Dhru Purohit Show - Cardiologist Shares The Real Cause of Heart Attacks, What to Do About Microplastics and the Top Tests to Assess Heart Health With Dr. Michael Twyman

Episode Date: April 24, 2024

This episode is brought to you by Plunge and Lumebox.  Heart disease stands as one of the foremost global killers, claiming the top spot as the leading cause of death among women. With numerous factors contributing to its development, the future lies in precision cardiology—individually, customized, and prevention-focused. Today's episode is a deep dive into endothelial health and the journey to becoming heart attack-proof. Today on The Dhru Purohit Podcast, Dhru sits down with Dr. Michael Twyman and Dr. Neel Patel to discuss endothelial and cardiovascular health. Dr. Twyman shares his approach to assessing an individual’s risk of heart disease, metabolic health, and the importance of nitric oxide. Dhru, Dr. Patel, and Dr. Twyman discuss the role of genetics and the bloodwork you can order on your own and through a traditional healthcare system. They also discuss the diet and lifestyle for optimal heart health, supplements that should be incorporated into your daily routine, and the role of statins.  Dr. Michael Twyman is a board-certified cardiologist focusing on the prevention and early detection of heart disease. Dr. Twyman completed his cardiovascular training at St. Louis University after he completed a four-year active-duty tour as an internist at Naval Hospital Beaufort. He has been in private practice since 2012 and uses the best of conventional, quantum, and Functional Medicine and biohacking to get to the root cause of his patients’ cardiovascular issues.   In this episode, Dhru, Dr. Twyman and Dr. Patel dive into (audio version / Apple Subscriber version): Microplastics and cardiovascular health (00:00:05 / 00:00:05) How to approach vascular health and what is endothelial health (3:42 / 3:42) Traditional versus Dr. Twyman’s approach to the risk of heart disease (10:00 / 8:10) Glycocalyx: what damages it and what supports it (14:32 /13:02) How to approach metabolic health (21:40 / 20:19) The role of nitric oxide (24:00 / 22:14)  Photobiomodulation recommendations (33:00 / 31:07) Nitrates in your diet, testing nitric oxide levels, and Dhru’s results (42:00 / 39:00) How does high blood pressure start (53:00 / 51:15) The role of genetics (57:00 / 54:36)   The three buckets of bloodwork and ordering bloodwork in the traditional system (1:01:00 / 58:33) Best diet for heart health (1:18:00 / 1:15:15) Optimal supplementation (1:26:00 / 1:22:40) Statins: who should take them and who should avoid them (1:37:00 / 1:33:50) Biohacking: blue light blocking glasses and sauna (1:58:00 / 1:53:10) Also mentioned in this episode: Lifeforce Digital Huberman Protocol post Image of Dhru's ApoB results  For more on Dr. Michael Twyman, follow him on Instagram @drtwyman or his website, drtwyman.com.  Right now, Plunge is offering my community $150 off cold plunges and their core products. Just go to plunge.com/dhru or enter code DHRU to revolutionize your wellness journey today.  Lumebox is offering my community $260 off their FDA-registered portable Red Light device! That's over 40% off! Go to thelumebox.com/dhru and get your Red Light device. Learn more about your ad choices. Visit megaphone.fm/adchoices

Dr. Michael Twyman, a groundbreaking and mind-blowing study just came out in the last couple weeks in the New England Journal of Medicine, and it highlighted the alarming link between microplastics, something super scary in our environment, and vascular health. Now, the study revealed that the individuals with detectable levels of microplastics in their blood vessels are 4.53 times more likely to suffer from heart attacks, strokes, or death within three years. Now, a little bit more detail. Among the 257 patients that were followed for about 34 months, 150 of them had detectable levels of polyethylene in their plaque. The individuals with detectable levels of microplastics also exhibited higher in

inflammatory markers and reduced blood vessel collagen. Dr. Twyman, I want to pop this over to you to get your big picture thoughts on this study and its findings. It's a fascinating study that we're exposed to these things nonstop, but this is the first time that they've actually caught it in somebody's plaque. These patients were getting surgeries known as carotid endodermidectomy, so they were taking severe plaques out of their arteries in the side of their neck. So these weren't people with just risk factors. they were already late to the game. And so then when they analyzed the plaque under special screening methods, they found these plastics in about 50% of the population.

And the macrophages, which are part of the immune system, are gobbling this stuff up, and that was causing a lot of oxidative stress and inflammation inside these plaques. And then they followed these patients after their surgery. And as you said, you know, there's a four and a half-fold increased risk of them having a heart attack, stroke, or dying over the next approximately three years from the index surgery. So it's fascinating that we're exposed to all these things,

but what are we going to do about that? And that's really going to be the thing that we all have to kind of figure out, because the plastics are not going to go away, but maybe we can be drinking out of more glass, maybe we can not have so many things stored in plastic, because we're not going to get it to zero, but we're going to talk about it today is like, what can you do to test your arteries? Like how much are you actually being exposed to this? Is it affecting arteries right now? Before we move on to that topic, let's first just go back for a second.

If we would just give people one, two, three, four, five things when it comes to my microplastics. We're not going to be able to remove them completely from our environment and our ingestion that's there. But what would be some of the top ways that we could protect ourselves? I know many experts on this podcast have come on and said, well, a lot of this is floating around in our water. So number one, either get a filter, preferably something like reverse osmosis, or your body becomes the filter. Do you agree with that? And is there anything else you would add in as we zoom in just specifically on microplastics? So that's a good point that we're probably going to have to more things. But it's my understanding is that they don't know exactly how these

microplastics got into the plaque. They don't know if these were ingested or were they inhaled. Is it almost like a, you know, smog type of situation where you're inhaling it in the lungs and this is getting picked up? Likely, it's probably from both sources. You won't be able to remove it all, but you could probably control the water that you drink. So it can be spring water out of glass bottles. You can do a reverse osmosis filter. That's going to get a lot of these total dissolved solvents out. But then we're also kind of be mindful of the air we breathe. especially probably while you're sleeping, that seven, half, eight hours is the most key time that your body's repairing. So probably having a nice hepa filter in your bedroom might have the potential to help pull some of that out of the air that you'd be breathing.

That's great. So let's go back to the zooming out here and the bigger picture around this. Give our audience, you've been on the podcast before, but give our audience an understanding of how you think about vascular health. So vascular health is fundamental to longevity. That's what I'm kind of talking about in the past year. There's a lot of great technologies that help you live longer. People want to talk about stem cells and hyperbaric oxygen. But the basics are the basics.

If you don't take care of your vascular system, you're not going to get a chance that these advanced technologies are going to get you that extra five, ten years at the end. Approximately every 40 seconds, somebody still has a heart attack in the United States. And there's over 800,000 heart attacks every single year. Many of them could be preventable with not necessarily completely simple lifestyle interventions, but they are preventable if you start early enough.

early enough, looking at the endothelial health, looking at the glycochalics. If you know that the person's at higher risk, you make the interventions, they don't go on to be one of those statistics. So let's break down a few different things that you just mentioned over there. And this is all in the context of how to make yourself heart attack proof in the ideal world. And at least part of that is if you have had not the best lifestyle habits over the last however many years, how to also catch the presence of heart disease early so that you could do something about it. So let's break down a few words and sort of things that you mentioned. Endothelial health. What is it? And what do you want people to know about it? So for those that are listening, I'm showing a picture of an artery

cut and cross section. And the blood flows in the lumen. And there's a lining of the artery called the endothelium, which is one cell thick. That endothel lining, if you're able to strip it out of your arteries, is reportedly the surface area of six tennis. So it's actually your largest organ that you don't know about. But it's the endothelium when it gets impaired or dysfunctional. That's the first sign that there's something wrong with your arteries. And if you don't do something about it, there's more potential that the arteries will ultimately become inflamed,

and then plaque will start to form. So the endothelium is critical to vascular health, and that's what we do here is do multiple tests to look at the health of your endothelium. That's fantastic. You know, we're recording here in your office, Apollo Cardiology, based in St. Louis. You've been kind enough to host me,

my father and also my brother-in-law, Dr. Neil Patel, who's also a cardiologist, has joined us as well, too, and is here with us on the podcast. And what's been fascinating is to see that really we are in the midst of what I would call, you know, precision cardiology, precision medicine, functional medicine cardiology. We've had many functional medicine experts in different categories. There have not been as many that are out there in the world of cardiology. So we've sort of made the pilgrimage here, me and my family, to get the work up done, not only on ourselves, but to obviously educate our audience on all the advanced things that you guys get a chance to do. Now, I want to zoom out for one second here, because you've mentioned a few different things. And before we continue

on, and you have some great props for our audience here, some important things about cardiovascular disease that a lot of people don't know or sometimes forget. It is the number one killer in the world. In the four, you know, henchmen of the apocalypse, cardiovascular disease is number one. In the United States alone, we have around 800,000 plus Americans have a heart attack, and roughly 200,000 of those are reoccurring heart attacks. And I think of the 800,000 of Americans that have a heart attack each year, I think it's upwards of 40% it's their first heart attack, and they end up dying from it, right? I believe it's like somewhere around the stats, we'll fact check me afterwards and put the stats in the show notes. Globally, hard

disease is the leading cause of death, as I mentioned, and there are over 17 million deaths annually each year. And something that a lot of women, my audience, mostly women, that are listening, that they forget about, is we often think of heart disease is something that somehow skews towards men, but it's actually the number one killer for women as well, too. This is why this podcast is so important. The work that you're doing is so important. And the foundations that we're going to explain today is going to literally help save lives that are there. So I want to come back to you breaking down how you approach cardiology and how you think about cardiology in your practice and what you educate your patients about. When it comes to cardiology and people visiting their

traditional cardiologists and wanting to avoid a heart attack, some of the standard advice that they get, of course, are the basics, which are very important. Neil, I might even have you chime in on some of those basics, right, in terms of avoiding heart attacks. What are the standard things that you cover with your patients. Yeah. So is your traditional lipid panel, so specifically your LVL, not looking at any other specialized lipid particles or anything like that, what is your LBL number? Where is it at? What's your blood pressure at? What's your A1C are you diabetic? Super important to differentiate between diabetes and prediabetes, but the conversation around glucose. So the basics is lipid panel, blood pressure check, A1C, and then weight. Right. How much exercise do you do? Can you

tolerate a certain load of exercise. Can your heart accommodate that type of functional movement? And do you have any symptoms? So a very cursory way of looking at it, but it captures, you know, a good general audience. But yeah, that's that's the general approach on cardiovascular health and people even coming to us in our clinic saying, hey, I'm able to do X, Y, and Z. So I guess I must be okay. Right. Right. My LBL said it was okay based on my history. Okay, so I guess it's okay because I'm 34, my Ldeal is 100, not a big deal. I think there's deeper conversations that need to be had, but that's generally the approach or the conversation that happens.

Michael, take us from there. Obviously, you've been trained as a traditional cardiologist, but now in your practice, build and expand on those. I think you would agree with largely most of those things that are brought up, but why are they not the complete story and picture in terms of the latest advancements that we have with cardiology? And those were an excellent review of like the top five risk factors from cardiovascular disease, So high blood pressure, dyslipidemia, diabetes, smoking, and obesity.

They're very important, but there's a couple hundred other risk factors that could potentially damage your arteries and set you up for this. I'm sure we'll talk about APO being all the fancy lab stuff that we can do later, but it really comes down to what is the health of the arteries. And that's something that I did not necessarily get in my conventional training. I was an invasive cardiologist for many years, taking care of people in the middle of night, having heart attacks. It's very rewarding, but you sort of thought like, well, this person was already on his stadden.

They're already on an aspirin. They're already on a beta blocker and acinibur, the standard of care. They just had their second heart attack. What did we miss? And I was just getting curious, okay, what is the missing link? A lot of times it's inflammation or now that I know it's more low levels of nitric oxide is a big role. And so I just got curious and go to different conferences and kept finding new ways to think about vascular health. It's not that the conventional system is necessarily wrong.

They're just set up more to kind of take care of it when it's near the end game. Like most people honestly are not going to a cardiologist. for screening. They're usually doing this with a primary care doctor or if it's a woman, sometimes they're OBGYN. Because most time you see a cardiologist when you're having chest pain, short breath, palpitations, or maybe you have a very strong family history and you want to go like, hey, I don't end up like dad. And the general cardiologist will say like, okay, well let's do a stress test, an EKG, and maybe they'll do an echo to look at the heart function and they'll say, yeah, that looks generally low risk. But they didn't directly look at your

arteries. They were looking at kind of downstream effects. And I wanted to kind of focus more on like, Let's look at the arteries directly because just having high cholesterol is not necessarily a guarantee you're going to have plaque, but having normal cholesterol of the converse is the same. Half the time people have heart attacks, they have, quote, normal cholesterol. So it's part of the equation, but it's not the whole equation. So you were talking about the health of the blood vessels, right? What are some of the other things you explain to your patients and that you want to explain with our audience here on the podcast today about what other things make up healthy blood vessels in the body? So we talked a little bit earlier about the endothelium, and that's been known about for many years. But in the 1960s, they actually discovered some called the endothelial glycochalix.

That's a protective gel coating that lines the endothelium. And so think about taking a fish out of water and it's slimy. That's the glycopalics of the fish. Your arteries have that type of lining. It's a protective coating. If that coating is healthy, then the things that flow through the blood tend not to stick to the artery lining, like Velker. I got a picture in front of me that has Velker on it. So if you have a damaged glyco calyx, then it's much more likely that the lipoproteins full of cholesterol

and triglycerides are going to stick to the artery like Velcro, or that the white blood cells, or the platelets that are floating through the blood stick there. The glyco calyx is a shield. It prevents certain things from sticking to the arteries. There's different antioxidants in it to prevent the arteries from basically rusting from the inside out. There's different quagulation molecules in there so that if you get a cut, the body can instantly respond. And then there's different things that help with the immune response. But it's one of the things where it's like if the glycochalics goes down and you don't do something

to repair it, you're set up to go down this pathway where inflammation and plaque will form in your arteries. And so I think sometimes, you know, cardiology and primary care, they get to lipid-centric. And the lipids are important, but it's downstream. It's four or five steps downstream from when the glycochalics and then the thelium are getting impaired. Let's talk about the glycochalics. you know, what are the things that damage it the most that everybody should be paying attention to

and should know about in this conversation of catching it away sort of pre-heart disease? The glycochalix is fragile, but it is easy to repair if you get out of its own way. So again, think of it like a protective gel coating. The big things that damage it are going to be smoking, which nobody should be doing these days, even vaping is a problem. You know, there's heavy metals and other things that are going to be inhaled that could damage the glycic. glycolalics, high insulin and glucose. You know, there's approximately like 80% of Americans are not necessarily metabolically

that healthy. So just having high insulin glucose is enough to damage this protective gel coat, which is a lot of its carbohydrates and polysaccharides. We talked about the microplastics. That's likely the mechanism in action. It's damaging the glycopalics. Air pollution, oxidized lipids, heavy metals, COVID. The spy proteins had a predilection to damaging that coating.

