43)

Exactly. And preventative benefit, too, I think. Very, very much so. So, okay, so we're looking at the microvasculature. 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 just as important, if not even more important sometimes. Then we don't talk about it.

B (19:06)

Well, we don't. And this is. I mean, this is why when you look at women's health and women's cardiology.

A (19:11)

It'S huge in women's health. It is.

B (19:13)

I mean, easily, we'd call it. You know, there's a ischemia or 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. Or they would get cast. They wouldn't find an answer, and they would say it was anxiety. I mean, it's bullshit. All right, we know now that this is bullshit. So if anybody tells a woman that they have anxiety, 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.

A (19:51)

Right.

B (19:51)

You know, we've got to take people seriously for their symptoms.

A (19:55)

Right.

B (19:55)

Another. Another issue with microvascular disease in women. Spontaneous coronary artery dissection.

A (20:00)

Yes.

B (20:00)

This doesn't happen to men, 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 men do.

A (20:17)

Absolutely. Yeah. And I think the important thing to highlight there too is women's symptoms are so different than men's symptoms. Right. Because microvascular heart disease symptoms, which can lead to heart attacks.

B (20:28)

Absolutely.

A (20:29)

But in these micro insults or these micro heart attacks, they don't present like the left, traditional left sided arm pain and crushing chest pressure. It can be misdiagnosed as anxiety. Right. And so back pain, sometimes shoulder pain.

B (20:44)

Sure.

A (20:44)

There's all different ways that it manifests itself. That's very different than what we think about as a traditional heart attack symptoms.

B (20:50)

Absolutely.

A (20:50)

And especially important in women because women also suffer from heart disease and they get cathedralized, they get their LDL managed with statins. But really we're barking up the wrong tree.

B (21:02)

Yeah, yeah. We have to look at them in a much more diverse manner.

A (21:05)

Right.

B (21:05)

You know, I mean, it's there. They have multiple hormones play a role in this too, because they have their protection, microvascular protection, getting up into menopause. Once they lose their estradiol and progesterone and even testosterone, they start getting these, this microvascular disease and it gets ignored.

A (21:25)

Right. And just so we are complete here, microvascular disease doesn't just affect your heart.

B (21:30)

No, it doesn't.

A (21:31)

It's every organ of your body. It's your kidneys, it's 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. So let's talk a little bit more about some of the biomarkers here. So you mentioned two biomarkers. Say those again.

B (21:55)

Ace, ADMA and sdma. Okay, Those are. Those. It's asymmetric dimethyl arginine and then symmetric dimethyl arginine.

A (22:05)

These are blood tests.

B (22:05)

Blood tests and then blood test or urine tests.

A (22:08)

Blood or urine tests. Okay, great. Now there are some nitric oxide test strips that you can do under your tongue. Are those useful at all or valuable at all?

B (22:15)

You know, those are. Those have some value. But when we're looking at serum levels, I don't think they're as useful because what happens is. So 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 stomach, absorbed, and then recirculate into our system.

A (22:39)

Okay.

B (22:39)

All right. That nitric oxide or those nitrates make their way back up into our saliva, but it's a different. Those are precursors, and they're also more of the nitric oxide arginine reservoir instead of the actual activity of the enzyme. And what's on the actual. What's in the. In the lining of the artery.

A (23:04)

Okay.

B (23:05)

So when we look at the enzyme and the Enos enzyme, it sits on the lining of the artery, and inside what's called the glycocalyx. And the glycocalyx is a gel, like, layer that sits around the artery, sits between that endothelium and the blood. It's like a Kevlar coating, and it protects the artery. It will shrink and expand depending on inflammation. It's very dynamic. It'll be different sizes in 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 variable. Enos will have different expression and different tissue. So what we try and measure in the saliva and in a test strip, it doesn't give us an idea of what's going on in the coronary arteries or, say, in the muscles or in other arteries that need, you know, that have different expression.

A (24:02)

Got it. Got it. Okay. Because, you know, one of the things that I've been given before at some of our conferences are these test strips, 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.

B (24:17)

Probably not. I think it gives you an idea of how much reservoir you have, what your arginine reservoirs are, your citrulline, that type of thing. And because the. The precursors that they're giving you are to. To replace that. They're arginine based. Yeah, 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 cell, and then the cell's got to. Into Right. Cell, and then the cell's got into usable compounds, and that's where the measurements like ADMA and SDMA come in. There's other ones. There's Homo arginine there, you know, which. Look at precursors. So this test from Vibrant is extensive, and it looks at all of these compounds, the precursors 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. And that's better than anything that we had so far.

