The Hidden Biology of Vascular Aging (Why Your Arteries Determine Your Age)

Welcome back once again to Made for Health. We are back, Dr. Hartman and Dr. Christian Jansky, once again to share our insights, our experience, and lots of nuggets with our audience. We are finishing up over the next couple episodes our vascular series on big fancy term vascular biology, which is a basic concept that you are no older than your arteries and that knowing actually how your arteries work and actually the wall within your arteries, and then literally the slime, the glycocalyx within your arteries, which is where all vascular disease begins and all aging begins and neurological issues begin. It's actually a pretty cool thing that we can now test, we can measure, and we can actually modify. Yeah. And so I want to recap what we've talked about so far. So I'm going to let my esteemed colleague with the photogenic memory to remind us of what we recapped. Because I feel like life is so crazy these days. I forget what I did like 5 minutes ago sometimes. Yeah.

So I mean, the, the best way to go through the recap would be maybe to start with a description of kind of what we're talking about with regards to the vascular lining and then how it gets hurt. And then what some of the risk factors are, and then maybe some of the therapeutic interventions. And I think that'll give a good general overview and then we can kind of get more detailed as necessary. But, but ultimately these are things that when you and I were in medical school, we didn't really know about. So these are relatively newer concepts. I mean, the concept of you are as old as your blood vessels is not, it's very old, but, but the reality of it is new. The, the endothelial glycocalyx, that slime that you were referring to, that's newly discovered. So the blood vessels, tens of thousands of miles of blood vessels in our body, they are essentially pumping blood, oxygen, nutrients to all these tissues that are incredibly important, whether it be your brain, the heart itself, your liver, your kidneys, et cetera. They just make the system run. And as that ages, you too age. And as they get older, you too get older. So there's a way for you to be biologically older than your chronological age. And that's a little bit concerning and scary, but it can be the opposite as well, which is younger than your chronological age. The lining of the blood vessel is this kind of sugar coat called the endothelial glycocalyx, which is basically, um, a bunch of different proteoglycans and glycosaminoglycans, which is basically carbohydrates and sugar that also houses all these anti-inflammatory and inflammatory molecules and things that thin out your blood or thicken your blood. These reactive intermediaries, that's where we start to make nitric oxide endogenously. So in our own bodies, the ability to make nitric oxide to dilate blood vessels. So it's, it's interacting with the blood as it's flowing through the vessels all day, every day, and it's modifying, regulating, and doing all the things necessary to make it as healthy as possible, or unfortunately diseased. So the glycocalyx sits on top of the lining of the blood vessel called the endothelium. The endothelium makes up that superficial lining of the blood vessel that has 3 layers itself. And when it's healthy, all things are working like they're supposed to. When it's damaged, we start to get a biological bandaid placed, and that's called a, a plaque. And, and so it typically starts as soft plaque. The soft plaque over time can get larger. It can rupture. That soft plaque is the more dangerous plaque because it's unstable. So a piece can break off and embolize. Meaning it can go from one area and shoot distally to a different area, get into a smaller blood vessel, not be maybe a problem in this big vessel, but in a smaller one gets stuck. And now all of a sudden you have an occlusion and the heart's taking a hit. Or over time that soft plaque can calcify, which is actually your body's biological mechanism of stabilizing the plaque. You hear about calcified plaque and you're like, oh my God, that's so bad. The reality is, is that it's, it's a way your body's trying to prevent that soft plaque from breaking off and getting worse. And interestingly, some of the mechanisms by which statins work is that they actually accelerate that, that calcification process to stabilize those plaques. So soft plaque is the beginning. It starts to push into the lining, push into the wall of the blood vessel. And as it's pushing into the wall, there's still no issue with flow. Blood is flowing appropriately. So you have disease without any clue that you have disease. You have disease without any evidence of that disease per se. and then as that plaque starts to push more and more into the wall of the blood vessel, it then hits that outer layer called the adventitia, and it starts to push the other way. Now it's starting to push into the lumen, which is where blood is flowing. And so think about it like a pipe. Now that pipe is starting to get a clog in it, and as that plaque buildup gets bigger and bigger, we say things like stenosis, meaning that blood vessel's getting tighter. The percent stenosis determines how symptomatic you are, how at risk you might be for a future cardiovascular event. And so as that plaque's getting bigger and bigger, it's either calcifying or it's embolizing, or it continues to cause more stenosis. And then eventually you have your event, which could be a heart attack, a stroke, or some other thing related to your vascularity. So that's in essence how you go from things are working well to things aren't working well. Everything's fine to my glycocalyx has been stripped. To my endothelium is inflamed and leaky, to now I have plaque formation, to now it's pushing into the lumen, to now it's getting tight, to now it's getting calcified, to now I have diminished blood flow. The three finite mechanisms of injury that lead to that in every single patient are inflammation, oxidative stress, and vascular immune dysfunction. So no matter how you slice it, that end product is the end product of one or all three of those diseases or, or, or those three mechanisms, let's say. So when you look at it through that lens, the, the 5, 6 different things that conventional cardiology pays attention to— are you overweight? Are you sedentary? Do you smoke? Do you have hypertension? Do you have dyslipidemia? Do you have diabetes? Maybe 7 things. Do you have family history? That's great. Those are important. We're going to talk about those, but that's just 7. What else can cause inflammation? What else can cause oxidative stress? What else can cause your immune system to be dysfunctional? So many things, hundreds and hundreds of modifiable risk factors. So we talked a bit about hypertension, high blood pressure, and what that means and what we should be doing about it. We talked a bit about dyslipidemia, so high cholesterol, high LDL, but took that deeper down that rabbit hole of it goes beyond that traditional panel where you have to look at LDL particle number and these other subtypes. Some of the genetic markers like Lp(a), we talked about some of the plaque markers. We talked about metabolic dysfunction. We talked about chronic inflammatory states. I mean, we even touched on to some extent things like autoimmunity and toxins and heavy metals, chronic infections, all these things that affect those three finite mechanisms of injury that lead to an inflammatory immune response that puts a bandaid on it that leads to plaque that eventually leads to disease. So that is really how you get from A to B when you go from I'm healthy to now I have vascular disease. And, and I mean, clearly there's a lot of steps along the way. Every one of those things that I just mentioned has a point of intervention. And, and that's not necessarily medication. It could be for some of them, and it is for many, but there's also nutraceuticals, there's dietary, dietary modifications, there's lifestyle modifications, whether it be stress management or exercise or diet, obviously. So there's so many ways to make this better, to go the other way, to prevent disease, but also reverse it, which is a cool thing that we'll talk about as well.