So many, many things can damage it. You just had to figure out what's damaging and try to remove those things. Unfortunately, we have ways to kind of test how healthy the arteries are. And then there are products, supplements, and sometimes medications that can help regenerate the glycocalyx if it's been injured. You know, one of the things that you didn't directly say, but is part of your answer, is in a way ultra-processed foods. Where do those fit in?

And where does diet fit in to the glycics? The glycocalyx is heavily hydrated. It's like a carbohydrate shield. If you're eating high, you know, fructose corn sap, or if you're eating trans fats, you're eating things that are going to cause a lot of oxidative stress and inflammation, the glycocholix is going to get damage from that process. I'm sure we'll talk more deeply about food, but, you know, my idea is that, you know, photosynthesis has to touch, you know, your food web.

You know, food that's made in a factory is not really food. And so sunlight is growing your food and you go eat that food and your mitochondria then break that down, or you eat the animal that ate that plant and then you reverse that process. Whatever you're putting into your body, your glycochalix is going to sense that. So if it's fried fats, if it's tons of high fructose cornstub, your glyco calyx is going to likely get damage from that process. And how does the damage actually take place? If we were able to look inside, you know, is there an analogy or an idea, is it rubbing

up against it? And now all of a sudden that glyco calyx is exposed and everything underneath it is exposed? Like what's actually happening inside of the body? So, you know, think of like, if I have a little artery here, I'm showing in cross-section, or think of like a garden hose that's, you know, a circle and you're slicing it. Well, the blood's floating in the middle, but the glycochalix extends out into the room where the blood is flowing. And it's basically an invisible gel coat. But if you actually use an electron microscope, it's going to look more like grass at the bottom of a riverbed.

And it's just sensing the flow of the things floating by it. But there's little things that live in the grass, you know. It's kind of like the reeds in a, you know, like a marsh, you know, like the crabs, the shrimp, they're all living in there. Well, there's different clotting factors and there's different antioxidants like superoxide dysmutase and just sensing what's floating through the blood. But if you have high blood pressure or, you know, high sugar, it's going to basically do a haircut, knock those glycopalic tendrils off, and then what's floating through the blood basically starts

sticking there kind of like a pothole. And then your body can repair it and you go back to the normal. But if you don't repair it, then these things continue to kind of go further and further down into the sediment. So you can breach the endothelium. Then you get into intimal space, and the intima starts to swell. And then the white blood cells are coming in, and they start gobbling up what's coming into the intima. And then that cascade will lead ultimately to plaque formation. So it's really something where you think of it as kind of like seagrass, and whatever damages the seagrass is the problem. Try to withdraw that. And then the arteries can generally start trying to heal themselves. So if you wouldn't mind,

Just a quick recap of some of the top things in sort of a listical order that you want people to know that damages this very delicate coating inside of the body, which is a big part of how you see hard disease starting in its earliest stages. So the glycochalics is damaged by many things. Aging, which you can't necessarily control, but high insulin, high glucose, high oxidized LDL. Not all LDLs are necessarily problematic, the ones that have been modified. We've just talked about microplastics at the top of the hour, heavy metal, air pollution, you know, those are probably the top things that are going to be damaging glycochalix. We talked about what damages the glyco calyx. Let's talk a little bit about what actually helps us protect it, what strengthens it. And this really gets into sort of your approach to your

interventions that you recommend on the lifestyle side for people strengthening their blood vessels and their mitochondria. So what supports this coating inside of the body and leads to healthier blood vessels. Always start with trying to withdraw the things that are doing the damage. And so taking a thorough history, like, hey, the person's smoking, get them to stop smoking. They do no exercise? Get them to do exercise. They don't eat green leafy vegetables.

Get them to do that because there's precursors in those green leafy vegetables that ultimately that become nitric oxide. If they're using antiseptic mouthwaters that disrupts their oral microbiome, get them off that. So a lot of times it's trying to withdraw the things that they just didn't understand would be impacting their arteries. And then since a lot of it's metabolic, it's affecting glucose and insulin levels, whatever lifestyle intervention you want to try to do to improve their insulin sensitivity.

So, you know, I'm with your friend, Dr. Lyme, you know, this is muscle-centric medicine. You know, 80% of your glucose is destined to go to your skeletal muscle. So what do you got to do that? Well, you got to get this person doing more resistance training. You got to meet high-quality protein so that they can lay down more muscle units to be able to burn that glucose. So doing anything you can to get them to be more metabolically healthy is key. And then you can do the other advanced testing that looks at...

things such as high homocysteine, high uric acid, high oxidized LDL, and then there's different supplements and medications that can be used to dial those things back as well. And then if that's still not working, there are different glycochalics promoters, different supplements that basically give that protective gel coating, building blocks to try to lay down a better gel coat, and there's different antioxidants to try to prevent that gel coat from rusting in the first place. So there's a couple of commercially available supplements that have been shown to help improve the glycoccalyx. You know, the last few years has been an explosion of research and awareness about metabolic health,

which is also in those four horsemen of the apocalypse, right? Number one is heart disease. Number two is cancer. Number three is metabolism disorders. And then number four is Alzheimer's and dementia, neurological issues that are there. There's been explosion in focus on metabolic health. If you just look around to the population, you wouldn't think so necessarily. But it's a little bit of a delayed thing.

there's more and more physicians that are out there that are talking about the importance of metabolic health at the earliest stages. There's more people that are ever been talking about pre-diabetes and having higher than average blood sugar and how we need to start paying attention to this. There's been more people that have been looking at continuous glucose monitors and companies like levels and other places that are out there. Neal, you know, being in this sort of quote-unquote traditional system, even though Kaiser does a great job to be a little bit ahead of the curve, what are some of the things that you talk to your patients about when it comes to metabolic health and how important it is for them.

The way I kind of tell them is very similar to what Dr. Feynman was saying is it's really just about how do you build your body's resilience to all the things that it is exposed to? Externally, there's a lot of things with microplastics, these are water filters. Internally, which is the metabolic health, is what are you doing regularly to kind of help promote the health and the resilience of your cells? So I usually tell people cardiovascular health, so getting some degree of cardio in a week, and then resistance training to help kind of build up those muscle reserves to kind of handle the glucose load, to handle things such as frailty and to help you kind of just move through life a little bit better.

A lot of the times those exercise or those interventions can actually help with pre-diabetes diabetes control. It can also help you increase nitric oxide synthase, which helps you increase your nitric oxide, which can over in the long term only contribute to a lower blood pressure, contribute to better metabolic flexibility is what I call. So I'll generally tell people is you want to schedule this like you schedule anything else in your day. You want to schedule your exercise time. You want to schedule your sleep time. You want to make those priorities just to make it a lot more fluid.

And the key to all of this is just sustainability. How long can you do this and picking at the different levers that you know you want to get involved with? Because that will keep you consistent. That'll keep you happy. That'll keep you wanting to keep coming back for more. You know, both of you talked a little bit about nitric oxide. and we really haven't gone into just how important of a role it plays on everything that we're talking about today. So Michael, I want to pass it over to you, right?

You are one of the biggest champions of why nitric oxide is so important and why it's so problematic that its production lowers especially as we age, especially if we're living like most people do in the world. So what is nitric oxide and how does it play a crucial part in cardiovascular? So nitric oxide is a gas. It's very short-lived, but in the vascular system, it's a vasodilator. And while, you know, I learned about it in my traditional training, I didn't understand how mission critical it actually was. When we have patients come into the hospital with chest pain, we're also giving them, you know, nitroglycerin. We're just flooding them with an agent that's going

to give them a ton of nitric oxide to dilate their blood vessels. But nitric oxide, normally, it's produced right on the lining of the arteries. So if the glycochalix is healthy, then the lying endothelium is going to be able to release nitric oxide. So in the presence of oxygen and arginine, there's an enzyme called endothel nitric oxide synthase. That enzyme will then convert it to citroline and nitric oxide gets kicked off. The nitric oxide gas then diffuses into the muscle into the artery and then that causes the muscle artery to relax. That keeps the flow normal in your artery. And nitric oxide also somewhat repels the lipoproteins and the white blood cells from sticking to the artery in the first place. So you have healthy nitric oxide levels, you should have healthy arteries.

But after the age of 40, that endothel nitric oxide synthase enzyme tends to slow down. It's just not as functioning as it was when you're 20 years old. So Mother Nature built in a backup pathway, this intersaliary pathway. When you eat your green leafy vegetables and your beets that have high nitrates in it, if you have the right nitrate reducing bacteria in your saliva, it will convert that to nitrites. Those nitrites that get swallowed go into your stomach. If you have stomach acid, there will all of them be a process where nitric oxide gets produced. So if you use a lot of antiseptic mouthwash, or if you use acid blocking medicines, you're going to

disrupt that backup pathway. And so it's sort of kind of like a two strikes you're out. If one pathway is working, you probably still have enough nitric oxide that your arteries are going to dilate and your blood pressure will be normal. But if that salivary pathway never worked or you broke it and you're now 70 years old and your endotheliotic oxide synthesis inside and doesn't work very well to begin with, then that's when you start seeing these stiffer arteries and higher blood pressure. And if it's long enough, like that they're going to have more and more plaque in their artery. So nitric oxide is often the canary in the coal mine is that there's a lot of tests that we did today that showed us like

how healthier levels are right now. But the signs and symptoms, if you don't have this type of testing is you could just have fatigue, you could have brain fog, you can have erectile dysfunction. I probably said it many times, but ED equals ED. If you don't have enough nitric oxide and the penis tissues, you won't maintain erections. That's the big canary in the coal mine that there's something wrong with your vascular system. Oftentimes, you know, patients take the little blue pills. It's not that that's the problem, is that you don't have enough nitric oxide going into the system. We have to figure out why you don't have that and try to replete that as possible. Just a reminder of some of those things that you mentioned, the healthy

lifestyle habits that people have that lead to high levels, especially as we age, of nitric oxide. If you can give it a little bit of a recap on that. The biggest one is probably going to be exercise, is your exercise and you're forcing blood across the endothel glycopalics, and then the underlying endothelium will release nitric oxide. So exercise is one of the best anti-aging drugs, partly because it's releasing nitric oxide. The second one, One is going to be sunlight. It's the UVA spectrum of sunlight when it strikes your skin that nitric oxide is going to get liberated from the blood vessels.

And then dietary-wise, it's mostly the green leafy vegetables, the spinach, the rougolas, the cales, and beets, those just have high dietary nitrates. And then if you have the right situation where you have the right bacteria in your saliva and you have stomach acid, more nitric oxide will get produced. So I want to talk about sunlight just for a quick second because there's so many different misconceptions about it. You're talking about wanting to have us in place. our exposure to the sun to support the production of nitric oxide.

Talk to us about why that's important and how that actually happens and why do so many people have this idea that we generally want to be avoiding the sun outside of vitamin D production. And that's the challenge is that people think the sun is all about tans or vitamin D production. And it's so much more. I tie back into the photosynthesis. We would not have any of these plants and foods to eat if we did not have sunlight. So to think that the sun is all bad is definitely misguided. But it is a tool.

You do not want to burn. You do not want to be fried. You don't want to cause all this oxidative stress and inflammation to your tissue. So if you've avoided the sun for years, it is not the right answer to go out at noon and start baking. Your skin needs to build up a solar callus over time.

So I always lead it back to like, what would an optimal day be? If you're up before sunrise, you want to keep your light very dim because you don't want to basically disrupt your circadian biology. The first bright light that enters your eyes, should be sunlight outside. You get that light into your eyes, and it sets the body's supercosmic nucleus, which is the master clock on the brain

to tell the rest of the organs, hey, it's daytime. So cortisol, your sex hormones will start to rise. But in the morning time, there's no UV light. Your skin is not going to burn. But somewhere between half an hour to an hour after the sun rises, the spectrum of UVA light will get through the atmosphere. Typically, when your skin starts feeling warm,

that's when UVA is getting through the atmosphere. And then depending on how high you're off of the equator, will determine when UVB is going to be available. And when UVB strikes your skin, then that's what's going to sulfate the cholesterol and ultimately become vitamin D. And so there's free apps out there that will tell you, where the sun rises at your local location,

when is the UVA window open, when is the UVV window open? And here in St. Louis, there's two months out of the year where the UVB window is completely closed. The sun never rises high enough in the atmosphere to make vitamin D for two months in St. So you have to know what are the proper times to go outside for these different wavelengths. But from the nitric oxide standpoint, it's really when that UVA spectrum's out.

So it's going to be half hour to an hour from when the sun rises, about that half hour to hour before the sun sets is the main window. Do you need to be out there in the entire time? Absolutely not. You have to kind of build up that solar callus. But if you have high blood pressure and you're not getting proper light exposure, no, the light basically is acting as a natural calcium channel blocker. You can lower your blood pressure if you're getting proper light signals.

So one of the most famous protocols that's out of right now is like the Huberman Protocol, where people go out and they get that morning sunlight and that evening sunlight primarily for the regulation of our circadian rhythm, and then also to support more energy in the morning and also deep, restful sleep at night. And I can't remember exactly you could probably pull it up and put it on the screen here, but I think he generally recommends, you know, five to 10 minutes first thing in the morning when the sun comes. A lot of people like to sit outside and drink their coffee and just enjoy and get a little bit of sun exposure. And another really cool thing is, you know, you can use if you have an iPhone or the weather app, you can see that

the UV spectrum doesn't really start to really pull up in that first hour of the day. So people who are really afraid about sort of aging their skin, it's not going to be at the place super early in the morning and super late at night where that's really going to be taking place. Is that accurate? That's accurate. And it's mostly the lack of burning. You do know what to burn because that is what's going to cause the DNA damage and the rapid photo aging. But it's the unbalanced light that tends to cause some of that photo aging. So you get a lot of melasma of your skin. If you're just in front of these devices all day long soaking in 5,500 Kelvin blue light from your devices, it's the red spectrum of light that balances that out. The red light is anti-inflammatory. The red light

stimulates collagen production and prevents wrinkles. So the balance of the light tends to prevent that. That being said, you're right. People are more sensitive to light that more. morning light is preconditioning your skin. If you get into that habit, you know, five, 10 minutes a day. More is fine. You know, if you're sicker, you're probably going to need more. But if you're generally healthy, you know, it's instantaneous that effect that light hits that melanops or something the eye. You set the clock. But it is a peaceful time of the morning. You know, you can also stack your hacks. You know, you can be grounding outside. You can, you know, do other things while you're out there. Think it as like a sunbreak throughout the day. Your body's always trying to

crave what time of day is it. And you're giving it those signals, those zeitgebers, the light that enters your eyes and the timing your nutrients come in are the two biggest ones. And so the body wants to figure out that there's a light cycle and a dark cycle. And so once the sun sets, no more blue light is supposed to hit your melanopsin receptors. Your body gets a big signal. Oh, it's nighttime. And three to four hours later, you should be going to sleep. Your cortisol levels are dropping.

