Real Patient Stories: What Actually Reverses Cardiovascular Risk

Welcome back once again, everybody. We are ending our, our series on vascular aging, cardiometabolic stuff. You are as old as your arteries. You have 60,000 miles of arteries in your body. The surface area of those are— of the endothelium, it's called— the size of 6 tennis courts surface area. The mass of it is the size of 6 hearts, making it the largest hormonal-creating organ in your body. And so, it's really cool. We've had a lot of great conversations about things. We're going to end things up just talking about some patients we've seen over the, for me, 25 years, Dr. Jansky, 23 years. So, almost 50 years between the two of us. So, it makes us sound, we are getting old. We're both getting a little gray these days. So, I know, I know. I can't grow facial hair. It doesn't work on me. I look like a high school kid who can't grow anything. So, It's kind of embarrassing actually. My son actually makes fun of me.

Oh man.

Yeah.

He can't grow anything either. It's the only place I have grays. So I'm not missing out.

I'm not missing out.

I don't have much gray on my head.

And so we'll talk about some cases. And so this is just to put things in people's idea. This is not just theoretical. It's real world stuff. And I'm going to talk about one of the first. This is actually when I first started some of my training. When I first started doing things with Anna. One of the first things I understood was the whole methylation pathway. I had a patient, late 60s, who had a series of 3 strokes over 6 months. And first stroke, she recovered relatively well from it. Second stroke, she had to stay off work for a couple months. And third stroke, she like developed memory issues, developed ADHD, attention deficit problems. And she was on, like did bookkeeping type stuff. So you have to be able to pay attention, like do numbers and stuff. She smoked, horrible diet, all the usual things. But why was she getting repetitive strokes? And this was— she was not a functional medicine patient. She was a regular world patient. And but I knew enough to do some additional testing on her. And I did my labs, etc., etc. Cholesterol numbers were great. She was mildly pre-diabetic, you know, but her homocysteine level was almost 40. It was sky high. And I knew enough at that point in time. This was probably 15 years ago to be like, wait a second, this is a marker for cardiovascular disease. It wasn't that long ago. It was 10 years ago because actually I gave her some Homocysteine Supreme. So I started using that a little more recently and got her homocysteine level down to 15. And the stroke, the stroke stopped. We also got her to quit smoking, clean her diet up, et cetera, et cetera. But the big thing when the strokes stopped was actually getting her homocysteine level down. It wasn't normal. You know, I look for 6 to 7, you know, still high even on a traditional lab. But 15 was the difference for this patient between having these little small mini strokes repetitively 6 over, I'm sorry, 3 over 6 months and not. And that's the point of that patient's story is that, you know, when you have a vascular event, that sure, she smoked, had a bad diet. She was late 60s. Typically those people just overlooked for this is what we expect. But she had one after another after another. She had quit smoking after the second one before she had the third one. The home assisting was a game changer for her. It wasn't anything ridiculous. The supplement was like a $30 a month supplement. For her, a game changer. Over the next year, she was able to get her cognitive function back enough that she could actually go back to work. As, um, through like accounting type stuff. So interesting case. Um, do you have any qu— I guess if you have a question about that.

Yeah, so I think maybe for the people listening, um, assuming maybe they haven't heard the other podcast, just touch briefly on why the homocysteine is important. Um, and what was in the supplement that you gave her that helped lower it so that they can kind of understand why 40 was bad and why 15 was better and how you got there.

Well, lab normal ranges depends on the lab. It can be like 12, less than 12, optimal 6 or 7. And so typically on a patient, you might see a 15, maybe an 18. Yeah. I don't see a whole lot of 20s.

No.

So this was like—

40 is ridiculous.

This was like—

You look at that and you say, maybe I should retest this because it's probably lab error. Like it's that high, right? It's scary high.

Yeah. And so as far as homocysteine, you know, you last episode did a nice job of going into the details, but basically it's a marker for methylation. Can you recycle your B vitamins, specifically folic acid? And it correlates to inflammation, endothelial inflammation, but specifically to cardiovascular and neurovascular events, i.e., heart attacks and strokes. So there's a direct correlation. If it's too low, you have an increased risk for cancer. And this is one of the markers that moms with autism have been asking for for years. Because, you know, in the autism world, that this is a big thing.

Yeah.

Um, the OCD world's a big thing. And so knowing that she's having these events, I needed to test for it. I did. It was that simple.

And genetics play a role, and diet plays a role, i.e., nutritional status. But then, you know, if this person's already, in her case, exhibiting end organ damage, you got to intervene. So you intervened with something that you supplement and what was in that supplement?

It had methylfolate acid. It had B12. It had riboflavin, which is vitamin B2, choline, and TMG.

Yeah.

But it was basically a— there's a lot of fancy supplements out there, but the ones that have the biggest bang for your buck are a high dose of methylfolate acid and B12.

Yeah.

And they'll have some other things in there as well. Yeah.

Other methyl donors or associated cofactors. And really, So essentially the presumption that can be made in a case like this is that when, when someone's homocysteine is that high, clearly they're not methylating well. That's obvious. Why are they not methylating well? There's gonna be a genetic component in this person, whether you test it or not. There's no way your homocysteine's 40 without some SNP or, or typo in the gene that codes for the enzyme that converts these, these B vitamins. So Dr. Hartman knew this, and, and I don't know if you tested her genetics or not, but either way. He delivered the end products. He basically hacked her system and said, I'm gonna, I'm gonna address your issue by leapfrogging over your biological inadequacy and just delivering the end product. Here's some methylfolate in super high doses so that the rest of that cascade can work. And here's some methyl B12, assuming that might not be working. And here's some cofactors that help the enzymes that are working slowly work a little bit better. And here's even more methyl donors in the form of TMG. And now all of a sudden her homocysteine drops by 25 points and, and she stops having strokes. Like, that's not a coincidence. That's a huge deal. But what's lost in that translation is this is a basic lab that's not tested routinely, and you picked up on it, intervened with a supplement, not a medication, which is just basically B vitamins, and this woman stopped having strokes. Like, that's ridiculous.

