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The Dr. Mary Louder Show
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The Dr. Mary Louder Show
Cardiogenomics
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Explore the world of cardiogenomics with Dr. Mary Louder and Amanda Archibald, RD as they discuss how genomics play a role in heart health, both in terms of specific genes that cause disorders and in terms of a buildup of genomic variants that add up to cause problems with vascular health. They discuss the role of diet and nutrition, hormones, and more in this comprehensive, holistic look at the different factors that impact cardiovascular wellness and our health overall. Listen to find out more!
Hello, everyone, this is Dr. Mary Louder. And you're listening to the Since You Put It That Way podcast. It's the show that examines various health, wellness and medical topics from unique perspectives. We will be having discussions and guests that will cause you to pause and consider, "Well, since you put it that way."
Mary Louder:Hi, and welcome to today's episode of Since You Put It That Way. We have a special guest with us today, Amanda Archibald, you'll see her shortly coming on the screen. Amanda--I want to give you a little bit of background about her again. She's the founder of The Genomic Kitchen, which is widely recognized, as among--her, herself--as one of the foremost leaders in Translational Genomics, connecting genomic science to everyday health. She's doing that through cooking, through the gut, through the kitchen, she's got a great book called The Genomic Kitchen. And she's also a global pioneer in nutrition, genomic nutrition. As an author, educator, and consultant, and public health advocate. She founded The Genomic Kitchen in 2017, to showcase the relationship between genes, food, and health. She's worked at the corporate level in public health, she's worked with hospitals, helping them reorganize their foods to help patients heal better. That's the very easiest way to say that. So we welcome back today, Amanda Archibald, to Since You Put It That Way. Enjoy this episode. Hey, hi, everybody, and welcome to our next episode of Since You Put It That Way. We have a guest with us today. She's a repeat guest, because she's that good of a guest. So this is Amanda Archibald. And Amanda Archibald is a specialist in nutrigenomics. And she's a specialist as a dietitian and a researcher and an activist. So she's definitely on your side. So I'm glad to have her in my corner. Welcome, Amanda. Welcome back.
Amanda Archibald:Glad to be back.
Mary Louder:Exactly. Well, we're going to delve into something called cardio genomics today. And I'm going to give a little introduction, it's going to be a little heady. So everybody, hang on, because I'm actually using notes to make sure I'm on par and on--on speed. Because we want to talk about the genetics and genomics that affect heart disease. Now remember, 13.7 million people die annually from this planet, they leave the planet because of heart disease, stroke, congestive heart failure, but primarily coronary artery disease or stroke. And so it's the number one killer, it's the number one morbidity maker. So we need to take heed with this, as we call it low-hanging fruit. So what does that mean, if you've got things that are keeping you awake at night, wondering about your cardiovascular health, we've got answers. And so going way upstream to look at genomics is super important. So just to understand a little bit of what genomics are, and I'm taking this directly from a lovely article in the journal from the American College of Cardiology, and there's about 6.4 billion nucleotides in the double-strand, human genome of our DNA. So 6.4 nucleotides, which means these two bases come together, we form the helix. Okay, that's the stuff we learned in science class way back when. That hasn't changed, what's changed is we're able to unravel that and analyze it like never before. And we analyze it better now than we did 5 to 10 years ago, which is amazing. And that's all because of technology. So we learn more because our technology improves and our ability to evaluate the DNA improves. Because until recently, we thought that most of the DNA was considered junk DNA. And now we know that virtually all of the DNA gets transcribed into RNA, which is a subset, and that helps with making proteins, and then coding again to make the cells replicate and do their work. So, that's really, really important because the coding DNA is doing its job going down the assembly line, the non-coding DNA is all the features on the assembly line that make it go down the conveyor system and work. And if we look at that, there are--let's see if I can find the number--in the human DNA, 6 billion bases, that they replicate their self every few days. So every few days, our DNA is renewed in our body. And it makes only one error per 1 billion bases created. So that's about six errors. That's amazing out of a billion. I mean, I can't even comprehend that. And--but those can accumulate over generations. So that's kind of fascinating. So now there's two parts of the of the DNA that's super important. There is what it is, and then there is how it's expressed. So we look at both of those things when we analyze DNA. And it's our job, meaning Amanda's and my job, to look at this from different perspectives. Now, for cardiology, we're going to look at two things, what is a cause, meaning this gene occurs, therefore this condition occurs, or what's going to be susceptibility, meaning risk factors, what comes together as risk factors in our genes that then play out. So you've got these genes that make an expression, you've got a gene that, that disrupts the heart, or disrupts the blood vessel, you've got a group of genes that disrupts the entire cardiovascular system. And the effect upon that is really from the environment. So that term we call epigenetics. It's the influence of the expression of the gene, as it's working within our body. Now, I use the word genetics, genomics interchangeably. Why? Potato-Potato, I look at genomics as the applied genetics to the systems in the body. So we're going to look in the cardiovascular system, therefore, it's cardiogenomics. So, I got a couple of questions. So what would keep you up at night as a listener? And wouldn't you want to have most the most information available to you as possible? So what keeps you awake? What are you preoccupied with? Well, we've got answers for that. Well, what are my true risks? What--what about my family? What about my mother and father who had heart disease, and now what are my risks? They just say, Gosh, your cholesterol is elevated, take this pill? Well, really, where are my risks? What did my arteries look like? We've got answers for that. We've got tests for that. Well, where do I stratify? And what do my genes tell me that I could maybe use for, or for sure use for, prevention? Well, we got answers for that. What if I need a statin versus not having a statin? Well, we have a test for that, and answers for that, too. And what about the score, literally the score of my coronary arteries? Well, we get a test and answers for that. And how about early changes? How early do my kids or my younger self since I'm really in my 20s right now, do I need to know? We've got answers for that, because heart disease we find begins in, ready? Teenage years.
Amanda Archibald:Really important point. Really important point.
Mary Louder:Exactly. And so then what's the vessel health versus cholesterol? What's more important? We've got a test and answer for that. So I'm feeling kind of smug about that, I have to say, Amanda, until--
Amanda Archibald:It's true.
Mary Louder:No, but it's true. Now until--I was smug until I went down into the depths of the genes and then I saw the different function, and I saw the interrelatedness. And I thought, Okay, I'm just going to throw a vitamin at that? It felt kind of like a sledgehammer trying to fix a beautiful Rolex watch, you know, it felt a little heavy-handed. But yet the elegance of the genes that are there, the beauty and for--the ability for you and I to study that, and then come way back up again to like, not necessarily 36,000 feet, maybe 21,000 feet, and begin to look at how it's all programmed together. And that's where you come in with the nutrigenomics. The, the switches going on and off, remind me kind of one of the like, those Wurlitzer theatre organs, that you've got this beautiful sound, but all these different ways the music is coming out, based upon what sit--what switches, poles we have, foot pedals, the whole thing. So it's just beautifully orchestrated. So give us, and remind us just a little bit about your background with the nutrigenomics and what work you're currently doing right now.