Great, great review. So if you want, people want to learn more, just basically you summarized in about 6 minutes what we talked about over 2 to 3 hours previously. But a couple things to think about to add on to that is, you know, if someone comes in, we are medical doctors. We went to university, I'm sorry, Medical College of Virginia undergraduate, did our residencies both there. And so if someone comes in with a 99% blockage of their LAD or whatever, and they have chest pain when they do stuff, that person's probably going to get a stent. And we have amazing cardiologists that literally can now do that through an artery in your arm. Basically a little conscious sedation. You close your eyes, you go to happy place and you see what's going on and you leave the hospital. Like we are awesome at that. That is 30 or 40 years after the first insult that might have been an infection when you're younger. It might have been a chemical exposure when you're younger. It could have been a life, a life of a horrible diet. And so we're talking about is not replacing these experts that we 100% need.

Yeah.

When you have angina and you have, you know, cardiomyopathy and you get a pacemaker put in because you might have sudden cardiac death. We're not, you know, we need these people. We're talking about before that and even complementing this because after they put the stent in, you have 60,000 miles of arteries in your body. They stented a little thing. It's maybe, you know, 5 centimeters. What about the other you know, 59,999.9 miles, right? Yeah. That's where all this stuff kind of comes into play.

And what about those that have disease but aren't bad enough yet? Right. Well, that's— this is a huge subset, right?

This—

these are the individuals that have multivessel disease or single vessel disease that isn't severe enough where they require stent or require bypass surgery. And so they're essentially a ticking time bomb. And the cardiologist will quite literally say medical management, come back when you're worse, come back when you're symptomatic. You know, there's blind spots in these stress tests, as you know. So if there's evidence of end organ damage, you gotta, it's emergent. You gotta intervene. We are excellent at that. I agree. And whether it be a stent or thrombolytics or both, depending on what the scenario is, that's huge. That's life-saving. That was my other life in the emergency department. I saw that all the time. And, and we jumped on these cases and we saved a lot of lives because of it. This is that middle ground that's really kind of scary. This is the demographic that gets gaslit, like women and people that don't have a lot of high risk. This is the atypical presentation demographic. And then this is all the preventative stuff.

Yeah. And that's where this shines. And even, you know, some of the stuff, um, we're both in the process of finishing up a vascular biology certification. Um, which is really cool. We're learning, um, it's actually reinforcing a lot of things we already knew, which is really good to hear it the second, third, and fourth time. But one of the speakers, uh, Dr. Mark Houston was talking about in their clinic in Vanderbilt, they're now seeing 8, 9, 10-year-olds with diabetes that they're doing, you know, ultrasound testing on, and they already have plaques.

Yeah.