And one thing that I've been— I've learned in the last 5 years, I've been reading a lot about nutrition. Medicine literature, and we have an epidemic of micronutrient deficiencies in our country because of processed foods. But also, you have a higher need if you're chronically inflamed, if you're chronically exposed to toxins, you're going to need more vitamin C, more B vitamins.

Overutilization.

Yes. And then if you have stressors, and so this is actually known in Japan, they had this, um, palagra. They had this, you could actually get sun-induced thiamine deficiency. People had mainly rice. Say all these B vitamin deficiencies, they would get in the sun, which would increase the B vitamin levels and they have all these weird neurological issues happen. And so, like the idea of like having malnutrition in a population is this old concept. And then stressors uncovering those in an acute way, a chronic process being uncovered in an acute way, it's not a new idea. And so, you know, well, I've read an interesting book recently about vitamin C. And you might appreciate this. When you look at sepsis patients, you look at what happens with sepsis patients, they usually die from bleeding complications. And you look at the process of sepsis at cell level when they start breaking down and clotting and thrombosis.

They go into DIC.

Correct. Yeah, that's a similar process to scurvy. And it's interesting how what happens is all these individuals get radical, crazy vitamin C deficiencies. So maybe, just maybe, this is the reason Dr. Paul Marik's research using vitamin C in sepsis patients had 80% response.

Interesting.

It's because there's a stress. And if you have a population that has low levels of vitamin C and you get pneumonia, oh my gosh, now she's bleeding and people die. Why'd that kid die? Why'd that person die? And it's typically the infection and they typically bleed out, right? The hemorrhage and that process at the level of the small microvasculature actually looks just like It's an acute process. It looks like scurvy.

It's like scurvy. Yeah.

And so the point being is that after reading these weird stuff, realizing that we, and there was a real interesting book by Dr. Lawnders, who's a pediatrician at Cleveland Clinic. It was actually about kids with weird dysautonomia things. And the point is like in the pediatric population with countrywide microdeficiencies in B vitamins, and then you get a stressor. Point being, this patient I was referring to had a horrible diet. Lots of processed foods. She smoked.

Yeah.

So she had all these micronutrient deficiencies.

Yeah. And then started getting strokes and heavy metals from the smoking, cadmium and things that were— so it's, so sometimes it's, it's lack of supply. Sometimes it's increased demand. Sometimes it's both. Um, sometimes it's the gut not functioning and you're malabsorbing and you're not getting it. So there's lots of reasons for that. And we see this and, and we are, I mean, there are food deserts in this country, but we are an overfed nation and, and yet we're seeing micronutrient deficiencies all the time, which is crazy. And one that comes to mind when we're talking about cardiovascular disease, magnesium, right? And in this case, I don't know if you also gave her mag or if she even needed mag, but like magnesium's also important for methylation. And, and I try to push everybody's red blood cell magnesium level above 5.8, closer to 6, because if you think about just what is magnesium doing beyond the 300+ processes that it's a cofactor in, from a cardiovascular standpoint, it's gonna help with her blood pressure. It's gonna help with methylation. It's going to help insulin receptors work better. Now all of a sudden, just by taking magnesium and optimizing it, you're taking other risks that this person might have had and making them a little bit better. And, and the symptoms just continue to improve. So there's, there's just a lot to be said about something as severe as a stroke and, and boiling it down to something as simplified as this person needed aggressive methylation support, which is vitamins, right? Vitamins and minerals. That's insane to me. Awesome case.

So what you got for me?