Amanda Archibald:Yeah, so you know, I work in the space of Wurlitzer theatre organ. nutrigenomics and it's sibling nutrigenetics, right? So we put Theater organ. Yeah, so we now know we can use information from the two together, where nutrigenetics is really looking at the impact of, really, how genes influence nutrients in the body, how that--and things like how they conduct or interpret food to steer your biochemistry which is absolutely brilliant the environment, like you mentioned, how they react to different forms of exercise. So it's sort of looking at pattern recognition. And then nutrigenomics is what can we--what can we find in our nutrient and food ingredient toolbox that can help, what is it, turn that--turn the handles on the what did you call it a Wurlitzer? and we know how, we know why. We don't always know exactly how much, but we know what you know, as you mentioned, Mary, we know, when we're looking at genes, we know which labs, which tests, it'll tell us, okay, what we need to target. And then if we retest say, Yep, we're on target, or we need to switch directions or adapt things. So my work is working in this space. So I have a clinical practice I continue. I do teach and training all over the world, so, and mentor clinicians in the space, and consult as well. So soup to nuts, genome is my thing. Right? And you've got a book called what? The Genomic-- The Genomic Kitchen, yes, yeah, that's my contribution. And it's to the science in the kitchen. And I wrote it really from a public health perspective, meaning very clearly you, you don't need a DNA test to start to be able to influence how your genes behave, you do if you want to go to the--you know, the n of one, to look at yourself in the mirror. But in other words, there's things you can do in your life and in your kitchen, that work for all of us, because we basically all have the same genes. It's these nuances that change our response, and that's the work you and I do, Mary, is like looking at the nuances and how they're impacting you. But regardless, most of us can pretty much eat the same way. And that's what The Genomic Kitchen is, it's a little, it's that last mile that makes a difference with our genes. And that's the work we do and, you know, in the testing that we're looking at.
Mary Louder:Yeah. And that's, you know, that's really the most important thing, because daily, I get questions, what how should I exercise? What should I eat, hey, look, I've tried these supplements, I saw this guy online, and I'm doing this and I'm not getting any different. And I'm frustrated, not getting--gaining any results. And so I'm frustrated. So I think the best thing to do is go up to the genome, as I call upstream--so that's why I call it up to--and then from there, apply tests that we know where we can find real life answers. Those are lab tests, like blood tests, those could be stool tests, if we're looking at gut function, those could be hormonal tests, if we're looking at how our hormones are not only functioning at what levels, but also how they metabolize through our body. And neurotransmitters as well. Yeah, so there's a couple things, you know, if we look at the two aspects of the genetics for heart, their single gene
disorders:dilated cardiomyopathy, that's where the heart muscle gets big, and the contractility the ability for the heart to compress, and pump blood out, is diminished. So we have a formula called stroke volume plus--times heart rate, is cardiac output. And so a lot of Cardiology is fluid mechanics. And what they're finding as they're digging into the human genome, that there's literally single genes that determine some of this. And there's actually even a hypertrophic cardiomyopathy, and that's something that, as a physician I've looked for in athletes. They have certain symptoms. And unfortunately, one of the first symptoms is sudden cardiac death, in participating in athletics, and it's usually a young male, late teens, early 20s. And it has to do with how the heart's functioning or not functioning, and you don't know it, until they drop dead. And that's very, very traumatic if you're in the sports world, because that's where you see it, usually in athletes. And so now we're finding things where we've got these single gene disorders with this, and even like with a thoracic aortic aneurysm, which honestly, runs in my family, and that's what my mom passed away from. And so you can darn well bet that I'm getting tested, you know, do I--am I testing for the gene? I haven't found that test yet on the market. But what I know I can do is do the monitoring for the screening. And I can modify my risk factors, I can know what my cholesterol is, what my inflammatory markers are, and know how to maintain good blood pressure, and then monitor to the best that we can with ultrasound, cardiac ultrasound, the thoracic aorta. So you begin to see a bigger picture, knowing if there's a familial trait, that that might be a single gene.
Amanda Archibald:You know, it's listening to a podcast yesterday, I--of all things, it was a cardiovascular really fascinating, deep into the bowels of research and how they come up with the assays, et cetera, et cetera, which is fascinating in and of itself. But I was learning with the aorta that over time, it makes sense, it gets stiffer. You know, when we're born, it's really soft and supple. And so it's interesting for people who have high blood pressure, you know, you're kind of firing. It's almost like you're firing in formation at a really stiff wall right, which is what happens to our endothelium to our blood vessels too. So it's, it's interesting, we're doing that testing, you know how we've advanced in testing to understand the, kind of architecture of our heart, and our, our system.
Mary Louder:Yeah. And what we're finding with the endothelium, which is the lining of the blood vessel, any artery has an endothelium, any artery in the body. And remember, folks, arteries go out away from the heart, veins come back into the heart, okay? So the arteries are thicker, and they have higher pressure. And so as a result of that higher pressure, that's where they get into more damage. The veins are more compliant, they relax more. And they have valves that help the blood stay going upward, because it's always going against, exactly going against gravity. So veins get problems with clots, arteries get problems with blockages and thickening and stiffness. So that's the two types of vessels that we've got that do that. So--
Amanda Archibald:I think that's where genetics is really interesting, we'll probably get into it here, we can see a lot of patterns that give us like, we might want to look at this, you might want to take a look at that. Because anything that, yeah, that impacts or causes injury to the arteries is going to cause injury upstream or downstream, you know, on your cardiovascular system.
Mary Louder:Exactly. Exactly. And so, you know, and then they say, Let's talk a minute about the heart healthy foods that the American Cardiology Association is putting out there. Give us your thoughts on that, Amanda.
Amanda Archibald:Well, I didn't know they were putting out any food, I have to say, and you buy something that's delivered to your house. What are you talking about? They're very specific recommendations--
Mary Louder:They're recommendations, recommendations.
Amanda Archibald:Yeah, which are changing in our lifetime, the time we've been in the business, right? Like, oh, so saturated fat isn't such a demon than it was before. So there is no such thing as a broad brushstroke for food, when it's in our work, everything is personalized. And so we do know, in general, when we're looking at genetics, and there's pictures that we put together in terms of diet, the kind of diet that you might want to move yourself towards, there are the genetics is going to determine that for you. So there's, it really doesn't matter what a governing body is saying. Because how you and I translate it on the ground floor is what actually matters to you. But in general, if I'm going to look at complications from the diet with heart health, it's going to be the type of fat, maybe, and we tend to sway more to poly- and mono- unsaturated fats. And we tend to go more to a lower total carbs, but that's different for all of us. And maybe at some point in time, but probably not. Today, we need to talk about keto. How do we now, if you can have a higher fat diet, which would go against all conventions, right from from the history of like, I don't know, the American Heart Association, some people can actually handle it, and it works for them. So yeah, so there's no broad brushstrokes anymore. Is that, is that a good answer?