A (25:22)

Much. I mean, this is all brand new. I just sent mine in, actually, 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 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.

B (25:50)

Yeah. I think that it's my humble opinion that anybody that focuses on LDLs 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 and is the solution, and now the most complex disease we have that kills more people on the planet is solved. It's a little simplistic.

A (26:20)

Yeah, exactly.

B (26:22)

I mean, there's easily four or five different systems that interact to cause this disease. And this is what we know. There could be more, right?

A (26:33)

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 the APOB kind of system with the more macrovascular disease plaque 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.

B (26:49)

Not really.

A (26:50)

Okay, great. I love it. That's. I'm so happy to be here with you. You're like, I'm done with that topic. I 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 newer biomarkers, the Enos 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 dilate.

B (27:21)

Yeah.

A (27:21)

To open up. Yeah. And so can you talk a little bit more 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 at a good. You talked a little bit about some lifestyle factors. You mentioned beetroot extract a few times. So I'm sure People are like, wait, what are you talking about beetroot extract for? Can you tell us a little bit more about that whole system of nitric oxide?

B (27:43)

Yeah. So when we, when we talk about so nitric oxide, there are three different enzymes that make nitric oxide. There's Enos, Inos and then there's one for your brain also.

A (27:53)

Okay.

B (27:54)

All right. So the two that make anti inflammatory nitric oxide are. The two, 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 in 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, foreign objects and quell inflammation. It's one of the powerful things that macrophages and, and other immune cells use to try and attack invaders.

A (28:40)

Got it.

B (28:40)

It'll control inflammation, but if it gets out of control, it will create too much inflammation. Enos and inducible. Well, the Enos endothelial nitric oxide is used in a different manner. So it has anti inflammatory properties when balanced, but it also dilates the blood vessels 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 you get down to the capillary level, but, and 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.

A (29:32)

Got it. Got it. And to improve nitric oxide levels, beet juice extract is a supplement. One of the ways. And this is available in pill forms?

B (29:43)

Yeah, pill forms in all over the place.

A (29:46)

And a lot of companies.

B (29:46)

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 will need at least about 400 milligrams. You know, this is what weightlifters used for years to get, get a pump. You know, they use arginine or citrulline and you know it gets, improves the vascular system, makes the blood, the, the veins look bigger and it also, you know, 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 weight lifters, this is what they're doing it for. Improve their, the amount of activity they could engage in and then the, the speed of their recovery. So that's, you know, 400 milligrams is really the minimum dose to get to that point. So, you know, I love weightlifters because they experiment on themselves to a detriment and we get to learn from them.

A (30:39)

This is the second podcast today that we've talked about weightlifters. We talked about them with Angelone and some of the other growth peptides. And yeah, we've learned a lot from weightlifters, which is great. They definitely, like, push it to the nth level, 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.

B (31:07)

If you're not, if you're, if your diet isn't balanced.

A (31:10)

Yes.

B (31:11)

Then that's, then it's something to use.

A (31:13)

Okay.

B (31:13)

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, that have enough arginine in them that your body can use to convert into, you know, into the precursors that you need.

A (31:31)

Right.

B (31:31)

So it's not something that we need to supplement. I mean, I think that if, if you're getting your greens, which, it sounds silly, but I have to emphasize that to all of my patients.

A (31:41)

Yeah, for sure.

B (31:42)

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 know, you're a bodybuilder and you want to get a pump and you, you know, or 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. But 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 uncoupling 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. All right? 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 uncoupling, 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 of a sudden all the nitric oxide goes to making inflammation.

A (33:00)

Oh, okay, got it.

B (33:02)

So. 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.

A (33:18)

Them, is one of the. One of the problems. This is another way chronic inflammation can be detrimental as it uses up all the nitric oxide.

B (33:24)

Yeah.

A (33:25)

And then you don't have enough, so.

B (33:27)

Or you're making too much. Yeah, from Inos.

