Why Your Blood Vessels Are the Largest Hormone Organ in Your Body

Welcome back once again. We are back to finish up our cardiovascular series, finding out your true age. How do you know what your true age is? Which is you're only as old or young as your arteries. 60,000 miles of them, by the way. It's a lot, a lot of mileage there.

Tennis courts.

Tennis. It's, yeah, it's like 6 tennis courts.

Yeah.

It's also, it's also bizarre. It's also on the, the endothelial lining. Is the largest hormone endocrine organ in your body.

Yeah.

It makes hormones. And so people don't realize it's actually hormone producing.

Yeah.

And if you took it and took, peeled off all the endothelium, it'd be the size of 6 hearts. So it'd be like, yay, 6 hearts.

Yeah.

And you think about how big is, is your adrenal gland? It's like, how big, how big are ovaries? Ovaries are the size of a thumb. Yeah. How big's your thyroid? It's like a little. And so to have like an endocrine organ That's the size of 6 hearts.

6 hearts and the surface area of 6 tennis courts.

That's kind of—

Yeah, it's crazy.

Big. So who are the specialists who specialize in that?

Yeah. Us.

Us. Yeah. It's vascular biology. So, so what we're going to do this session is we're trying to close things up here a bit and we're just going to walk through risk factors and a routine evaluation. Then we're going to divide the risk factors. And these are things that, now having said that, you know, I wrote 200 plus, but there's like 400 different risk factors if you kind of get into the literature. Probably 200 and change we can measure. So we're going to divide into traditional risk factors and some other ones people might not be aware of.

Yeah.

For the purpose of just to know what you should look at. And these, these— I try to keep it simple. These are things that you can do with a typical provider who's willing to do a deep dive with you. Yeah.

This is, this is Quest and LabCorp. This is not fancy functional testing.

Yeah.

You can get this at just about any lab in the country. It's just whether or not they're willing to do it and how, if they know how to interpret it.

The biggest thing is willingness to do it and then interpretation. I have some people, I have some people that are, well, treatment, obviously you have to have all the training for that part. But some people actually will self-test and go, there's online things you can actually, there's bulk lab places where people can go and actually order their own labs at a greatly discounted rate and get them to check. Now obviously you have to figure out what to do with them, but there's, you can do this if you either work with someone who's curious and still learning and wants to help you as best they can or on your own or come see a functional practitioner like us.

Yeah.

The thing about a lot of these I'm finding, I'm surprised about a lot of functional people don't do a lot of this stuff, which is kind of to me a little like bizarro. Like why, you know, but.

Yeah, I don't understand it. But, but on the flip side of that, what I'm finding to be kind of cool I'm seeing a couple, at least of our local cardiologists doing some of the advanced testing. Yes. And hormones maybe being tested a little bit more by some of the local OB-GYNs. Yes. So it's like if you say you're functional or integrative, you should be doing these labs, period. 100%. And if you're not, then you need to learn how to do these labs. But it's nice to see that, that the conventional docs are dipping their toe in it a little bit because then there's continuity. So that when I send someone to a cardiologist for a stress echo, they are also commenting on the LDL particle number or their Lp(a) and coming up with a plan with me instead of just like, well, we don't, we don't acknowledge that weird test that's so important for you.

Correct. Yeah. Yeah. We don't, we don't recognize that whole field of that. There's literally a textbook on vascular biology.

Yeah.

This is pretty standard stuff. Yeah. But the other caveat to that is in our local environment, there is a I don't want to say too much, but there are practices that are ordering this kind of test, but the treatment is a standard of care treatment. So they'll order, you know, NMR and Lp-PLA2 and the ApoA, ApoB, Lp(a), and the treatment for all those is still a statin.

Statin and metformin.

Or PSK9 now or bimsipoic acid or some of these other drugs. Not recalls, not do you have lead, not do you have infections, not—

Not what's going on in your gut, not do you need hormone balancing, not what are the nutraceuticals that we can use.

So as we go through these risk factors right here, these are things that will alter people's cholesterol markers. But more importantly than that, that will alter your risk for cardiovascular disease.

Yeah, that's the big one.

I ultimately don't care what the numbers are. I want to care your disease risk.

Yeah.

If your cholesterol is 200, my cholesterol runs 220. My LDL is about 100. My HDL is about 80. My HDL particle function is 45. My LDL particle is a little high though, but my hs-CRP is normal and all my inflammatory markers are normal. My, even though the total number looks a little concerning, underneath the hood is all fine.

Yeah.

And so that's where you have to like get into some of these nuances.

And so it's a timeline, right? So we've talked about this. I talk about, I use the Goldilocks analogy a lot and I use timelines and the way that I use the timeline is if you're all the way down to the left, you have no risk, you have no disease. Then you have some risk, then you have some more risk, and you have to identify what that is. Now you have some early disease or damage. Now you have more disease. Now you have dysfunction. Now you have your event. So just getting labs isn't enough. You need some anatomical data to know where that person is, to be able to put them on that point in the timeline to then say, hey, let's see if we can push you back this other way. And then the Goldilocks analogy is just basically like a lot of these things, there's a sweet spot. Too high, problem. Too low, problem. Just right, just right. Cholesterol is that, that as well, right? Like cholesterol being high can be a problem. Doesn't mean it is. In your case, it's over 200, which is technically abnormal, but it's not a problem for you. And if you were to get on a statin and drive your cholesterol down to 120, you would probably feel like crap. And that actually paradoxically would increase your risk for other diseases, including cardiovascular. So it's, you have to understand the person sitting across from you and understand their biology and figure it out together. And is this number that's deemed abnormal truly a risk for you? That's where the personalization comes in.

So the categories we're looking at today are nutritional risk factors, hormonal imbalances, inflammation, environmental, and others, which is a, you know, and this is basing out—

bucket.

It is a bucket. Yes. So nutritional risk factors, you know, everybody knows about glucose, about blood pressure, about cholesterol, sleep, obesity. But it's interesting, nutritional risk factors also homocysteine level, which is not routinely checked on people. But yet, homocysteine is a risk factor for neurovascular, cardiovascular disease. And actually, if it's too low, it can actually be a risk factor for cancer as well if people are hyper—

Hypermethylated.

Yeah. So, talk about homocysteine. You know, I don't think I need to talk about blood pressure and glucose and—

Sleep and obesity.

Yeah. But to briefly give us a spiel, like, because this is actually a traditional risk factor, not a—

Yeah.