Mary Louder:Right? Yeah, I think it is. And I think you know what some of the things American cardiology and American Heart Association said, you know, low fat, and they were leaning towards low sugar, but if they're doing low sugar, they're putting on the artificials. So then we're getting into the package, pre-packaged, processed foods, because anything that's an artificial is a processed food. And so I literally call those Frankenfoods, like they're, you know, you've got some molecules somewhere that might be a food, then they've got all these bolt-ons of what these other ingredients are, and so becomes like a Frankenstein of a food. So what happens, then, our body sees that and typically goes into inflammation.
Amanda Archibald:Exactly.
Mary Louder:And so we've we've got these causal genes, meaning these groups of genes that tend to go somewhere, because all the--all the sway is that way. So you've got artificial things coming in, maybe saturated fats, maybe trans fats, right, that trans fats are just super stiff. And they're just fats that are flipped in their molecule configuration. So instead of it being super fluid, it's rigid. And our cells are made of fats and cholesterol--which we need, by the way, we got to have a certain amount of cholesterol in their body to function and function well, so we can't knock that down too far--but the cholesterol has to be fluid. I wish I could dance like that, but--maybe we do the hula, it has to be fluid, right, and not stiff. And so our cells need to be fluid, our arteries need to be fluid, the cell walls need to be fluid, the arterial walls need to be fluid and not stiff.
Amanda Archibald:And I can't, you know, talking, I'm just kind of watching you do the dance with your hands--
Mary Louder:Did you like that?
Amanda Archibald:Fluidity, one of the things that lends huge fluidity to the cell membrane are phospholipids and long chain fatty acids, which guess what? You get in seafood. Right? And this is super, super important to fluidity to the cell membrane, the integrity of the cell membrane. So yes, I think there's one thing I spent a lot of time talking about is the need to find EPA and DHA--DHA, which are the long chain fatty acids, so instrumental to cardiovascular health, cellular health, and immune health, right, you know, because they're huge immune modulators. So if you're not a seafood eater, you really need to be working with, with a specialist, a, you know, physician who understands this, or, you know, someone in nutrition and nutritionists that can help you evaluate how you're going to work that into your diet, because, critical building blocks to health.
Mary Louder:Yes. So there's studies that show that the EPA-DHA, the fish oils, essentially, omega-3s, help with rhythm, heart rhythm, help with inflammation inside the blood vessels. They-- Absolutely. Yeah, they help with the cells communicating one to the other. And they quiet an immune response, which is inflammation. When everybody says, well, that's just because of inflammation, we might as well say, well, that's just because the sky is blue, that really doesn't mean anything. It doesn't mean anything, unless you really have markers that drive, that drive inflammation in your body. And some people have the big ones, IL1, IL6, I've got both of those. And they're just, they just love to be turned on and irritated.
Amanda Archibald:And give them an inch, they'll take a lot--these are locked and loaded genes, right? Give them an inch, they'll take a mile, then you add CRP and TNF-alpha into--into the mix, a little bit of a hum--histamine dysregulation. And it's like a, it's a very powerful storm in the body that we can see through genetics, so.
Mary Louder:Yes. And so what happens is these causal genes work like a gang, they come together, the more that they're triggered, the more join in. And so if they're not triggered, if they're quiet and turned off, they're just like nice neighbors living next to each other, a nice little fence between them, the grass is green, everything's good, the flowers are nice, but if it gets, if the neighborhood gets stirred up as it were, then you have much more of a problem. And--yeah, and so what happens is, then these genes influence our biochemistry. And that's the effect. So by the time we see an elevation in blood pressure, an elevation in cholesterol, a change in highly sensitive CRP or homocysteine, those are like the canary in the coal mine, hey, there's been changes already happening. So to say that your labs are all normal, might be okay. But I dont, I don't know that anybody's normal. I'm not sure what normal is. So are you without symptoms? By the time, the same thing, by the time you have symptoms, the horse is well out of the barn, the boat has left the dock. And everything is well downstream that we need to work extra hard to bring back into more homeostatic balance.
Amanda Archibald:Exactly.
Mary Louder:Now, the neat thing of with all these genes, how they're, you know, as is I went down into them, I thought, oh, my gosh, I you know, it's amazing how we exist. It's amazing how forgiving our body is. And it's amazing because our body's always seeking balance and homeostasis. And yet, it's also amazing that it carries us through when we aren't always good stewards of what our genes are all about. So let's go into a couple of the genes. Let's pick on a couple of the genes here. Let's pick on a gene of highly sensitive C-reactive protein. Let's talk about that one. We hear about that, but I'd like to hear from you, Amanda, what you feel. And again, it's one gene but that's going to be one of the major ones that triggers other ones. So don't think we're isolating a gene but we're just going to pull things out for illustration and discussion during our time together. So tell me what you think the biggest thing we need to know about the highly sensitive C-reactive protein gene?
Amanda Archibald:Well, I think you already said it, you know, if it moves into the wrong neighborhood, or it doesn't like the neighbors, it's going to let you know. So we call it, if you will, like a gain-of-function gene. So it's, it's, in the way I explain that, again to patients or clients like we just said, is, give it an inch it'll take a mile. So it's already up-regulated. It's all ready to pounce. With--and you may see it more than me, Mary, because you're measuring, but these are people that may automatically have slightly higher CRPs anyway, and I think one of the things that's important is to put that in perspective, like, okay, it's--but what other markets might we look at to see whether it's actually an issue, which is why I love genetics, because you and I would automatically say, Well, what else? What else we can look at? Maybe homocysteine or I say, too, I think the homocysteine is fine. So are we good with that? Or--but then you pick those two up, and if you're looking in the cardiovascular system, which is where we're gonna go, we're going to look at a whole slew of other markers, right, which is the power of genetics and the
Mary Louder:Right. power of testing, so. So you never look, I think it's a key point, you never look at one gene.
Amanda Archibald:And you as a doctor would never just look at one inflammatory marker, right? Say, okay, that's it. You need this,
Mary Louder:Right. And in fact, that actually--the elevation of highly sensitive C-reactive protein is, like, nonspecific.
Amanda Archibald:Exactly.