All right, I got one. So it's not as cool as that, but this is, this is one of these like cool success stories. So I have a patient, um, she is, uh, 54 years old and she is, uh, she came to my practice for, um, optimization, concerned about cardiovascular risk. Cause she had had a CIMT study about a year ago and her CIMT study when she was 53. Showed her vascular age to be 59. So she was 6 years older than her chronological age, had a CAC CT done by me that showed a zero. So I said, okay, you don't have calcified disease, but you do have soft plaque based on your CIMT. Bare minimum, you have endothelial dysfunction. So we got to get to work. And in the process of working her up, she knew that she had high, high, uh, LDL. I wound up getting an NMR on her that showed that her LDL particle number was elevated. Her ApoB was normal. Her total cholesterol was normal. Her HDL was great. Her triglycerides were great. Her A1C was great. Her plaque markers were great. So if you get where I'm going with this, a lot of her numbers look really good. And the question was, well, why does this woman have vascular disease? No one had tested an Lp(a) on her. Came back elevated. And so we worked on her Lp(a). In addition, she was newly postmenopausal. No one had talked to her about hormones. In addition, she was stressed out. So we worked on her stress. We worked on getting her cortisol better. She had a dysfunctional HPA axis based on a salivary cortisol panel. She was hypercortisolemic. So we worked on stress reduction techniques. We worked on adding some adaptogens. We worked on sleep hygiene and making sure her circadian patterns were established. She's a typical female patient that I have that are the caregivers that carry the stress of their family and their loved ones and their children and are just carrying the weight of the world on their shoulders. So we worked on compartmentalizing and delegating some of that responsibility to other people in her life. And then I got her on bioidentical hormone replacement therapy. She started to feel better. She started having less hot flashes. So she was having hot flashes, which are vasomotor symptoms associated with this vascular risk. She started sleeping better. She started feeling less stressed, less tired, started exercising more. Her diet was pretty, pretty good already, but we honed in on that. So a year goes by. We added a couple nutraceuticals to kind of help with some of the other things and to go after the Lp(a). And she just did a CIMT study recently, and her score is now showing that her vascular age is 56.5. So she aged one year and reverse-aged vascularly by almost 3 years. And so we're seeing reversal and regression of her plaque in the process of her getting older, and we're going to continue until those numbers sync up, until we get to the point where her vascular age is even younger than her chronological age. But just in the course of one year, she went from a vascular age of 59 to 56.5, which is reverse aging that you don't typically see, and this was stress management, bioidentical hormone replacement therapy, and a couple of nutraceuticals, like a little bit of niacin, a little bit of NAC, a little bit of vitamin C to deal with the LP(a), combined with just some fine-tuning of her lifestyle. And she feels phenomenal. She feels really great and is really happy with the results. So much so that she said when she was on the table and they were doing that ultrasound, the tech was like, wait, what's going on? Uh, this, and he didn't know what was happening. And she was like, she was scared. And he was like, this can't be you. And he was looking at it and he, he had never seen this before. He had never seen someone's age go the opposite way on a CIMT study. It was the first time that this personal tech had seen a score that he had previously done be younger a year later. And she just had a big smile on her face and just kind of walked outta there feeling like, you know, the best.

That office should be hopefully by now getting used to that. 'Cause we send all of our CIMTs there. Yeah, we do.

I'm actually going to get one myself at the end of this month, next month.

So a couple things about that, you know, that the menopause like that, individual, female caregiver. You know, I have this, this type of person I'm visualizing, the phenotype, right? The appearance of the person, you know, hard worker, type A sometimes, but they have this low estrogen appearance, like their skin, they get some of the fine wrinkles. The way their skin looks like has a low estrogen appearance to it. They'll have like arthritis, like they get like all my joint aches and stuff, osteopenia, you know, on their DEXA scans. But it's like calcium's going in the wrong places, right? It's going in arteries and stuff. And it's interesting how that phenotype, which is really common at this presentation, you know, what's the treatment for that?

It's estrogen.

Yeah. Hormones. It's like hormones. It's like a base. Well, obviously, I'm sorry, it's balancing your hormones. Sorry.

Yeah.

Better way to say is balancing hormones. As far as the Lp(a), that's becoming more popular right now. And that's a genetic marker, right? Well, let me phrase it. It's genetically influenced marker. You tend to be high or low. I'm not sure what your experience— I've been pretty, pretty good luck getting people's numbers down 40, 50% with like 200 to 125, still elevated. I'm not sure what your clinical experience is with those numbers, getting those.

Yeah, I have too. It's been pretty great because typically when you're taught about this, you're taught that you can't move it. You're taught that it's about 20 to 25% of the population that has this. If you get it tested and it's normal, it's usually going to be normal for the rest of your life. There are some that are kind of like on the fence and sometimes it'll go up a little and sometimes it'll be normal. That's rarer. And then there are those that it's elevated and sometimes really elevated. And those are the ones that you have to be really concerned about because this is atherogenic and thrombogenic, meaning that you're at risk for clots and plaque. And ultimately the goal is to lower it any way you can because there's no, there's no direct pharmaceutical on the market yet, although there's apparently one in the pipeline. So cardiologists are aware of this. Cardiologists that we work with are aware of this, and there are off-label use for certain drugs like Repatha or Lekvio that can help lower this, but it'll only lower it by about 20%. And I get better— I get better percent lowering with, with nutraceuticals and lifestyle modification. So sometimes it's a combination of all the things. Sometimes they'll get on the drugs and you'll add in whatever you're going to use, whatever you like to use for that specific individual. I tend to go towards niacin. I like— obviously they all get vitamin C. I like using NAC for this. But, but yeah, the numbers budge for sure.

That's interesting. The 15% reduction in Lp(a) with your PSK9 Repatha.

Yeah, it's about like 15 to 20% because statins will increase your Lp(a) about 15%, which is the problem because in order to qualify for Repatha, you have to get on a statin first and, and show that you fail therapy. And next they will add Zetia, which is basically a pharmaceutical plant sterol. To decrease cholesterol absorption in the gut and gives everybody bad GI side effects. So now you're on a statin and Zetia and, and your, your Lp(a) is actually not budged or gone up and your cholesterol, which wasn't a problem to begin with, is even lower and paradoxically increasing risk. And now all of a sudden you might qualify for Repatha, but they don't want to take you off the statin and it just becomes a nightmare. It's rare that someone gets the ability to leapfrog those two drugs and goes right to Repatha. I do have some that are just on Repatha or Leqvio, but most of them in in order to get to that point have to be on at least like 5mg of Crestor. And, and to me it's like, how much of that is pushing the number the wrong way? And how much of that is creating a problem when her cholesterol, her LDL cholesterol, her ApoB, her particle number, none of that was really the issue to begin with. So why, why put that person on a statin, right? Like, and that person didn't have a CAC CT that was positive, so doesn't have calcified plaque, although has some soft plaque, not documented by traditional cardiovascular ways. So she's technically, in my world, secondary prevention, but in their world, maybe primary prevention. And the number needed to treat is 1 out of 100. So like, she's not even gonna get benefit from that statin unless she's that one person, right? So it's just, these are the, these are the things that you and I are navigating. These are the waters that we're trying to navigate with these patients, hopefully with, with the help of a cardiologist that knows what they're doing. But like, this is, this is one of those cases. The whole point of the case was not only to show that you can regress soft plaque, and you can calcify plaque, by the way, as well. But you can regress soft plaque because it's basically a biological band-aid the body's putting there to address a wound that was insulted secondary to inflammation, oxidative stress, vascular immune dysfunction. There's 3 finite mechanisms. Address the root cause, no longer insulting. Now regress the plaque. Now that band-aid's better and you can put the glycocalyx back. The endothelium gets better. Everything moves in a positive direction. But the other thing is that this was an atypical presentation. This woman was hormones. This woman was hormones and a genetic marker. And, and most people were missing it, right? Kind of like your homocysteine story. Like no one was really looking at that. So I just thought that that was kind of a cool case.