And so it's one of those crazy things with disease can start decades before. And so we want to catch people ideally when they feel great, they're awesome, you know, and, oh, look, you got the small plaque here. Oh, you don't have this flexibility in your arteries that we can measure. All of a sudden you have low nitric oxide levels. And then intervene and actually prevent or even reverse, you know, having people's calcium scores go down, having people's— I've got a patient who had— he's in his 60s and his, his CIMT says his carotids are 90. And so we've actually been able the last 3 years to drop that age about 5 years as he's gotten older. So we're kind of closing that gap down.

Yeah.

So, so cool things we can do.

It's incredibly cool. And just to kind of summarize what Dr. Hartman was just talking about, like, so a CAC CT is a coronary artery calcium CT score, and it's basically a radiologist measuring the calcium that they perceive in your coronary arteries that gives you a score, and then by that score gives you risk for future event. The CIMT study is a carotid intimal-medial thickness study. It's basically an ultrasound that's looking at 2 of the 3 layers of your blood vessel, the intima and the media, and calculating a thickness ratio. And that then estimates your vascular age, which if older than your chronological age means you have vascular disease and you have inflammation, you probably have soft plaque. So we do these tests on patients routinely to risk stratify the biology, to risk stratify the anatomy that, you know, seeing risk in lab isn't— is not enough. You need to know what's going on on an anatomical level because again, a lot of these patients fall into that window of blind spot where they may have some disease, but not bad enough where they can still crush a stress test. And then everyone's like, you're fine cuz your stress test was normal.

Yeah.

But you need 70% or more stenosis in a single vessel to have a positive stress test. I mean, that's kind of like an average, but the reality is you can have 50% of an occlusion of a blood vessel and still pass a stress test. So that's kind of scary. So doing these other tests allow us to see, but also track progress, right? He was talking about a case where he had a guy who was, it was older. He did some things that intervened, and I think we're gonna talk about case presentations and we'll learn about some of the stuff that Dr. Hartman did, but then the score went the other way. Like that's, that's not routinely spoken about in conventional medicine. It's like you're stuck where you're at. Let's hope it doesn't get better. Here's a bunch of Band-Aids. And when you're really, really symptomatic, we'll do something interventional.

Another, and also another angle to think about this in the functional medicine and Grave world, um, the online social media influencer world, we hear about biohacking and what's the newest fancy anti-aging thing. And the thing I want to stress to people is you are no older than your arteries. If the arteries going to your kidney are old, you have kidney disease and you might need a kidney transplant or you might pass away. If the kidney— if the arteries going to your liver are old, your liver's old. If the arteries going to your brain are old, guess what? You get dementia. And so the idea that the 60,000 miles, we can actually measure, you know, the 3 finite responses. We can actually measure inflammation. We can measure immune dysregulation. We can actually measure, then anatomically measure flexibility, all these things. And then, do interventions and watch that stuff change. And that is the ultimate biohack. It's the ultimate anti-aging thing. And what I also tell people is, you know, this is all cool fancy stuff, but most up-to-date literature tells us that 80% of heart disease and 70% of most cancers can be prevented by diet and lifestyle. So what I tell— we're going through all this really cool stuff, but eat real food, exercise, get adequate sleep, have a purpose and meaning and value in your life, be a part of something bigger than yourself. Like, that's the super sauce that makes people in Blue Zones live to be 100 without fancy technology. And then roll this on top of it, and that's where you see, yeah, the magic happen.

That's, that's the foundation. I mean, I know you do this, but just for the sake of devil's advocate, like, we do this for every patient, right? Like, every patient that comes through our clinic has to have a foundational lifestyle plan. Like, 100%, it The other stuff doesn't matter if you're not doing that. It's like painting a burning house. Like, you don't put a coat of paint on a burning house. It's— you have to work on the diet, you have to work on— and that's different for everybody. It's not the same. It depends on genetics, it depends on, you know, how their gut's working, it depends on their deficiencies, it depends on what their body says it needs, you know. And then you got to be active, you got to manage stress, you got to prioritize sleep, all these things.

And it's— this is the ultimate personalized precision medicine where you take this, you know, you've been practicing medicine for 20-something years. I'm at 25 now.

You're, you're 20, 20, 2003 was when I started residency. So from MD, it'd be, this is year 23 from end of residency. This is year 20.

So you've created this buffet compendium and you've got a, you scare me sometimes. You have a really, really good memory, man. Because you have a really good memory. So it's a lot to keep up with you. But you've got this compendium and then all of a sudden now when someone comes in front of you, you have the time to basically figure out. And of course, that's over sometimes over a year or two or three.

Yeah.

This idea, you know, you are as long as you're— I'm going to quote somebody. Longevity is a vascular question. A person is as old as their arteries. So the question is, who said that and when? You know the answer. That's right. What's the answer?

Sir William Osler.

In 1892. 1892.