Mary Louder:Where's that coming from? That's, you know, and so then, could it be an infection? And if so, what kind of? Viral? Bacterial? Fungal? Is an autoimmune driven? Is it backdoor because you also have high histamine? Is it front door because you got auto immunity? Is it, is it you got, you know, inflammatory bowel disease? Do you have--is it associated with Lyme? Is it associated with Epstein-Barr? Is it associated with COVID? Is it asso--you know, there could be many things it's associated in, and what we know is when we, on some of the autopsies, they've literally found in the arteries of the coronary vessels, in the plaque, they found bacteria, viruses, and spirochetes. So those are there causing havoc. So then we've got this environmental toxic burden, that one of our first things we may see is fatigue, coronary artery disease, elevated CRP, that most often is typically, I'm trying to couch this, blown off, as--
Amanda Archibald:Well, yeah, no, you're right and--and I think, too, there is when you see a high CRP, exactly what you said, you know, where are we going to investigate to see what else is going on? And you know, looking at the lymphocyte to neutrophil ratio, that kind of thing that gives us this little idea? Yeah, there's some upregulation. Okay, let's go to the immune system. And, you know, obviously, I'm not a doctor, I stop at a certain point. But this definitely, it's like a trigger point for thinking, and you want to work with a clinician who's thinking.
Mary Louder:Yes, you do. Rather than following an algorithm, or rather than following an insurance policy, or rather than following what they're trying to do to get good marks or just trying to get you out the door, you've got to spend time. And this is why I left the clinic, you know, and I left the clinic never to return. So I can work with folks, one on one with no barriers, no boundaries, because it's just time to really get the real answers to folks who want them. And that's really, you know, so important. So we've got--so let's put a kind of a group together. So we've got highly sensitive C-reactive protein, we're looking in the inflammation part, that that highly sensitive C-reactive protein can influence two things
with cardiovascular:can influence cholesterol, can influence the blood vessels. So those are some of the two
things:we've got what fixes the the blood vessels, which is the cholesterol, and you've got the vessels themselves, so you've got structure and some function going on. Right? And then you've got homocysteine, well, homo--
Amanda Archibald:My favorite.
Mary Louder:So homocysteine, okay, if it's your favorite, tell me what you like so much about this one, when you're measuring. Well, we use it, as you and I with our training, we use it as a marker for so many things. You know, we're looking at methylation, it's, it's, that's one of the things we're looking at, whether the body's optimally methylating is one way, we're also looking at a pathway to detoxification. So it's like a jump-off point. That's number one, or number two, that's one and two, but number three, and I find this really interesting in the cardiovascular system, a really elevated homocysteine can activate the ADMA receptor, actually, it's not. It's a byproduct or a downstream metabolite called his--homocysteine thiolactone, I think. So HDL, that activates this ADMA receptor. Why that's important is because that will then block a really important enzyme called eNOS. eNOS, guess what? So it's called an endothelial nitric oxide synthase. When that doesn't work, guess what? You don't produce potentially efficient amounts of nitric oxide, which is a vasodilator right? Yes, vasodilator, get it all the way around. Keep the endothelium very, very comfortable.
Amanda Archibald:Exactly. And when it's not functioning, the connection between homocysteine and heart disease is in the end, it's oxidative stress. Because it's basically causing a lot of inefficiency in a number of different biochemical reactions we described, we describe one that in the end will be disruptive. If you bombard any wall in the body or any tissue, any cell, with enough reactive oxygen species, you're going to do damage. Right? Right. So that's one of the ways I explained it, Mary.
Mary Louder:That's very good. So essentially, your pipes are gonna rust. That's what we're saying.
Amanda Archibald:Rust or burst, we're gonna--or we're gonna create, we're gonna create injury. And then that's really interesting, because then you start--we haven't even talked about cholesterol yet, that's coming, right? But, and this is more your area than mine, for sure, but one of the things when we cause injury to any vessel, particularly in the endothelium, then we activate a gene called VEGF. Right? And so we know with people who have had heart attacks, the, the, I think it's one of the tests that run, Mary, that looks at levels of VEGF, because this gene it causes--it's a protein, right? VEG--I forget what it what it all means, endothelial or something, factor, that basically that, it does two things, it promotes repair. So it promotes angiogenesis, which, particularly if you had a heart attack, it's really good, right? Because you need new blood vessels to deliver oxygen to the heart. But the problem when you in when you're in a state--more stable situation, is this will grow new blood vessels, but it also creates permeability in the vessels, because what it's doing is attracting cytokines. And it, to--so let me back up. It creates permeability because there's injury to the wall. So what comes with injury, comes with inflammatory molecules. Well, we've already got a situation of injury, right, potentially from homocysteine. Now we're creating permeability, and in the blood vessels. And guess what gets attracted to that? Good old oxidized HDL--LDL, right? It's gonna come along, and that's sort of like this formula for plaque formation, or atherosclerosis, you just see these weird, we're talking about genes and markers, but you see this playground of, hey, let me stop by to the injury and see what more damage I can do. Is what how we look at this. And we're looking--
Mary Louder:Well, let me reframe that, so do you think the body is--let me reframe that, do you think the body is saying let's see what damage I can do? Or let's see what I can repair of the damage.
Amanda Archibald:It's the body's saying, What can I repair, right? The genes tell you and I what we need to look for that could be causative to the situation. Right? And VEGF is interesting, because in a different space, in cancer, we don't want this gene upregulated, because what does it do? It causes growth of new blood vessels, which would promote tumor, tumor--tumorigenesis, right? So. So it's a really kind of diff--it's got a Ying--Yin and Yang in the cardiovascular system.
Mary Louder:Yes. So the VEGF is the vascular endothelial growth factor.
Amanda Archibald:Thank you. Yes.
Mary Louder:You're so, you're so welcome. I have a list of them here. I don't have them memorized. I have a list. I work from a list. So, yes, the eNOS was endothelial nitric acid--oxide synthase. And then for methylation defect, we're looking at the MTHFR. And I remember, gosh, 15, 20 years ago, I have MTHFR. I'm gonna die. Oh, no, no. That's not true. You know, I--I'm a poor methylator, I'm gonna die. No, well, we're all gonna die, I finally started saying. It's just, but not from this.
Amanda Archibald:One of many teams. It's just one on the playground.
Mary Louder:Exactly. And so there was a lot--there was a period of time where there was a lot of testing done where that was the only gene tested.
Amanda Archibald:And it's still is, Mary, I'm still seeing that.
Mary Louder:You're still seeing it?
Amanda Archibald:Yeah, I still seeing that, it's just, yeah.
Mary Louder:Yipes. Okay, yeah, that is so 90s, folks, that needs to go. So if anybody offers you an MTHFR test, do not take it, it is of no value. And so I say if you're going to study one gene alone, leave the genes alone. And if you're going to study genes alone, leave the gene alone. So what I mean when I say that is, just the genes, remember, is a blueprint for what you can build and what you can restructure and how you can put the design on the building, which is our body. So we want that but if you only have the blueprint and no supplies for building and you don't have quality building, it doesn't matter. You've got--you can't just say the genes, and you cannot study a single gene and figure out--a single gene does not a disease make unless it's literally listed as that, that we found in the research, but not for cardiovascular disease as we're talking about it. So then the other thing, so we've got homocysteine. And so homocysteine was also looked at, interestingly, with methylation, and there's a lot of that now, looking at, you know, because methylation has over three--300 different pathways that it's involved in, in the body. And so that's the other thing, is when you say we have a methylation defect, well, what are the other ingredients to methylation? There's things like zinc, phosphatidylcholine, Sam-E, Magnesium. Add to it, if I'm missing anything.