So tell us about—

Yeah. So I think the lens through which most people might know what homocysteine is, is the MTHFR gene and how that affects it, how that affects methylation. Methylation— homocysteine is kind of a surrogate marker for methylation. And methylation is, to me, it's kind of akin to a light switch. The body, trillions of times a second, in every cell in the body, it's flipping this light switch, turn on, turn it off. It's activating, deactivating genes, enzymes, pathways. Affecting change in a way biologically that allows for you to function well or not well. What are the functions that are being affected? Am I making antioxidants, in particular my master antioxidant glutathione? Am I making nitric oxide to dilate blood vessels? Am I controlling inflammation? Am I making neurotransmitters to balance my mood? Am I helping with gut function and detox? So there's so many facets to what methylation is. And then it gets a little bit more esoteric when you're talking about methylation of genes and how that leads to transcription and downstream products, but the, the quickest way to understand this is that if your homocysteine levels are high, you're not methylating well. If they're really low, you're over methylated. If they're in the middle, then you're good. And for me, optimization or optimal homocysteine levels are 5 to 8, 6 to 8, somewhere around there. I'll take 'em if they're less than 10, but I like 'em in that 6 to 8 sweet spot. But again, it's gotta be individualized cuz if I have someone who's got a homocysteine of 7 and they're super anxious, they might be overmethylated, and if we scale back, they might feel better. So it really depends on the person. But these are, these are influenced by genetics and, and nutrients, in particular B vitamins and magnesium. And then there's some minerals and some other things. And the MTHFR gene codes for an enzyme that takes folate and converts it into methylfolate. And so that's a domino that falls, and there's a cofactor nutrient called vitamin B2. So B2, along with a functional enzyme, converts folate into methylfolate, which then causes the next domino to fall, which is B12 being methylated by a different enzyme called MTRR, and that cofactor is B6. So B2 and B6 adequately taking B9 into methyl B9, which takes B12 into methyl B12, spins the wheel and takes homocysteine, reducing it to methionine, methionine can then go down the sulfation pathway. You could make antioxidants, goes down another pathway to make neurotransmitters, goes down another pathway to make nitric oxide. And all these things just work or they don't. In the middle of all this is cardiovascular risk. You see stroke risk, you see cardiovascular risk, you see cancer risk, you see dementia risk, you see IBS, you see miscarriages, you see clots, you see mood disorders. All these things can be problematic if you're not methylating well. So, a homocysteine should be checked in every single patient. In my opinion, should be the standard of care if you're a vascular patient for sure.

And, and just, we could, I could go off what you said for a while, but to a point you mentioned briefly, fleetingly, some mental health issues.

Yeah.

And it's funny how there's a drug called methylene, which is a prescription for 5 to 7 minutes, 5, 7.5, and 10 milligrams. I think there's a 15 as well of methylfolate acid.

Yeah.

That's FDA approved to treat recalcitant depression. So what does that tell you? That tells you that, huh, pharmaceutical companies spent, who knows, millions of dollars to take this fancy methyl B vitamin and, and brand it to, um, Deplyn. Deplyn.

Deplyn.

Yeah. Deplyn. To turn it into a drug that now is, you know, available in your pharmacy.

Yeah.

And it's funny how in the pharmaceutical world, once you can do that, it becomes a known entity in the medical world, but it's been known in our world forever. So, the idea of this concept and even, you know, kids with different pervasive development disorders, et cetera, et cetera, the neurodevelopmental pediatricians are now giving them methylate, B vitamin, methylfolate acid, particularly autistic kids. Last—

Leucovorin.

Leucovorin is like, you know, One of the— this is going off track here a bit, but last, end of last year, some things became political and talking about Tylenol and da da da. But one of the things about autism, but one of the things that was missed in the whole conversation because it came political unfortunately was leukovorn for autistic kids. When I heard that, I'm like, brilliant. Like we're actually coming out into the public sphere mentioning there is a part of autism that has a folate receptor antibody. And what happens is they, it's an autoimmune process. They attach it there. And now these kids are developing neuro— autism, tics, behavior issues, and literally you can bypass that with leukovorin, just bypasses the receptor. And so, what we're talking about in cardiovascular health, we're being very, very super narrow here, but the reality is these things, the whole body, it's really kind of cool to see how interconnected everything is. So, risk factors, traditional. Now, let's talk about hormone imbalances. You know, I'm so glad we removed the black box warning off of hormone replacement therapy.

Yeah. Thank you for your most recent post. I mean, like, After 23 years, they finally got it right. I love that headline. That was great.

Yeah, only got like 300 clicks on that one. Yeah. Yeah. But, but it's, it's crazy. You know, you can't make these, you can't make this stuff up.

Yeah.

You know, half of all in women, menopausal women, if you put them on hormone replacement therapy, you can lower the risk for cardiovascular disease 50% more than treating blood pressure, more than treating cholesterol.

Yeah.

And you can lower the risk for dementia 35%. So all of a sudden, these hormones, you know, estrogen, progesterone, testosterone, pregnenolone, yeah, um, are a big deal. Could you talk a little bit about vasomotor symptoms? Because I don't think people realize that, yeah, actually vasomotor symptoms are cardiovascular risk, are a risk factor in women, yeah, for cardiovascular disease.

Same as ED in men, right?

No way, Dr. Yeah, Dr. Zinski. Yeah, there's no way. Yeah, explain to me this, this, this. Yes.

So, so this is what gets lost in the shuffle is when you're looking at just traditional risk factors and you're not paying attention to whole-person medicine, systems biology, um, vasomotor symptoms like hot flashes are essentially a risk factor for, for cardiovascular disease, or maybe a harbinger of already present cardiovascular disease. So when a woman goes through perimenopause and she's starting to have hormone withdrawal as the ovarian production goes down, if that's not buttressed by replacement, of bioidentical hormones, these symptoms that they're having that are just treated as symptoms, you know, here's some drug, here's some herb, here's something, you know, get a chili pad bed, turn the thermostat down, like deal with it. That's garbage. The reality is, is that that should be taken seriously as this person has risk for cardiovascular disease if they don't have it already, because that's, that's akin to arteriospasm. And ultimately, if that person has plaque or stenosis, That eventually can lead to an occlusion. Same thing with erectile dysfunction. Erectile dysfunction in men could be due to arterial disease already present, or is it a vascular disease in general? Because it's either blood flow to or venous return from engorgement in that area. So if a young man is in his 30s complaining of erectile dysfunction, you have to take that seriously and work him up for cardiovascular disease. That's probably not happening. And so they're getting Viagra or they're getting Cialis, or they're maybe getting put on Clomid and having their testosterone tested or something along those lines. But these are the things that you really have to pay attention to as in our world, not so subtle signs, but maybe in conventional medicine, subtle signs of that this person already has cardiovascular disease. Not to jump, jump to the conventional stuff, but like going back to blood pressure, when someone comes in and their blood pressure is high in the doctor's office and at home it's normal, we call that white coat hypertension. And we dismiss it. You just have white coat hypertension, or the patient says, I just have white coat hypertension. We know that that's actually a risk factor now, the same way that if your blood pressure does not dip at night, you should dip by about 10%. If your blood pressure stays the same at night as it does during the day or goes up, paradoxical dipping, that's risk for cardiovascular disease. So these are the things that are swept under the rug or not even considered. It's the same vein with hormones. I mean, anything you want to add on that?

Well, the whole thing we mentioned with nitric oxide, we use nitroglycerin to treat angina. Yeah, we use isosorbide dinitrate for heart failure patients.

Yeah.

Yet our body makes our own nitric oxide. When that breaks down in some way, you can have erectile dysfunction, you can have hot flashes related to these things. But the thing is, like, if you— and I remember this popping up probably 10 years ago in some of the conventional literature, and it kind of fizzled out because these people go to a cardiologist and get a stress test and the stress test is normal. Because it's small vessel disease, because it's like glycocalyx, it's endothelium, it's endothelial dysfunction. It's earlier, it's early stuff that's not going to like rear its head for 10 or 20 years.

Yeah.

And won't be picked up by end-stage disease tests like a stress test, like a catheterization, like an echo.

But pulse wave analysis or endopad. Yeah. Arterial stiffness studies.

Or even doing a 24-hour blood pressure monitor.

Yeah.

