Your Arteries Are Your Age: Introducing Metabolic Cadiology

Welcome back once again to another episode of Made for health with myself, Dr. Aaron Hartman and my partner in crime, Dr. Christian Jensky.

Hello.

We're back again. We're back again. Back again. Yes.

I'm excited about this one.

Yeah, I am super excited. We've been talking about some kind of sort of esoteric stuff. For us it's bread and butter. For us it's what we see all the time. You know, mold, Lyme, mast cell hypermobility, pots, things that aren't on the typical integrative functional medicine person's purview, but we see on a daily basis and actually, actually ridiculously common. Yeah, I refer to mystery illnesses because they're a mystery to most and we see them literally on a daily basis. But we will switch gears a little bit because we'll go back to the basics, go back to the good old fashioned stuff which is foundational. And we're talking about the concept of, you know, we were discussing what do we call this And I think the current term that were that we're landing on is metabolic cardiology, which is the idea of your vascular health or your vascular age. And so the concept is this, you are no older than or younger than your arteries being, you know, your arteries, arterials, capillaries, the stuff that actually feeds blood to your entire body literally is your age. And we have a lot of shiny objects, you know, peptides, stem cells, which are helpful. I've done those with myself, patients, my daughter, hyperbaric, which I love. But these are treating downstream things that ultimately affect that one cell lining, endothelium, the lightning of skin basically inside your arteries, your capillaries, where literally your age and everything happens. It's the largest actually hormone endocrine organ in your body. Actually. It's not your thyroid, it's not your adrenal glands, it's your endothelium.

Yeah.

Which is really fascinating. So we're going to talk about that over the next several episodes. This is the ultimate biohack. When we talk about how do you, how you affect your age? You know, is it how your skin looks, is it your, what biomarkers do you have? The ultimate marker for age is actually your arteries.

Vascular age.

Vascular age. A hundred percent. And something that a lot of people aren't talking about because once difficult, it's. You have to be a clinician, you have to know how to actually deal with blood pressure and a lot of things, you know how to have to deal with these markers, you have to know how to measure them. So it requires someone who actually has a clinical expertise. It's not a, you know, one size fits all on the, the one true, you know, one trick pony show kind of thing. You have to actually be able to do some stuff. And so it's not. It's hard, it's not fashionable, it's not great for social media, but literally it's a foundation of absolutely everything. So any.

The other stuff doesn't matter. The other stuff doesn't matter without this. Right.

100%.

It's. This is the core. This is truly where anti aging, where optimization of health, where all the things that we are seeking to obtain when we're on our health journey starts and stops. And the reality is, yeah, it's not sexy, it's not shiny, it's not new. But there's new information, there's new ways to test, there's old ways to test that still aren't done right. There's new ways to treat, there's always to treat that we repurpose. The key is to always take a step back and say, what can I be doing differently? What can I be doing better for my patients? What's at the core of every problem? You know, we talk about inflammation at the core of every problem, or mitochondrial dysfunction, or oxidative stress. Well, all those things affect vascularity. They affect the vascular age. So I think this is a huge topic that I don't know why, but for some reason flies under the radar. And I love that we're giving it a reboot and putting it back out there to really kind of unveil what it truly means and what can be done about it. Cause I think it's going to be absolutely eye opening.

I think these are just introductory comments as we. Because we're both kind of excited about this, actually. But when you talk about metabolic syndrome, that's your diabetes, that's your gout, that's your high triglycerides, that's your obesity, sleep apnea, hypertension, hypertension, pcos, osteoporosis, like, you know, fatty liver disease, fatty liver disease, low testosterone, men. All these things in metabolic syndrome, ultimately, where they increase your risk for heart disease, neurological disease, brain and heart is actually at this endothelium, at this, this layer of skin around your arteries and capillaries. And so you have to realize that it's trendy right now to talk about, you know, energy and talk about mitochondria and talk about, you know, metabolic stuff. And. But where that exists, where it does us damage, is that your endothelium, is that this One cell layer of thick skin.