Amanda Archibald:B12, and folate of course, I always say, Mary, all the Bs and the ones that are so instrumental, we always focus on folate and B 12, but when I'm looking at labs, B2, riboflavin, and niacin, which is often used, you know, in working with, with heart disease, which is a kind of precursor to working with a statin, maybe, you know, red yeast rice or whatever, you know, B3 and B2 are often highly deficient. So, yeah, there's a whole gang of nutrients or betaine, right? If choline and betaine, we might use into--interchangeably for methylation.
Mary Louder:Yeah, that's right. And so when we do something like supplement, we actually do what the word says, we supplement. And so we aren't, so we're supplementing what nutrients, we're supplementing with foods that we know support these different pathways. And we're not just saying here's a bowl of vitamins with some milk or plant-based milk, and here's a spoon and you're going to eat vitamins. That's not it. Nutrition first through food. And then, if needed, supplementation to support the body's repair process, homeostasis, return to normal. And sometimes, I, you know, more often than not, I can bring back and restore health 3, 6, 9, 12 months depending upon what the needs are, and the need for supplementation diminishes significantly.
Amanda Archibald:Oh, absolutely. I always say that supplements help get the body back on track, you know, get the, the teeth of the gears to reengage, because the body has innate intelligence, but sometimes, because the environment we live in emotionally, environmentally, or whatever, stress, really is depleting, but the body knows how to rebuild. We just need to help it. They're helping hands.
Mary Louder:Exactly, exactly. So then, you know, what I did was put these components of the cardiovascular disease, and I came up with 36 different genes, but we're not going to go through them one by one. You're welcome. So you're welcome. But what we're going to do is we're going to, I'm going to post this document in conjunction with the podcast today. So folks can get an idea of what they are and what's going on. And they're in different, they're in five categories that are main components of cardiovascular disease, but then I'm going to give you actually that the fact that there's more, so we've got blood pressure, cholesterol, vascular health, or the endothelium, and I even needed notes, inflammation and clotting. Now, what we haven't put in there is metabolic, which is insulin, which is our metabolic flexibility, obesity, inflammation, according with that, it's--
Amanda Archibald:Hormones. Hormones.
Mary Louder:Yeah, hormones. And all of a sudden women, you know, losing hormones, losing estrogen and progesterone, and all of a sudden their risks just skyrocket because those are actually vasoprotective and antiinflammatory. And so, and we've got genes and genetics and genomics that looks at how we detoxify those. So if we were to really do a thorough workup, and look at genomics for cardiovascular--so say, somebody came into me and said, Hey, Doc, you know, I want to know my family history. I'm adopted. Don't know. Can't find anybody, have no clue. Okay? I would start by what? Hearing their story first, their history, any current symptoms, dietary history, exercise history, stress history, job history, relationship history. Why? Because emotions drive our feelings, emotions drive our hormones, emotions drive our diseases. That's just how it is, because we're emotional beings. So I would take that as a history. We look at any of their vital signs. Why? Because they're vital. That's why we call them vitals. So heart rate, blood pressure, oxygen level, pulse. Okay? Then we look at basic labs after we do an exam. So we listen to arteries, we listen to heart, we look at how the fingers look for circulation, the ankles for swelling, we--it's just really, the patient will tell you what's wrong with them, if you let them. And so we don't have to say, oh, heart disease, fine. Here's, here's a test, off you go, you come back in a month, okay? Your cholesterol was 220. Here you go, take a pill, see you in a month, see you in six weeks, see you in two years, who cares? That's not what this is. We really listen to what the patient's history and needs are, what their desires are, do they want to go food-based? Do they want, you know, what type of diet do they eat? What type of stress level are they dealing with? And then after the physical exam, we order appropriate tests. And I would start with a genetic-genomic test. And there's companies that I use. And then while that test is cooking, they're getting modules about learning how that works. And then we would get a specialized test I've worked with, with Boston Heart. And that's the best test on the market right now. And they've made one specifically for our, for my practice, to put together with exactly what I wanted, with what I thought was the best stuff. So that's great. So it's top on the market. And then we look at GI health, why? Amanda, talk to us about how the GI health, pulling in the nutrigenomics, affects the heart.
Amanda Archibald:You--it effects everything. You are what you--well, we used to say you are what you eat. In my opinion, you are what you absorb. And that's it, you know. So I mean, the gut is instrumental to how your body functions. So, eat a crappy diet, you're going to have a crappy gut, basically, got a crappy gut, you're gonna have a crappy heart, brain, just name the system. So to be honest with you, my knowledge for the microbiome is and the gut is more gut-brain than I think of gut-heart, which is interesting, of course. And then I guess the whole field of Heart Math, the heart has--is its own brain as well, this is--this, you could speak on a lot more than me, but I have not really connected that. So if the gut talks to the brain, the gut has to talk to the heart, so--
Mary Louder:And we've done, what the heart, the heart having And it's the best test. The best test on the market. Critical. its own nervous system, we've covered already in a podcast with Carol Ritberger. So yeah, and so we've talked about how that is, and as we really are driving the emotions into our our illnesses and into our everyday living and how we're emotional beings. So yes, there's a whole section on that. But I think you bring up a good point, what we see, so, if we pick up on the issue of inflammation, or high blood pressure, you know, can we tell genetically if a person tends to be salt-sensitive or not? Yes. Can we tell if they are cholesterol-makers? Yes. And then we can measure that with a Boston Heart test. Do they make cholesterol or do they absorb your cholesterol? Exactly. And so the thing is, if they don't make cholesterol, but they absorb cholesterol, a statin is not the drug.
Amanda Archibald:Exactly. The biggest misnomer. Yes.
Mary Louder:And so that's why a statin is not a one-size-fits-all for everybody.
Amanda Archibald:And you know what, Mary, like we are in my favorite space now.
Mary Louder:Okay, all right.