Yes. So there are other ways to And that's where a person could hear this, be like, okay, I went to my doctor, they blew me off or did a stress test and I was negative, so I'm fine. It's like that was an end-stage test, not a early upstream.

Yeah. Yeah.

So the other thing to think about with hormonal imbalances, PCOS.

Yeah.

Polycystic ovarian syndrome.

Yeah.

Is a risk marker for future cardiovascular disease.

Yeah.

And that's, and if you had PCOS when you're 18 or 16 or whatever, and when you're on Metformin and had a couple babies and moved on with your life, that's still a risk factor, you know, sexual dysfunction, which is getting more and more common. And so it's interesting how closely related hormones for— in order for your sexual organs to work, they're very nuanced organs, more so women than men, but they get dysfunctional. There's a lot of downstream stuff related to that. And cardiovascular disease is one. So it's something that, you know, isn't on the radar for us, but it's a hormonal non-conventional thing people need to be aware of. Inflammation. So, you know, the three finite responses, endothelial dysfunction. So, it's dysfunction of that lining, immune dysregulation, inflammation. So, autoimmune, autoantibodies, chronic stress is actually can lead to inflammation, which is high cortisol. If you have high stress, you get leaky gut.

Low DHEA. This goes back to the pregnenolone that you talked about.

Autonomal memory hormone, DHEA. It's really interesting. I'm not sure if they're still doing the study, but I read about this 5 or 6 years ago about a study to treat lupus going on at Johns Hopkins. And they're using 200 milligrams of DHEA as the drug to treat lupus. And I'm like, autoimmune disease, immune dysregulation. And they weren't checking people's levels. They're just giving them. But the point is, in the research world, we know these things exist. We actually have studies that look at this stuff. But part of translational medicine is taking that and then how do I apply that to the male, female person in front of me to minimize the risk.

But like the autoimmune one, like if you have rheumatoid arthritis, you have increased cardiovascular risk.

If you have— 1.5x. Yeah.

If you have inflammatory bowel disease, you have increased cardiovascular risk. This is well documented.

Yeah. Rheumatoid arthritis is a coronary risk equivalent, meaning it's the same risk as being diabetic or having had a first heart attack for having a second.

Yeah.

The thing I didn't realize was lupus, that's like a 2 to 2.5x. So, that's even a higher risk than being— than having rheumatoid arthritis. And so, all of a sudden, and you can screen for this, you know, the whole field of predictive autoimmunity, which we put in all of our standard panels have, you know, thyroid antibodies, rheumatoid antibodies, celiac antibodies. ANA, then sed rate, hs-CRP, looking for these things. And if someone has a positive antibody, like a thyroid antibody, they have something like a 50 or 60% chance developing Hashimoto's in 8 to 10 years, an 80% chance of getting lupus in 20 years.

Yeah.

But these are also markers for inflammation, for cardiovascular risk.

Yeah. And then what about antiphospholipid syndrome, anticardiolipin, you know, seeing these things and we see these, this is stepping into the next one, but like the toxin-induced antiphospholipid syndrome that we see a lot in SIRS patients. I mean, I see cardiolipin and we see clotting issues and—

Okay. I want you to take a deep dive there. So what Dr. Jansky's talking about is when your cell membranes get exposed to toxins, they'll actually flip inside out.

Yeah.

And expose this thing called a cardiolipin. And if it gets exposed to your immune system, you can then develop anticardiolipin antiphospholipid antibody syndrome. We know it's a risk for strokes in women. We know it's a risk for infertility, for miscarriages. Yeah. But it's toxin-induced. So, it's this very well-known phenomena related primarily to environmental chemicals, which in the lipid medicine world, we can treat with all some cool stuff.

Yeah.

No time for that here. Yeah. But talk about that, about that's a bridge between environmental factors, which is the next post-factor thing with chemicals inducing autoimmunity, inflammation inducing heart disease.

Yeah.

Take us down that little pathway.

They're tied. I mean, it's the In our world, the typical patient that I see that in is a biotoxin patient. So chronic inflammatory response syndrome. So it's a toxin-induced chronic inflammatory response. It's also an immune dysregulatory response. It's also an oxidative stress-induced response. It's also mitochondrial dysfunction. So just biotoxins alone kind of scratch all 3 itches that lead to endothelial dysfunction, to be completely frank. And in this case, if someone has anti-cardiolipin antibodies, and they meet criteria for antiphospholipid syndrome, they tend to get put on blood thinners, right? And it's to prevent or treat the presence of a blood clot. They may have had miscarriages, but they might also have PEs, pulmonary emboli, or DVTs. And so they're either walking around on a baby aspirin or they're walking around on Lovenox or some other fancier drug. The reality is, is that toxins affect the cell membrane, affect the mitochondrial membrane, cause an immune response that leads to new inflammatory response that leads to vascular disease that leads to a potential future event. And as you treat that patient and work backwards, you're taking that risk and making it go the other way. Ultimately, by treating their biotoxin illness, you can actually put that autoimmune into remission.

And the thing about that made this common knowledge for— this should sound familiar to the average person listening to this because of COVID Because during COVID because of endothelial dysfunction, induced by the spike protein. We saw people having microclots, the shortness of breath phenomenon. I'm short of breath 4 to 6 weeks after having COVID. I was short of breath for about a month after COVID. My D-dimer was up. It's about 0.7. I was getting microclots in my lungs. And that was, we realized that in the COVID world, but the thing is that happens in the regular world as well. And the perfect example of that is this antiphospholipid antibody syndrome, the SIRS phenomenon.

Yeah. I mean, COVID causes an endotheliitis, causes your blood vessels to be inflamed and damaged and leaky. And, and D-dimer being elevated typically means you gotta rule out a PE, a pulmonary emboli, and you get a CTA and it's negative, but you're still short of breath.

I did that.

Yeah. But what if it is and it's negative and then like, okay, you're good, but you're not.

Not good.

Right?

Yeah.

So it's, you then gotta dive deeper. Does that person need to be on, on some natural fibrinolytics, especially if their fibrinogen is elevated? Do they need some nattokinase or lumbrokinase? Do you start to add some proteolytic enzymes like bromelain? Like, do you boost their mitochondria? There's, there's ways to get this better. You just have to dive deeper. But like the other environmental stuff, like extreme weather, you'd put fires or PTSD and some other toxins in. Last time you kind of touched on metals a bit. Dive into some of the environmental stuff.