A (33:29)

You're making too much from Inos. 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 I partnered with ima. IMA powers that cellular battery. It's not just another multivitamin. It's a comprehensive 92 ingredient formula designed specifically for cellular health and longevity. I'm talking 900 milligrams of vitamin C. That's like 20 oranges worth of DNA protection, the clinical dose of CoQ10 that you need to power your cellular engine. You also get zinc, selenium, vitamin E, alpha lipoic acid. All of these work synergistically for cellular repair and protecting your telomeres. So instead of taking a handful of pills every day and all these supplements, Im8 actually gives you everything that you need in one scientifically formulated system. And this isn't just a theory anymore. IMAID had partnered with Oxford University, the International Space Station San Francisco Research Institute, and they've done studies and they've gotten this NSF certified to truly power your health. Most people are aging twice as fast as they should. Unfortunately, you don't have to be one of Them Try Imate. I actually have a discount secured for you if you go to DrShaw.com IMA or go to ImaidHealth.com discount DrShaw. And you can get 20% off with my discount code DrShaw. You can also find the link below. You mentioned the glacocalyx a couple 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. Right. And I remember I used to do, like, carotid endarterectomies, and in one of 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 glycocalyx.

B (35:48)

That's the glycocalyx.

A (35:49)

Got it. Okay.

B (35:50)

And you know what it is, is it's a gel layer.

A (35:54)

Yeah.

B (35:54)

And what's fascinating about this layer is that it's composed of the same things that we find in our joints.

A (36:00)

Huh. Interesting.

B (36:01)

It's got hyaluronic acid, hyaluronate. It's got chondroitin in it. And then it's got something. It's got an anticoagulant. It's got heparin in it. And so, though. And then it's got albumin. It's one of the largest reservoirs of albumin.

A (36:15)

Wow. Okay.

B (36:16)

So it houses so many different vital compounds. It will open. I mean, it'll thicken and shorten depending on need, depending on inflammatory exposure.

A (36:27)

Got it.

B (36:28)

And it serves as a bulletproof layering.

A (36:31)

All right, so an additional layer of protection for endothelium.

B (36:33)

Yeah. And this is one of the things that. That are. It's integral to controlling the effect of LDLs and even things like LP.

A (36:43)

Sure.

B (36:44)

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, the obvious things that. That reduce it. Smoking and then standard American diet. Anything that causes a lot of inflammation, inactivity, and then uncontrolled 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 glycocalyx.

A (37:20)

Really? Okay.

B (37:21)

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.

A (37:28)

Yeah, It's a very important piece of the puzzle for Covid and cardiovascular disease, for sure. Is the glycocalyx.

B (37:34)

Yeah. Yeah, it is. It's our body's own bulletproof layering for the endothelium, because the endothelium is only a cell layer thick, and it can't really manage everything that it needs to protect itself.

A (37:47)

Right.

B (37:48)

It's got these adhesion molecules on it. They're receptors. And this is what the immune system activates and sticks to and is the beginning of plaque formation. So when the glycocalyx is healthy, it's thick. It covers those up and doesn't allow the immune system to bind onto 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 get in underneath the lining of the artery. Same thing with the LDLs. Same thing with, you know, with macrophages or any other inflammatory compounds.

A (38:25)

Yes.

B (38:25)

So that's the. Like the. It's the gatekeeper.

A (38:28)

It's the gatekeeper that protects the endothelium from plaque development, basically. And so how would one thicken and create a healthy glycocalyx? Obviously, you want to avoid smoking. Make sure your metabolic health is under good control. Is there anything else you can do for glycocalyx health? This is like a hot topic right now in cardiology, I think. Right.

B (38:49)

I don't know that it's. To be honest with you, I don't know that it's a hot topic.

A (38:51)

Really. I keep hearing about it in longevity circles.

B (38:54)

We're hearing about it. Longevity. But in cardiology, I mean, there's 30 years worth of data, maybe more. And this is not something that was ever taught in fellowship.

A (39:05)

Wow.

B (39:05)

This is something that I'm learning now on my own.

A (39:08)

Oh, my gosh.

B (39:09)

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 an aside.

A (39:21)

Even macrovascular health, right?

B (39:23)

Yes.

A (39:23)

Right. Any other techniques to improving glycocalyx health?

B (39:27)

Yeah, 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 glycocalyx. Take a step back and talk about it. Is it's got that compound called heparin in it.

A (39:40)

Yes.

B (39:41)

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. If 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 fibrin. It's the fibrin and the microscopic clots that are the drivers of atherosclerosis more than say LDLs and cholesterol.

A (40:21)

Oh, so interesting.

B (40:22)

So when that layer wears down, that compound called heparin 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 heparin to stay in the art in the vascular area too.

A (40:41)

Another reason it's super important.

B (40:43)

Yeah. So. And this is where things like. So there's. So there's supplements that can help support that anticoagulant function. One of those is nattokinase.

A (40:51)

Yes.

B (40:53)

Another one is lumbrokinase. Yeah. Nattokinase is from. Is. Is from Anatoly Annatto plants.