Amanda Archibald:Cholesterol and hyper absorber versus hyper Right. Yeah, who knew? And so plants have cholesterol, folks, producer, like absolutely critical, but one of the things that I noticed, and you see it all the time too, is there a lot of people eating a very heavy plant-based diet, let's say I'm eating Mediterranean. Well, Mediterranean traditionally, is actually a higher fat, very plant-based diet, but it has a good amount of protein in it, too. So a lot of people can be eating and even be vegan, 100% plant base, and have very high levels of cholesterol, and oxidized LDL. In fact, some of the worst panels I've seen have been people eating a very well-meaning, beautifully balanced vegan, or highly vegetarian diet. And guess what, they're eating tons of plant sterols. Well, body's like, that's a cholesterol, very, very high levels of beta sitosterol, right? And so they have hyper, what do we call it? A stero--a steroli--the plant plants have cholesterol. It's not about the french fry. Right? sterolemia--hypersterolemia, but it's coming from plants, right? It's not about that. It's about avocados and nuts too, I mean, they're beautiful food, doesn't really say you can't have them, but you can see when we're looking at genes, and we're looking at very sensitive labs, like the Boston Heart, we can start to see how to redirect or orient the diet, and then we should talk really about treatment for these individuals, because you brought up the statin. And--are we allowed to talk about that right now?
Mary Louder:Go for it!
Amanda Archibald:You got in that space, because it is so important to understand absorption versus hyper production, because it's different, but as a physician, you would treat that differently, too, right? It's, it's so important.
Mary Louder:But they aren't even finding it.
Amanda Archibald:They're not finding it. And yet, it's so easy.
Mary Louder:They're not looking for it. Because, I'm going to throw out the L word. They're lazy. Okay, so call me on it. Say you hate me. I don't care. It's true. I mean, when they get into patterns where they're doing so many patients that they just can't think outside of the box. And I've always said, Is there a box? I've always questioned? Where's the box? And don't put me in it. So I've never been in the box. But when I saw the difference to literally some person having a cholesterol of 313, I kid you not. And they go on a statin and it made no difference and not only that, it made them ache all over and the doctor didn't believe them. Right?
Amanda Archibald:Lying. You need to lose Weight.
Mary Louder:Yeah, yeah. And there, they are a slender person, and they have excellent cardiac output. Then what happened was I said, we need to do this test. And we found out everything was over in the absorption. And what they're eating was exactly what you were saying: avocados, plants, nuts, things like that. And so what we did was altered that diet. And what we did was change that amount of fat that was coming in, went more towards some proteins and fiber, and modified those fats a little bit. And then we are using a medication. Why? In that situation, we have to protect the heart valve that was put in. So we've got things we have to protect. And so does that require medication? Right now it does. Absolutely.
Amanda Archibald:Just such an important point, like you and I were talking before because obviously, I'm working in an overlapping space. But there's a point when you see these risk factors, it's, and a patient may say, but I really don't want to take medication that, Well, I think you need to talk with your physician who's--can manage the risk, explain the risk and manage the risk. So there's, I feel there's only so much we can do with natural intervention like Berberine, bergamot, whatever, niacin, red yeast, rice, but the risk and management has to be in a physician space, it has to be. So if you're listening and say, Well, I want to go the natural route, providing it's managed, and you've got a point in time, say, Okay, we've done this for three months, it's not working, you must work with your physician, you know, it's,
Mary Louder:I would say physicians make it look easy. it's-- It's not. It's not, and I had 11 years of training, and I've practiced 30 years. So, where are we? Close to 44 years of whatever I've been doing. And you know what, it's not easy. And, and, and the thing that's most important to know that, no, And so this is probably our public--this is my public you can't just substitute something, especially if you service announcement right now, to all the noise that's on the internet, filter it out. To all the folks who have a really good don't know what you're treating, accurate diagnosis leads you to idea but have literally no credentials, they don't have a license, they aren't in a space that's regulated, they can't be held accountable for their words, and their decisions, and accurate treatment options, and a natural route. Because we all directions, it's not the folks to get the information from. They're well-intended, well-meaning. I won't say they're the most well-educated, though. And so I think it's really super important to understand health and wellness naturally die. I mean, I often, you know, at some point, I mean, coaches cannot diagnose labs, they cannot interpret labs, they cannot prescribe medications or supplements. They cannot tell you to stop supplements. They cannot tell you to stop that's true, not meant to be sarcasm, but that's true. We all medications. They can work closely with a health team under the guidance of very good direction. And what they do as they coach people to continue with really, really good naturally die of something. You know, whether it's prematurely lifestyle changes. And it helps the consumer, the customer, the patient, the client, get on board and make the changes they need to make. But it's not up to them to lead the team. And whether it's on time, or whatever. But we have to anybody that's doing that in that space that is not licensed, not credentialed, I don't think they're in the right space. And understand that in this space, there's a lot of folks, there's I don't think--and I think they're beyond their scope. And I think that's dangerous and I think it's--I know it's out there. I get confronted with it all the time. And I get my stuff a lot of noise on the internet. second guessed, because it looks super easy. And-Amanda's laughing. I'm kind of chuckling. But I'll tell you what, what we're talking about is not easy, to care for a patient and to accurately diagnose them, and to accurately give good information. And the fact that, and here's, yeah, so I'm going from public service announcement to soapbox here really quickly, the fact that, that we offer genomic-genetic testing, we offer the highest and the best testing for cardiovascular health, and for gut health, and for hormone testing. And for all this, and we listen and spend time with people, I don't know why they would want to trade that for something that's less than, or to try and figure it out themselves. I don't understand that. So I would encourage everyone to just, this is the bandwagon you need to get on. Right, Amanda? This is the bandwagon you need to get on with a--with a doctor, a provider who's licensed, who knows what they're doing. Doesn't have to be me, be great if it is, it's always fun. But someone who is really, really certified and knows what they're doing. Because, you know, it would be awful that going the natural route would lead to a premature death or morbidity, meaning you didn't die but what you got leftover isn't all that good. And--
Amanda Archibald:Well, I think the perfect example of this is, and I watch this all the time, you may be sitting on a large Facebook group, and it's dedicated to health, and even clinicians can be in there. Somebody posts, I've got this, and I--it's like, wait five minutes, you'll have 200 responses, either on, I took this and it worked for me, which is absolutely irrelevant to you. Or you're throwing 200 different concoctions, right? There's no training, I don't know what all those concoctions do. But when you're working with, you know, I don't do physical exam, that's not obviously something I'm trained to do, you do that. And we have genetics, which is a signpost. You put that together, it tells you what labs to validate your impression, right, that tells you what to do. But I can't think of one time where somebody comes to me and they leave and I've thrown them a bucket of supplements. I might make some general dietary adjustments, right? But we use this, it's not even an algorithm, it's the process of critical clinical thinking to get you to the best outcomes. And like I said, I can only go so far, so I flip to a physician or will always work side by side with their physician. Because there's a lot of things I personally can't do. So if somebody's trying to play physician and your life and they're not, move on.
Mary Louder:Yeah, because you know, it's, like I said, I think we make it look easy, too easy, but--oh, it's just a little blood pressure, it's just a little cholesterol. Okay. That's two big things right there that we need to treat and understand and take care of. Yeah. So alright, soapbox put away, public service announcement over. But I think--important. Very, very important. Very important. Okay, so what do you--when you--so you're looking at, when you--let's bring the nutrigenomics back into the cardiogenomics.