Well, it's— this is one of the things that, that became super obvious to me during COVID I was actually traveling with— it was family vacation to the Cape Charles with my family and actually ran into a teacher from Arizona and, you know, talking about like, hey, why are you out here by the way? He's like, oh, well, you know, COVID. And by the way, the fires are going right now. And I'm like, in the 20, whatever, 2021, I'd never heard of that before. I'm like, fires? He started explaining to me, oh yeah, the fires in California and then all comes out to Arizona and you can't see anything. And I was like, at that point in time, COVID was blowing up. In Arizona and the light bulb went off. Oh, we have NHANES data on smog and microparticles, PM2.5 and strokes and dementia. The environment can do the exact same thing. And fires is a big one on the East Coast. We don't really experience that a whole lot. We did a couple of years ago with Canadian fires on the West Coast. They have a fire season. Yeah, L.A. has a fire season where literally people— and I'm getting patients from California now coming to see me here and it's like, and you have to start or have moved here and you're like, Okay, where'd you live? LA. Where'd you live? You know, Mexico City is another great example of a place that's horrible air quality. So all of a sudden, environmental thing, not just fires, but what's going on? Well, right now, I'm not sure when this will be going out because we record a lot of these in advance, but we now know the Potomac River is horribly polluted right now, probably the biggest pollution event in our lifetimes. And what's that going to do to the people who live around the river, but also that feeds into the Chesapeake Bay, which is the biggest bay in the world. It's where a lot of seafood comes from. Like all of a sudden the environment becomes a big issue. Knowing, living on a farm, having, you know, I call it Jimland's farm. We kind of, you know, have cows and chickens for, you know, fun, not for a living, but you become aware of the environment. You learn like when it's frost and you learn like that part of the yard's lower, it's like wetter, moister, that part. You see like that part grows this, this part doesn't grow that. Super. And so I actually got really good at predicting people coming to me for respiratory tract infections based on the environment. It's a big deal where you live, the environment, and fires or something. You know, when I was in the military, I actually was stationed at Travis Air Force Base, which, you know, it's kind of desert-ish, and I had a horrible reaction there. Well, there's this unique mold spore thing there that I had a horrible reaction to. This was 20— this was 20— 2021, May 2022. I'm sorry. 2002. And all of a sudden, like seeing patients around the country, you get really, your spidey sense you talk about goes up to learn which areas in the country have different issues. If you're from Long Island, you have an increased risk for cancer. If you're from the Annapolis, Maryland area, lots of pollutants. And all of a sudden, not just fires, but the environment plays into this risk. And so that's part of, I love, like I've actually had to become like, we've had to become experts in environmental medicine. Because all of a sudden now, not just fires, not just pollution, but just, you know, in Richmond, Central Virginia, we talk about this a lot. There's a lot of endotoxins in the air because we live in a swamp.

Yeah.

And so we tend to see more CIRS, chronic inflammatory response syndrome. We also see more PANDAS and PANS. We also see more autism because of environmental factors. And so when someone that has a concern for cardiovascular issue, you have to, have to, have to have your radar up for You know, oh, my granddad had heart disease and my dad had heart disease and my uncles and aunts. And where'd you all grow up?

Yeah.

What'd your dad do?

Yeah.

What'd your mom do? What'd your granddad do? Oh, he was, you know, from Appalachia, Virginia, and he was a coal miner and smoked. And well, okay. And your dad smoked and you grew up in a smoking household. The person's 50. And like, I don't smoke. Did you grow up? I ask this question all the time. Did you grow up in a smoking household? Yes. Okay. You smoked for 18 years.

Yeah. Yeah.

And like people like, what? Like your dad smoked, right? Well, your mom, when you inside your mom, when you were like, went from one cell to two cells to however many trillion cells you were being exposed to smoke. Smoke.

Yeah.

Came out and exposed to smoke for the next 18 years. It's like that affects inflammation. And so I love the environmental piece because I'm more, I geek out about that way more than the genetics things. I feel like the genetics was overblown.

Yeah.

And environmental is something we really, really, really, really do not focus on enough in general. Even in the functional medicine world, we're supposed to be experts and we get our lectures on and people forget that it's a big deal.

Yeah. And there's the paucity of quality testing too. It's almost kind of swept under the rug. You have to really seek out, I mean, you can get heavy metals testing, which you have to really seek out other environmental toxin testing. I mean, we see a lot of CIRS patients, but there's only a couple hundred of us trained in the country, CIRS certified, you know, like, and it's one of those—

Couple hundred?

Couple hundred. Yeah. Yeah.

It's so it's two, two of that couple hundred are sitting here right now.

Yeah.

It's a lot.

It's a lot. But then others, obstructive sleep apnea. I mean, that's, that's okay.

Well, let's, so we're transition. Well, let's, I'm sorry to interrupt you. Yeah. PTSD.

Yeah. Yeah.

This is something I'm not sure. I think we've had the same experience, but where patients are getting stuck in their healing process and you, you work with them for 1, 2, 3 years and finally comes, you had a traumatic life event. Whether it's your illness or whether you grew up or something happened to you. And we now know from, you know, MACE events, major adverse childhood events, if you had something bad happen to you when you were a kid, increases your risk for all-cause mortality. And so, with our patients, when you kind of start getting into risk factors, non-traditional, beyond hormones, behind all this cool stuff.

Yeah.

You know, what was your childhood like?

Yeah.

What was your adulthood like? Have you had, if you had horrible relationships and also traumatic brain injuries, you know, you can have an environmental stressor, a lifestyle stressor, a mace event, and it can act like a traumatic brain injury on your brain. And you can do MRIs and see these things, chemical exposure as well. But the thing as well is that concussions also leaking brain, leaky gut, inflammation. And so all of a sudden this PTSD that used to be like, you know, only military recruits, you know, only if you were sexually abused, it's— there's capital PTSD and then there's lower, in my mind, lowercase.

Yeah.

It's a big, big tent that is hugely neglected that can lead to inflammation, that can lead to autoimmunity, that can be a part. And there's direct correlation between these adverse events and cardiovascular risk.

Yeah. For sure.

That's my, sorry, I ranted a little bit.

No, it's the truth. It ties in. I mean, it winds up, it winds up being a root cause for some of these factors and they're all tied together. And then there's sleep apnea, genetics, mood disorders, and then infections. I mean, the infection component, I think that's another one that kind of gets swept under the rug.

So we've just finished the same, I'm finishing it. You already finished it. I'm a little behind you. Sorry, my friend. That's all right.

Yeah.

So, but it was interesting. Autopsy patients who died from cardiovascular events, autopsies, 80% of the autopsies had oral bacteria in the plaques. I read another thing looking at, this was a dementia thing with dementia, but having, it was roughly about the same statistic, about 80% of, it was a small, it was like 20 patients that passed away from dementia and diagnosed Alzheimer's type. About 80% of them had spirochetes in the brain biopsies, which people think syphilis, but spirochetes are also Lyme. But a lot of these oral bacteria are spirochetes as well. So, all of a sudden, and this is something we haven't really honed in on, oral health. We look at infections, not just Epstein-Barr or Lyme or whatever, but—

Or COVID.

COVID, yeah. Or oral. Or having horrible oral dentition. There's a direct correlation with your oral health and cardiovascular disease.

Yeah.

This is a fun rabbit trail.

I mean, also the nitric oxide. I mean, that's where they do that for us. Do that trick for us.

Talk. Do this trick.

That's where the dysbiosis comes in. I mean, like that, that to me, when you say dysbiosis, I think everyone's brain goes gut and okay, great, that's true. But your microbiome for your GI tract starts in your mouth and so you have to factor in the oral microbiome. Yeah, the, the, the trick, the oral dysbiosis component, and I think the bug that, that you were talking about is P. gingivalis, and there's some others that are being isolated, is how your body does or does not make nitric oxide. Nitric oxide is a vasodilator. Nitric oxide is essentially something that is inherently important for your vascularity to work properly. For your blood vessels to dilate, to be able to deliver oxygen and nutrients and things to move in the right direction. We have endogenous nitric oxide that's made at the level of the endothelial lining. So the glycocalyx plays a role, the lining itself plays a role, nutrition plays a role, all these influences. And then there's exogenous nitric oxide that we can make through foods that we eat. So we eat nitrates, the oral microbiome converts them into nitrites, and then they get into the stomach where hydrochloric acid converts them into nitric oxide. And now all of a sudden, by eating dark leafy greens and beets and having the right mouth bugs, you're able to have less cardiovascular risk. The flip is also true. If you're using a nuclear bomb mouthwash every day to destroy your oral microbiome, your blood pressure goes up, your cardiovascular risk and stroke risk go up. You are now not able to convert, even if you are still eating those foods, those foods into the products that I was just mentioning and make nitric oxide. So you have to solely rely on your endogenous production, which also may not be good if you already have some vascular disease and some glycocalyx dysfunction. And now you're just a ticking time bomb. And it all goes back to proper dentition, proper cleaning, proper mouth hygiene, making sure that you're not going nuclear on your oral microbiome. All these things that we pay attention to, also ruling out things like cavitations and pockets and You know, things of that nature, but super duper important.