So, um, had an interesting case with a gentleman, um, had retired recently, young, young retired, closed down business, sold it. He was doing great, but, um, started getting, um, stress, another stroke patient, but he had actually had about 5 strokes in a period of 2 years. Went to the Cleveland Clinic and got diagnosed with autoimmune vasculitis. Got put on statin, the best they could do for him. And that was kind of it. And came, saw me, and he was obviously super anxious because he's having like these— his were more mini strokes. So they would, he'd have a stroke and he, you know, within a month would be back to normal, but he had 5 of those. And so, interesting. So we started doing the usual stuff. And so because of where we are and where we live. I started going down this. And so he had no chronic fatigue, no fibro, no typical mystery illness symptoms that you think about because we've done a bunch of mystery illness kind of things.

Yeah.

Did SIRS labs on him, chronic inflammatory response syndrome labs, and his C4a was off the chain. He had Marcons. His MMP9 was off the chain. Is TGF-beta, which is not an official SIRS marker, but it's a marker for inflammation causing scarring, right?

Yeah. Fibrosis.

Exactly. And it was ridiculously high. So we went down the, I think this is an autoimmune phenomenon related to an environmental biotoxin, a water-damaged building, commonly referred to as mold illness, but it's actually not mold. It's the biotoxins. It's all the company mold keeps, right? Yeah. It was about a year process to encapsulate his crawl space, start on lipid therapy, which now we're doing IV phosphatidylcholine here to treat actually a lot of these things with great results. But I'll start with oral therapy, start using Tutka as well as butyrate. Those actually, it's interesting, those nutrients, if you've had a biotoxin exposure, speed up the— your body has a natural trash dump burning. It's almost like a trash fire called the peroxisome, but they take the trash to the peroxisomes and they burn it up. And so you can speed that up with butyrate and TUDCA. So we gave him those things. So started doing binders, et cetera. And he went without stroke for like 3 years and he was obviously elated. Of course he got super anxious because now he's like mold. Yeah. And he's a super bright guy, so he researched it and he's like, isn't this everywhere? It's like, yeah. But it was, but it was one of those things where, um, he'd gone to probably one of the top, if not the top places in the country, um, been diagnosed with an autoimmune vasculitis. And, and for me it was like, okay, you've got, it was kind of nice to be honest with you. 'Cause it was like, you've been the top place in the country and they're like, here's your statin, go home, have a good life. Um, they put him on, um, some Plavix as well, like blood thinner. Yeah. Um, and they came to me, I'm like, well, they gave up.

They stopped asking why.

And, and for me it was like, Well, cool. Like, I can do whatever now because you've been to the best place and they're so— we're done. And so it was kind of nice to have that freedom to go and do whatever with. But also found he had some heavy metal issues, also had some lead issues. Of course, his gut was a wreck. Of course, his omega-3 omega check was low. So we needed to balance his omega-3 levels. Of course, his vitamin D level was like in the tank, which is related with autoimmune vascular issues. But With autoimmune things, if you have an autoimmune problem, regardless of the name for it, you have to have 4 things. Genetic predisposition, which I can't change. Increased gastrointestinal permeability known as leaky gut. Chronic infection of some sort. And a triggering event. And for him, the triggering event was the biotoxin. And he had some dental issues and gut stuff as well. Negative Lyme markers, negative Epstein-Barr markers, et cetera. But it was just really interesting.

And any coronary artery disease, any cardiovascular disease, just the stroke stuff?

Just the stroke stuff. He had like an elevated calcium score. I was like, you know, 100 and change. And his CIMT, actually we did that and that was elevated. So we're, you know, working on that. Yeah. So, but as far as he came with like a big, big issue. And for him it was like interesting because he wanted to like start another business and he was like, I still got my mind. I'm in my mid-50s and Obviously, if you're having strokes every couple of months, it's— Yeah. You can't plan for stuff. And it's really like we collect these rare, interesting kind of oddball cases, but you learn from those and then you realize this is going on at a much lower level, like the entire population.