Yeah, kind of like the gut, right? Like we talk about the gut all the time. When in doubt, heal the gut. Kind of the mantra of, of functional medicine. Hippocrates famous for saying all disease starts in the gut. When I talk to, to my patients about their GI tract and try to explain to them like intestinal dysbiosis and leaky gut or intestinal permeability, it's always, hey, there's this one layer of cells and they sit together and they're stuck like a tight junction and they should be locked in place, but if they're not, it's called leaky. And on top that there's a cushion and that cushion is protective and it houses the microbiome. Well, the blood vessels are the same. It's a cell and a cell stuck together. And on top of that there's a cushion that we now know is called the endothelial glycocalyx. And it houses all these little mediators of inflammation and anti inflammation and thinning and thickening of your blood. And it's just kind of like the quarterback for the football team, like sending out the signals and ultimately as that gets damaged and then the blood vessel itself gets damaged, that lining now maybe you're forming a plaque in the wall and that's how all this stuff kind of starts and stops. So it's literally that little microscopic wet paper towel, that layer that we need to work on to get these individuals moving in a better direction from a health standpoint.

And I think another thing that's really interesting about this topic is when we talk about, yeah, you have a heart attack, you have a stroke, your, your calcium score is higher, your CIMT is thick. Whatever the test you've done that shows you have disease, the infiltration, embedding of fat, fatty plaques into the walls of your arteries occurred 20, 30 years before that event. And what we now know is these changes that we can measure now in the compliance. The compliance, the stretchableness of your capillaries can be measured 10 or 20 years before that point in time. So literally we have the ability now to an 18 or 20 year old to measure the stretchiness of their arteries. These other Zealand markers for inflammation, biomarkers, genetics. We'll talk about a couple episodes from now gene markers and you can say based on these, we're going to start preventing this disease 20, 30 years later. If you don't do that, what can happen in 20 years is now the blood pressure goes up a little bit and we use a blood Pressure medication for that. If someone's measuring hscrp, which is inflammatory marker, if you're diabetic now, we'll lower that with the statin drug. Right. If you had a stroke, small vessel disease, and have high blood pressure and cholesterol, then we'll start dealing with those 34 years later. 30 or 40 years later. But the reality is we now have the ability to find these things way earlier. Way, way earlier.

Yeah, it's upstream. It's what we're attempting to do in just about every aspect of health. There's root causality in upstream medicine. And as diagnostics have improved, as the understanding has improved, our ability to detect earlier and intervene earlier has improved. And that always is important.

And there was an interesting study that NIH put out last fall, November timeframe. And this is important to all the females out there, men as well, but it was particularly women, and showed there are three biomarkers that could predict a female's risk for cardiovascular disease 30 years out. 30 years out. Those markers were LDL particle number, HSCRP and lp, which many functional people are kind of familiar with those. Yeah. But now we know there's markers 20 or 30 years before that as well. And all of a sudden, this is truly like longevity, anti aging. Just. This is like what we're supposed to be really good at.

And those are three. Just to be even clearer, those are three uncomplicated labs that you can get at any lab. This is not fancy functional testing. This is Quest. This is LabCorp. And your doctor can order them, should order them, and. And then you get that result and you know if you have risk or not. And then you can start to figure out why they might be elevated and what you can do about it. But it's. This should be the standard of care, in my opinion. I mean, the days of the basic lipid panel, cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides is archaic and quite literally not enough, not good enough. We should be doing better. And when you're adding in LDL particle number and particle size and you're looking at LP and you're looking at apolipoprotein B, and you're looking at the functionality of hdl, because not all HDL is actually good. And so if it's high, don't assume it's protective. You now then get a better understanding of the true risk stratification of this patient. And you can say, these are what your numbers show. This is what it means. This is what we're going to do about it. Here are your targets. And let's work at it. And you just get to work.

And we also have an understanding about our arteries that they all have these things called mast cells associated with them as well as neurovascular bundles, which is a way of saying arteries and nerves that surround these arteries that protect them.

Yeah.

And we now have ways to actually look at the integrity of that doing. Looking at your sympathetic nervous system, your parasympathetic nervous system with a measuring device that also can measure the stretchiness of these arterioles. And so now you can measure the pressure on your heart, pressure in your extremity, and actually figure out what is your actual nitric oxide level. Not a spit on. It's not a spit test on a. Yeah. On a strip, which we don't quite know if that correlates with actual heart disease or not. But we can actually measure that and then address it and change it. And so super excited. Because these are. These are things that aren't. I guess I shouldn't. They're complicated but not difficult. You just need to do the training. And I've seen the patients and. And cut your teeth and be able to address it. Um, yeah. So let's. Let's transition a little bit. That's our introductory notes or introductory things to say. We're super excited. Great. So. But I love the idea of everything's, as I understand things, deeper and deeper and deeper, and they become more complex. Complex and more like awe inspiring. They also become. The concepts become more basic. And you and I, one of our. I think I can say this for both of us. I know I can. One of our many Heroes Mentors is Dr. Mark Houston, who literally wrote the textbook of vascular biology, who runs the St. Thomas Hypertensive Clinic at Vanderbilt. So he's like, he's the guy. He's the man. Yeah.