And even like one step down, taking certain medications like proton pump inhibitors.

Yeah.

It's a correlation with proton pump inhibitors and increased hypertension, cardiovascular disease, renal disease.

By inhibiting the conversion, right?

By this, this process. You know, I, I was interviewing Dr. Chalmers, who's like one of the top, if not the top functional dentists in our country. And she started this amazing organization and was talking about, and she said a number that just blew my mind that the average person swallows about 5 trillion bacteria a day. And when we were talking, I was like, wait a second, so like my fancy probiotics that I spend a bunch of money on, and like this is the most powerful blah, blah, blah, it's like 100 billion CFUs.

Yeah.

And I'm swallowing trillions, 5 trillion a day. Yeah. All of a sudden it's like, you know, do I spend a lot of money on a fancy probiotic or do I floss my teeth, brush them, if I've got chronic gingivitis, I get that taken care of. Brush my tongue. There's a certain back— it's like all of a sudden, like Americans love flashy new things. We like simple fixes. Like, you know, and sometimes it's just like a clean mouth.

Yeah.

It's ridiculously powerful. And it's funny, historically we knew back in the day, if you look at someone's mouth, you can tell how healthy they are. And we were, you know, back, back in the day during slavery, et cetera. So you'd look at someone and look at their mouth. If they had poor, poor dental hygiene would actually affect how much they were worth on the slave block. And not to get into that stuff, but the point is we've known about this for a long time.

Yeah.

That oral health in the diabetes world, in my primary care world, I learned very quick in MCV, you know, Medical College of Virginia, you have your diabetics come in. The people with horrible mouths had worse diabetes, more strokes, more heart attacks, all kinds of stuff. And so how many cardiovascular experts are hammering the oral environment for cardiovascular health?

Not many. And I mean, it's also the potential source of inflammation, infections, infections.

Yeah.

And, and, and a host of other things. I mean, you can look in someone's mouth and sometimes determine if they have gut dysbiosis. You can look in someone's mouth and determine if they have nutrient deficiencies. You know, if someone's got a big shiny tongue, you got to be worried about B vitamin deficiencies. If someone's got aphthous ulcers, maybe some chronic viral infection. So there's all kinds of layers to this that ultimately lead to those 3 finite mechanisms. But the most important is that that oral microbiome needs to be robust and diversified and appropriate, i.e., balanced with the right bugs. I mean, I like coconut oil pulling. I like doing, you know, simple things that have been around forever that just keep your mouth the way it needs to be to get your health back.

And, and there's over 200 others.

Yeah.

And so we're gonna skip those. Yeah. 'Cause we only, we, we, I mean, this, this is enough. Yeah.

But the point is like, this is enough low-hanging fruit for people to start plucking.

But these are all risk factors for heart disease.

Yeah.

And if you know, are older than your arteries are, you need to be looking at these factors. And these, the things we just talked about are things that people can do.

Yeah.

Look at. Yeah.

Start low and go slow. I mean, keep it simple. You talk with your doctor. I mean, we're gonna talk about how we evaluate these in a minute. Yeah. But like, Talk to your doctor about some of these or, or do some of the work on your own. I mean, obviously everybody can improve their diet a little bit. Everybody can move a little bit more. Everybody can work on their oral hygiene a little bit better. But like now know that by doing that, you're decreasing your cardiovascular risk. You're improving your vessel age and therefore your age, your longevity.

So, so the risk factors. So someone comes in our office, they see us, we kind of go through their history. It's, 2, 2.5-hour process.

Yeah.

We go through all the stuff. We get this history down. We look at traditional factors. So evaluation. So we're now evaluating someone through complete history and physical. What are, you know, it's really interesting in the functional medicine world. Like we have lectures about the importance of a physical exam and how you can use that literally. And that's one of the things in primary, in my primary care world, we got pretty, I got pretty good at like doing a physical exam and figuring out if someone has in my world, it's supposed to be physical exam gives you 80% of your diagnoses and you fill it up with fancy labs, et cetera, et cetera. But it's often overlooked more so now in the traditional world, but also in the functional world. So what are some things when you're doing a physical exam, and I'll give some of mine that you look for, and we're trying to stay in the cardiovascular risk world, okay?

Yeah.

When you're doing an exam, what are some things you like you'll see, look for?

Yeah, so I think for me, You are clearly a skilled clinician when it comes to physical exam findings. You know, as someone who came from the ER where you have seconds to make decisions, you're going to pick up on obvious stuff, but we're not necessarily looking in every nook and cranny until we maybe have a minute to do so. So this is a skill set that I feel like I still will work on for the rest of my career. But some of the things that are obvious to me, I mean, we just talked about it a bit, look in someone's mouth. Like, don't skip an oral exam. Look at their teeth, look at their gingiva, look at their tongue, smell their breath. I mean, these are all things that are giving you tons of information. We didn't touch on this when we were talking about the oral exam and things like ulceration and how the tongue looks, et cetera. But like fissuring and scalloping, coating on the tongue, metal in their mouth, these are all things that are going to be important to me. Listening to their carotid arteries, do I hear turbulent flow that we call a bruit? Looking at their lower extremities, do I see edema? Do I see swelling? Do I see peripheral vascular disease? Obviously a thorough heart exam. Am I hearing murmurs? Am I hearing gallops? Am I hearing a thrill? Listening to their lungs. You know, do they have hepatojugular venous distension? When I push on their liver, does that neck vein pop out? Like, there's just the touch of their skin. Are they perfusing well? When I touch their arm, it's warm. When I touch their fingers, they're ice cold. Do they have Raynaud's? Which is an arterial spasm. You know, these are the things that I'm kind of paying attention to. What are some other things that you might be paying attention to?

One known risk factor is a horizontal crease in your ear. You know, if you have— it's a small thing to miss.

Is that for heart failure or myopathy?

It's for cardiovascular.

Cardiovascular in general. Okay.

You know, when you look in the mouth, you know, do you have— I call crooked teeth. You don't have enough space for your teeth in your mouth. Do you have these things called tori, which are these bumpy, bumpy things in your mouth? Do you have a high-arched palate? Those are all risk factors for sleep apnea, which, as you know, we need to worry about that. You know, I'm doing the physical exam also. Typically, when I listen to people's heart, I'll feel their pulse. Then I'll feel both pulses. And you can actually get kind of good at it where you'll, like, notice a disparity. Like, okay, I hear— I feel the pulse. And if you see— you hear the heart, like, I hear the heart, I feel the pulse. If there's a delay— yeah, you want a little bit of delay, but not a lot and not instantaneous. If it's instantaneous, it's like, The arteries are hard, you know, and then traditional Chinese medicine actually, this is a diagnosis all the time.

Yeah.