Yeah.

So what we're talking, this is, this is one of my newer, my newer things. I mean, my newer things, my newer thing is my newest thing is the old thing that's been around for 100 years.

Yeah.

So lipid therapy is half a century old. Neural therapy is 100 years old, right? Vascular biology is, I mean, what's that, 138 years old, right? Everybody's looking for the fancy, shiny, fancy, fancy, super new thing. It's like literally the basics are the new thing.

Yeah.

Perfecting the basics is the new fancy thing.

Yeah.

Not, you know, peptide, you know, XYZ123, that's going to like, you know, blow your number this much. It's like the old school stuff.

So it's the difference between Bitcoin and cash money, man. Give me, give me some cash.

Oh, that's controversial, man.

I know it is.

I own zero Bitcoin because I still don't I understand it, but it doesn't feel—

I can't afford Bitcoin.

You buy like, it's like, it's like in the old day they have gold, you like cut a little thing off of it.

It's like, give me a shaving of your imaginary money.

We don't have Bitcoin, we have bit shavings.

Yeah, it's, it's, but it is, it's repurposing. It's, it's going back to the drawing board. Why not? Right. And for some of these things, if it ain't broke, don't fix it. It's just these core concepts is really what you're talking about. It's not, it's the evolution of medicine and our, and our better understanding of some of these things that were proposed centuries ago, they were right, but now we know why they were right. And that's really, really important because now we can hone in on here's the evidence behind something some dude said. And oh, by the way, here are the interventions and here's our way of measuring it before and after so that we can prove that there's a better outcome. That's huge.

Yeah. And it's, and not to say we don't learn new things. Literally the idea of the glycocalyx, the literature was back to the early like 2010, 2012 timeframe, studies on using the rhamnosin. What's the seaweed extract?

Rhamnosulfate.

Rhamnosulfate. RS. There we go. Rhamnosulfate. That memory again, I'm telling you, man. It goes back to like 2012 to 2015. And now, we actually have a product that we can actually use. So, the idea is we're still using really cool new things. At the same time, it's still vascular disease from late 1800s. So, a couple of couple of statistics I want to say before we kind of—

I can't wait for you to do this part. This is crazy.

This is crazy.

I was reading this list and I was just like, this can't be true, but it is.

Well, you know, because you've heard it from the exact same place, you know?

Yeah.

So 70% of people with a heart attack had no previous symptoms. So if you wait for symptoms, you know, 70% of people have no symptoms.

I mean, what does that say? Prevention, right? Prevention. Be proactive.

75% of those people who've had a heart attack had a normal LDL cholesterol.

Yeah, that's—

and I remember, well, the old number I remember hearing decades ago was 50% of the people who go to the ER with the first heart attack have a normal cholesterol. Yeah.

So now they're saying 70. So say that one again. 75%.

Well, this is a normal LDL.

75% of those with a myocardial infarction heart attack had a normal LDL cholesterol.

And half of people who go to the ER with the first heart attack have normal total cholesterol. Yeah. And so Point being is if you're just looking at a standard cholesterol panel, anywhere from 50 to 75% of the time you're, you're missing it.

And the flip side, if you're just treating lipids, then you're not treating that patient because obviously these cholesterol numbers are not the main cause, right? These patients had other reasons for their heart disease. So, so treating their lipids is not going to be a game changer.

And this is where you get the game-changing statistics, 75% of cardiovascular events are due to a plaque rupture, which you start to mention. So, you have these plaques, the Band-Aids.

Yeah.

They're trying to fix something or unstable. And when you can actually measure a marker to measure for unstable plaques, they rupture and you go from, you know, 50%, 40%, 30%, maybe even 5% occluded to vroom.

Yeah.

And that's what kills people.

Yep.

75% of deaths are due to a plaque rupture. Which you'll miss in the cath, you'll miss in a stress test.

Yeah.

And if it's not significant, 75% of people admitted to the— okay. And this is, this is where, you know, when you talk about data points, this is, you know, we read a lot of literature and articles and one article will say 50%, one will say 69%, one will say 70%.

Yeah.

The gist is the majority. But yeah, this data point is 75% of people admitted to the— with an MI, and this is admitted to the hospital with an MI, had normal cholesterol.

So it's at least 50%.

The point is, is that majority.

Yeah.

Majority. So if you're only looking at cholesterol, you're missing.

Yeah. You're missing out.

Half of all, and this is, this is a lovely statistic. Half of all heart attacks are silent.