Your melatonin level start to rise. And melatonin is the hormone of darkness that helps you stay asleep. But melatonin is also critically important as an antioxidant is essentially the fuel that repairs the mitochondria that had been potentially getting damaged during the daytime. And you're making all these different hormones based off the light signals that hit your eyes and hit your skin, but they get released during different times of darkness. So going back to what I was sharing about the human protocol and we'll fact check it afterwards, but I think it's like five to 10 minutes in the morning. You know, he's trying to give the minimum effective dose for what he's talking about.

What is your recommendation when it comes to this category? And, you know, I learned this phrase from you and you talked about on the podcast last time, photo biomodulation, right? That's the practice of getting this sort of red light and other light spectrules, but in particular we're talking about red light in a way that's therapeutic for your body. So what are you recommending to individuals? And I know it depends on sort of where they're at, but as a base level, what's your recommendation? So always want to use natural sunlight because it's always going to have the right wavelengths of light. And so if you're somebody who's very, you know, pasty white and you burn easily, start very slow and build yourself up. But that morning light will get that skin condition for later

when UV comes out. So if you do this for a few weeks to months, you're much less likely to burn high noon in July wherever you're at. But back to your question about photobondulation, I often joke as a sun plement. You know, it's not supposed to replace the sun. You use it when you don't have access to the sun. Or you have an acute injury and you're just trying to get more photons of light into that injury. So in my office here, I have multiple of these different red light panels. The best way to think about these panels is that the light is absorbed into of the mitochondria and three big things happen. It's going to release nitric oxide from the mitochondria,

and that's going to dilate blood vessels. It's going to decrease reactive oxygen species, free radicals. You're not going to rust as much when this light therapy is being applied. And the third big thing is it's going to produce more ATP in the mitochondria, more energy. Then your body takes that energy and does what it does. Your brain works better, your heart works better,

your musculoskeletist system works better with more energy. So photo modulation, multiple use cases head to toe, but it's mostly to charge up your mitochondria and then they know what to do with that energy. So we got on this topic of light therapy, photobiomodulation because we're talking about nitric oxide. You know, and to recap there, there was a few things you mentioned, exercise, which what is your dosage that you talk about with patients, you know, from your end, Michael, and then we'll go over to Neil. What's your recommendation? I mean, it always depends, like, where's the person starting from? Like, if they're basically just coming off the couch,

trying to get them to doing resistance training like twice a week, and then trying to get, you know, a couple sessions of zone two type training initially. And zone two is the low and slow cardio where you're just trying to build mitochondria efficiency at being able to burn fat for energy. And then once you've got enough of a base of the zone two, then you can start teaching them how to do some of the interval type training. But if somebody's more fit, then it's really what are their goals? Like, if it's really like longevity, well, there is a minimal effect of dose. You know, you probably want at least 150 minutes of moderate activity a week and that resistance. component two to three times a week, that's the minimal effective dose, but I've also worked

with people who are professional bodybuilders and athletes. That's a different skill set. I think of that more as like a skill versus a health promoting activity because a lot of the times the challenges those guys face is that they're overdoing it. They're overtaxing their nervous system. They're short sleeping themselves and they don't have the ability to recover from all oxidative stress and inflammation that they put on their system. So they can be very, very fit looking on the outside, but they've thrashed their vessels.

There's just been so much in the field dysfunction because of the lack of recovery component to it. So that's why often I tell people like, show me, I'm from Missouri. You've got to show me that your arteries are healthy. And so exercise is the greatest drug, but it is a proper dose effect. Yeah. And generally for the vast majority of people who are listening, they're not going to be overdoing it. They're probably underdoing it a little bit. That's really a conversation for like professional athletes in some sort of, you know, context.

And maybe even sometimes like people who are regular marathon runners. I've heard this from a lot of individuals. In fact, David Promo was on the podcast last week. And he had been struggling for a few years with some sleep issues and other things that were there. And he went in to get diagnosed. And I think he was at the Mayo Clinic or Cleveland Clinic. And they found out that he had AFID. And then his doctor had asked him, you know, let me guess, you're a long distance runner.

And they said that a huge percentage of his patients that have AFib, I don't know if either of you have seen this, are individuals who are overdoing the sort of long distance running, the marathon running. Is there any truth to that? Yeah. Do you get an adaptation with exercise where you can see in young patients, their ventricle, which is the pumping chamber of their heart, gets a little bit thicker. So that by itself is not abnormal. If you have really uncontroll high blood pressure, then the thickness can become abnormal and that can lead to other issues.

But the top chamber, the atrium, that's where the atrial fibrillation starts, and that's where the terminology is, that can actually stretch in accommodation to all that extra blood volume that you're getting as an athlete. So we see this a lot in football players where they will come in an a fib, but it's because of that long adaptation where the top chamber of the heart stretches out, and that predisposes people to having an irregular heart rhythm or atrial fibrillation in this case. And it could just be, again, like anything else or diabetes or LDL or high blood pressure, how long were you exposed to that? We'll call it an insult even though it's not necessarily

a negative connotation. How long were you exposed to it? And under what conditions? Anything else that? No, very much so. And I have the little heart somewhere I'll show you guys. All right, so those of you that are listening, Michael just pulled out a heart model that is going to walk us through and you'll describe what we're talking about. Correct. This is not life size. This would be more like a, probably a cow. Like the human heart is about the size of your fist.

But as he was mentioning, like the atria are the top chambers, the ventricles of the bottom chambers. But in patients who are high level athletes, you know, they're going to increase their stroke volume and improve their cardiac output by stretching out their atria and sometimes even stretching out the left ventricles. So there's pumping this blood around this circuit so much faster to deliver all the heartic muscle. deliver all these oxygen nutrients to their muscles. But this top chamber is much thinner than the bottom chamber. The bottom chamber is relatively thick. But the top chamber, it's kind of like a balloon. The more it gets stretched out, the more it may not actually shrink back down.

And so there's different echo criteria to tell you, like, do you have mild, moderate, or severe left atrial enlargement? It's one of those cases where the larger the atria are, the more likely there to have more of this atrial fibrillation. And it's, you know, something I learned from some of my attendings was that like, aphib begets a fib. So the longer you're in a fib, you start basically burning in different pathways in of atria that you're just more likely to keep going in and out of this.

And people who tend to be younger, they tend to be much more sensitive to going into atrial fibrillation. We've definitely had older patients who have no idea that they're in it. Partly, they're just not that active. But if somebody's very active, the loss of their atrial kick could be a big problem for them. So about 20% of your stroke volume comes from the atria. So there's a valve, the mitral valve, between the top chamber of the left atrium and the bottom chamber of the left ventricle. So as the blood comes back from your lungs, it's just passively

flowing through this atria into this mitral valve into the ventricle. But then the atria contracts and squeezes about 20% more of the blood through the valve, the valve closes, and then your left ventricle pumps and sends it out through air-ed up to your brain and the rest of your body. But in H-ferbilation, instead of an coordinated pump, that atria is quivering like a bag of worms. And so it's not going to be pushing that extra 20% down to the left ventricle. Well, at res, that's probably not a problem for most people. But if you're a high-level athlete trying to sprint, you know, 18 miles an hour and you lose 20% of that, you're just not going to be able to go anymore. And so that's why they're so symptomatic when they get that loss of the at atrial kick.

So again, zooming out, we were talking about exercise because of its role with nitric oxide and nitric oxide with its role with a healthy vascular system in general. And is it fair to say just so everybody really connects the dots because we're not dealing with probably a lot of professional athletes on this podcast or marathon runners, a few of you out there. to you. If people don't use it and actually exercise on a regular basis, they're going to have low levels of nitric oxide most likely, right? If they're not regularly active in the blue zones that are out there, they're not exercising necessarily, but they're active all day long. They're squatting. They're getting up and down. They're gardening. They're doing things. They're getting

a ton of steps in. And so as we age, the less active we are, that's going to make us more at risk for cardiovascular disease. So I want to jump out to another topic that you mentioned with nitric oxide, which was making sure that we get our nitrates inside of our diet, right? What do you generally recommend for people who are listening when it comes to getting the minimum that's needed to make sure they support their nitric oxide? This gets where it's a little bit challenging is that it's going to depend on where they're getting their foods from. And the part that isn't as fun to know about is that organically grown food is going to have 10 times less nitrates than conventionally grown because of the soil

conditions. So you almost can't eat enough organic greens they actually get a load of nitrates through your diet. And so in those people, if they start having a lot of issues, they're probably going to end up on a concentrated beetroot supplement that actually has that amount of nitrates in it, or they can take various other supplements to promote nitroxide if they don't want to do the juices. But you always want to try because even if you can't get all the nitrates through the vegetables, there's other polyphenols and other things you want to get from the vegetables, but you may not be able we get all your nitrates from your diet. Okay, great. So we have exercise. We have making sure that we have our beets and our dark leafy greens, if not, you know, potential supplementation. We'll get

into a whole category on supplements. But just so we don't leave people hanging, is there a favor that you like when it comes to some of these beet supplements or nitric oxide support supplements? The beat elite has been studied a lot. It comes on like these little plastic bottles, unfortunately. But maybe the nitric oxide can block some of the microplastics, I'm not sure. But Beta Leed has a concentrated dose of either 300 to 400 milligrams of nitrates. It doesn't taste that bad. I have some in the fridge for patients to try if they're interested. And then if people really don't want to drink it, there are other concentrated lozenges or

capsules that can kind of help promote nitric oxide production. Great. We'll chat about some of those. So we have making sure we get our nitrates. We have making sure that we have exercise. we also talk about making sure that we have proper exposure to the sun. And then if you're not, supplementing with things like red light therapy can be components that could be helpful.

Are there ways to measure nitric oxide and talk about some of the things you had, me, Neil and my dad Kumar, who's here with us today? Talk about some of the things you had us to do to see how healthy is our nitric oxide production. So that's what we're all set up here to do at a biocardiology, is look for vascular disease at the earliest stages. Now, there's not really any commercially available testing to be able to directly test the endothel glyco-calyx. Now, there's some microscopes that are in development, but there's nothing that can directly look at how healthy the glyco calyx is. So you have to kind of look at, like, what is the layer below that?

Because if the endothelium is not working well, then you already assumed that the top layer is not working either. So we did some testing that looked at your nitric oxide levels that you could produce through your saliva. So there's a test strip, you put the test strip in your mouth, get the test strip wet, then you kind of close the little plastic strip. and it's kind of like litmus paper, it's going to change a color. And the brighter red it is, the more nitrates that you're getting through your diet is the first part of the test. And the second part is, do you likely have the right nitrate reducing bacteria in your saliva? Because there are certain people that just lack that bacteria, or they're using antiseptic

mouthwashes and destroying those bacteria. And so they can eat all the beads and the greens they want in the world, but it's the bacteria in their saliva that breaks those nitrates down. So we did those tests on you today. were a little bit low on that part, but the later test showed that you make plenty of nitric oxide. So it all has to kind of rhyme. We just know that, okay, we got to do some blood work to figure out is there high uric acid or homocysteine or something else that's sort of breaking that pathway.

Then we did test to look directly at the arteries themselves. So a device that does pulse wave velocity, it clips to your finger, and it gives us your heart rate, but it's also looking at the elasticity of the arteries. So the blood leaves your heart, goes in those arteries, and if your arteries are healthy, they're going to expand and then contract. And it's going to be kind of like an accordion snapping back and forth. They're not going to be like a little lead pipe. And this test takes one minute, not painful, and it gives you a score between one and seven.

The lower the score the better. So you are type two today. Most are type two, but half of them are almost type one. So you're almost completely excellent on that test. So very good pulse wave velocity. So that tends to me that the Arbdis probably can release nitric oxide efficiently if they can stay very elastic. So that's a quick and easy test that we do on every patient.

walks in here. There's no real special prep you need to do for that part of the past. Can I add in one more item before you continue? Neil scored a type one, I believe. He did. What is he doing right that I'm not doing? I need to aspire to his level. What do you think are some of the things that he's doing that I could be incorporating? We'll have to actually see what the blood work shows because I don't think it's actually going to be a major lifestyle thing. I think it's going to be removing something that's in your blood work that has the effect. I think you probably have more lipid issues than he does and that might be the differentiator. He does also work out

pretty much every morning. So I know there's a higher degree of probably cardiovascular fitness that's there. He also goes rucking on the weekends as well too. Neil's been a big inspiration to our family when it comes to all things fitness. So I need to start incorporating some of those things inside of that. And he beat you by like that much. It wasn't like a big deal. But he also outscored me, you might be getting to this in a second, on the endopat test.

He did beat you a little bit on the endopat test. Can you talk about that test? And does that help you at all in understanding how much nitric oxide production is going or if the blood vessels are healthy. So the endopad test is a non-invasive test. A lot of calibration work was done at the Mayo Clinic, which is one of the world's expert in cardiology facilities. And I first learned about this device back probably in 2013, 2014,

from Dr. Mark Houston and Dr. Nathan Bryan, who did a lot of the research with this type of device and some of the early nitric oxide lozenges. But the way that this device works is that the person has to come in fasting, no caffeine, because you don't want anything that's vasoactive that would constrict their arteries. There's a five-minute warm-up period

with the test. So you have probes on your finger that's measuring the flow in each fingertip. It looks like a little seismograph as the flow is going through the finger. So the five-minute warm period, make sure all the devices are working well. And then there's the test part. So you have a blood pressure cuff on your brachial artery. We pump up that blood pressure higher than your systolic blood pressure, and you do not have high blood pressure by far. And so that temporarily cedes the flow to the arm. And so that probe then doesn't sense any more blood flow, and the line just goes flat. The other arm access the control and you keep seeing it going up and down like a little seismograph or metronome. After five minutes, we then release the stopcock and the blood pressure

cuff and the blood's going to rush back down into your arm. And that's basically the stress test for the arteries. That blood flow comes rushing back down into your arm. It's going to flow over the endothelial glyco-calyx. The glycocalyx senses this sheer stress, oh, here comes a big slug of blood, tells the underlying endothelium, release nitric oxide. Here comes the blood. The nitric oxide gets released, the smooth muscle and artery relaxes, and the blood rushes back down into your hand. and your hand wakes back up because it kind of feels like sometimes your hand fell asleep, like you had your arm on your arm and cut out the flow temporarily. So some people get that tens of needle sensation.