And so, and is there a difference between the left and right pulse? If you have a coarctation, you might actually have a little bit of a pulse difference, you know, to the point of looking at your hands, looking at nails.

Or dissection, even worse.

Oh yeah. Hopefully have some symptoms of having dissection. Yeah.

Nails. That's a good one.

Yeah. Nails. Like, do you have splinting? Do you have markers of low protein?

Clotting.

100% clubbing. Sometimes people will get their luna, will get a, which is the, the white part of the nail, will get a funny discoloration to it. Splinter hemorrhaging. But even like just like capillary ref— I do this thing. I know people think I'm weird 'cause they're like, why is he playing with my hands? But, but you're like looking at how quickly does your, your nail bed revascularize after.

Yeah.

Which one of the fancy tests we talked about, the endopad test, right? You, you cut off the blood flow to the arm for 5 minutes, you let it go, and then you look at they met— we measure how dilated do these arteries—

you're checking hyperemia, basically reperfusion of vessels.

So this is a poor man's— I mean, not really a poor man's, but it's like same concept, but you'll cap refill.

Yeah, it's more reliable in children, but you can use it in adults as well.

Yeah. Other things, you know, to your point, feet, you know, people when they get poor vascular flow to the feet, the feet start getting these funny discoloration to them. They'll actually have like almost a hewing down to their feet. And it's interesting as you get—

mottled.

Yeah, mottled. And when people have— it's really interesting. It'll get mottled initially, but there's— then it can actually get red. And that's like this inflammatory response before you start getting like really nasty looking. But the feet are— the longest arteries in your body are going to your feet. The longest nerves in your body go to your feet. So you actually will pick up things like peripheral neuropathy in people's feet before you pick it up other places. Same thing for the vascular stuff. I also will do blood pressure, pulse. If someone's numbers are off, I'll do sitting, laying, sitting, standing, a nasa lean test, which is looking at if I lay your body down, what's your heart do? If I sit it up and you can see if someone's blood pressure skyrockets, that can be a marker for adrenergic POTS or a sympathetic overdrive. If it bombs out, it can be more of neuropathic POTS. And so—

Or hypovolemia.

Yeah. So all of a sudden it's like, This physical exam that is throwaway now that, you know, all these online people and I have some colleagues in some of the groups I'm in who pay lots of money to see fancy people and they are non-medical trained individuals that don't even do physical exams. And I'm like, and we have, there's literally a Bates Tech, remember Bates book in medical school? Yeah. There's literally a textbook on physical exams.

Yeah, I still have it. I think it's in my office.

It is, actually it is, yeah. And it's like, That's part of our training. How can you use the physical exam to make a diagnosis? And I feel like that is a lost art.

Yeah.

And it's important. And if, anyway, we could ramble.

It's obviously important, especially if you are in a situation where you don't have access to testing or don't have the funds or logistics to do a bunch of fancy testing. You can gain a lot of information from an exam that allows you to make some decisions. And then you have a dialogue with your patient and you can maybe do some therapeutic interventions. Like, it's the totality of what we're talking about. It's take a history, that gives you info. Do an exam, touch your patient, that gives you info. Get objective data, that gives you more info. Collectively, that gives you all the info that you need to then intervene and then track that over time. That's how it should be.

And the entirety of that is clinical medicine.

Clinical medicine, yeah.

Yeah, so it's a combination of science personal expertise, clinician experience, and that intellectual curiosity. Yeah, that's—

yeah, yeah, lost.

So routine evaluations, a physical exam and labs, you know, doing a blood count, a comprehensive metabolic panel, fasting insulin and A1C. We've talked about these a lot.

I like also looking at leptin and adiponectin. I go upstream with my metabolic markers. So I like uric acid a lot too. Uric acid is is clearly something important for cardiometabolic disease. The leptin adiponectin component is just telling me more information about maybe a downstream abnormality like an A1c. Because if I have a patient whose A1c is pre-diabetic and their fasting insulin is normal or optimal and their glucose and their adiponectin and their leptin look good as well, that A1c is not traditional insulin resistance. It might be related to chronic cortisol dysregulation or toxins or something else. But if you just get an A1C, you don't know that.

Yeah.

And you assume it's IR and you put 'em on metformin or whatever you're gonna do. So the more you have upstream, the better off you are. And you can kind of see those things subtly change before you see the downstream stuff.

Yeah.

So it's reassuring for the patient. Your adiponectin is now finally above 15. Your leptin is finally going down. You are losing weight. Your A1C hasn't budged, but it's 3 to 4 months before it budges. Let's just give it some more time. Next time you look at it, it drops by 0.5 points. And then they finally understand how that's connected. Yeah. But then lipids, so lipid fractionation, which is the NMR that you had talked about, like LDL particle number and all the different sizes. TMAO, talk about TMAO. What is that and what does that even mean?

Well, TMAO is interesting cuz you, you, it's a byproduct of certain bacteria in your gut when you consume carnitine or, which is a protein in that comes from red meat, egg yolks, and tends not to be as much in fish and poultry, that if you have the wrong bacteria in your gut, they'll actually make this product that actually is inflammatory that's associated with an increased risk for cardiovascular disease. So in my mind, the TMAO being elevated, it's a direct marker. Your gut microbiome 100% is a part of your risk for cardiovascular disease. And I have a data-proven data point that tells me this is so.

Yeah, the gut-heart axis, right? Like, so now we have all these axes and this is one where This is my favorite one. When someone's like, hey, doc, I want to do a— I want to do a caveman diet. Hey, doc, I want to do— I want to do like, you know, a carnivore diet. Or I'm like, okay, okay, fine. Do you have some risk? Can we check a TMAO level first? Or can we look at your gut first? Because if their TMAO level is elevated, they have dysbiosis. And by them consuming tons of red meat every day for the next 3 months, you're increasing their coronary artery disease risk. Whereas they might be doing that to cut weight, they might be doing that to shave points off their A1C. Paradoxically, they're increasing their cardiovascular risk through another mechanism. So you have to look at it through all these different lenses in order to get it right. So that's one that I think is a little bit of an unsung hero. So I'm glad that one, that one was on this list.

Yep. Let me go back to the A1C, your little snippet you said.

Yeah.

A1C represents the area under the curve. So what do I mean by that? When you, if you can think about, you know, fasting insulin, less than 84, whatever. You have a meal, it goes up, it comes back down. Meal, it goes up, comes back down. Snack, et cetera, et cetera. So it's like roughly 3 times a day your sugar comes up and comes back down. If you think about all the space underneath that curve, you can have a normal fasting insulin and have an elevated A1C. Why? Because your sugar, whatever you eat, will skyrocket and take a long time to come down. It might normalize in 4 hours versus an hour, an hour and a half, your sugar should be mostly normal within an hour after eating. If it goes but stays up, you can have someone with normal fasting insulin, but because of what they're eating and how it's interacting with their body, which could be an issue with postprandial endotoxemia, which is a fancy way of saying you release toxins in your gut from the foods you eat, or insulin resistance or a whole host of things. And so that's where in our world when people like, oh, A1C, fasting insulin, Like, I want people to understand that to us, when we think fasting insulin, we think aponectin, leptin, we think A1C, when we think a C-peptide, you know, 1-5 AG, which is a postprandial estimation of dysglycemia.

So if you're 1-5 AG, and I don't remember what AG stands for, it's a big fancy word. It is, if it's low, you're having spikes postprandially in the 200 to 300 range.