So he's Oz. He pulled me behind the curtain and said, this is how it goes, man.

And you're like, oh, yeah.

Seriously. That was the biggest light bulb moment I've had in my functional journey. I mean, you and I, I think we have light bulb moments all the time. That's why we love what we do, because we, we will constantly be learning. We're never going to know enough. We'll always have to dive deeper. There's always going to be something new, learned. There's always going to be some different modality of intervention. And that's what's cool about it, especially if you have the intellectual curiosity that we have. But a lot of the aha moments that you and I have had, at least I could speak for myself, have come from the understanding of the complexity of human biology and how these interwoven systems kind of connect. And that was the difference between our conventional and our functional training is like, ah, that makes sense now because I understand them as a whole person versus the compartmentalization. But this was one of those light bulb moments where it was like I understood a system better than I was ever taught in a way that I never thought I would by someone who's been doing it for decades. And it was just this moment of clarity. Okay? Now I understand what cardiovascular disease is, and I understand what I can and should be doing for my patients differently and myself and my family. And it was just a light bulb. It was a switch. It was literally akin to Oz pulling you behind the curtain and being like, listen, Dorothy, this is how it really works. It's just smoke and mirrors. This is how true cardiovascular medicine should be. Should be implemented.

And so one of these concepts we're gonna talk about right now that I'm gonna have you explain, the three. The three finite responses. It's one of the things where that Dr. Houston talked about an infinite number of insults.

Insults? Yeah.

Calls in your body and your vasculature calls three finite limited responses. So what? That means it doesn't matter if it's mold or Lyme or heavy or mercury or arsenic or smoking or drinking or diabetes or high blood pressure or. Now we know you can have prevotella. You can have spirochet infections from your mouth, dental cavities that actually will literally get in your plaques, in your heart. H. Pylori as well. Doesn't matter what the cause. Okay, Chemical, napalm, Asian origin, Vietnam. We could go on.

Right?

The responses that your vascular arteries have are three. The infinite number of insults cause three finite responses. Dr. Jinsky.

Hey, what are they?

What are they? And enlighten us as to what these three finite responses are.

So this was that moment that I was referring to. And it was, you know, you understand the traditional risk factors that you're taught. You know, the family history, diabetes, hypertension, smoking, obesity, dyslipidemia. And it's like, okay, that's it. That's not it. There are hundreds and hundreds of modifiable factors that you were just alluding to. And you. You listed a bunch of them, and there clearly are more. And they all lead down one of three paths or two of three, or all three. And it's inflammation, oxidative, Stress and vascular immune dysfunction. These are the three finite mechanisms of injury to a blood vessel. So ultimately said differently, no matter what the cause is, the reason it hurts your blood vessel and potentially causes a plaque or stiffness or stenosis or any of the disease is because it creates inflammation, or because it creates oxidative stress, or because it creates vascular immune dysfunction, or all three at the same time. That then lends itself towards a response that leads to the process of events that happen that we know that lead to a plaque and ultimately tightening of those arteries. So you have this blood vessel, it's patent, it's, it's got good blood flow, there's no obstruction, there's no stenosis. You have this lining that you were talking about, kind of the skin on the inside called the endothelium. On top of that is this kind of carbohydrate, sugar rich glyco. They're called glycosaminoglycans. That kind of sit in this endothelial glycocalyx, which is why it was named. We didn't even learn about this in medical school. This was just discovered within the last five to 10 years. So like literally in the time that we've been practicing functional medicine, this new knowledge about cardiovascular disease has kind of come into play. So we learned about the glycocalyx, and that's sitting on top of this endothelium. And the endothelium then has this basement membrane that's kind of at the base. And then you have three layers to your blood vessel wall. It's the intima, the media and the adventitia. So it's the wall of the blood vessel, which is collagen and elastin and muscle. And then there's the basement membrane, and then there's this wet paper towel, and then there's this little sugar coat, and then the actual internal portion where blood is flowing. And as inflammation or as oxidative stress, or as vascular immune dysregulation occurs, the glycocalyx gets damaged. The glycocalyx then gets stripped away. Now you've exposed that endothelial lining. Now perhaps that gets damaged. Well, now a signal goes off and this signal is saying, look, something's wrong here. So the immune system gets wise, comes to the source of that injury, one of the three finite mechanisms. And you have these cells called macrophages that show up, they become a foam cell. They put down a biological band aid called a plaque. That plaque is there to protect, doesn't want to hurt you. It's there because something's wrong. You figure out what's wrong. You figure out what insult has occurred. And you can repair that plaque the same way that if you cut your skin that will heal over time. It might leave a scar, but it's going to heal. It doesn't stay open. Plaque can regress. Plaque can heal if you figure out what the problem is. So ultimately that plaque is put there. It's typically a soft plaque. It's first deposited into the wall of the blood vessel. So you might have vascular disease without any stenosis and not know it because it's not yet pushing into the lumen or the internal portion. As it pushes into the wall of that blood vessel, it eventually gets to a point where it realizes it can't go any further. Now it'll bow back out into the. Into the lumen. Now you get that classic plaque picture where you have disease that's visible on a catheterization or on a clearly study or on some modality of testing that shows you your arteries. And as that plaque is pushing more and more into the blood vessel, you get more and more what we call stenosis or tightening. So less blood is able to flow because that. That there's a clog there, so to speak, that soft plaque can break off and embolize and go into a distal or further down smaller blood vessel and occlude it. Or you can get calcification of that plaque that stabilizes it over time that can still also push in. And then tick, tick, tick, eventually it tightens up enough where you have diminished blood flow, you feel chest pain or whatever your equivalent is, and now you've had your event. So this is kind of the continuum of what happens. But ultimately all of that starts and stops with those three finite mechanisms.