But when that blood rushes back down into the hand, that's called reactive hyperemia. So the test will calculate a score known as the reactive hyperemia index. We're essentially looking at we stressed your artery, how well does it respond to that stressor? Normal is greater than 2.1. That means your arteries dilate 210% over the baseline. That tends to mean your body's pumping out nitroxx. on demand. If the score is less than 1.68, that's abnormal. That's evidence of end-to-field dysfunction. The arteries can't release nitric oxide very efficiently, and that person's more prone

to developing plaque in their arteries if you don't fix that condition. But optimal is between a 3 and 4. The arteries should triple or quadruple in size. And yes, he did beat you. I think you got 3.2 and you were 2.4 or 5 or something in the range, but you're both normal and he'd beat you a little bit. So it's often the case where you just had to figure out what's still floating around in their blood and withdraw that so they can get to optimal. But sometimes people start out near one. You've got a lot more work to do in those individuals. Super fascinating.

Anything else that you want to say about nitric oxide in terms of measuring it or things that you look at here or education that you provide to your patients that come to apollo cardiology? Sure. So one of the things that we did today that anybody could do is just your blood pressure. Your blood pressure is a good surrogate for is that likely that your body can make nitric. First start off like how to properly take a bloodbusher. Your feet should be on the ground, you should be in a rested position, your back should ideally be supported, and your arm should be at heart level, and you should use some type of blood pressure mining device that goes on your break your artery.

Now there are devices that can go on the wrist, but those sometimes aren't well calibrated, so you want to steer clear those when you're trying to get a true baseline. But ideally, your bloodbusher should always be less than 120 over 80. I think Drew's central bloodbushers were like 90s over 60s. That's what mine is. It's normal. There's no too low of a blood pressure unless you're symptomatic. If you were light-headed, dizzy, had exercise intolerance, okay, are you taking any supplements or medications that are going to be pushing your blood pressure down? If you're not, if that's just naturally how you are, I'm not as concerned about that blood pressure being that low. But typically, 120 over 80 is kind of the cutoff you want to start looking at.

If you're consistently 140 over 90, that might not be high risk, but it is a marker that you already don't release nitroxide very efficiently, and we've just got to figure out why that is. I know we get this question a lot in clinics and so maybe the viewers are having the same question is hey my blood pressure I've checked it a few times last month and it was quote unquote normal I saw my primary care doctor or saw a specialist and I generally tell people like more data can sometimes be helpful in this realm especially with blood pressure if you agree with that dr. Simon so it's like check your blood pressure every day the same way do it for a few weeks keep a log then you get a trend because I generally don't make a decision off of just one number

Would you? Very much so. I mean, like, unless somebody comes to my office, then they're like 180 over 90. Like, okay, I got to act now. Like I put out the five-a-long firewall and figuring it out. But correct, more data and especially at home, like under your normal conditions. You know, there is a circadian rhythm of your blood pressure. It changes throughout the day.

And one way to really kind of see that fluctuation is to do a 24-hour blood pressure monitor. And there's a couple different vendors that we have a newer device called the BioBeat. And it's kind of like one of the holter monitors that just, sticks on and it uses photoplasmography or PPG to non-invasively measure the blood pressure and it's well calibrated towards the brachial cuffs. So this little monitor sits on your chest and every 15 minutes it takes a measurement. And so then you get a full on 24 hour average blood pressure but more importantly then you can see like what times of days

are some of these spikes when the blood pressure load goes over 140 over 90? Well you're stuck in traffic you know you just drink five espressoes and an energy drink like you'll figure out like what are the triggers that tend to spike it? But the key time is really saying like, does your blood pressure drop while you sleep? Because your nocturnal blood pressure should drop 10, 15% while you sleep. If it doesn't, that's sometimes a marker of sleep apnea. You know, you're putting a lot of stress on the vascular system when you're not opening your airway, and your blood pressure won't drop at that point. Okay, well, figure out how to get their blood pressure to dip appropriately, and you really take a lot of that vascular stress often. But yeah, a lot of times I get that

question a lot like, oh, I just have white coat hypertension. And today I'm wearing white, but often I don't wear wideness off because I don't want to influence people's ideas on the blood pressure with the colors. But white coat hypertension is just stress-induced hypertension. And we didn't talk about it today so much, but yeah, when we were doing that max pulse device, I need to look at your pulse wave velocity, how elastic the arteries are. That test also looks at heart rate variability, which is just an instantaneous measurement, how much stress your body is sensing.

So sometimes we get an idea that if the person comes in and the blood pressure is elevated And they say, like, it's just only high when I'm here. I'll look at that part of the test. And when I see that they have really high sympathetic tone, I'm like, it's possible. But I just tell them, like, your body doesn't know the difference between your blood pressure's high because you're sitting in doctor's office than when you're out in public, when you're, you know, in line for something and you get cut off in the traffic. Like, the body doesn't know the difference.

The arteries are going to respond the same way. And it's really the load of it. Like your blood pressure is up for one minute a day, not a problem. But if it's hours and hours, that glycolycolics and underlying endothelium, it's just going to get damage to that high shear stress. Yeah, I just find daily blood pressure checks allows people to get involved in their health. Correct. Something easy, simple, and you can trust yourself, and you can go to your doctor and you guys and have that thorough conversation.

One of the top things that's searched on YouTube, just in general, is why do I have high blood pressure? I think it's a good opportunity here to just cover something very basic. A lot of people that are listening today are dealing with high blood pressure or have a family member who has high blood pressure. What's going on? I mean, they call it the silent killer for a reason because the majority. majority people don't feel any symptoms with that. I mean, by time you have symptoms, you know, you're having headaches, vision changes, chest pain. It's been going on for quite a while or you have a really, you know, kind of bizarre kind of like secondary reason why you have high blood

pressure. But that being said, you know, you want to start early in life and get a baseline, you know, your blood pressure should throughout life consistently be less than 120 or 80. Just because it tends to go higher when you're older doesn't mean that it's actually normal or good for the vasco system. It may be common that people, blood pressures are 150, 160 when they're 70 years old, but the blood pressure and the blood vessels, they don't care. But often we'll talk about patients that, like, high blood pressure is not necessarily a disease. It may have an ICD-10 code and we can quote bill for it, but it's just a maladaptive response to the arteries trying to provide profusion to the vital organs. But I often look at it as that you have to make sure that

it's not a nitric oxide issue to begin with, because that is just so common. If you fix nitric oxide issues, often their blood pressure tends to improve significantly. But I think we're talking offline about it's like, you know, how do you do a good workup for hypertension? Well, first, take a good history, you know. Most of the stuff is lifestyle induced. Like, what is this person fueling with both mental activity and food-wise, you know? Are they watching like toxic news and eating toxic food? Their blood pressure is probably going to be high from that. Is this person completely sedentary? Their blood pressure is likely to be high. They have level 10 stress. They're type A. Okay, well, you need cortisol for some things, but if you have cortisol that's high all the time,

it's going to raise your blood sugar, it's going to constrict your arteries. You're going to age faster from the inside out, having high cortisol all the time. And then the forgot one is how well do people sleep? I mean, most people are not sleeping seven and half, eight hours and feeling super well rest of the next day. If you don't sleep well, there's almost no change you're going to have really great optimal blood pressure the rest of your life. So kind of work on the low-hanging fruit lifestyle things first, then you can do these type of testing, like monitor your blood pressure at home and keep it long. If you have access to somebody who can put a 24-hour monitor on,

that's really the gold standard to tell you what your blood pressure are doing out of the environment. Then you can do a whole host of blood work to figure out, like, is it a metabolic issue? Is it high homocysteine, high uric acid? You know, some of the tests you guys did today, like is it a nitric oxide issue? Genetics, there's many, many genes that affect, you know, blood pressure and they tend to stack on each other. So often night patients come in saying, like, I'm doing all those lifestyle things. I still have high blood pressure. I'm like, all right, well, check the gene.

check the genetics and they'll have like eight, nine, ten genes that tend to kind of be polygenic. It's not just one gene raising. It's eight genes interacting. Okay, well, try to fix what you can with lifestyle and nutrients that are deficient, but sometimes medications are the right choice to lower the risk. And often these genetic testing will give you that kind of precision medicine. Oh, an asinibur will work best in this individual. A diuretic like spurnal lactone will work best in this individual. And so just be very precise with your treatments,

and the blood pressures tend to come back down to where you're. want them to be. So we'll get into blood work in a second, but let's talk about genetics since you brought it up, right? One of the things that you offer here at your clinic and with the patients that you work with is genetic screening and to look at specifically do you have certain genes that make you, in my case, for example, hyper reabsorber of cholesterol and lipids inside of the body. You mentioned some other examples of why, you know, you're looking at genes.

If you could expand a little bit on that thread of some of the insights that you've gotten to personalize a patient's unique plan that you're putting together for them. So patients that come to see me often are asymptomatic, and that's the goal. They don't want to go on to have a heart attack stroke or be on medicines for blood pressure per se, unless it's something that really needs to be done to reduce their risk. So the genetics that I typically offer initially for almost anybody, there's four big ones. LPLLA, lipoprotein LLA, which approximately 20% population has, is a type of LDAL, but it's more athergenic and thromogenic. It's more like it it called plaque in the arteries, and more likely it calls the arteries to clot.

And so you want to know do you have high levels of this genetically inherited lipoprotein? So I check that to everybody. I will check apolyproprotein E as an echo because that has an effect on your lipoproteins, your metabolic flexibility. People have an APOE4 tend to have more risk of insulin resistance, diabetes. And the APOE4 carriers also have an increased risk of Alzheimer's, which may be diabetes type 3 of the brain. It doesn't mean you automatically get those diseases, but you're at higher risk. but you're at higher risk, and so maybe you need to be more aggressive with your exercise

routines, your nutrition needs to be a little more locked in. 9p21, that's colloquially known as the heart attack gene, 9p21, mostly has an effect on the endothelium and underlying smooth muscle. So some people have this gene, and that's the cause of why they have low nitric oxide to begin with. So people end up more likely on supplements and medications to support their arteries. And then the fourth gene I often will check is KIF6, K-I-F, and the number six. People who have one abnormal copy of that gene have a 50% relative risk increase of cardiovascular disease.

So they're more likely that plaque in the arteries if they have this gene. But the carriers of the KIF-6 gene also tend to be able to tolerate statins better than people who don't have that gene. So I'm not telling people that stenters are for all, but if you have certain genes, certain meds may work better for those individuals. But Kif-6 is also associated with erotic aneurysms. And the order is the blood vessel that lets the blood out of the heart and it takes the blood down for the rest of the body. the rest of the body. But in some people, their erudic dilates out, and that's an aneurysm. If it gets to a certain dimension, there's more risk that that irritate will tear and cause a dissection, and that potentially can be a fatal consequence. So patients who have a KIF-6 abnormality,

they may be at higher risk for that, so they probably need more closely to be followed up with certain types of imaging, CTs or ultrasounds to look at the erotic dimensions then. So that's the genetic component of looking at a patient to further personalize for them, especially if those are individuals that are coming in in a more preventative way, right? If somebody just had a cardiovascular event, you're not necessarily first going to genetics. You're just trying to treat that situation and deal with that situation. But it's nice for our audience here who is in the same bucket often as me. You know, I just turned 40, you know, a year or two ago.

And I'm really thinking about cardiovascular disease runs my family. I've had a history of high LDL. The first time I got my APOB measured, many years ago, when I didn't even really know what it meant. I don't even think the physician who was ordering it really fully understood. It was like 160 or something. I remember sending it to you saying, oh my gosh, my lipids are like totally jacked. And you're trying to make sure you're doing the right things

and you're heading in the right direction, especially with heart disease being the number one killer. So the genetics is on the more advanced side of personalization. Not a lot of people are doing it. You're doing it here at Apollo. Let's talk about some of the things that is part of, the standard sort of bucket of blood work that people are getting and then taking it to the next level beyond standard of some of the other things that you look at from some of these advanced

screen. So let's talk about blood work for a second. Sure. So we'll go down kind of like three buckets of blood work. But then I'll layer on that, like depending on what this blood work shows or the patient's concerns, there's two other big genetic panels that we can do. One that looks a little bit more at kind of the lipoproteins like what's affecting their lipid metabolism. And then there's a bucket that tends to have more effect on their blood pressure, which I kind of mentioned. a little bit ago. But the three ways that I think about looking at these advanced cardiovascular labs is what are the ones that affect nitric oxide pathways? What are the ones that affect inflammation and oxidation? And then the third bucket is the libel proteins. Because on these

vanes panels from Cleveland Heart Lab or Boston Heart Lab, which are kind of the two most common ones that most patients would utilize for this type of testing, you know, there's hundreds of markers on these tests. And I can tell you that unless you've seen these panels before, you know, they're sometimes overwhelming. It's nice that they're color-coded, you know, green or optimal values, yellow is borderline, red's higher or low. But if you took this to your doctor

and they've never seen one, they're not gonna understand how this all fits in. So back to bucket one, the nitric oxide promoting ones. There's a urine test called urine microalbumin cratine. This is a standard of care test that patients get when they have high blood pressure

or diabetes. The more protein in the urine, the more likely that your kidneys are failing because of diabetes or high blood pressure. Those are the most common causes. There's some infections some other rare causes, but those are the most common. But if you're leaking protein into your urine, that's a marker that the glycopalix to the

lining of the kidney arteries was getting impaired. And then you're peeing out protein into your urine, which is not supposed to be there. So it's like a quick check on are your arteries healthy? If you're leaking protein, maybe not. Homocysteine is in amino acid. The higher the levels of homocysteine that you have, the more it's going to increases the level of a compound called asymmetric dimethylrogenine or ADMA. ADMA lowers endothel nitric oxide synthase, and then that lowers nitric oxide.