Okay. Educate me. What is a 1-5 AG?

It's exactly what I just said. So basically it's a post— it's an estimation of postprandial after eating dysglycemia. So your glucose spiking after a meal, if it's persistently spiking, because this is what we're not measuring because no one's doing a 3-hour glucose tolerance test. So nowadays we do an A1C, we do an insulin, we do a fasting glucose, we do adiponectin, we do leptin. If you're doing a continuous glucose monitor, you're getting this data. If you're doing a 3-hour glucose tolerance test, you're getting this data. But if you're not, and you have someone who says, you know, I don't feel well after I eat, or I don't feel well after I eat excess carbohydrates, but their A1c is fine, their insulin's fine, their glucose is normal but maybe not optimal, and you get a 1-5 AG and it's low, they're having significant postprandial spikes in their glucose. And that way you can say, look, this is maybe an issue with some early metabolic dysfunction. Maybe it's due to endotoxemia and the endotoxin's getting into the portal circulation causing problems.

So is this a blood test?

Blood test.

Okay.

Blood test that you can get through Quest.

Oh really?

I don't do it a ton, but I've started doing it more. 1,5-AG. And it's a postprandial—

I'll have to look into that—

postprandial dysglycemia. If it's low, you're spiking your sugar after you eat.

Interesting. Yeah. Okay. Look into that. So, ADMA on lipid particles.

What about salivary nitric oxide? Do you test this a lot? I don't do this a lot.

People do it at home. Well, it's different because this is— I thought you were— when I said go Take us there, Dr. Jansky. I thought— I was hoping you'd go this pathway, but yeah, with— you have to eat the nitrates, you have to have the saliva, you have to have bacteria, the acid. But what happens, it gets in your body and then it goes in your mouth. Your mouth secretes it. So maybe 20, 30% of what you're eating and gets in your body actually gets secreted. So the nitric oxide in your mouth is telling you, hey, this whole process is working. Is working.

Yeah.

The ADMA and SDMA is actually at your cells saying, is it working at your endothelium?

Yeah.

So, so this is like a more general, like it's Well, the pathway, you're getting enough. Okay, cool. But then the question is, got it. What are the arterioles doing and endothelium doing?

Yeah.

And so you want both of those. And so the idea is that, and there, there's interesting, there are some of these oral test strips that actually also test for the, the bacteria associated with, um, breaking down the nitrates in that mouth. So you can actually test for that.

Are you doing these on patients that, that only have an elevated ADMA or are you doing these on like Like do you, if you think someone's oral microbiome is right and that their diet is right and there's some way to quantify that and you suspect they might have low stomach acid, but we're not getting a Heidelberg pill challenge and like their nitric oxide's still low, like that would be interesting, but I don't know how you would do that study.

Well, the, quite well, the thing is like if you're consuming excessive amounts of green leafy, you could overpower that, you know?

Yeah.

I, I know I've got some hypochlorhydria issues.

Yeah, I know I do too.

Insensitive issues, but I've been able to get my, oral salivary numbers up. So, um, I think this is where clinical medicine comes in. No one's paying millions of dollars for that study. Yeah, but no, you know, when you get these questions and you start doing with patients, yeah, and you get the data point back, um, that's—

well, the cool thing is that, I mean, I'm sure your patients are the same way. My patients are game for all this. They're just like, they love it. They love the data points. You know me, I test like a lunatic. So, so we have tons of data. We've had it for days, man.

Days.

What else? Um, thyroid, vitamin D. Vitamin D, vitamin D.

For cardiovascular risk needs to be over 50. For autoimmune issues, needs to be between 60 and 80. And if you have a history of breast cancer—

Even higher.

Closer to 100.

Yeah.

And so vitamin D is super nuanced, just like an A1C is super nuanced. Yeah. You know, being accurate at 32 is not enough.

No, I try to push everybody above 60.

Yeah. And then a routine evaluation. I wrote down like ANA, rheumatoid factors.

Yeah. So autoimmune stuff.

Thyroid antibodies, fibrinogen. These are just the markers. For the hormones, FSH, LH, estrogen, sex hormone binding globulin, prolactin, pregnenolone, estradiol, all these things will probably be in the show notes if people want to look at them.

Yeah.

These are— I don't want to belabor time, but the neurocognitive labs I think is interesting because when we did our training, Dr. Houston's stuff was my very first, the cardiovascular module.

Same.

It was a very first. It was, it was just like, it took me 3 months to digest that there was 3 days of information. It was just—

He's the only, he's the only functional clinician that I've gone up to personally after a lecture to shake his hand and say, thank you. Oh, like everyone else, I just like sat and listened to their lectures and like took notes and was like, okay, this is cool. I'm learning a lot of new stuff. I was so in awe. It flipped everything I learned on its head that I had to go up and be like, thank you. Like my eyes felt open. That's why I call him Oz.

I just had—

he pulled the curtain and was like, this is how it really works.

For me, I was like, I'm taking notes. I have no idea what you're talking about.

Yeah.

I had to go back and like read and read and read.

He's the GOAT, man.

Yeah. But, but anyway, so we did, I did his thing and then did Dale Bredesen's work, which he is the expert on dementia. It was really interesting because the evaluation's like 89% the exact same thing. And so the point is like if someone's got cognitive markers like their beta amyloid is off, the beta amyloid 42/40, their p-Tau 217, which we can now measure. We, as of, as of 3 months ago, we can now test these things.

Yeah.

I think the point to what people are listening to right now, literally I've changed some of my testing in 3 months because this is now available.

Yeah.

Like that is really cool.

Yeah. It's called AD Detect. You can get it through Quest and these are included and you can also get ApoE status on there. You can also do neurofilament light chains, um, NFL. And, uh, and this gives you information because this is the kind of stuff that you're going to see abnormal years before evidence of cognitive decline. And, and you want to catch it because it might have vascular pathology behind it, you know, or be tied to the other risk factors that lead to vascular pathology, right? Is this person's amyloid beta secondary to chronic infections, which will inevitably become vascular? Is it tied to toxins? Is it tied to heavy metals? Is it tied to chronic inflammation? Now you're getting a different target end organ data point saying there's something wrong with me. Go figure it out.

And one thing I'll tell people as well, that it's interesting in the kids with, um, every— these, these kind of tests are not determinative. They're helpful. One of the reasons why these tests are now available is because some of the treatments now, beta amyloid treatments, they require this to be positive before insurance companies will pay for stuff. So that's part of the reason why these become more commercial. The other thing to think about is that, this is something I learned recently, that in the Down syndrome world, Alzheimer's is much more common. I've had one patient that had Alzheimer's when she was like 28. And there's interesting studies looking at, so they, because of their genes, they're way, way more prone to heart disease, dementia stuff. But it's interesting in that world, you might have two brains that have the same pathology in one Down's patient or one, child, adult will have dementia and one won't. And this one study I was looking at, the difference was their diet. The diet with this increased beta amyloid laying down could make the difference between this 40-some-year-old needing to be in a memory care facility with their dementia and this one not.

I wonder, did they check ApoE status on those patients?

It was still—

The diet would play a role there too.

100%. It was— and obviously part of Down syndrome is they have methylation issues.

Yeah.

Which is how, which is one of the reasons why diet is so ridiculously important in that population. Yeah. Because if you have a methylated deficient diet, hyperprocessed inflammatory diet, you're gonna go around the—

All those processes that we talked about.