And I think it's something that. I like what you said that a lot of people don't realize is initially that that soft plaque is actually a healing process. Yeah, your body's trying to protect itself from a damage. And if you remove that endothelial dysfunction, immune dysregulation, inflammation, that your body will actually heal itself. We'll do what it's made to do. But because it's usually related to something in the environment like smoking or drinking.

Or obesity that's ongoing.

Chemical or horrible. Processed food, diets, trans fats, seed oils, high, sugar high. Yeah, I actually had a conversation with someone. I'm trying to think it was a very interesting conversation, and they had a really good point. And it wasn't a conversation, actually. I'm not remember where it was. But the idea is smoking and heart disease. And you look at cultures that smoke a lot, Japan, Italy, they don't have that much heart disease in those countries, though. They smoke like chimneys. And we have all heart disease here. What's the big difference between. Now the argument was being made, therefore smoking is not as bad for you. I do not agree with that statement. Okay. But the point of this discussion was the difference that we don't smoke as much as them, all the sugar and processed food in our diets, and they don't have that in their diet. So therefore they can smoke. Point being is that if you have a horrible diet and. Or smoke or whatever, you have to remove that insult. But the thing I think is also really cool about this is you can measure inflammatory markers, you know, you can measure the inflammation, you can measure the immune dysregulation, you can measure genetic predisposition towards both of those things. And then we can also measure when the arteries start to get thick. You can actually measure compliance, how stretchy they are. You can measure blood pressure at night, when you're sleeping, daytime, et cetera. And now we have the ability to measure at every stage of this. Our current system waits there until you have chest pain, angina, shortness of breath, which is when, like you said, it's so narrow you have less blood flow to your heart or you have a release and you have a stroke to your brain. That's a little too late.

Yeah.

To be measuring stuff. And so I'm really excited about the ability to actually find these things, measure them, and then see that they're improving. Which we, we do this already. We've done this already. We, we've been doing the patients for years. I've had patients, calcium score goes down, scores go down. I've had just this past week, a patient who had a stent who was still the angina and a shortness of breath after a stent, a month after a stent. And we started using some, you know, some newer things we'll talk about a little later on. Yeah. And within fourth and four infusions, basically her shortness of breath went away. Yeah, she was really excited about it too. Yeah, she was actually just thinking clearer. But the point is, like, these should be readily available to the population at large. And what I'm hoping we can do over the next couple sessions is educate people so they realize this is not just make believe, it's the real deal. It's tomorrow's medicine today.

Yeah.

But what just blows my mind Is that guys like Dr. Houston, Dr. Slotel, Dr. Garani, that you. You actually went to her clinic? Yeah, yeah. How many years of that was that when you do your training?

At the beginning? Yeah, 2017.

They've been doing this for decades. There's a lot of smart people doing this for decades. And this is not new. It's actually older science and older information that is now just accessible and we can now learn and practice in our clinics. Instead of it being three to five people in the country doing it, now there's maybe 20 people. Yeah, the country doing it.