So high homocysteine sometimes is associated with different methylation issues. There's mTHFR genes that some people inherit that affects this pathway. So you have high homocysteine, it's usually a relatively easy fix using a methylated compound to bring that homocysteine down. High levels of uric acid is associated with the glycocalyx being oxidized and damaged. uric acid often associated with if the person doesn't metabolize fructose well, if they're drinking more alcohol, then their body can tolerate. Those are probably the most common reasons, or they have kidney impairment to begin with,

and they can't clear the uric acid through their kidneys. Those are kind of probably the most common nitric oxide promoting ones that I will initially look at. Then bucket two is going to be the oxidative stress and inflammation. So we're sitting here breathing oxygen and we're breaking down the lunch that we ate through hermotic andria. But there's always going to be reactive oxygen species when that is happening. Your mitochondrial engines are making smoke as they're consuming those food

stuffs. So your body's always trying to make different antioxidants to prevent that from getting out of control. But on these blood panels, the oxidized markers that you would tend to look at is GGT, gamma-glotyl transferase. It usually shows up on like the liver function markers, but if you have high GGT levels, you're going to have relatively low levels of glutathione, and that's one of the master antioxidants that prevents all this oxidative stress. So if you have high GGT, that's often a problem for your oxidative marks. You can look at oxidized LDL, and then there's a test on Boston Heart Lab called the oxidized phospholipid apobie.

It's more sensitive at looking at which lipoproteins already started to kind of rust or be oxidized. Those are the ones that tend to get trapped in the arteries more. That's the oxidation standpoint. Then the inflammatory ones, high sensitive ECRP, you know, normal should be less than one, but if you've had a recent infection, musculoskeleton injury, you know, it can shoot up 50, 60, 70. It's not that your immune system turns on when there's a problem, is that doesn't turn off. That's really the concern. And if it doesn't turn off, well, that's kind of the next thing.

Maybe you have an autoimmune condition, you've got to go hunting for that. But there's some vascular specific inflammatory markers. Two big ones I look at as L-P-L-A-2 and myeloproxidase. If either those ones are elevated, that tends to mean the arteries are more inflamed, and there's more ability for the plaques that are in the arteries to rupture. Your body's always trying to take care of plaque, just kind of seal it off, put a cap over it, calcify it, but if there's a lot of inflammation in the plaques, the plaques are more likely to rupture, and that's what leads the person having a heart attack.

So those are kind of the inflammatory and oxidative stress markers. And the third bucket is a lipoproteins, and this could be like an eight-hour podcast probably. But if you're going to make it simple, you do want to look at the traditional lipid panel, but you're only looking at for make sure the person does not likely have familial hyperlipidemia. So if their total cholesterol is over 300 milligrams a deciliter, and their LDL cholesterol is over 190 milligram decilator, it's possible that they have to me a little hyperlipidemia. That being said is that they had a normal, quote, normal cholesterol in the past and it shot up this way, that's not going to be full on genetic.

There's probably going to be some metabolic reason why it shot up like that. But if you've been since a kid, your numbers are over 300 and 190, you likely have a big genetic preload that's driving this. Then you can do a genetic test to figure out which gene that person inherited. They made their lipids look that way. But that's not very common in the general population, maybe one. 1 in 200, 1-3 in people have that type of genotype. On the traditional panel, the main thing I would look at it is triglycerides.

And in pretty much all comers, I generally have to see that triglycerides less than 80. It's not a perfect test, but if it's less than 80, they're likely not to be severely insulin-resistant. So it's a starting point. I really don't look at HDLC as much of a predictor. It's much important to look at the particle count of HDL. Then that gets into where we're really kind of looking at these advanced panels, is looking at the lipoproteins themselves. And so the arteries, they have this lining called the endothelium and then the underlying intemot.

This plaque only gets in the arteries if an APOB-containing particle gets retained here and leaves its cargo here, and then the plaque starts building up like a pimple in the artery wall. I often use this tennis ball is the analogy of what a lipoprotein is all about. Cholesterol is a waxy compound that is produced in the liver. It's produced in many of your cells, but the liver produces the ones that are going to basically be transplanted. in these lipoproteins. Cholesterol is a critical nutrient. You're not going to be alive without cholesterol.

You make your sex hormones with it, your cell membranes, your bile acids, your vitamin D. Without cholesterol, you're not alive. But cholesterol is waxy, so it's not going to float in your liquid blood, much like oil and vinegar won't. So the liver makes these lipoproteins, these lipid protein carriers.

And I use the tennis ball now because the lipoproteins are generally spherical. So the cholesterol is going to go inside, triglycerides, which are energy for the cells, go inside because not every cell is making its own energy supply. The fat soluble vitamins go inside. Phospholipids, which are building blocks for the cells, go inside, and there's different immune complexes that all go inside.

And then the liver pumps these things out, ships them through your liquid blood, and then the organs that need something are going to bind to it, take out what it needs, and then it has to ship it back to the liver. And this is where often you can figure out what genetic issues are going on in this person. Is it that their body is producing too much cholesterol and thus too many of these lipoproteins? Or is it an issue that they don't make enough receptors to get them out of the circulation? Kind of think of like a docking station. They don't have many docking stations.

These are the LDA receptors. And these things just keep circulating around the blood vessels trying to find an off ramp. If they eventually find the off ramp, no harm, no fall. But if the glyco calyx has been damaged by these microplastics or air pollution or metals, then it's more likely that they end up sticking to the artery lining like Velcro, and then they could kick off this cascade. So back to the long-winded answer, is that you do want to look at the actual number

of the particles carrying the cluster around because it's not necessarily the cargo that's a problem. The cargo, you know, if it doesn't end up in the arteries, no harm, no fall. It's the lipoproteins that get stuck here, and that's what you want to measure. And so the test is the LDL particle number is the line here that most people will have,

but you can encapsulate it by looking at apo-liper-protein B or APOB. So if the L-DL-D particle is the tennis ball, APOB is this white stripe on the tennis ball. The white stripe is basically what holds this thing together in a sphere. It also acts as a ligand or a key. So when it's coming back to that LD receptor, it's going to bind to it and then it gets pulled out. So APOB is on the outside of all the particles,

the LDL particles, the VLDLs, the ILDLs, and LPLA, if you got it, it's on the outside of them. So you can just count up all the particles that potentially get second arteries by looking at the value of APOB. And then there's different graphs you can look at it and say like, okay, if your APOB is 170, well, compared to your peers, that's going to be well above the 90th percentile. 90 percent people will have values lower than that.

And then you want to go look at the arteries. Okay, is this actually causing damage to your arteries? And that's what all the testing you guys were starting to do here. Some of the testing you've had done in the past, such as that clearly scan. That's fantastic. Thank you for that, Michael. Neil, I want to have you kind of chime in a little bit.

There's a lot of people that are listening today who have insurance through their job or part of, you know, a hospital group like a Kaiser or some other group that's out there. And even just getting the basic labs at a young age to be more preventative sometimes can be a little bit challenging. Any suggestions of how people can ask their doctor, or physician, or find somebody more open-minded within the system? Maybe not everybody has access to a Michael or can make it out to St. Louis. And what are beyond, you know, Most people just know cholesterol LDL. They don't know about a lot of these other things like APOB, lipoprotein, LP, L.P.

Any suggestions of which ones are starting to come out that people can start to ask for a little bit? They might have to do it really nicely with their doctor. But yeah, just navigating the system a little. Yeah, so that's always a challenge because as more data comes out over the years, you want to kind of tailor health care toward that new data to kind of help either prevention and or secondary prevention. EKG is very basic that I think most people will get in a traditional lipid panel you'll get your LDL. But recently over the last maybe a few months, we're kind of debunking some myths that an APOB can't be ordered because it's too expensive. I looked into it in our lab and it only costs $3.

So it is possible to get ABLEB. I think that the traditional viewpoint was what do I do with this information. Yeah, the doctor may not know how to interpret it or what to decide. And that, I think, is what's limited. So it's kind of like, okay, a 40-year-old has a normal stress test. Okay, great. So I can tell them that at this moment, they don't have a significant narrowing in their heart artery to cause them pain or limitations when they're exercising.

Now, that might have some value. Hey, great. You can continue to do your exercise. But the questions that patients are asking and getting to your point is, you know, are there other ways or metrics of trying to capture when we, are younger, or even when we're older, a little bit more representative picture of my health or my vascular health. So just know that having an NMR also, like in our system, I think it costs $40 or $50. Not really exorbitant, but doable. And especially with the APOB,

APOB is more causative as opposed to correlative. So you can get that. And if it's just a few dollars, it does actually give you a lot more insight into what is happening. The other thing that I have ask people to do because this is a traditional panel is add fasting insulin, right? That tells you a lot more about your ability to handle glucose and then that whole kind of interplay between that and the vascular health. So the things that I tell people to add are just to kind of recap. You can ask for the NMR, the APOB, because the NMR, just to be more clear, it'll tell you the particle number and the particle size. Which is what Michael was talking about earlier. Correct. So the small the particle number, the more damaging it can be, the more particle numbers, the more damaging can be.

The analogy, you use a tennis ball, I use cars on a highway. The more cars on a highway, the more likely you are to have kind of pileups and accidents. So NMR, ApoB, and then the fasting insulin. And I think that's a pretty good starting place. Now, one of the common comments that I get, I think we got some last time, Michael, you were on the podcast, was people saying, my doctor just doesn't order a lot of these. So anything about, you know, I've often found that sometimes it's about being nice, but then also, and, you know, Neil, I want to see how many tips,

because you're more recently sort of in the sort of traditional system. Any ways that people you recommend sort of finagle to get their doctor? And is it ever okay to just say, all right, forget it. I'm just going to go find somebody new. Well, I'll tell you what I just said is actually on AHA guidelines. There's the traditional route. Metatryman had mentioned if your LDL is above 190 milligrams, deciliter that automatically is red flag to kind of really start things but if you look at their

workflow and their protocol CBD risk enhancers they call it and under there is lapar protein little a and there is APO B so it's in there it's in the guileas that I guess what I'm hearing is that people are saying my doctor just doesn't want to order this yeah or again it could be a legitimate I think it's too expensive and they just don't know so we just stop there but I would encourage people to say hey these are a part of the actual guidelines that, hey, this is a risk enhancer. I just want to know my risk for the next 30 years and I'm 40 years old. I think that a lot of doctors have actually taken to that. Yeah.

Michael, anything you want to add to that? Sure, like two points. One is that there's a lot of great direct consumer lab companies now. Yeah. Some of them are just even finger sticks. It's going to be a little bit more than $3 or $40 sometimes, but not terrible. And you can do this test at the comfort of your own home and the results get sent to you. Now, the biggest challenge is just how do you interpret it?

And hopefully you're learning stuff through here and you've seen other videos. And you have an idea of like, okay, my numbers are high. I might want to do something about this. But you should be able to get any of this testing pretty affordable at home and just have an honest conversation with the doc. Like, hey, I can make it easy for you. Like, this is the test. This is how you do it?

It's often just lack of knowledge. Like, how do I order this test? If it's not in their electronic medical system, it's like foreign to them. And your point is that most doctors are very well meaning, but they don't know cost of things very well. Like I wasn't trained this way. They don't tell you like, well, not it's going to be this many dollars. I cast this much. You have to figure that out later. And so the patient has to like,

well, how much will this be? Most doctors just literally don't have an idea because they were never taught at themselves. Yeah, and the price may vary greatly depending on the insurance, cash pay, et cetera. Michael, since you mentioned it, any of your favorite sort of direct-to-consumer labs that you want to mention or give a shout-out to? There's a company called Sy Fox, S-I-P-H-O-X. They are the first one that I have seen that does APO-B at home, and it was very easy to do. There's a lab called Empower. They actually will do the cholesterol balance test that you can get on that Boston Heart Lab panel.

So the cholesterol balance test is the one that tells you, are you a hyperproducer of cholesterol, or you're of cholesterol, or are you both? I often get that question like, well, how can I get it? Because I don't have access to Boston. This Empower is direct to consumer. You do the finger stick at home, send it in, you get the results.

The side note is they actually send it to Boston, and Boston runs it for them. But you at least can have access to it if you're interested in that type of information. That's great. I know one of the sponsors, and I've used them well before, they were a sponsor of this podcast. It's called Lifeforce.

Tony Robbins and Peter Diamantis, big fans of them. They have a company. It's not an at-home test per se that you do yourself, but every quarter they send a phlebotomist to your house in most major cities across the U.S. They take your blood work. They put it in. I love their interface.

I've shared before, you know, sort of my breakdown of everything. They do do APOB and some of these other items that are there. Yes, full disclosure, they are. sponsor, but even well before they were a sponsor, I was using them, I was recommending them. And I think it's a monthly subscription. It's about like 120 bucks a month. So not like super, you know, cheap. But as part of that, you also get a doctor interpretation as well, too. Every quarter you get a 30-minute call. So we'll put the links for all those in the show notes below. So we covered, you know, some of the top laboratory test, things that you'd be doing here,

how people can approach it and ask their doctor if they don't have access to a functional medicine and cardiologists like yourself, Michael. We also covered genetics, and we talked about some of the other key components that play into healthy blood vessels. I'd like to take a moment here and just talk about this idea of, I'm going to come back to diet, because even though you shared your ideas and thoughts, often people ask, what is the best diet to protect the heart? And there's a lot of different messaging that they get out there.

They'll talk to somebody who's in the carnivore space, and they'll hear one thing. They'll talk to somebody who's a little bit more what I would call in sort of the evidence-based camp. They're going to hear recommendations like keep your saturated fat to less than 10% or 20% of your calories. Eat a diet that generally keeps your LDL down and keeps your omega's high and make sure you have enough fiber and a few of those recommendations. Are there any fundamentals besides staying away from ultra-processed foods? that you recommend to your patients. So we have the nitrates and making sure you get ample amount of nitrates

as part of that. We have staying away from ultra-processed foods and greatly minimizing them as part of the diet. Is there anything else that you feel strongly about when it comes to dietary recommendations when it comes to protecting the heart? Absolutely. I have this conversation with every patient

is that, you know, the timing of your meals and the seasonal portion of meals is probably as important as what you're actually feeling the body with. Now, the data in the conventional cardiology world is going to talk more about the benefits of a Mediterranean-type diet. And that's always a good template. If you don't know where to start, start with a Mediterranean type template.

But if you're going to be more kind of data-oriented, well, first start with the time of day. My general rule is you want to eat during daylight hours wherever you're at. If it's dark out, stop eating so that the gut and never know it's time to go to bed. Second thing is that we're not designed to eat the exact same foods 365. you know, until 100 years ago, if food wasn't growing outside your door, you didn't hold on to it, you know, canning it. You didn't have access to it.

So in St. Louis, there's four seasons. So I get the question about, like, I want to do keto diet. Like, well, if you do keto diets, evolutionary, it would only make sense to be ketotic in the wintertime in St. Louis, because there wouldn't have been a lot of fruits and vegetables growing at this time. But now we're starting to have into spring and summer, that's when you would have been having more carbohydrates. So having a seasonal approach is also very important.