Yeah.

Go sideways. And just to be clear on these labs, this is not how you diagnose dementia.

Correct.

These labs give you a likelihood score or low, yes, intermediate or high likelihood of PET scan positivity. So it's just a guide. It's just a tool.

Well, actually the, the way it came about was they were doing, like how can we, because previously the way was we'll do a spinal tap for beta amyloid, which who's going to, I mean.

Yeah. Who's going to volunteer for that?

Yeah. I'll come. Yeah. Screening for dementia, spinal tap.

Come on down.

Yeah. And so they eventually got the test fine-tuned enough that they could actually do the blood levels and it would correlate with the spinal tap. And therefore this correlates with central nervous system. So it's a correlation. It's not determinative. Doesn't mean you're going to get this, but if you have it, you need, And just like the whole thing, like the— my point of mentioning the whole Down syndrome world, you can have the brain pathology, but what is it? What are the downstream things that are leading to that? Is your diet horrible? Are you inflamed? Do you have an ApoE4 status and some of these other genes, a 4q21 and blah, blah, blah. That makes— if you have these things, it makes the diet and lifestyle stuff even more important.

Exponentially so. And then what about functional testing?

Functional testing.

You know, I Sounds like we just talked about functional testing, but believe it or not, all those are regular labs through Quest and LabCorp. Like, doesn't it? Like, it seems like we were just like, like, that's like, that's the, that's the irony of all this is like every clinician has the ability to order these tests quite literally. You don't need to have access to some functional lab. But, so let's talk about functional lab testing.

But, but to keep things in perspective, we also have each Between the two of us, we have 6 board certifications. So it's maybe not fair.

It's a lot.

It's a lot. Yeah. So that's kind of crazy when you say it like that. Anyway, functional testing. So this is actually in the functional medicine world, looking at doing advanced stool analysis where you can actually— there's a newer test I'm actually— I just did on myself that actually would analyze and say if I had oral bacteria in my gut associated with some of these things.

Yeah.

The HPA axis, we talk about trauma, we talk about high cortisol. Yeah, we talk about your brain with your thalamus, with your pituitary, hypothalamus with your pituitary going to cortisol, going sex hormones. We can test that, do HPA axis test.

I do a poop test and a spit kit on every new intake. You can't get through the gate without it.

Yeah. The methylation is just, could be, MMA, methylmalonic acid. That could be genes. COMT could be gene testing.

100%. But also there's a lab that I use that does a methylation panel where you can measure SAH, SAMe, serine, glycine, homocysteine, methionine, all these things. So you can see not only the genetics, but literally it'll map out your pathways.

I tend to do that on my neurodivergent kids.

I do that on somebody whose homocysteine is like 30, and then I throw the kitchen sink at it and it still doesn't come down. And I'm like, what am I missing?

Okay, fair enough. Yeah. That's a good— that's a— we're going to talk about that in cases next.

Yeah, cool.

I've got one of those. Sleep apnea. I feel that every patient, period, should be checked for sleep apnea.

100%.

We say— this is like falls into the medical blind spot, medical gaslighting world kind of sort of where maybe even medical— becoming a medical feminist. I kind of stole that from you, by the way.

Yeah, it's all right. We can share it.

We can share. Yeah. But the idea is that obese males with thick necks is how their standard Aries evaluation is based on.

Yeah.

And so it's like obese males with thick necks, but can someone who's slender, who has a poorly developed midface, underface, who has dental crowding, has an Irish palate, can they have upper airway resistance syndrome, which is a kind of sleep apnea? Yes.

Yeah.

And that's where most of my diagnoses of sleep apnea are coming from.

Or hypermobile patients.

Which is a part of their thing, 100%. So all of a sudden, Everybody's getting this.

Yeah, same. I think it's underdiagnosed, undertested. I'm about to get an updated test as I was talking about with you earlier. I mean, I was, I had moderate to severe sleep apnea when I was 230 pounds. I used CPAP, I lost the weight and I thought I was done and I had, I had mild sleep apnea. So I wore an oral appliance. I've stopped using it and I'm going to get an updated test to see where I'm at.

And then there's some of the cool things which we are hoping to add here in the future, which are the Endopat. And pulse wave analysis. Tell us about what is an Endopat briefly? Yeah, that's a pretty cool test.

Yeah.

And what is a pulse wave analysis, which is another pretty cool test.

I mean, the shortest version is they're both kind of giving you input about the arterial stiffness and essentially another term we use is compliance. And so basically how compliant is the blood vessel, how, how able is it to expand and dilate and contract when necessary, if necessary. Or is it too stiff? And as it gets stiff and calcified and plaque-laden, hardened arteries is the term that people use, then you have vascular disease. And the cool thing is that this is very upstream of those larger or the larger vessels, which means we're now detecting small vessel disease.

And the key to that is this is where you're finding the stuff 20, 30 years before. Correct. So you address this, fix it. And even if you have heart disease and vascular disease, if your cholesterol is fine, blood pressure is fine, and this is off. Yeah, it still needs to be addressed.

You got to be aggressive. CAC CT and CIMT, we've talked about at length. CTA is pretty great if you can get it. It's a coronary CTA or CT angiogram. And then typically it's with something called FFR, which is fractional flow reserve. And then there's an AI overlay with a specific study called the CLEARLY study. And the best way to explain this is that it's a, it's like an external catheterization. I mean, it's literally giving you an analysis of your blood vessels, your coronary arteries, and where you have plaque and what type of plaque it is and an estimation of stenosis. So it's quite literally like a cath without the invasiveness of a cath. I mean, you are getting contrast and it's expensive test that's not covered by insurance, but it'll tell you if you have soft plaque or calcified plaque. Is it lipid rich? Is it necrotic? Where is it? How distributed is it? Is it one vessel? Is it multivessel? How stenotic are they? And it just becomes a nice way to kind of understand if you're in one of those blind spots where I have risk. I had a CAC CT that came back with a score of 100. I got a stress test. It was normal. They told me I'm good, just take my statin. And then you get a CCTA and you got soft plaque everywhere. Like, that's clearly got to be more aggressive there.

And using things like K2, MK-7.

Yeah.

Garlic. Using the things that help with the glycocalyx. Nitric oxide. All of a sudden you can actually help these soft plaques improve, regress. Yes.

Yeah, yeah, yeah.

So that's kind of it as far as— now this is the reality. We do a lot more than this. We do a whole lot more than this. So I don't want people to think this is all we do because we can't say everything we— I was actually We're already like in an hour. I'm like, oh my gosh, we, I can't believe we—

It is a long one.

Yeah, I know. So, but the point is that the risk factors are pretty standard. There's a bunch of basic stuff you can do and then there's really cool things you can do. But I always like to end it on, you know, 80% of heart disease, 70% of most cancer can be prevented by diet and lifestyle alone.

Yeah.

So perfect the basics, then do all the cool stuff.

Yeah. And individualize it.

100% has to be individualized based on the person in front of you. Not based on, you know, 10,000 people in some random study that was in a different part of the country and on different ethnicity group that happened 20 years ago. Right. And you're like, but yeah, well, hopefully this was helpful. We're going to end up talking about some cases of real people that we've seen. That's how we end this series up, hoping people can realize and give people the tools to take charge of the real age, which is the age of their arteries. And to help prevent the number one cause of death in our country, which is cardiovascular disease. So anyway, take care, bye, and we'll talk to you soon.

Care.