Yeah. I mean, the other thing that comes to my mind when I think about these SIRS cases, because I see this a lot. I mean, we treat a lot of SIRS patients because we're both certified and not many are. And so they, they tend to flock to this, to this practice. But I personally am a SIRS patient. So I also have this kind of attachment. Um, I see cases where you, and this is well documented in the SIRS literature, where you get pulmonary artery hypertension. And so when you have chronically low VEGF, chronic tissue hypoxia, maybe compounded by that person might also be anemic or have low ferritin or something like that. You, you eventually develop a little bit of tricuspid regurgitation, then you develop pulmonary hypertension, then you develop some right heart strain, and then these patients go into dysrhythmias. So we talk a lot about the vascular issue in the way of a plumbing problem, right? You know, does this person have coronary artery disease? Do they have a blockage? Are they going to have a heart attack? Are they having strokes? But we also previously discussed some of the electrical stuff like the arrhythmias, and I've had some cases cases of patients where due to pulmonary artery hypertension secondary to SIRS, they've developed AFib and now require multiple medications or ablation that then fails and then ablation again, or some sort of, you know, pacer, defibrillator, whatever, depending on the dysrhythmia. And it all ties back to a biotoxin issue, right? Whereas if they were to just present with the arrhythmia to a conventional cardiologist, they would just treat it as such. And never look for a root cause. My question is, as I get this gentleman towards VIP and SIRS reversal, can we reverse pulmonary artery hypertension? And is there any way to remodel the heart? Is there any way to make the arrhythmia go away permanently? So there's so many layers. There's so many layers to this. But I think that that's kind of fascinating. I'm sure this guy's very, very grateful for you finding this out.

Well, it's interesting you ask that question about the cardiomyopathy stuff. I have a patient, um, that I'm working with right now who, and it's going through a lot of stuff with him, has a pacemaker, EF like 20%.

So heart failure.

Yeah. And so, yeah, I'm sorry. Yes. Heart failure and had a dual pacer and then had a defibrillator placed because the standard of care, which is appropriate, is these people have a high risk for sudden cardiac death. So you kind of put the defibrillator in there. So if the heart stops, they kind of, gets shocked back. Yeah, shocked back immediately. But with his numbers going down, he started developing edema. And so, you know, the typical thing is you get on Lasix for that and then double the edema, then that causes more potassium micronutrient deficiencies. And so I offered him actually some exosomes and stem cells. And so we ended up doing inhaled exosomes, IV exosomes and stem cells, repeated an echo 4 months later, and his EF is now 40%.

Oh my gosh.

And so, so we're early in this right now. And because the question is, do we do this again? Because they're expensive.

Yeah.

You know, he's doing great. It's funny now because as he's gotten better and you've probably had this, I'm not sure if you had this experience, but having done a lot of primary care with heart failure patients, whatnot, when people get better, it's almost like the medications work better. So it's like put all stuff on, right? And then they get a little better and all of a sudden now their blood pressure starts dropping.

Yeah.

So he's at the stage now as cardiologist weaning off some of his medications.

Yeah. It's awesome.

And so, But the question is, which doesn't happen with heart failure.

It's typically progressive. Like you, you typically don't go backwards with your medicine.

I've had patients go backwards with medicine. Typically, yes. Yeah. But for it to go backwards, the person has to be willing to do a lot of stuff and lose weight and change diet, et cetera. But then what happens is the medications work better and all of a sudden their blood pressures are dropping. But the question with him now, which I don't know the answer, I'll ask you, you know, you know, do we do another round of this at 6 months? Because they tend to think of 4 to 6 months. You know, right now I'm trying to get him off some of the medication because I want to see what he'll look like at the end of this. But exciting because, you know, we were concerned because like at his age, I mean, next step would be a cardiac transplant. Yeah.

That's crazy because, you know, the other thing with the diuretics is that you're starting to tax the kidneys. And then when the kidneys go the wrong way, then you're just going to get even more dependent edema. And you don't know if it's related to the kidneys or the heart. And it just becomes a vicious loop. And then how do you diurese if your kidneys aren't even working? So that person just becomes a ticking time bomb of flash pulmonary edema. And these are the cases I saw in the emergency department all the time. That's where my, they tend to not go backwards comes from. So I'm glad that you're seeing that because we, I mean, these were literally, we'd call them frequent flyers. I mean, they were just in and out of the ER all the time. They'd come in, we'd put them on BiPAP, we'd diurese them. They'd get admitted, they'd get tuned up, they'd go home and then they eat their high salt diet and they'd come right back. And it was just, it was insane. All right, so I have, this is like one of my cardinal cases and, and we're still working hard, but this, the main reason for me telling you this case is because of how hard we had to fight for her. Um, because I want to make sure that people are aware that, that you need to be an advocate for yourself and, and that, um, don't assume that, that anyone has your back other than you. Until you get a good relationship with a provider that you trust. She moved up here from Florida. I actually treat her husband and previously had treated both of her daughters. And I don't treat kids anymore, but one of her daughters is still in my practice, grandfathered in, and they're a wonderful family. And she came up, joined my practice. She was in her 40s and had a known CACCT that was elevated in like the 200s.

40.