After that, then you can use this blood work to kind of guide you. We talked a lot about insulin resistance. You can look at your fasting insulin level, your glucose levels, your Homo IRC scores, are you likely insulin resistant. You can also backtrack it and look at some of the lipoproteins. If they have very high triglycerides, you know, over 80, they have a lot of these small, dense LBLs, if they have low HDL particles. That's often a mark of insulin resistance. That person is probably going to need to be more careful on the volume of carbohydrates. Because carbs are neither good or bad.

There's just a tolerance that people are not. that people have, lastly based on their skeletal muscle help. And so that is somewhat of a non-negotiable. I have multiple copies of Dr. Lyons' book sitting there is that people have to get their high quality protein so that they get enough leucine to trigger muscle growth because the metabolism is happening in the muscles. So the protein is basically the same for everybody.

Like you need at least 90 grams, figure out what sources you want to get it from. Then the fat component to it, there is a big variability as well in that. The APO E genotype also has a big role. so you're an April E4 carrier. Sometimes these higher fat diets don't always work as well from them. From a lipid standpoint, it may be great for reducing body fat or their brain works better. Great, but they're probably going to have the side effect of we've got to fix their lipids

potentially. And then on this Boston Heartlight panel, you can see, like, well, how well is this person absorbing the saturated fats that they've been eating? Trans fats, which are, you know, margarine and really fried oils. That should be minimal in your diet. You shouldn't be trying to actively add that. But sometimes you eat packaged foods, you're eating out, you're going to get exposed of those type of oils.

And then the omega-3s. The mega-3s are critically important for vascular health, that lowering inflammation. And the DHA component, very, very important for brain health. You need DHA for the neurons to work together well. So you think of DHA is your cell phone charge. The higher DHA, the better your brain tends to work. And then there's the monounsaturate fat.

So this is the bedrock of the Mediterranean diet. So you're getting a lot of mono and saturated fats in the diet. So you kind of guidepost by this lab, like, hey, this person's pretty carb tolerant. So whatever they're doing is working for them. Or do they need to dial back not only the total grams, but their meal threshold. And then the fats, it's pretty straightforward.

Like if they come in, like, hey, I'm following a high fat keto diet or I'm a carnivore and their saturated fat numbers are through the roof and their apobies, you know, 190, well, you got out of the conversation like, are you going to plan this diet and be at higher vascular risk potentially, or are you going to switch and take less saturated fat and do more monom polyod saturated fat like omega-3s, is not seed oils and C, and C, like, okay, what

What does their lipid panel look like on this new type of fat concentration that's coming in their diet? What are the arteries doing? Again, like I said, I'm from Missouri. Show me that it works for you. Like, I'm pretty flexible that, you know, there's not a perfect diet that everybody should be doing. It's very individualized, but you have to test and retest to make sure that you're not kind

of putting yourself behind the apoll from a vascular standpoint. So just to recap here, would you say this is a fair statement? Every diet from an advanced precision medicine, cardiology, functional medicine cardiology perspective, every diet out there can be supportive for heart health and every diet done incorrectly for your sort of background genes, metabolic health, skeletal muscle masks could actually be worse for heart health. It's about personalizing it to make sure that it fits for you. Is that a fair statement? Very much so. Yeah, it's individualized the person who's sitting in front of you. Like one of the first questions I have on my intake form is, you know, do you know your maternal haplotype?

You know, you can get that off the 23 mean data. Your maternal haplotype tells you where did your original mitochondria come from? So if you're more equatorial, some of these higher carb diets probably would work better for you. But if you're more northern European, maybe these higher fat diets might work for you. And so it gives you a starting point to have the conversation with people if they know the maternal haplotide. That's great. Neil, anything you want to add in on the dietary side for the conversation? Yeah, I mean, and I think it was just be a point of, so like omega-3 and

There's a recent study when they analyzed the Framingham data, and they said that people who had a higher omega-3-6 ratio had an equivalent amount of lower risk for CVD or cardiovascular disease. So in which form that you get it, you know, obviously is your personalized decision, but having a higher omega-3 intake compared to your omega-6 has been shown to be vascular protective. Yeah, being high on the omega index. Yep, that's right.

Yeah, that's right. We've had Dr. Bill Harris on this podcast here, who is the venter of the mega-quant, And I always share with my audience, that was actually the pivotal test that got me to stop being vegan. Not that you can't be a vegan and have high omega-3s and sort of moderate levels of omega-6. And obviously there's 369. I was sort of flip-fop. I had super high omega-6s, very low omega-3s, which also probably describes that why, you know, I was starting to feel like my brain wasn't turning on.

And obviously there's plant sources of omega-3s. There's allergies and other things like that that I wasn't sure. Do they actually move the needle forward? And Dr. Bill Harris did say that in all their research they've seen, these plant algies that people are using to get omega-3s do work. And so whether you're plant-based or something else, just making sure you're in the ideal omega index range. But if somebody works with you, Michael,

and they get the Boston heart panel done, they have the omega index also inside of there too. Correct. Fantastic. Since we are on the topic of amegas, obviously let's move over into the category of supplementation. If you're not eating enough fish, you can supplement with omega-3s, fish oils or algae, as we just mentioned. And would you say that that's one of the supplements that you might recommend for individuals if they're trying to protect their heart

as they age? It's potential, and it will be based off the blood work. But I'm always going to recommend getting it from the root source whenever possible. Diet first. Died first. Is why you took us to the best seafood restaurant in town over here in San Luis. Correct. I took us to a seafood place and we loaded up on the seafood tower and I always want people try to get through dietary sources when they have access to it. Can you supplement? Yes, but it's sort of like the same question with like Reli therapy. You always use that after they've kind of exhausted their regular ways of getting it. And it's theoretical. The omega-3s that come in supplementation, you know, they might make your blood levels look better, but are they always actually getting into the cells and activating things that

you want them to activate? And that's sometimes a moving question. And I don't know the answer to that. Like, does it actually cross the blood and barrier and get into the neurons? I don't know. Maybe there's probably some smart people watching this. And I can tell me I'm wrong on this. But I always would say, like, supplement if you need to, but it's preferred not to. Yeah, you see that this is a very vocal group of people online who talk about phospholipids and things like, I forgot the main one that's out there.

This company called Body Bio that makes a particular type of phospholipid. And they're saying that it's not just about the omega-3s. you've got to have the right type of these phospholipids. Does this spring a bell at all? Right. And it's like the omega-3s, you know, are on a triglyceroric backbone. There's the S-N-1, S-N-2, S-N-3 position.

And my understanding is that, like, it needs to be in the S-N-2 position to actually be like a key and get into the receptors. And nobody knows exactly if, you know, once you take it out of the fish and put it through the process, does it stay in that position?

Got it. Well, at least from the data that we have right now, being in the optimal omega index, we know is good. So however you get their dietary first, what are some of the other top supplement recommendations that you have for individuals? And you mentioned a few of them earlier on the topic of nitric oxides. You mentioned the beet supplements that are out there, but there are also some advanced nitric oxide lozenges if

somebody's not producing enough. And here's my question. For somebody like me who's in a good range based on some of the testing that I went through today here, but once again in the optimal range, should I be considering some of these nitric oxide supplementation? I think the answer is probably yes. I think once you have any evidence of the arteries are getting stiff on one of these tests, or you have evidence of plaque on a carotid scan or calcium scan or a clearly scan, then you would do everything possible to stop the process right there. And so think of as things that are trying to help put the force field up higher so no further

damage happens. Yeah, could you kind of use it like an antibiotic where like there's a lot of issues you use it, kind of put the fire out, you could, but you also say, like, my goal is not to, you know, live 10 years, I want to go 40 more years. And so it's kind of a risk-reward thing. It's like, if vascular disease is still the number one thing keeping people out, then do everything you can do to protect the vascular system. And often it's doing something that boost nitric oxide, if it's not optimal. There's a couple different companies that make lozenges, Dr. Nathan Bryan, who I know you've had on the show and I've had a pleasure to speak with at

multiple conferences, you know, he has a few different pads on different lozenges that have signs behind them that actually shows that nitric oxide is getting released when it dissolves in the saliva. And then when you swallow it, it helps kind of recouple that endothel nitric oxide synthase enzyme so that your body's natural production starts working well. So he has a company N101 that has those lozenges. And then there's a company in full disclosure. I speak for them sometimes just educationally. It's Calroy. They have a product called Vasconox. It's a capsule. And it has about a 24-hour duration of action. It also releases hydrogen solace and that hydrogen sulfide in of itself is a vasodiliter, so the arteries get bigger.

But hydrogen sulfide acts somewhat like the phosphodicerase inhibitors, so the biogro-type medications. So you're putting more nitric oxide into the system, and then the hydrogen sulfide keeps it around longer so that works better for longer periods of time, let's say. So those are kind of the workhorses that either use your own with these lozenges or this Vasconics product if the person that's lower nitric oxide needs to be supplemented. On the topic of supplementation, one area that's come up a lot on this podcast here and on our newsletter is the idea of anything that can help people address the plaque buildup that happens in the arteries. One of the tests that you send me in for was the Clearly Test.

You mentioned it earlier. We did a whole podcast that was a breakdown of my Clearly Test, what people can learn from it. But just big picture of people didn't listen. The Clearly Test is really one of the first sort of, I don't know what the right term is, but predictive, you know, earliest sort of diagnosis. of heart disease that would be there? How would you describe it? I think it's the most sensitive test that's been invented today. Because by the time somebody normally comes to a cardiologist with symptoms, chest pain

with exercise, they have a 70-80% blockage in their arteries. I'm holding up a diagram of an artery, and this is what it would look like. Your artery is severely 80% senosed. You're likely going to have symptoms when you're exercising. You can't get enough oxygen and nutrients past this. But this didn't happen overnight. These plaques usually are harder plaques and they're generally more stable. You'll have symptoms every time you exercise at a certain heart rate for the most part,

but these aren't the plaques that necessarily rupture and cause heart attacks. It tends to be the less severe stenotic plaques, the softer plaques that tend to be the problem. And those are the plaques you can't feel until it's too late. Half the time somebody has a heart attack, they had no symptoms until that heart attack occurred. And so the clearly scan helps try to find this plaque at the earlier stages. You start with a CT cornea angiogram. So you have to have an IV placed. If you don't have a low resting heart rate, they often give you a beta blocker medication

to slow your heart rate down. That just helps cut down a little bit of the motion artifact as your heart continues to beat, and they're taking a picture of a moving object. They take a picture of your arteries and it looks at the degree of stenosis. You know, do you have a blockage in your arteries? That's not the best case for the Ctangio for the clearly. You're mostly looking at like what's going on on the walls of the artery. You know, how much plaque is like in an iceberg below the surface?

That's what you want to look at with the clearly. And clearly it's basically just an AI software algorithm that they upload the CT angiogrammages into and then the machine learning software. Voxyl by Voxel slices the artery and looks at what's in the walls of the artery. And it quantifies the total plaque volume and it will break it down to three buckets. Calcified plaque, soft plaque, and low density soft plaque. And it's those soft and low density plaques that more likely you go on to rupture and cause a heart attack. And while Calcum Cortest is an outstanding test, it cannot. see that soft plaque. And that's really the question is like how much soft plaque does somebody

have in their arteries? Because that gives you an idea like that person's had a lot of endothel dysfunction. Their glyco calyx has been trashed for years and they've had a lot of the smoldering fire in their arteries and they're laying this plaque down. You can still intervene before they had their events, but you have to know that it's there first. And in your situation, it was more about that. You had these high apeobes. This is why if you do all the right lifestyle things, you can still have a relatively low total plaque volume. You didn't have a lot. You didn't have advanced plaque in your arteries. You already didn't have 90% plaques them just because you had a high apathy. That tends to mean you had healthy nitroxide levels for years and years and low

inflammation. Your arteries never developed this problem. So clearly just really helps quantify people who are higher risk, more likely to go on to have a heart attack, need stents, bypass or die versus people, no, stay the course, lifestyle, supplement, Medicaid when necessary. And in all fairness, when I got it done, I was 40, so I'm still pretty young. Correct. And so things could happen over a period of time. When I was younger, I was on a vegetarian diet, probably not a healthy vegetarian diet initially. Then I went on a very processed vegan diet, and then I went on like a raw food diet when the whole raw food movement was, you know, very popular. So a lot of my adult life, I was either young with a very healthy body that could kind of deal with a lot of this.

And for a period of 10 years, from 18 to like 28, I was on like a very clean vegan diet towards the end of that. So I'm also paying attention to individuals that are out there that are saying, hey, okay, now that I'm 40 years old, I am mindful about how much APOB is floating around between the ages of like 40 to 100, right? We'll talk about that in a second when we talk about prescription interventions that are there. So going back to the topic, we were talking about supplementation. We went into clearly. We were talking about soft plaque. If somebody does find that they have some soft plaque built up inside of their body, are their supplement recommendations that, you know, they could possibly undertake to help potentially address it.

So we've talked about some of them already, so the nitric oxide boosters are going to be helpful to basically stop doing damage, you know, put the force fields up so the body has a better shot at improving what's below the surface of the water, you know, the iceberg. The omega-3s, that's also very important. You know, help basically put a thicker cap over the plaque, decrease the inflammation in the system so the plaque doesn't rupture. Kiloa garlic, it's a particular type of garlic. It's a Japanese garlic and has been studied.

There's trials at UCLA that they're doing looking at arteries with calcium scores. Those patients, calcium scores test, tend not to get worse. And sometimes the calcium score test was actually backing up or improving with chylo garlic. Usually the dose is like 600 milligrams twice a day. And before I get asked, like, well, can I just chop it up and put it in my spaghetti? Of course, add garlic to whatever you like, but it's the dose that is the drug. And so you want to have the exact dose. And that garlic, I believe, is we wrote a newsletter on this we'll link to in the show notes.

It's an aged garlic. So that seems to be playing a role in it as well. Correct. It's the aging process that has the effect on some of the compounds that then the actual garlic releases. It's not just the, you know, the polyphenols and other stuff that comes in it. Great. Anything else that you've mentioned? I think that there's a few sort of more advanced supplements that are there that you offer in your practice. You recommend individuals. Yeah, I mean, I've been the arterosil.

It's a glycoccalyx promoter. You know, it's mostly been studied in carotid plaques at helping the soft plaques basically delipidate or shrink. there's no reason that it wouldn't suspect that would help with the coronaries. It just has not been studied. But, you know, personally, taking arteriosil, just in the hope that it helps any soft plaque I have in the system, and then I have multiple patients on it for other reasons, and we'll eventually repeat clearly as on them to see.