A (41:00)

You know it's like a Japanese soy plant, right? Yeah, yeah.

B (41:04)

It's a soy that's got like some sort of. I think it's a fungal growth on top of it.

A (41:09)

Yes. I might be wrong.

B (41:10)

I don't know if it's fungal. But anyway.

A (41:12)

Yeah. As fermented.

B (41:13)

Fermented. That's fermented natto.

A (41:16)

Yeah.

B (41:17)

And that's what nattokinase is. And it helps to maintain the heparinine. It will. In the glycocalyx. So it doesn't cause anticoagulation but helps your body regulate it because it either keeps it in the glycocalyx or releases it when it needs it. Other so. And that's one aspect of controlling, of maintaining the length of the glycocalyx.

A (41:39)

And there's a recent study in nanocannas that said, you know, most people have been taking too low of a dose. You need 10,800, I think.

B (41:46)

Exactly.

A (41:46)

Units of it to get the true anti plaque effect. And it could actually reverse plaque. Right. Is what the studies show as well.

B (41:55)

That's what we. That's what some of. Yeah. In animal models we're seeing it can reverse plaque.

A (41:58)

That's incredible.

B (41:59)

Particular kinds of plaque. It's a soft plaque. Yes, 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, other therapies with nattokinase that may be able to help loosen up hard plaque. I don't know, is still sort of something we're thinking about.

A (42:18)

You know, you look back at all Ornish's studies and you know, the plant based diets and reversal of plaques and it just makes me think that it was the green leafy vegetables the whole time 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, but that one direct biochemical mechanism.

B (42:37)

Yeah, definitely. And so other things to help strengthen the glycocalyx. This goes back to what I was saying, that there's multiple things in the glycocalyx that are the same as what's in our joints. So taking something like chondroitin sulfate.

A (42:51)

Chondroitin sulfate.

B (42:52)

Right. That helps your glycocalyx. Taking hyaluronic acid or hyaluronate, that helps potentially collagen peptides. So there's taking some of those supplements and there's studies that look at glucosamine, chondroitin sulfate and showed that there was a cardiovascular benefit. Not talked about much, but there was, you know, there was a study that looked at chondroitin sulfate and glucosamine in joints and there was an arm that showed significant cardiovascular benefits.

A (43:20)

Oh, that's incredible. So these joint health supplements can actually help with your cardiovascular health because of the glycocalyx. Will this new cardio zoomer, is there a test for glycocalyx health or thickness?

B (43:31)

There's, there are some tests that look at, there's some, some, some visual tests like radiology or. It's not radiology. They're ultrasound based.

A (43:40)

Ultrasound based. Okay.

B (43:41)

And they look at it underneath the tongue.

A (43:43)

Oh, okay.

B (43:44)

So it's, it looks at an isolated spot for your glycocalyx. 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 the glycocalyx, they're like little hairy projections and each projection is a different length.

A (44:12)

Okay.

B (44:13)

So it's like a. Yeah. Hairs.

A (44:15)

Yeah.

B (44:15)

Like a shag carpet.

A (44:16)

That's.

B (44:17)

That's a different length. So it's really, you know, I think that it would be difficult to really quantify where it starts and sometimes where it ends, too. So 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 syndicin, and I think it's syndican one. You'll have to off to check that. But anyway, it's looking at breakdown products of the glycocalyx.

A (44:43)

Okay.

B (44:43)

So every time when we see degradation of the glycocalyx, 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 glycocalyx and Covid, this is how they were. This is how they determined that Covid was breaking down the glycocalyx significantly because syndicin levels were elevated.

A (45:06)

Wow.

B (45:06)

During acute Covid and then in long COVID patients.

A (45:10)

So interesting. I hope that test becomes more available. Is that going to be in the cardio zoomer, you think, or not?

B (45:14)

I don't see it in the cardio.

A (45:15)

Zoomer, but you got to call them up. That's right, Exactly. That's really important. I mean, I think having an indicator of glycocalyx health could be another dimension of what we look at. Yeah. Okay. So we talked about nitric oxide, we talked about the glycocalyx, microvascular damage. What are some of the other. Not too often talked about mechanisms around cardiovascular disease.

B (45:37)

Well, we touched on it looking at the thrombotic effects.

A (45:41)

The thrombotic effects, right, Exactly.

B (45:43)

And that can be looked at in a couple of different aspects. I mean, you can look at fibrinogen directly, and that'll give us an indication. There's a test from Cleveland Heart Labs. It's called aspirin works.