I mean, I've been on, I've been on both sides of that coin, right. I was an ER doc for 20 years. That's all I was dealing with end organ damage. It was. What happens when you don't address these issues? What happens when you already have heart disease and now it's bad enough where you're having an active heart attack? What happens when this is your third stroke? So, yeah, what you're measuring at that scenario, in that scenario are the, the, the measurements of injury, right, which is typically irreversible, some reversibility, but typically irreversible. So you're measuring a troponin, which is, you know, a blood marker that basically shows that your heart is being hurt. And, and so it's an enzyme that's being leaked by myocardial tissue. So you're measuring a troponin, you're looking at an EKG or you're measuring, you know, these other markers. And really what we're trying to do now is can we get some markers, can we get some data before that happens? Can we figure out where you are on this continuum of all the way to the left? I have no disease and no risk, and that's where I want to be. All the way to the right is I have all the risk and all the disease and I already have comorbidities. Where do you fit and where can we go from there? Is some of it fixed or is all of it reversible? And bare minimum, can we hold space while we're working on these things and try to move the needle a little bit more to that left? And the answer is usually yes. I mean, a lot of these things are just easy to order labs. It's just understanding what it all means and then what you can do about it. You should not feel that you're locked in. You should not feel that, oh, my dad and my dad's dad, they all had heart disease. So I'm going to die. Of a heart attack. If that's your mentality, change it now, like immediately rethink it. Because it's not the truth.

Yeah. I mean there's, we have so much information data about different people groups in the world. You may have heard the Nigerian paradox. It's the population has the highest amount of the ApoE4e4e4 allele, but low dementia. Yeah, low dementia, low electron with no heart disease. So they have the gene that here we associate with a four to five fold increased risk of dementia, double or tripling of your risk for heart disease.

Yeah.

And it's really funny as well because we talked about arteries, vasculature, neurovascular, cardiovascular, so brain arteries, heart arteries, which between that's number one killer and number three killer. Right. So if we three to four, you know, I'm saying right now, I'm saying medical errors, number three killer, which you may have heard about that. So. Yeah, well, but for today's conversation, we'll kind of keep it simple. But the point is, if you can eliminate those, it's like you've eliminated like the, some of the biggest issues we have as far as aging is concerned. Longevity, keeping your mind is concerned and it's a big deal and it's actually addressable. But back to the Nigerian paradox. So this, this gene, one of the many genes you can actually measure if you, if you have that gene in Nigeria, guess what? Yeah, Nothing. You bring it to America, guess what? Whoa. And so that's what people don't realize is you can even have these genes and have this predisposition, but it not express itself.

You know, you can't predestiny.

Yeah. In the, in the cancer world, the BRCA, the BRCA gene. In the 1950s, if you had the BRCA, the 1 and 2 gene, you would have about a 20, 20% chance of breast cancer today to 80%, 400% increase risk for breast cancer if you have the gene now. And so now the standard of care for those young ladies after they've had children, cystectomy, hysterectomy, oophorectomy, softomy, depends on now they're kind of realizing you can. It's actually ovarian cancer is actually fallopian tube cancer. So trying. But even now, still it's like eventually remove the ovaries. You wouldn't have done that rewind decades ago when the risk was much less. And so the point is our genes on our destiny environment plays a bigger role than we've thought. And even if you have disease you mentioned bypass. I've had patients who've had blockages, weren't surgically amenable to fixing, but the person worked out, they exercised, and they actually. The body made collaterals, they made workarounds, and after a while, their symptoms went away. They stabilized this. They made workarounds. Your body is pretty smart if you can kind of find what's lacking, give it some help. It wants to heal, it wants to self repair. And that's a basic concept that most people these days, I think, buy into.

Yeah, I agree.

So that's our introduction, I think. I think we'll stop there with this introduction. I think what we do next is take individual situations and start with hypertension, because that's like the big elephant room, so to speak. Talk about how it starts, where it starts, how you can treat it. Maybe talk about uric acid levels and colchicine for blood pressure and the difference between central and peripheral. You know, some really cool topics, but the idea is that even something as basic as high blood pressure can be done 100% differently. And then throughout the next episodes, we'll walk through heart attacks, strokes, neurological issues. What else do I have written down here? And all that one finished with arrhythmias and afib, which is a newer thing that we're seeing that we can address as well from a metabolic cardiology perspective.

Sure.

Cool. All right, well, I'm excited to keep.

Me too, man.

Take care. We'll talk to you soon.