Did those soft plaques regress with that? But then getting into, like, pharmaceuticals, you know, the ones that have the best data are generally going to be the statins for those that can tolerate it. And a lot of that data, you know, is with resubastan or crustwork. You don't necessarily need to go all the way to 40 milligrams every day to get the benefit. You know, often many patients I have just on five milligrams daily or twice a week and just try to get some of the anti-inflammatory lowering benefits of the statins. There's some data

that it helps with the glycopalics. It doesn't make it so impermeable, but it does tend to make it thicker. And then it also is going to help with keeping down some of the oxidative stress that the glycocalyx is sensing. So you stop doing damage when the statin is on board. It's not all about just lowering the cholesterol particles with it. Let's talk about statins in the category of prescription interventions that are there. Generally, there's been a lot of confusion about statins. You address some of this here. There's also been some concern in the wellness community of like, oh, I don't want to deal with statins. I don't want to take them because of potential side effects, mitochondrial issues, muscle issues that are there. What's real and what's not

and what's a little bit in between? It's a great debate and it's one thing's where it's like, no, I don't believe that statin should be in the water and we shall be taking them. And I don't believe that they're poisons that nobody should. If it was all magical and nobody had heart attacks, we would have already seen that. Because almost every patient I ever saw when I was in my fellowship that came in and having a heart attack was already on a lot of these medicines because the majority of heart attacks are repeat. It's not all the first time we're having heart attacks.

So if it stopped all the heart attacks, we would have been done, we'd all be taken on. So what was the part that we're missing? It was the unmitigated oxygen stress, inflammation, and this end of the field dysfunction. Those things aren't fully responsive to stats. It's why it's not a magic bullet. It's one tool. And the major side effect that's across the board, even in the trials, it's going to be muscle-related symptoms.

Muscle pain, weakness. I've honestly, in my 20-plus years of being a physician, I've never seen a case of rabdomiolysis from a statin. I was in the military cell hundreds of cases of rabdomysis from exercise, and the July heat in South Carolina, the DIs would go a little bit too hard sometimes. But rabidinlysis is when the muscle cells die. It looks like you're peeing out blood when that happens. I've never seen a case of that from a statin.

That being said, the muscle symptoms are real. In the trials, they may see it's only a couple percentage points that people have it. In real life, it's, you know, 10, 20, 30% of people might have some symptoms if you really dive into it. But is it sometimes bad enough that they have to stop it? Not always. But I would often do some of these advanced testing

say, like, who's the person who's more likely to have side effects than not. And the people who tend to get more of the muscle symptoms across the board, it tends to be the people who are vitamin D deficient, So they have a level under 30 milligrams per deced a liter. I usually shoot for a level 50 to 60 on vitamin D to reduce the risk of muscle symptoms of stans. They have low co-inzyme Q10 levels. COQ10 is produced in your liver, but it also gets depleted with statin use or beta blocker use. If you're going to supplement with CO10, generally you want to supplement to get your level back over three.

It's never been fully elucidate that if you supplement people just routinely with CO210 that they don't get muscle symptoms. But some people benefit and there's no harm in supplementing with COQ10. If you're hypothyroid, if your thyroid's underactive, you're much more likely to have muscle symptoms with statins. And then there's some of the genetic reasons why. So if people have an apo e4 allele, they tend not to tolerate the highest dose of statins. They tend to get a lot more muscle symptoms or glucose dysregulation issues with it. If you're pumping it at 40, 80 milligrams of some of the higher potency statins. And then there's some genes you can look at on some of the blood tests and then there's also the Bucco swab, that G.B. Insight panel that you

time that looked at, do you have certain genes that tend to cause four to five times increased risk of having muscle pains on stands? And you had one abnormal one that has the effect on carnitine levels. So those are the people that like says that if you're going to use a stand, it should be very, very low dose and maybe intermittent dose. But there's so many other good tools out there right now. So I don't understand the debate where like I don't take a stand. Okay.

What are you willing to take to lower your risk? Because if it's just like the stands off the board, I have a lot of other tools we can use but it's a different conversation when they're like I don't want to touch my cholesterol levels at all okay well then we have to have that conversation if they're just concerned about the muscle symptoms we can find something that will work for them you know anything you want to add to the prescription intervention conversation here yeah i mean you know a zetamide i think to be honest in fellowship wasn't used as much statins were like the mainstating can describe what that is sorry yeah yeah absolutely so zetamide are also known as zedia um the difference is that statins will

actually reduce the production of the LDL or the carrier, the tennis ball in your analogy. A Zetamib or Zetia will actually block the reabsorption of the cholesterol to kind of, in a way, reduce how much LVL your liver has to make. A lot of people will tolerate that a little bit better. Sometimes you can get some GI side effects, but depending on where you fall, whether you're hyper absorber or not, Zetia might work enough to get your APOB down and then in surrogacy, your LDL as well. One of the things you recommended for me was a Zetamide, Michael. Just talk about that intersection. What did you see that you suggested that?

And generally, I don't know if it's, somebody told me that a Zetamide is not truly in the category of a statin because it's blocking the reabsorber, but I generally think that people put it in that same category. Is that correct? They may, but it's not a statin. It's flat out it's not. It's a cholesterol reabsorption inhibitor. And it's working in the intestine and in the kind of the bile ducts. The analogy you think about is, are you a hyperproducer of cholesterol or are you a hyper absorber?

So sometimes I will use an analogy of a bathtub filling up with water. So if the bathtub's filling up with water and you don't want to overflow, there's three big things you can do. You can go to the faucet and shut the faucet off. If you're a hyperproducer of cholesterol, then you have high levels of lanthostrol, desmosterol, and those compounds get produced into cholesterol. So that's the location where statins work, where if you're stand intolerant or just, hey, I'm not taking this stuff, Thimpiddoic acid, which is nexlatol, works in the pathway two doors down from where the statins work. If people are intolerant medications or they're trying to go supplements because their levels weren't so high,

this is where red yeast rise in Bergamount work. They're HMG co-reductase inhibitors like statins that does not as potent. So you're just dialing back the amount of cholesterol produced in the liver, less of these tens balls get shipped out. The second thing you could do is you could open up the drain in the bathtub. This is where the PCSK-9 inhibitors would work. These are mostly rapatha, preluent, and there's Elysmlion. There's companies working on oral forms, but they're a year or two away from my understanding of hitting the market. But PCASK-9 is an enzyme.

It's an enzyme that breaks down your L-Bore receptors. So sitting outside of your liver, these cargo docking stations, grabbing these particles, these APOB particles as they go by and brings them back into the liver. I told you guys last night that I had a great grandmother who lived 106 years old. I have multiple family members who have very low APOBs in the 40s on no medications. And when I did the testing on them, they had loss of function PCSK9 genes. They basically got built in rapatha. They're never going to have high lipoproteins because their body just clears these things

very efficiently. So it's basically like the water can be blasting into the bathtub, but the drain is wide open. Water goes straight out. The water is now out. Well, the only way cholesterol leaves your body is through your intestines. And about one in five people, there's a gate essentially, the Neiman C1, like one receptor. It basically is open and keeps letting a lot of this cholesterol reflux back to the liver. It's basically like, hey, we made this stuff, took us a lot of energy to make it.

We don't necessarily want it to leave the body. Let's just save it. Everybody resorbs a little bit, but about one and five people sends back a lot. And that was in your case. You were hyper-absorbing a lot of these sterols from the gut. So with a Zetamide on board, it's basically like making sure that once the water gets, out of the drain, it's going to go into the main line and go out to the sewer. And it cannot come back. Okay? So three big levers. You can either shut out the faucet, open up the drain, or make sure

that the water in the mainline goes out to the sewer. Yeah, I think we started on a Zetamide last year. It was June. I started taking it. My APOB last year before I started on a Zetamide. So this would be February 2023 was 144, which is still not the highest that it's ever been. It's like, was like 17, I'll fact check that and go check that old test. And then by June, end of June, early July, it had gotten down to 86. And I think that I was around like mid-70s-ish through this time period. And then about last month, I, one of my buddies, Mark Mayhew House, who's part of my men's group in Los Angeles, he like got me hooked on this beef chili.

from Air One. You probably heard about Air One. It's like that most expensive grocery store in Los Angeles. And I literally was eating this beef chili for like breakfast, lunch, and dinner. And even while I was on azetamide, I don't know the dosies, you probably know better than me. We can find out and kind of put it on there. Obviously, everybody needs to go talk to their doctor, see what they're a good fit for. But I'm just using it as a reference.

Even though I was still on azetamide, but I was eating this chili for breakfast, lunch, and dinner. My, it will be jumped back up to like 100. Right? That was there. But I was literally having like saturated fat for like breakfast luncheon and that it's mostly ground beef or bison and that's like 80% fat, 20% lean typically. And a lot of that being saturated fat, I kind of got off the chili for a little bit. I know we did a test today. It still may not be long enough of a time period for it to sort of lower, but I'm hoping to bring it back. What should somebody like me who's generally had a, you know, a good clearly scan, right, in the optimal category, pretty good endopat.

You know, you've seen the rest of my labs that are there. What should I be shooting for if I'm trying to not roll the dice as I continue to get older? Where would you like to see my APOB? It's going to be nuance because I'm always going to go back to what is the health of the glycopalics and the nithelium? Because if your force fields up, you're much less likely that these APOBs are getting through the glycocalyx and getting retained. So if you have a healthy endothelium glycalaics, I care, but not.

not nearly as much as if you have severely damaged glycopalix. The reason that this is important is that the glycocalyx is heavily structured water. It essentially is highly negatively charged because all the sulfate glycosomino glycans that are in the glyco calylax coating. That negative charge repels the lipoproteins, the apobes as they're going by. Negative charges on the lipoproteins, negative charges on the robot itself, negative repels negative. So it's kind of like a maglev terrain.

So if you have healthy glycopalics, these things don't get in there to begin with. And that's what already been shown on your prior clearly scan is that like not a lot of these things had gotten in there and set up shop. Today, your testing shows that you have relatively good nitroxide availability. Your endothel function is very good.

So if your APB is a little bit higher, maybe still not necessarily having a problem. And this is where the question is, is APOB causative of atrosis? Very likely, yes. But at what degree? And I think the missing piece is, what is the health of the glycopalicine

and the endothelium first. Because we all know there's these lean mass hyper responders out there that, you know, have LDL cholesterols of 200, 300, 400, and they will say, well, if I have a calcium score is zero, it doesn't matter. I would say, show me, like, show me that you don't have vascular inflammation, that you don't have endothelis function. If you don't, then maybe you are that one individual where this diet is not impacting your arteries in a negative way. But I wouldn't want to wait to your calcium score is abnormal before you say, like, hey, I want to dial back on this nutritional strategy. It may turn out that, they'll do these studies and they'll show that, like, and these people who are, quote,

bio-healthy, the LDL particles don't matter as much. But in my mind, I think it's because these people probably have very healthy glyco-calyxes, and they don't have that issue. The quick sidebar on that was that, I know in December they presented some of the preliminary data from the keto trial versus the Miami heart trial, and they were looking at baseline CT angiograms. And they basically said that, like, well, the people who were on the keto diet for, I think it was about four to five years beforehand, did not have more plaque in their arteries than the people from the Miami heart trial who were mostly following a Mediterranean type a template. But if you actually dive into the details, the patients in the Miami Heart

trial, there was, I don't remember the exact percent, just 20, 30 percent of people were on lipid lowering therapies, but their average LDLC was 123. Well, that would put somebody in like the 60th percentile. That doesn't mean they treated them aggressively and that they should have had lower plaque. It's just that you're comparing two groups that had super high lipoproteins and one that had high. They both had plaque because maybe they didn't fix all the reasons that their glyco galaxies were impacted. But they're not doing the prospective studies where they're going to stay on these diets

and they're going to repeat a scan and see, like, the interval, did it actually change? That'll be great data. But in the interim, you are kind of playing Russian roulette because you don't have that data. You have a lot of data that your arteries are really healthy right now. So is your APOB actually causing a problem?

It does not appear to be so. That being said, where would you like your levels? I think trying to keep less than the 20th percentile would be a good starting point. So that's generally about an APOB of 80, maybe 70 would be a good starting point. If you want to be extremely aggressive, then that's the fifth percentile. That's like 55.

I don't know if April B of 20 is a reasonable goal for the average person. Actually, it's not. If you've had multivessel bypass surgery and strokes and stuff, okay, maybe you've got to do everything possible, throw the kitchen sink at that person. But if you're 41 years old and low risk otherwise, no, I don't think you need to use three pharmaceuticals to drive you all the way that low.

But I made some say from an adult sample, I was like, yes, I have these family members who have naturally low APOBs in the 40s, and they're living into their hundreds and very low calcium score test. It makes sense that you can have low APO B and live a long life, but do we need to use lots of pharmaceuticals to drive down there? I don't know that answer yet. Because you'd be concerned about what is the sort of side effects of that? Partially the side effects. And, you know, is it necessarily overkill? Do we have to give you this many medications and drive APOB to zero? How about we focus on the things that really are the problem, the oxidative stress,

the inflammation, the autoimmune dysregulation? Those are the like things you focus on. Like we're talking about, you know, high blood pressure and diabetes and lipids and smoking obesity. They're important, but like what are the arteries doing with that information? That's what you really care about. Yes, APOB particles are going to drop cholesterol off in the arteries and plaque can build up. But it's not the only thing. And that's the thing that I just wanted to be able to share on this is like,

Look at your APOBs, but the target's going to move somewhat based off of what's going on in your particular arteries at that time. One follow-up question, you know, in the case of somebody like your grandmother, right, you may have the information or you might have to just speculate. So you know that her APOB levels, even without medication, were low. How do you think her endothelial health was? Knowing that she passed away at 106 on no medications, probably pretty good. She never had hypertension as far as we know. The only time she ever stuck cardiologist is like in her 90, she developed complete heart block. She ended up getting a pacemaker placed in, and she lived long enough that the pacemaker was end of life and was supposed to be replaced.

She's like, I'm pretty old. I don't need to replace. She lived in her eight, nine years without her pacemaker working. So I think she probably had a pretty decent endothel function. That being said, she was the exception, not the rule. She did not exercise. She did not eat clean. She ate tons of processed food and soda.

She lived under an airport. There's no way she slept well. She was the exception. But I get to say that, you know, she had some lucky genes. Not everybody got them. So sometimes if you have what you don't expect, go in. Yes, blame your parents maybe a little bit, but there's so many things you can do from lifestyle

that can mimic what some of these octogenarians have. So if you need to lower your vascular risk by lowering APOB, great, we have multiple tools. If you can't tolerate sands, there's multiple tools. We'll use those instead. So I think she was lucky in ways, but I still throw it out there like my gauntlet, I'm still trying to beat her longevity record,

even though I don't have the same APOB targets. genetically, I still think I can figure it out because I know what I know now. One last question of the APOB topic since we're on there is I've heard individuals like Dr. Peter Atia say, you know, we generally want to be bringing the APOB levels back to down to where people were when they were like in their teens. Have you generally seen that people in their teens have lower APOB levels? Obviously, in my case, I'm somebody who probably had elevated levels with the familial hyper-cholestraleemia.