I knew. And this is one that hits home. I saw this in the ER all the time. It's, it's the atypical presentation. It's the, I didn't know I had a heart attack. What do you mean? My EKG is abnormal and shows that I had a previous heart attack or They come in for some complaint and they get admitted and they get worked up. And part of that workup is a cardiovascular workup. And they're told that they have wall motion abnormality on an echocardiogram. You had a previous heart attack. What do you mean I had a previous heart attack? It's just crazy how often that happens. In this case, the statistic is half. So silent heart attacks mean you didn't feel that elephant on your chest. You didn't have that, that, that anginal equivalent of, you know, jaw pain or numbness in your arm or shortness of breath or sweaty or chest pain or chest pressure. Pressure or that boring sensation in your scapula. It's the atypical presentation of I'm fatigued or I am not recovering from exercise or I just don't feel right. They're silent. They're not obvious. And so it's, that's kind of concerning.

Well, my question is how many of those are women? Because we know women present so differently than men. Yeah.

Women, diabetics, and elderly all present atypically.

Yeah. And so the question is, and I don't know the answer to this, I don't know if you know, but is, is this silent? Is this atypical? Skewed towards that population.

I think it is. And I know for a fact that plaque rupture is for sure. Statistically, women typically present with a soft plaque that ruptures. Men typically present with that, but more so calcified plaque and worsening stenosis over time.

This interesting— I'm going to throw this in here real quick. It was a patient early in my career that came in and was having some liver pain. This was a male actually having liver pain. So I did, you know, Typical workup for abdominal pain is the liver enzymes are up. So, okay, liver enzymes are up. He's a little tender over here. I don't know why, in hindsight, why I ordered a CAT scan versus something else, but I ordered an abdominal CT. Liver was fine, but it picked up the bomber's heart. And the bomber's heart was inflamed. And I was like, well, that's weird. So I ordered an echo and a troponin. And his echo was off and his troponin was sky high. And so it took about, it was about a 10-day, 7 to 10-day window from when he came in, I saw him, labs, to get this figured out outpatient. Yeah. But his heart attack, and this was a young, he was like late 40s. His heart attack looked like abdominal pain, looked like hepatitis.

Yeah.

Oops. Yeah. And so it was, it had to be an inferior wall. It, it, 100%. Yeah. Yeah. Of course. Yeah. Inferior wall. But the point is that you gotta be inquisitive. Don't give up. Keep on looking. Yeah. But this stuff is, according to these statistics, these kind of atypical presentations are everywhere.

I mean, I had in the, in the ER, I had women coming in saying something just doesn't feel right, or intuition, abdominal pain, or nausea, or I'm dizzy. I mean, it was, it was rarely textbook chest pain and you just have to have a high index of suspicion and you gotta trust your patients, which for some reason is not the norm.

Yeah, actually, in the book, in my book, I talk about this, the science, the neuroscience behind your gut intuition sense.

Yeah.

We now, now there's actually fields of medicine that say that it's a real legitimate thing. Yeah. So here's another great statistic. In those who have with a low risk of heart disease based on traditional factors, blood pressure, cholesterol, diet, you know, all that kind of stuff. The 7 things you mentioned previously. On a cardiac MRI, which is a fancy test, half of them will have plaques and 25% will have multivessel disease. So if we do traditional risk factor evaluation with your primary care doctor, all the usual, usual stuff in your, in your low risk, half of those people have a plaque. 25% of those people have multivessel disease and insurance will not pay for that cardiac MRI. And so how do we pick that up? Other things we'll talk about later, but it has to be preventive, preventive cardiology, metabolic cardiology, vascular, whatever you want to call it. Vascular biology cardiology has to be the standard.

Yeah.

Not wait till you have symptoms, wait till you have things. 20 to 40% of heart attacks, and this is, these are different statistics to say the same thing we've said already. 20 to 40% of heart attacks occur in undiagnosed heart disease. Here's an interesting, 20% of heart attacks are in undiagnosed hypertension. This hits home a lot because in the primary care, in the primary care world, my first board certification is in family medicine. You know, this thing called JNC 6, JNC 7, JNC 8, Joint National Convention. They, give the hypertension recommendations. And you start treatment, you know, stage 1 hypertension is 140 over 90 to 160 over 100. Stage 2 is 160 over 100. You know, stage 2, you start medications. Stage 1, you start diet and lifestyle.

Yeah.

Prehypertension is 130 over 80 to, you know, technically 139 over, um, 89. We don't have to treat those, just da da da. But yet, Dr. Jenske, what is the, What's the blood pressure? And I know you know this number. What's the blood pressure above which the risk for heart disease starts going up?

120 over 70s, maybe even lower.

Wait, wait a second. Are you saying that 120— I think the most recent thing I heard is like 115 over like 72, 75. So we'll say 120 to be less controversial, but it's actually 115. Let's say 120. So between 120 and 140, what do we do?

Intervene. No, what, what, what does conventional medicine—

what's the standard of care do?

Nothing.

Nothing.