A (45:55)

Okay.

B (45:55)

And that is looking at 11 DH thromboxane, and looking at. If you. If. If those are. That's what aspirin inhibits.

A (46:04)

Okay.

B (46:04)

So it looks at thromboxanes, and it gives you a fibrinogen antigen.

A (46:07)

All right.

B (46:07)

That's useful in more than just assessing aspirin, because if thromboxane is elevated, your fiber, your clotting mechanisms are going to be a little bit more active. And then if you have a high fibrinogen antigen, that's another indicator that you're. You have a high clotting state.

A (46:20)

Okay.

B (46:21)

So you may, you know, It's a, it's a test to determine if you need or would benefit from aspirin. But it'll, it'll. You could use nattokinase on these kind of patients too.

A (46:30)

Yes, absolutely. So that brings up a really important question. The aspirin recommendation, baby aspirin recommendation is kind of come and gone and come and gone. Come and gone.

B (46:38)

Yeah.

A (46:38)

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 nattokinase can also solve the issue.

B (46:50)

It could, yeah. Nattokinase 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, I feel like aspirin's had the same, same problem that statins have had. You know, the recommendations are based on wide populations.

A (47:10)

Yes.

B (47:10)

And it's just, this is something that you've got to use in particular people. You got to know if the person's 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.

A (47:27)

Absolutely.

B (47:28)

Which they didn't do in these older studies.

A (47:30)

No.

B (47:31)

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.

A (47:54)

Taking an aspirin, maybe aspirin. Right?

B (47:56)

Yeah. And then in patients, in my patients that have heart disease that don't have contraindications to using aspirin, I will use it whenever I can.

A (48:05)

Okay.

B (48:06)

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, I'll cut it back. I'll do it maybe every two, three times a week or something like that.

A (48:19)

Okay, got it. And are 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 at a high risk for like stomach ulcers or bruising or any other things. And probably, you know, risks outweigh 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 aspirin.

B (48:48)

Yeah, that's right, yeah. It's never as binary as that. It's, you know, there's a. There's a reason why these things have gained such a purchase in our. As 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 evidence.

A (49:03)

Right.

B (49:04)

Not just the one study.

A (49:05)

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 data and the latest knowledge, which it sounds like in cardiology, it's. It's hard to find that it is.

B (49:18)

Yeah, yeah. And then, I mean, going back to the things that affect, you know, our heart disease, I mean, the big one is metabolic disease.

A (49:26)

You know, let's talk about that.

B (49:27)

You know, and that's not just your blood glucose, it's hepatic health. It's, you know, it's liver inflammation, things like that. And this is where I really appreciate what GLP1s have done for. For the. 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. And it's even trickled its way into cardiology. So this is the gateway that is going to make cardiologists become more sort of cardiometabolic doctors.

A (50:05)

Right. I love that.

B (50:06)

Yeah. And when we're looking at the root of a lot of the problems, a lot of it is going to be the most common problem. The root of the most common root of cardiovascular disease is metabolic issues. Now, 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 glycocalyx, they're going to wear down the glycocalyx 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 if we just call it glucose dysregulation, it will wear down the lining of the arteries, it'll increase production of enzymes, proteases that wear down the lining. That glycocalyx expose the artery and then a CAB plaqueform.

A (51:15)

See, I never knew the mechanism of why the liver formed small, dense LDL particles. Like why, why, why does it choose one or the other?

B (51:23)

Yeah.

A (51:24)

And it's metabolic disease is the reason.

B (51:25)

Yes.

A (51:26)

So GLP1s can be an incredible part of the treatment algorithm for cardiovascular disease. And yeah, I agree, like, you know, people need to stop thinking about GLP1s as just weight loss drug is really about metabolic health and metabolic control. We started doing the fibroscan liver scan on our patients and it's mind blowing. The number of people that have fibrotic 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. So I think it's really important for people to get their metabolic health right.

B (52:02)

Definitely.

A (52:03)

And reduce alcohol intake as well. All those things.

B (52:07)

What else have we also seen on purnuvo scans?

A (52:09)

Yeah, yeah, that's true. On a full body MRI.

B (52:11)

Full body MRIs, 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 know what's going on. And we see fatty liver where it's unexpected.

A (52:30)

Yeah. And they're like, wait, I have no idea that fatty liver, why, what happened? And then the hemoglobin A1C might even be in an acceptable range sometimes. And you just don't know how metabolic disease is going to manifest itself. 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 when they're thinking about their heart health?