Amanda Archibald:Right.
Mary Louder:Nuance this, bring me through, somebody comes to you and says, Hey, I want to eat the best for my heart health. What do you do? How do you approach this? Share with us.
Amanda Archibald:Well, it's rare, they would say that, right? It's usually, they'll come blank canvas with unrelated complications. But we through genetics can say, Wait a minute here. I know you want to focus on losing weight, for example, or the best preventive plan. But the way I am looking at genomic systems, and we could get into this, there are certain things that are going to be like flashing red lights that would alter the conversation I would have with someone about where I think we need to place a priority to get you where you want to go. Which is what's brilliant about this work, you come in thinking, Well, you know, I got a sleep problem. And I may say, Well, it looks like you have a dopamine issue, which could be a gut related issue, right, which means once we fix that, we can get to, you know, helping you sleep and then lose weight. But I think from a cardiovascular perspective, of course, we're going to look at those genes. The pattern I see that is like such a flashing red light, and I bet you see it a lot too. We'll look and we'll see dysregulation from two--it's one--it's two genes plus one and the first one is cholesterol esterase transfer pro--protein CETP. And it's sidekick LPL. As soon as I see those two lit up, I can almost guarantee even with a basic cholesterol panel--this is where we can talk about going deep--these individuals are going to have elevated LDL, often low HDL, and of course, elevated total cholesterol. And these are the poor people that end up going ah, you need a statin, and like, wait a minute, Mary, can we look at this please? Because they probably even need to look at, like you say, advanced testing. LPA, MP, Lp-little-a ApoB.
Mary Louder:Yes. Which is totally different, a statin does not take care of those.
Amanda Archibald:Totally different.
Mary Louder:Yep.
Amanda Archibald:So I see that. And first of all, I'm like, okay, we probably need to--and there's one more gene, right? That's so important to us. But I see that and automatically, like, well, we probably want to check this, almost always it comes back the way we think, and then that drives thinking in terms of reorganizing the diet. And this isn't necessarily so much nutrigenomic at this point in time as it is kind of macros, looking at how to organize the diet. And those genes don't work by themselves. So is there an inflammatory background? Usually. Are these people that, they, okay, they may be on a vegan, or they don't eat seafood, but they have problems with fats, genes, so fats genes help the body produce those omegas that we were talking about. If that's missing, until we fix that, we can do whatever we want with the vasculature. But as you heard us talk, these omegas are critical, you know, for cognitive, cardiovascular, immune regulation, and on and on and on. So, you know, you--what do you hear me talking about is I'm reading genes that give me impression to validate before I give out advice, but then you and I always look there beyond that. And we're just talking very simple cholesterol metabolism here. We look beyond that and we say, Okay, what's the ApoE gene doing? Right? This is the, I don't know if you've talked about this on the podcast, probably every time, but ApoE gets our attention. It just does. And we're looking for a form of it. If it you know, you inherit, for each gene, you inherit what we call allele, one kind of variant from your mom, one from your dad, and we're looking to see who--if you got four. And if you've got four-four, you're sitting in front of Mary really fast. No-- And if it's three-four. We're also you know,
Mary Louder:That's right. That's right.
Amanda Archibald:Yes, it just is. it sets in motion a lot of thinking. There's certain
Mary Louder:It is. systems and labs, we're gonna chat. But the four is an absolute rabble-rouser in cholesterol metabolism, it, it is. And we get really serious, we probably already know, that, you know, there's going to be dysregulation. And if there Yeah, it's interesting, because some of the tests, the company isn't, we're still going to look, it's just that important. So what you hear her saying is, you would not show up at Mary's office, for sure. And mine, excuse me, you wouldn't show up your conventional doctor down the street, carries your insurance, and they're going to run a genetic test that tells you what you got a three-four, or a two-three, or a three-three, this is so important to cardiovascular health and cognitive health. So what your--again, just to kind of go back to, I didn't really talk too much about nutrigenomics, as I did about nutrigenetics. That tells us how these genes may be forming that drives what kind of validation, so you hear us say validation in laboratory testing, to say, Now, this is what we're going to do with diet. And here, we want to turn these genes on and off. That's where nutrigenomics comes in. But if it's a three-four, it's a rare day I'm going to, or a four-four, a rare day I'll work on that without that client knowing they need physician oversight. It's that important. that we use, it gives the three top genes, which I really appreciate, three top--not genes, but three top concerns, pathways, right, pardon me. Not genes, pathways, which are combination of many things. And then I go okay, fine, thank you for the heads-up. Then what I do is I, I sit, I sit with what the, the next phase information is, the next layer down. Exactly. And what I find is, instead of, you know, like you say, Amanda, that ApoE might not come to the surface with that first blush, as well. We peel the layer of the onion back, and it's sitting right there plumbed in. And then you know, and then they say, well, could have a methylation issue. So we look at those genes with that. And then it says, and no need for choline. And we're like, woah!
Amanda Archibald:Say what?
Mary Louder:And so, so what those things tell me as a physician, my brain just kind of rattles. It's like, because, what it's not--the methylation is not all about B-vitamins. So it's the supporting things to the structures to continue with omega-3s and choline to make those membranes continue to be very flexible, and very fluid. And the more fluidity the better the body functions.
Amanda Archibald:I mean, so, so what you're saying is we're actually, regardless of the genetic tests we work with, we were reading between the lines with, as I said, we're looking at the, the gaps in the data, because no one can read--there's no company that can predict the blueprint, they will hand to us a blueprint, say, you know, these are the genes. And this is how the hand is played from the lab. But the real magic happens in the setting when we're looking at that patient history and the asks and saying, Okay, now I'm seeing some patterns, you know, that I think relevant.
Mary Louder:And so by--and by definition, the SNPs which are the changes in the genes that we're looking at, which are these mutations we've talked about, you know, one in every billion, these SNPs, what happens is, they have little influence, sometimes no influence, but it depends on what gene they're on as to the amount of influence, and then how they're stacked, and how they come together in a cluster or group. And so if you have SNPs that are all again, in this neighborhood, or all points, just lean this direction, then that's where, you know, you and I get a little more excited, a little more on-edge, a little more, Okay, this is actually quite actionable, and we can actually influence that to go another direction, because the SNP by definition shouldn't be much of a change. But I was looking at an article yesterday that had, I think it was over 30 variations on the theme of methylation. And it had to do with cardiovascular. 30 different genes that affects methylation. I'm like, it's not just that--an MTHFR, MTHFR didn't even make the list, because they said in the summary, we already know. And so, and so, you know, there's so much more we're learning that when, as we look at the genomics, to for sure have the basics of what we're doing is certainly important, and certainly able to change for folks what's happening. And then, like you said, the follow-up testing, when we know that there's a tendency towards aortic change, we get a, we get an ultrasound, we know there's a problem with coronary artery disease and the cholesterol is elevated. Well, a non-invasive test is an ultra fast CAT scan, where we can look at the arteries of the heart. Without doing an angiogram without injecting dye into or going up through the leg into the heart. It's a non-invasive test. And we can then analyze the cholesterol much more closely, look with oxidize, what's not oxidized, absorption versus making of cholesterol, and then the inflammatory markers and--I can looking at the hormones, and then what's driving the emotions? Because that's also like a hammer or heavy foot on the gas as well.