Watch.

Watch. And the thing about it is this diagnosis of undiagnosed hypertension is legitimate 140 over 90 stuff.

Yeah.

Not this prehypertension world.

Yeah.

So I would probably say this 20% number is significantly lower.

It is too low. It should be higher.

It's higher. It's higher.

100%.

Yeah. Yeah. 30% are undiagnosed hyperlipidemia. 1 out of 3 young adults without traditional risk factors develops plaque before middle age. 1 out of 3 young adults without traditional risk factors. You don't smoke, you don't drink, you're not overweight.

No diabetes, no hypertension, no family history.

Develop plaque before middle age. So—

33%.

So we are missing the 8 ball horrifically. And right now it's not, it's changing, but right now still, as far as my understanding is, cardiovascular disease still is number 1 killer in our country. Yeah. Number 2 cancer, soon to be number 1.

I mean, if, if something infectious was killing as many people as cardiovascular disease does per year, we'd be in a constant state of emergency. It'd be, you would just hear epidemic, epidemic, epidemic, and all hands would be on deck. So I'm not sure why this isn't the case for this. I'm not sure why it's not more aggressive.

I mean, I understand why. The reason is because if you do this for every American, We bankrupt the country. You know, part of preventive, part of public health, part of, you know, this goes to vaccines, this goes to standard of care recommendations for cancer screening, this goes to mammogram recommendations, this goes to HIV testing. Why do we not start with a Western blot? This goes to Lyme testing. Why do we not start with the Western blot? We start with antibody testing that misses, by the way, half of all later confirmed cases of Lyme disease. So half of all confirmed Lyme, the initial standard, you know, antigen antibody testing is negative. Why do we have all these standards? Because—

so isn't the money saved on not getting the proper test lost on follow-up morbidity and mortality?

Well, the problem with data is that it lags reality. Yeah, that lags reality sometimes by decades. And so I remember when we were debating making the meningitis vaccine for college kids mandatory, um, earlier in my career. And the number was if you vaccinated all these kids, um, every college kid, because, you know, people come together, you get, you know, college recruits, I'm sorry, military recruits, kids going to college, lots of young people come together, you get meningitis, right? And this was, this status point's maybe 20 years old, just about, that it cost about, this is old dollars now, it'd be about $25 million to prevent one case of meningitis using the vaccine. So early on we didn't recommend it, and then the recommendation changed and we decided actually the life is worth XYZ, right? But you have to think about that, that $100 vaccine shot to save a life, you got to vaccinate a lot of people multiple times over years. And all of a sudden it's like, you look at prevention, you know, why is it that an A1C, which is a $25 test, is not standard for screening for diabetes? 'Cause AccuCheck is a $2 test. If you're doing a $25 test on 330 million people, that's a lot more expensive than a $2 test. And so that is in the equation. That is public health. That is standard of care, population-based medicine. When I see someone in my office, I'm looking at them, taking care of them. And all of a sudden, those limitations don't apply to my brain.

Yeah.

But when insurance says we don't pay for something, when the government says we don't do this or that or the other, you have to realize they're looking at 330 million people, not the person in front of them.

For testing, I get that, but there's no cost in teaching someone how to eat better. There's no cost in giving someone an exercise plan. There's no cost in, you know, helping someone manage their stress or help them understand it. Like just the lifestyle stuff alone, or stricter, a stricter guideline for blood pressure management, you know, all these things.

True. But there's no reimbursement for it.

Yeah.

Wow. I mean, my practice before I went—

Slam here.

Yeah. In my practice before I went full-fledged functional medicine, did I spend time with my diabetic patients? Yes. I had one patient who was a truck driver who, he came in for his annual physical because you have to, you may not have to, you didn't have to do these, but you fill out the little form every year for your driver's thing for truck drivers and bus drivers and whatnot. And his A1C was 10. So he couldn't drive. So his career was over. I'm like, look, He's like, Doc, you know, I can't not drive. I'm like, look, I'll give you a month. I want you to do this, this, this, and this. Don't eat this, work this much. And so he basically lived out of his, the bed of his truck and walked 3 hours a day, changed his diet. And when I rechecked him a month later, his A1C was 7.2. Wow. Now, with that 7.2, he can now drive. I put him on metformin. I didn't put him on insulin because you can't drive a truck on insulin. And we got, we actually got down to 6. And so did I do that stuff early in my career? Yes. But that was free recommendations I was giving to this guy. I was trying to help. When you're in a busy practice seeing 30 people a day, 8 to 10 minutes a slot, that's not going to happen. And so these are things people need to realize why this is not standard of care, because I don't know if it can be standard of care without tripling or quadrupling the number of providers in our country and increasing reimbursements some other way. And yeah.