In her 40s, not perimenopausal, still not borderline perimenopausal at worst right now, and was like, look, I have coronary artery disease. I know I have Lp(a). I had to fight for that to get tested. I had some heavy metal testing done and I went through some IV chelation, which is a little aggressive for me, but maybe wherever she was in Florida, that's something that they did routinely. And she's like, I just want to prevent further heart disease. So she had no other known risk factors. I labbed her up, checked everything that I could from a cardiovascular standpoint. Um, and it was the Lp(a) and the metals. That was all I identified at the time. And we worked on that and worked on that and tried to get her in with a cardiologist and tried to arrange for some further risk stratification. And that included trying to get a stress test with that CAC CT. And her insurance wouldn't cover it. So we continue to work because they said she had no, no risk factors despite a CAC CT that was in the 200s. So calcification in her 40s, which clearly means that she also has extensive soft plaque and Lp(a) and heavy metals, which they're clearly not going to acknowledge. So we're working on everything. We do the metals. Metals are no longer an issue. We're working on the Lp(a). It's getting a little bit better. We haven't gone to pharmacotherapy yet. She didn't really want to pull the trigger on that. and she's starting to get symptomatic. And we try again to get a stress test. Insurance wouldn't cover it. It says that she does not have any risk. So then she writes— with symptoms, with symptoms. She, she then writes me, um, through the portal, um, that she was short of breath and having exertional chest pain chasing down the bus, school bus, when her kindergartner was late for the bus and the bus was pulling away. And I said, you need to go to the emergency department right now. She goes to the emergency department. It's an EKG, gets a workup. They admit her, they do an in-house stress test. It's abnormal. They take her to the cath lab. She has a 90-plus percent stenosis in her LAD. This was 12 months after my initial attempt to get a stress test, which she would have failed 12 months prior. It's a miracle that she didn't have a massive heart attack and die at this point in time, but she didn't. They put a stent in. Now she's on the drugs, which she didn't want to be on, but she understood. She's on statins and aspirin, some beta blockers. She's on Plavix. So dual antiplatelet therapy, statin standard of care, even though her cholesterol was never super high. I get her on CoQ10 to combat some of the negative effects of the statin. We try to find the minimal effective dose. We're playing around with her numbers. It's driving her Lp(a) up higher, which is a problem. I get her in with a cardiologist that I trust who is trying to get her on Repatha now at this point in time. She's already on a statin. Insurance says no. She had 90% stenosis in her LAD, stented, on statin, has known coronary artery disease documented on a cardiac catheterization. Insurance wouldn't cover her Repatha. I write a letter. They probably threw it out. Cardiologist writes a letter. They say no. They want her to, to get on Zetia. So she gets on Zetia, gives her diarrhea, immediately comes off of it. Now the statin's causing her cholesterol to get too low and she's having symptoms, sexual dysfunction, brain fog. So we lower the dose, give her more CoQ10, finally gets approval for Repatha. But before that happens, she's symptomatic again, goes back, gets retested, goes back to the cath lab. She re-stenosed, winds up getting another stent placed. She's fine. And we're at a point now where she's been asymptomatic for a while, but this is a woman who's gotten stented twice. This woman who had significant disease. This is a woman who had heavy metals and Lp(a). We had to fight tooth and nail with her insurance to get a stress test, which is appropriate, that she eventually failed 12 months later and then couldn't get the right pharmaceutical coverage, the right pharmaceutical covered to treat her condition until recently. And then she wound up going out of state to see Dr. Twyman in Missouri. I think he's in Missouri to have like extensive, like genetic testing and all kinds of other treatment. Turns out she's also a CIRS patient. So she's got chronic inflammation from that, but this is a very atypical presentation at a very young age who clearly has significant pathology and significant risk. And the amount of, of, of stress placed on this woman, the amount of self-advocacy that she's had to do to maintain her health is, is only contributing to her disease state. And it's appalling to me at how hard we've all had to work, especially her, and her family to get to this point. But she's fine. She's fine. But there's still a long way to go. And these are, this is just one of probably many stories like this, that this is why we do what we do when we're looking at these cases that women, diabetics, and elderly present atypically. This wasn't even atypical. She was symptomatic. We couldn't get the appropriate testing because it wasn't traditional risk factors. Ad nauseam documentation of the risk that she did have and the literature to support it, and yet they still wouldn't cover it. So like, What do you do in those situations but just keep fighting? Thankfully she's okay, but like, this is why you gotta get ahead of it. This is why you gotta jump on it. This is why you gotta look at these atypical markers so that you can do something before you have 90% stenosis of one of your main arteries.

Like, and if you didn't have that calcium score, you wouldn't even have thought she was high risk.

It, it, as soon as I saw her Lp(a), I would've gotten a CAC CT and we would've gotten it. And seen it. But yeah, you wouldn't have, you wouldn't have known. You wouldn't even have known.

Interesting. What's your endgame with this individual as far as like, 'cause now she has a stent, so the calcium score's gonna be hard to track.

Yeah.

Like what other markers do you have besides the Lp(a) that you're tracking for like a clinical outcome? Like, okay, I know I'm going on the right pathway. Yeah.

So all of her cardiovascular markers we're tracking tightly, whether it's Lp-PLA2, ADMA, Lp(a), all of her lipids including lipid fractionation. I'm looking at homocysteine and methylation. I'm looking at metabolic markers. She's now dipping her toe into perimenopausal. So we're going to get her on some hormone therapy. We've worked really hard on stress. We've cleaned up her diet. I recently put her on a GLP-1. I'm microdosing a GLP-1 to get her some cardiovascular risk reduction. It was, it was our decision because she was also gaining weight. She was unable to exercise the way that she wanted to exercise. The goal is eventually to reverse her SIRS and then Twyman did a bunch of genetic testing, some of which helped, some really didn't. She's currently on Repatha. Our, our hope is that the Lp(a)-directed pharmacotherapy that's allegedly coming out comes out and that she qualifies for that. And then from a tracking standpoint, because I can't do a CSCT, CIMT studies, and then eventually if we get an endopat and other things that I can use to kind of track more closely, and then her listening to her body and symptoms and working closely with that cardiologist.

Have you thought about using PlaqueX with her?

I have. I've already talked to her about it. Yeah, yeah. She's on the list when we get it again to be able to do the IVPC.

The PlaqueX is really cool. It's an IV phosphatidylcholine that has really good literature, basically soap for your arteries. Yeah. And for it actually lowering calcium scores.