B (52:49)

Yeah, this is something I'm going to be focusing on this year and this is mental health.

A (52:57)

Ah, talk about that.

B (52:58)

Yeah. It is underrepresented in how significant mental health engages and adversely affects the Heart and the whole cardiovascular system really. You know, if you look back at studies pre Covid even there, the inter heart study is one of those. There's a Finnish study, Scandinavian studies that look at large populations, you know, double digit thousands, like I think the intra heart study might have been 20, 27,000 people. And it came up to the conclusion that mental health has about a 30% contribution to heart disease.

A (53:33)

30% contribution to heart disease?

B (53:35)

Yes.

A (53:36)

What's the mechanism?

B (53:37)

The mechanism is multiple mechanisms. This is what I'm seeing happening in a lot of my patients right now. It is activ 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 dysregulation. 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 prone to illness and then our whole system sort of shuts down to protect itself to go into a low functioning state.

A (54:43)

Yeah.

B (54:43)

So that's just two systems that kind of engage. So you know, 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 hard? How are you going to tell a CEO of you know, of a multi million or billion dollar company that he has got to slow down. He, you know, even though he's doing everything that he's supposed to be doing. And this is what's, what's really interesting about this time right now. CEOs of the past, they, we have reasons for why they showed up with heart attacks, why they, why they have poor health.

A (55:23)

Right.

B (55:24)

The new CEOs, these are sharp, well minded individuals that are focusing on health and they're still showing up with early heart disease.

A (55:32)

That's true.

B (55:33)

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 is.

A (55:52)

Yeah, yeah. They become numb to it.

B (55:54)

They become numb to it. And the system, our system is supposed to be cyclical. We're supposed to have stress and then have relaxation. So this is how we gain resilience.

A (56:05)

Right.

B (56:05)

If you're always in the top of that stress category, that just leads to system breakdown.

A (56:10)

And that's like you're lecturing me right now because this is me. Totally. I'm like, always up here. And you're absolutely right. Like, 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. No, but you got to cycle it for sure. And even like daily stress control mechanisms such as, like, meditation, breath work. That helps as well.

B (56:34)

Definitely. Okay, that helps. I mean, this is why fitness is so important, because it's. It's an outlet.

A (56:38)

Yes, absolutely. Yeah.

B (56:40)

Breathing techniques, you know, you need to. You need to have social outlets.

A (56:45)

Yeah.

B (56:45)

All right. There's got to be time to reflect. You know, time is such a commodity for all of us.

A (56:51)

Right.

B (56:51)

And there, you know, 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 gotta be something dialed in to do that. Of course, sleep is really important, you know, too, because you gotta recuperate. But, you know, this is me too. You know, I mean, anybody that is trying to perform at their peak level, you know, this comes back, this comes to a philosophical question. Are humans meant to survive at peak level for. For longevity?

A (57:21)

I don't know. I don't know.

B (57:23)

We're trying to figure this out right now. Is there, is there a hack to. 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, you know, they have the warrior gene that makes them live Exceptionally sure. You know, I don't, you know, these are just, these are stupid thoughts that come through my head.

A (57:43)

Philosophical questions that are that really do get down to, you know, as we continue to improve our understanding of the science of aging, I do feel that we may hit a brick wall here in, like, what is nature really programmed for us for? Once we get everything else right, we've 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.

B (58:10)

Yeah. You know, if I am a student of Carl Jung and I read a lot of philosophical books, you know, we 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 in 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? And I don't know if that goes contradictory to what it means to be human.

A (58:44)

Right.

B (58:44)

But we're going to find out.

A (58:45)

Yeah, absolutely. You know, there's so many Greek and mythologies around humans trying to be gods and that's exactly what happens.

B (58:54)

So history has one one answer.

A (58:57)

Yeah.

B (58:58)

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.

A (59:05)

Really. It's so true. Well, this was incredible. I learned 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.

B (59:32)

Thank you for having me. It's been a pleasure.

A (59:33)

Darshan can't wait to see you again soon.

B (59:35)

Thank you.

A (59:39)

Dr. Hussain is a massive wealth of information. Here are my five takeaways from this episode with him. 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. Microvascular 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 estradiol, leafy greens and beetroot extract all help restore nitric oxide function. Number three, the glycocalyx, is the 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, nattokinase, chondroitin sulfate, hyaluronic acid and collagen. Number four LDL alone is not the full story. Cardiovascular disease involves multiple inflammation, microvascular 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 dysregulation 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 like 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 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 it's always important to seek their guidance.