So the best thing to do is empower patients.

100%.

Educate them.

100%, which is what, which is why we do this, why we, why we do all the free stuff online, why we do all the education stuff. 100%.

Yeah.

I've said this one bazillion times before. 80% of heart disease is pre— well, I haven't said it this way, but 80% of heart disease is prevented with just 5 lifestyle factors. So, you know, diet, exercise, don't smoke, stress management. Yeah. I throw in adequate sleep.

Yeah.

Yeah.

Take your meds if you're prescribed them. It's, it's—

Well, actually here's, I actually, I'm sorry, I actually listed them out right below. Diet, physical activity, smoking cessation, stress management, and compliance with medications was the fifth. Yeah. Assuming they have blood pressure and other things. So, so let's repeat one last time. Dr. Jinsky. What, what is the cause basically of heart disease, of everything? And it comes down to it. It's vascular biology.

It's vascular biology. It's 3 finite mechanisms and all the myriad of things that can lead to it, right? The dysfunction of it. It's, it's a laundry list. And these numbers are staggering. These numbers show you the reality. I mean, we can throw stats at you all day long. These numbers show you the reality of how many heart attacks are missed, how many heart attacks are atypical, how much or how little some of these risk factors play a role. You have to be aggressive. You have to be proactive. You have to be preventative.

Yeah. And let's— one last thing. I, you know, I have a bunch of other notes here. Actually, these notes are from my— the vascular biology certification we're going through right now. Both of us are going through currently. But, you know, I wrote down the same thing, 20% Different statistics, 20% of heart attacks are undiagnosed hypertension.

Yeah.

30% are an undiagnosed hyperlipidemia. Tell us, you know, I'm going to take this undiagnosed hyperlipidemia and I want you to blow it up. Okay.

Yeah.

Don't, I want you to think non-conventionally. Yeah. Because if 20%, if 30% is in just a good old-fashioned cholesterol panel, the number's going to be higher if you're doing an advanced expanded. So I'm going to do that right now with you. I want you.

Okay.

Undiagnosed hyperlipidemia, but I want the vascular biology perspective.

Yeah.

Like keep it simple. Yeah. Because once you start talking about Lp(a)s and Lp-PLA2s, you kind of—

everybody goes to sleep.

Everybody goes to sleep. So try to, try to— don't go do it. Don't do them all. But when you say undiagnosed, what do you see? Undiagnosed hyperlipidemia.

Yeah.

What are you seeing?

The, the, the shortest, easiest, simplest answer is it's beyond the 4-lab panel that you get at your doctor's office. It's beyond cholesterol, which is total cholesterol. It's beyond LDL cholesterol, which is touted as bad cholesterol. It's beyond HDL, which is touted as good, and triglycerides. Those 4 are important. We pay attention to those. That is an— that is a non-issue, but that is not enough. That is the issue. So you have to look at LDL particle number and particle size. You have to look at apolipoprotein B. And then you can get into some fancier markers. But for me, my baseline workup is what's their lipid panel? What's the LDL particle number and size? What's ApoB? And then am I going to look at genetic markers like lipoprotein A? Am I going to look at vascular markers like Lp-PLA2 and ADMA? Am I going to look at apolipoprotein A? Am I going to look at oxidative stress markers? Because it's not enough to just say, these are the numbers and I'm going to assume these are good and these are bad. LDL is absolutely necessary for human life. Our body makes it, we need it, we consume it, we utilize it to preserve function. In excess and if dysfunctional, it can absolutely cause problems. It gets sticky, it causes plaque formation, it makes you atherogenic. That being said, not all LDL is bad. And if your LDL cholesterol is controlled and if your LDL particle number is nice and low and your particles are big and fluffy beach balls that are sweeping through the blood vessel, cleaning it out, they're functioning just like HDL. On the flip side, HDL is not all good. HDL can be dysfunctional, and if that's the case, it's going to damage the blood vessel and lead to plaque the same way LDL would. So you need to know, and someone that has HDL, that's, let's say 80 to 100, and they're patting themselves on the back saying, look how good my good cholesterol is. If that's dysfunctional, they don't know that they have risk. And they're assuming that not only do they not have risk, but that they're protected, which is the opposite. So you have to dive deeper to understand the details of the biology behind this, these lipids that you have to become like almost a borderline lipidologist. And then you have to look at LDL. Is it damaged? Is it oxidized? Is it glycosylated? So is it rusted or is it sticky? And if that's the case, it's just gonna— any plaque that's there or any denuding or stripping down of that glycocalyx exposing the lining, any inflammation and damage and white cells and these things that are getting recruited by the immune system, they're just grabbing onto these molecules and they're just forming these plaques and it's just getting bigger and worse. And that's problematic. And so you have to dive deeper into fully understand what's going on with these. And so I look at all those parameters when I'm looking at someone from a lipid standpoint, and I know you do the same.