I just saw her and we talked about that and I said, right now we don't have it. When we get it, you need to, you need to sign up for this. And finances are an issue, but she's willing to do it. And then ultimately I have her on glycocalyx support, nitric oxide support, like You know, vitamin K2, MK-7, aged garlic extract, resveratrol, like all the things. Like literally I, I have a kitchen sink of supplements that she takes religiously.

So a question for you, and this is something I'm, some of my patients having sticking points. So you have, you do your calcium, calcium score and it gives you multiple arteries like, you know, RCA, circumflex, LAD, et cetera. And they have like a score of, let's say, 400 for argument's sake. Yeah. I've got some people with 1,000+ numbers. So do I. Yeah. So it's elevated. They get a stent put in, RCA, let's say. How are you tracking those calciums after that? Something I've been looking at is just repeating the calcium score, but ignoring the stented artery and only looking at the other ones that have calcium.

We did that. We did that and we had to fight for it. The imaging center wouldn't do it. Post-stent because they said it's going to mislead and be artifactual. And I said, she has one stent in one artery, read the other arteries.

Yeah.

And they wouldn't do it. And then we went to a different imaging center and they did it.

Interesting. Mm-hmm.

So it's, it's, it's only been a fight. I don't know why, but it's only been a fight. But any data is better than no data, in my opinion. As far as I'm concerned, data is king. You just get as much as you can and you do your best, and then you, you have to track the markers. So it's, it's making sure that, you know, all of her biometrics look good, her blood pressure, her heart rate, her BMI, how she feels, her exercise tolerance, and then everything objectively that I can measure, anything anatomically that the places that I don't have control over are willing to do. Her cardiologist, an outsourced cardiologist, and then we just keep going. But it, it's been a nightmare. It's been a complete nightmare for this woman.

Yeah, I've got an interesting similar case from a while ago. It was an individual with diagnosis of hemochromatosis and he was diabetic and has cardiologist, has stress test every, you know, 2 to 3 years and started, and he had even had a stent placed previously and started getting, they called, he was traveling across the country and he called me like, hey, I'm having some shortness of breath, some pressure. It sounded very typical. I'm like, well, go to the ER. He went to the ER, went there, had a stress test done, it was normal. So flew back across the country, came back to Richmond area. I see him and it's— but it's interesting because it's like one of the things I learned in my training, my family medicine training, you have a diabetic and he had— he also had hemochromatosis, which is, as you know, just increases your risk for everything.

Yeah.

Hemochromatosis is an issue where you store too much iron.

Yeah.

And so iron is a heavy metal. It's probably more toxic than than mercury.

Yeah.

You know, one, the average person has about one penny's worth of iron in our body. You put two pennies worth and you get hemochromatosis. So, yeah.

And so, that's causing two of the three finite mechanisms of injury, right? Inflammation and oxidative stress.

And if you have like typical symptoms, you always go to cath. You don't just— you're not satisfied with stress testing because it's not 100%. It still misses stuff. So, him see his cardiologist. He's like, your stress test, I read it fine. So he called me back. I'm like, so I personally called the cardiologist. He's like, fine, I'll just cath him. And he had like a 90% blockage in the circumflex artery. You know, it was one of those things where—

And his stress test was normal.

Yeah, stress test was normal. The cardiologist actually called me back. He's like, you're right, I'm sorry. So it was really cool with the cardiologist. That's really cool. But the thing about it was, is that like, that's where listening to people advocating for them. But also, he happened to have someone who was on, like, the specialist was on his team as well who gave me a little bit of pushback, but not a whole lot. And that's one of those things where it's really hard. It's really frustrating when you—

He probably had a lot of collateral flow. If he passed his stress test, he probably had a lot of collaterals.

100%. Yeah. Yeah. Well, I mean, he also had hemochromatosis his lifelong. Yeah. The diabetes was like the last 5 to 7 years. Yeah.

But with 90%, you would expect a failed stress test unless there was the body figured out a way to circumnavigate it.

I mean, when my dad had his, it was a circumflex stent, it was 99%. And it was one of those things that, you know, this is when I was in the military and he like, Aaron, how you doing? You know, my reflux is, he's an old Marine. My reflux is acting up. I'm like, 'cause he always complains about his, his reflux was acting up one time. He has gallbladder removed. Yeah. 'Cause the burst.

Next time he had 99% occlusion.

Yeah. So he's like old Marine. He's like, you know, it's not dying. It's nothing, right? And so, so I had that in my head. I'm like, okay, well, what are you doing? I'll mow in the yard. What happens? You stop mowing the yard. Oh, the, the reflux goes away. Okay. And if you start mowing the yard again, what happens? Oh, it comes back. Well, yeah, you can just see.

Call the engine a dash.

Yeah. So, so he went to his, his primary care doctor and had an EKG done. They sent him to Chippenham, which is the big heart place here. They got a stent put in that night. And it was one of those things where it was just like, these kind of things happen all the time. Yeah. And there, it's, it's one of those things where it's so easy to miss.

Yeah.

So easy to just blow it off.

Yeah.

And the difference is, you know, you make it or you don't. And as a provider for medical doctor, we have to advocate for our people. Yeah. But people also have to be willing. This is where some of the, the gut stuff comes into play. Like if you feel off, you feel like things aren't right, you have ultimately, you are your own advocate. Yes, we come alongside and help people, but they have to be willing to advocate for themselves. And that's, yeah.