But generally, is that accurate that in our teens, we've had our, our, APOB levels would typically be lower? I don't know that for sure from personal experience because I usually don't see a lot of teens and have access to all their labs from that period of time. But I believe a lot of that data come out of the European Consensus documents that Brian Ferenson in the group put together

that really kind of linked together that yes, APOB from the Mendelian randomization trials, the statin drug trials, some of the other observation trials, is causative, it's not just a correlation. The higher APOB, the more likely will develop plaque in the arteries. But there are other things.

You don't necessarily have familial hypoglyphemy. You don't have the like one gene equals your lipids. You have kind of a more polygenic mix. And that's what that GBN site told us. It's like your issue was more hyperabsorption issue. Okay, well, Zetamide was likely gonna work better for your case. But that being said, is that yes, probably in your teens and 20s, even if you're doing a different diet than you do now,

you probably had higher apobes than the average 20-year-old would have had. You still don't have as much plaque as a lot of 40-year-olds have right now. So what was the difference? You did something right nitroxide wise. And so I don't think everybody needs to shoot for that goal of 20 to 40, which that's, you know, what neonates are supposed to be. I do have some patients that come into me. They follow Dr. T and others, and they're concerned about their family history, and they ask for help. Like, I would like to lower my APOB that low.

I will support them in that mission, but I'm not pushing that mission, say, hey, everybody's got to go down this far. And just so that people are aware, if people wanted to go down that route, what are the, the pharmaceutical interventions that you would be bringing in at that stage, even though that's not your primary goal with all the patients that are out there. Sure. So go back to like my bathtub analogy. It's often you're going to have to do something with the faucet. So statins or nexusatol, shut off some of the cholesterol production in the liver, maximum

tolerated dose, but you get probably about 80% of the benefit at the low doses that we're using resubstant. So I pretty much always will start 5 milligrams of resubstam and titrate up a little bit if I need to, but I'm rarely ever going back all the way to 40 milligrams a day. open up the drain. That's going to be a PCSK9 inhibitor. If insurance covers it, you're usually going to be good to go. But if insurance doesn't cover it, you know, it's $5,600 a month out of pocket for these drugs still. They just help support that LDO receptor. You know, open up the drain, get it out. You know, you'll have, you know, 40% reductions in your particle count with the

PCSK9 inhibitors on board. They're just extremely potent. But then, often you add the azetamine. Make sure that the water, once it gets into the gut, leaves. So often using triple therapy to try to drive people into those able to be 40 or less goals. And as you mentioned, you know, this is really about making sure that the piping is in good health. If your piping is in great health, it's less likely that these lipids are going to be sticking in the first place. If your piping is not in great health, even if you have lower lipids that are out there, you've been on a statin before, you're doing some of these interventions,

you will still end up with cardiovascular disease, ultimately, because the piping is not in great health. Very much done. And I said it earlier, but half the time people come in with heart attacks, they have, quote, normal cholesterol. People always used to be like, how is this possible? Well, that's the thing is that it's this endothel dysfunction was present from their metabolic disease that we weren't really paying attention to, or they're extremely vitamin D deficient, which we weren't paying attention to 15 years ago in the cardiology world.

There's something that was causing issues with their immune system. You know, we didn't put two and two together like rheumatoid arthritis and Hashimoto's. It's really just precursors that you're going to have a lot of vascular disease unless this stuff gets, bowed back. And so I think cholesterol is extremely important to this process, but just being lipid-centric, you're going to miss too much of the story. So look at the arteries first, like you said. When it comes to some of the areas that are around the world of biohacking, some of the fun sort of interventions that are there, we've already talked about red light therapy, how you're a big fan of it. Actually here at your office, you have this red light panel called The Beast.

The Beast. Made by what company? What's the name of the company? EMR Tech makes that one. The EMR Tech. The same one that makes my biohacket. or blue blocking glasses. Yep, yep. So in that same category, you mentioned the glasses, right? Through this entire interview, you've been wearing the glasses. Just give us your take on that, why you choose to do it. And generally speaking for your patients, how and why you recommend blue light blocking glasses?

So I've been doing these type of glasses since at least 2017. I was taking a very long trip from St. Louis to Bhutan and Tibet. And, you know, I was reading that jet lag was going to be pretty brutal. And so I was just trying to figure out ways to kind of mitigate that. Came upon an article that Dave Asprey had talked about. I'm wearing these biohacking glasses on the plane. Bought a pair of the original True Dark, the wraparound, Terminator ones, wore them on the plane. And I had jet lag, but it's maybe in my estimation, like one-third is bad as it should have been.

And then when I got back to the States, I'm like, I got to read up on this, like, how did that even work? And then went down the rabbit all like, oh, it's your circuatomy. It's the light signals that are hitting these receptors in your eyes that are doing that. So basically like when you're on the plane and you're wearing the red biohacker glasses, you just told your brain it's night time in Asia. And so your body's just getting synced up that like when you land there, oh, it is night time here and your body gets back on sync a lot easier. So basically since 2017, if I'm indoors and I don't control the light environments,

I just wear these to protect my eyes because I want my brain to know what time of day it is. These don't block all blue light and not all blue lights bad. Blue light from the sun is very, very good for you. That's what tells your body it's morning, noon, or the sun's about the set. But the light that comes off your technology or your overhead lights, that's set at the same color is basically noon time. And so if it's noon, okay, no harm, no fall. But if it's 9 o'clock at night and it's dark outside, but you turn on these lights, your body keeps getting these signals. Oh, it must be daytime.

Pump out cortisol, you need to keep hunting and go find food. Like, it's still daytime. So I don't want my brain to get confused as a day or nighttime. So I will wear these anytime on the front technology or lights that I don't control. And the yellow ones, these are essentially like daytime lenses, from sun up to sundown, if I'm indoor, they're indoor sunglasses. I do not wear these outside because I want the full spectrum of light to get into my eyes. But post sunset, the sun would set, no more blue photons hit the back of the eye and your body

should be going to bed in three to four hours. But we have all these wonderful devices and such, which is great to be able to communicate around the world, but your body's going to get confused as it's still daytime or not. So people are very sensitive. They may want to switch from the yellow lenses to the darker red lenses because the red lenses block a hundred percent of blue light and a hundred percent of green light. And the body basically gets the signal. Oh, it's really midnight.

But I'm very, very sensitive to those glasses myself. So I will only wear them maybe half an hour before I want to go to bed or if I'm traveling and you've got to be better at a certain time. I'll put them on. Otherwise, I'll put them on watching TV and I'll fall asleep with them on. I usually tell people like, any time post sunset, you could wear them. But about the hour before bed, if you throw them on and you're tracking your sleep at the end of the rings of the watches.

You'll generally see your sleep scores improving. So a lot of the biohackers keep using that just to kind of keep optimizing their sleep scores. You know, as a cardiologist as well, you got super into the blue light locking glasses. and you're like very meticulous about them. What did you notice firsthand when you started using them? Easier to fall asleep, wasn't tossing and turning. Just kind of like my sleep latency or the time when you get into bed and you fall asleep was falling between 10 minutes or less.

It didn't feel like I had to kind of struggle. I kind of did that just because I was reading obviously things that we were interested in and seeing different ways of modulating circadian rhythm. It's almost now my practice now when kids go to bed or once after dinner, I just put them on. And just keep it on. Yeah. It's been super helpful. When you put them on, like my nervous system is sort of trained to sort of start

like relaxing a little bit. Absolutely. What time do you put the red glasses, the ones that block all the blue light? What time do you typically put those on? Probably around like 8, 7.30 or 8. And you fall asleep at what time? Usually nine. If you can last more than an hour, then that's pretty impressive.

No, but by then it's like I got to go. Got to go to see. Got to go to see. Michael, anything else, you talk about the red light panels that are there, you talked about the glasses, anything else that's in that sort of biohacking space that you're a big fan of? So I think any of the ones that have plausibility on how they help the mitochondria, here's something I would focus on.

Photo by modulation, one of its major actions is making the mitochondria more efficient at making energy. This is where grounding or earthing comes in. Absorb electrons from the earth, the electrons go through the mitochondria, make more energy, lower inflammation. This is where potentially hyperbaric oxygen can help people. Not for everybody, but hyperbaric oxygen can have. help people, you know, heal faster from wounds or have traumatic brain injuries, you know, okay, it's helping the mitochondria make more energy efficiently. Methylene blue, possibly for some,

you know, it helps with making more energy than mitochondria, it helps with lowering oxidative stress. So that is a possible thing that would consider for certain people, not all. And then, you know, this is where kind of the cold plunging comes in as well. Cold plunging is obviously the rage right now in social media. You know, I often joke about, like, where do you keep a lot of your produce? You keep in the refrigerator so it doesn't spoil. Well, like the prevent spoiling in us, that cold therapy is helping lower inflammation. From a mitochondrial standpoint, it's helping the respiratory proteins in mitochondria come closer together. And when they come closer together, it's like a semiconductor. You can make energy faster through the system. That is probably the major benefit that cold

thermogenesis is having, is that just makes the mitochondria more efficient making energy. One of the ones that we didn't mention here is sauna. And obviously there's a ton of research that's out there on the topic of sauna. Is that something that you recommend or regularly use yourself? Correct. And it's just that it's one that I don't necessarily put two two together. Yeah, it's always demotocondrial booster that it is. But no, lots of data on sauna therapy. There's a lot of data out of like Finland and Japan using it for patients with heart failure. The best way to think about the sauna is that it's, you know, also kind of a sun filament. It's just different wavelengths of light that your body's absorbing. It's mostly the infrared spectrum, the heat. That heat helps

structure the water that's in your cells. That glycochalics that you have lining in 60,000 miles of blood vessels is a lot of this structured water. So that is probably one of the ways that sonnet therapy is benefiting your arteries is that it's making that glyco caly less things to stick to it. There's also the benefits of sweating. That sweating is to help you get rid of the heavy metals that you're getting exposed in your life. Maybe it's getting rid of some of these microplastics. I don't know if that's true yet. But the benefit also is that it increases your heart rate. So it's sort of like exercise without exercising. So, you know, a big fan of sauna, you know, three to four sessions a week for people

if they're really going to want to get the main benefits. And then for how long? Probably at least 20 minutes of a rolling sweat at whatever temperature it takes for you to have that sweat. You know, you're a huge fan of sauna. You have one in your garage. You've even got our parents on it on a regular basis. Is that about your dosage that you're shooting for?

Yeah. I usually do 20 minutes, three to four times a week. I generally couple it right after exercise. A couple other benefits, testosterone boost. There's some other recovery functions of that because you get vasodilitation, probably nitric oxide increase, which can be helpful. But I definitely tell people, if you get the exercise and the cardio dialed in, this can be a supplement.

This can be an additional boost to your regimen. Fantastic. Michael, you covered a lot here in today's episode. We've talked about, you know, what are some of the things that increase people's risk of cardiovascular disease? We talked about some of the top blood tests that everybody should be paying attention to. We talked about some of the advanced screening options that you guys have here, and some of the ones that you also recommend to people that you don't do here

but are a big part of your practice, like the Clearly Test. We talked about supplementation, and what are some of the supplements that could be supportive towards our endothelial health and potentially even removing soft plaque? We also talked about dietary interventions, some of the basics that everybody can be paying attention to, but how also personalization of the diet is most pivotal when it comes to truly reducing our risk of heart disease. Any diet could be done well or any diet could be done unwell

when it comes to the personalization of increasing or reducing our risk of cardiovascular disease. And we also talk about pharmaceutical interventions and what some of the top ones are for individuals. Anything that we didn't get a chance to touch on that you want to share with our audience? Now, first of all, I just want to thank you again for the opportunity of coming out to see us here at Apollic cardiology and going through the gauntlet of the testing to see how healthy your arteries are because they all have this goal of longevity, but it's really more about health span. It's how well are those years going to be? And vascular disease is still the number one thing that takes people out sooner than they want. And it's maybe not even the thing

that's going to kill them initially, but it may decrease their quality of life. But if you get a handle of this thing early, you can live your life a very long time without these events, even if you have bad genetics, even if you have high cholesterol. There's a lot of things you can do to take your vascular health back into your own hands. Your doctor's always there is kind of the but to guide you, but start with the things that you have in your own control. You know, it's how you fuel the body, how you move the body, how you deal with your stress, how you sleep. Those are all things your doctors aren't going to do for you.

You have to figure out how to do that every single day. Then working with somebody who can help you, you can get the right testing to look at what's floating through your blood, the biochemical, and then you can do the biophysical testing. Like what is the state of the arteries? You know, are there arteries stiff? Is there soft plaque building up? It's their heart plaque? you can figure out where you fall on those spectrums,

and then you can decide, okay, I need to be way more aggressive or what I'm doing is working for me. Your vascular health is in your hands. If you understand the basics, it's really not that hard to reverse this stuff. You just had to first go looking for it and know what you're dealing with. Well, Michael, on behalf of myself, my brother-in-law,

Dr. Neil Patel, we want to thank you and your team for hosting us here, taking us through the gauntlet of the test, getting us a chance to see sort of behind the scenes of how you organize your practice, why you use the test that you do, and mostly for just being an incredible person who has the heart of a teacher, who really wants the audience to learn.

There's not that many resources when it comes to the most advanced interventions and approaches when it comes to cardiovascular disease and functional and integrative and precision medicine. And your voice being out there as being one of the main ones has been a huge benefit to our audience. So thank you on behalf of myself, Neil Kumar, but also thank you.

Thank you on behalf of our audience as well. You're very welcome. Thank you, guys. Hi, everyone. Drew here. Two quick things. Number one, thank you so much for listening to this podcast. If you haven't already, subscribe, just hit the subscribe button on your favorite podcast app. And by the way, if you love this episode, it would mean the world to me.

And it's the number one thing that you can do to support this podcast is share it with a friend. Share with a friend who would benefit from listening. Number two, before I go, I just had to tell you about something that I've been working on that I'm super excited about. It's my weekly newsletter, and it's called Try This. Every Friday, yes, every Friday, 52 weeks a year, I send out an easy-to-digest protocol of simple steps that you or anyone you love can follow to optimize your own health. We cover everything from nutrition to mindset to metabolic health, sleep, community, longevity, and so much more. If you want to get on this email list, which is, by the way, free and get my weekly step-by-step protocols for whole-body health and optimization, Click the link in the show notes that's called Try This or just go to Drew Perot.com.

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