Yeah. And so, and so To say the exact same thing you said in a different way, you know, looking at oxidized LDL, we can 100% check that it's that inflamed burnt cholesterol molecule. We don't have a way to measure the glycosylated, but hemoglobin A1C is basically red blood cell membranes. So if they're elevated, you know you have the other one. Do you have vascular information? If you measure an NP, myeloperoxidase level, an NMP9 level, you literally are measuring an HSCRP. Which are all available through like Quest Labs, which is here in Richmond and across the country. You're now measuring that inflammation. So these are things that can actually be measured. And if you do an NMR lipid, which is that advanced profile you're mentioning, then you can guesstimate things like HDL function looking at the HDL particle number. So all of a sudden, a few extra labs and you can hit all these points.

And ApoA and myeloperoxidase also correlate to HDL. So if ApoA is too low and myeloperoxidase is elevated, then you know that you have dysfunctional HDL as well. So, so they all, there's ways to kind of put the puzzle pieces together.

And the last data point I want to say, and this is according to, I think, I forget that this was NHANES data or EPA data. It was one of the two of those that I was seeing this a couple of years ago. But 30% of all heart disease in our country can be directly related to lead exposure.

Wow.

And so that's a crazy number. Like when you go to your doctor and you've got artery disease, how often do you get a lead level done?

Yeah.

The answer is it should be every time. Yeah. And how much lead is safe in your body?

Zero.

Zero. It's, um, I have to, we've been doing this long enough that we actually now, I'm the old guy in the room. When I was your age, when I was younger, right? And so it's like, so the doctor version of that is early on in a career, you know, this is actually before my career, but a normal lead level was less than 50. And then when I started practicing medicine, they lowered it to less than 20. Then maybe 10 years ago they said actually a healthy, safe lead level is less than 5. But in the pediatric population, that's less, less than 10. But in the pediatric population, it's less than 5. And the reality is, is what level of lead in your body does at which you don't cause any inflammation. You know, lead in your body is a part of osteoporosis, osteoarthritis, osteopenia, basically calcium going in the wrong places, including arteries. And the answer— and the question is, what level of lead is healthy or okay in that? And from a vascular standpoint, the answer is zero. And so all of a sudden, if you're a patient with vascular disease— and oh, by the way, if you were born before 1991, you were exposed to lead. So how many of our— you know, right now, typically most people I'm seeing with issues are born after '91. I have a few actually I'm sorry, before— sorry, born before '91. I do have a few born after '91, but point is, like, a lead level is a simple test.

I test metals on all these patients. I mean, not just lead, mercury, arsenic, cadmium, thallium, especially if they're a smoker, cadmium. And I see positive levels and I do serum, but I mostly do urine provoked to see a body burden. And I just work on chelation and work on playing detective in their life to see if they have an ongoing exposure. Filter your water, eat clean, use proper cookware, use natural products. And then the numbers just get better and you're just taking one more risk and making it go away. There's no harm in that. And actually there's, there's treatment benefit and you see patients improve from it. So it's these are, these are the things we're talking about. I mean, we didn't even really touch on it, but like hormones are another thing that the risk of cardiovascular disease associated with perimenopause, like getting a woman on bioidentical hormone replacement therapy decreases her risk, period, hard stop. Like it's just there's layers to this that just aren't even considered in conventional medicine.

We're actually going to talk about that next. Great. Like after, we're going to close things out now. Next, I want to talk about actually risk factors, go through traditional risk factors, non-traditional, including hormones.

Yeah.

And then talk about a routine evaluation, what are some things we look at. So this is the way we're going to kind of, we're going to do 2 more episodes. Next episode is going to look at actual risk factors, actual data, actual routine evaluation, and then we're going to finish it up with some cases of people we've seen. That's the fun part. Yeah. And we're going to be— we basically wing most of these. I put some notes together and we just kind of—

I have one note. The rest I'm just going to try to pull from memory and we'll see.

Yeah, I've got one note as well and everything else is memory. So cool. Well, thanks for listening. If you've made it this far, if this information has been helpful, please like, share, subscribe. If you have any comments, we do actually look at those, so please put them below as well. We do take information from you all as far as future podcasts because we're always looking for topics to talk about that are relevant, not just to our patients in the office, which the reason we even started this was for education of our patients. So instead of spending all their time talking about this stuff, they can just listen to us and then we can spend our clinical time actually doing the real stuff. But if you drop some information, ask, you know, hey, XYZ, we can, if it's a topic that people are interested in, we can actually put that into the rotation of things we'll talk about. So otherwise, take care and we'll see you next time on Made for Health.

Take care.