Um, we just have to empower them. We have to— oftentimes for me, it's like, it's just coaching them on what they should be looking for outside of the obvious. And then verbiage that they can and should use when communicating with other providers, because they sometimes feel like they're stuck between a rock and a hard place where like, they don't really know what to say to maybe convince that person and they shouldn't have to convince them, but unfortunately they do to convince that person to maybe do the test that they want. And if I hadn't a chance to talk to them or advocate for them, you know, I just coach them up. I'm like, these are the kind of things that I want you to say. And I'll write it in their, in their summaries when I send them, like, when you see your cardiologist next month, say these things.

Yeah.

You know, like, and it's, and they do and they do and they don't care because they shouldn't. It's their life and they deserve to live it. Right. So it's just one of these things where these are not uncommon cases. I mean, we, we probably have hundreds and hundreds of these, if not more. And for decades I saw the end-stage stuff. I saw all the downstream stuff. Now I'm getting to see the upstream stuff and oftentimes finding myself in the middle ground where someone's presenting already with known disease. It's obviously a lot easier when they don't have disease and when it's just risk factors or maybe really, really early on. It doesn't mean that we can't do something even if you have active disease. I always tell patients, step one, figure out where we're at. Step 2, halt progression. Step 3, let's push it back. Yeah. And, and that's how you do it. That's how it is.

Cool.

Yeah.

How's— feels like we've been talking for 5 minutes. It's been like 45.

Yeah. So many lies, man.

I know, man. Especially when you're having fun. So anyway, I hope this was helpful. This— we are ending our series on cardiometabolic cardiovascular.

This is my favorite series.

So, um, Hopefully we'll be adding in some of these new fancy things to our office here soon, which will be exciting. Yeah. One of the reasons why we're talking about this is so we can educate people. But, and we'll continue on. If there's something you'd like to learn more about, please drop us a note on social media. Say, hey, talk about this XYZ. We pull people routinely. Like, share, subscribe, follow us on all the social media places that are linked in the links below. But the way you take charge of your health is get educated. Become your own CEO of your own health and then get a good practitioner to come alongside you to basically be your advocate, but also be your, your expert on you as an addition to you. So any other parting words you might have?

Yeah. If you get stuck, just say Dr. Hartman said so.

No, I don't say that.

Just kidding.

I'm not throwing you under the bus. That would just cancel that out.

No, I just, I, I think that's well said. Like, I like the terminology CEO of your own health. Like you have to own it. And especially in this day and age that the days of paternalism They, they, they're over. They, they still exist, but you have to advocate for yourself. You have to educate yourself, but you also have to go in open and, and, and, and hopeful and, and hopefully work with somebody who cares enough to, to do the right testing and to be an advocate for you with you. And, and that way you can, you can own your health.

We also have one of the resources on our website, which is how to talk to your provider. Mm-hmm. It's also a resource in the book, the book on Curable. Available everywhere, right? But anyway, sorry, I had to plug it in.

Yeah, man.

But, um, it's the resources, literally like a video and stuff like how do you talk to your provider? Cause they have like 10 to 15 minutes. How do you walk through it? How do you like navigate this and do this? Cause the reality is there's, you know, you said less than 200 CIRS trained physicians. If you look at, there's like, I think 7,000 people through the IFM that have done some sort of certification, most of which aren't practicing cause they're in these systems cause insurance doesn't pay for this. So the reality is like in Central Virginia, we're at— yeah, as far as doing this. So, um, it's the same place across the country. So people really need to get educated and find someone that can work with them. Yeah. So they can start doing this kind of stuff at home.

Going in with a game plan is really helpful. I mean, you know this, we, we, I mean, I, I have a 45-minute appointment with a patient. If you blink and it's done.

Gosh.

And then there's so much stuff to cover. So, you know, our intake is 2 hours long and you blink and it's done. So optimizing that time, maximizing that time, having a game plan, being organized, being an advocate, these are all important things.

And that's where with, with us doing a 2-hour intake with an hour first follow-up, additional 30 to 45-minute follow-ups, sometimes it's 2 years before things pop up.

Yeah.

With that amount. And then people are sending messages in the portal back and forth.

Yeah.

So the reality is, is that if you're getting 10 minutes. You know, what we figure out in a year or two might take a decade or two.

Yeah.

And so people really need to like be proactive. You know, one of the examples I give is my wife. It took us about 5 to 6 years. She had horrible fatigue. It was like so bad, literally I'd come home from work and she would just crash. And so she kind of missed that 5 years of our kids growing up and it still makes her upset and sad to this day to think about missing those 5 years. But it's, if she'd found like someone kind of like what we do here, just with the, all the free information online, could that 5 years, and that was not for, that was before I knew I was doing it. So that was—

Don't beat yourself up, man.

I don't, I don't, I know, don't worry. I don't, I don't beat myself up. I know my limitations, but, but could that have been 1 year? Yeah. Could that have been 9 months? Yeah. You know, potentially. Yeah. And so I think just one of my passions is to make the information available to self-starters, self-learners that are looking for reliable information that's vetted from experts in the field that then they can then learn. Because again, the reality is it's going to be hard. Yeah. You know, we have a waiting list. You know, there's only 4 of us in this practice here for a city of 1.2 million people. So real people that need to take their health into their own hands.

Yeah.

Find someone that can work with them, but they have to be educated. Yeah. So I think if That's all you get out of this, these 6 or 7 sessions for cardiovascular health, and it'll be, been worth it.

Yeah. I agree.

All right. Nerds. Take care. We'll talk to you elsewhere.

Take care. Good luck to you.