Amanda Archibald:It is, can you talk about the hormone piece, like, you know, why that's so important to the cholesterol picture, because it's fascinating.
Mary Louder:It is. So when we look at--when I look at the genetics of hormones, and how the hormone genetics affects the heart, I look primarily first at detoxification. The reason why I do that is because we are in a toxic world. And because so much goes through our liver. And we, a lot of women have been exposed to estrogens. So whether it's we've had estrogens provided to So if you're already shy in progesterone and that's dropping off, you're going to be more estrogen-dominant. If you're more estrogen dominant, you tend to, and you don't detoxify that us in birth control pills, or we have extra estrogen because well, that then goes down into what, more of the rogue we're estrogen dominant. And so if we're estrogen-dominant, by estrogens, it blocks the CY--or CYP1B1 pathway. And then that's definition, we're progesterone-shy. Those don't, where our need for sulfuraphane or indoles or other things come those are not a yin and yang they literally have two in to help clear that and then we look at phase two with different processes. Two different things. It's not this methylation, sulfation, acetylation, glucuronidation is is on, that's off. They literally have their own cycle within the month. And so but we, as we go, as women go into and one of the main ones for estrogens, glucuronidation. So we look at those pathways to see how you're, we're clearing those. Now, the other thing is then as that cholesterol, or, correction, as estrogen drops, cholesterol increases, because it responds to cortisol. Because estrogen drops, and so cortisol says, Okay, I'm just going to overshoot that. And it does that around menopause, that gap widens between estrogen and because estrogen is dropping around menopause. And, and the stress levels are still high in a person's life, and so as progesterone. Progesterone drops off faster. estrogen drops, cholesterol comes to the front, and that begins to blunt insulin, which is like putting a wet blanket on something. And then the liver, and the inflammatory markers,
Amanda Archibald:It's a good point. So it you said a couple try to fight through that if you don't literally just clear them out of the system. of interesting things with progesterone, what genetically, we can actually see there are genes that will really speed up progesterone production. But at the same point, they can--it's interesting, it's like this bifurcation, so they can really push progesterone, but the other route was to really push cortisol. So it's interesting. So you could end up having lower, like you said, lower progesterone, estrogen dominance, the worst, and elevated levels of cortisol, which can just come from your genes.
Mary Louder:That's right.
Amanda Archibald:Wow. And then you can have elevated testosterone, let's add that sort of ick. So you'd be all over the place, losing your hair, pulling your hair out, what little you got left, and feeling crappy, and weak, because your estrogen is through the roof. But you know, one of the questions I had, it came from one of the clinicians in one of the classes I was teaching, it was a really good point. I never thought about it. Well, when you go through menopause or andropause, midlife, you know you're losing these hormones, basically, hopeful--never always in balance, right? But they're made from cholesterol. So is part of the elevation of cholesterol potentially that, well, you're not making these hormones anymore, so cholesterol doesn't know where to go. I mean, is that a legitimate observation?
Mary Louder:Absolutely legitimate. Absolutely. And the fact is cholesterol is the mother hormone, mother molecule for the hormone. So, and I maintain cholesterol is actually a hormone not, not a molecule, not a--
Amanda Archibald:Oh, yeah. Because it making hormones, right? Yeah.
Mary Louder:It's taking a message from one place to another, and it's a fat soluble molecule? That's assigned a hormone. So I look at it functionally as a hormone.
Amanda Archibald:Yeah, no, that's a really good point. So it's interesting. So you hear us having this conversation about like midlife and observations, but what we're looking at is genetics, because genes tell us fast, slow, on, off, but symptoms and how do we validate that? And how do we test that? But you know, the other thing I thought was really interesting, reminded of recently, is cholesterol--we're talking about heart, right? So cholesterol is often what we think of. So cholesterol is the starting molecule for bile. And you don't emulsify fat if you don't produce bile. Cholesterol is the starting molecule. And yet you went through so many years with the American Heart Association, and probably the British Heart Association, low cholesterol, right? You need low cholesterol, well, yeah. You--
Mary Louder:And then digestion, which was, which then kicks off the whole issue with dysbiosis and gut imbalance. Which affects the gut-associated lymphoid tissue, which affects, you know, really, then that's your gut to brain axis, your gut to heart axis, your gut to joint axis, your gut to nervous system axis, really all begins in the gut with the microbiome. So yeah, it's, it really so it brings it back to the gut. So is there a pathway genetically, genomically, functional medicine-wise? Gut to heart? Yes. Is there one heart to head? Yes. Is there one head to heart? Yes. Is there heart to gut? Yes. You know, and so, yes. And so when you look at that, you've got to find, it's like a, like one of those merry-go-rounds on the playground, aren't quite sure where to jump on: green, blue, red, you know? When you try to get on. So that's what you do, you wait and you time it, you time it, and you get on. So you find where you can jump in, where the best access point is for that patient. Sometimes the key point, and sometimes it's a point that's away from that, interestingly. So, and it's probably my osteopathic training, because I just backdoor a lot of things and all of a sudden I'm there. And it's a very unique approach because all of a sudden I'm up in the biochemistry, as it were, without disturbing much. And then I began gently breaking it down, supporting, breaking it down, supporting, and all of a sudden, three to four months are like, their tests come back normal, their, their hormone tests that I use is much improved. They're metabolizing correctly, they're sleeping. We're using a little bit of bioidentical hormones. We're monitoring their cholesterol, plus or minus, we've had to treat it, sometimes it just sorts out, when we treat out cholesterol. And, or it sorts out when we treat the hormones.
Amanda Archibald:Absolutely.
Mary Louder:Yeah. And so what we're doing is working with the body, and I'll tell you what, none of that's easy. But it's absolutely beautiful. And absolutely driven by the genetic and genomic patterns of when they run in, as we say, as I say, in cahoots. They're running in cahoots.
Amanda Archibald:I think what genetics does, and you know, what, obviously, we're talking about heart, the heart here, but what it does, honestly, is it saves you as a patient time and money because you're not running around, you know, trying to find out what's wrong, it really gives us this amazing matrix that helps us fine-tune, okay, where, where might, where might the weaknesses be, and as you said, oftentimes they're far removed from what we're looking at. The issues you experienced in heart disease, may have their roots in gut, or inflammation, or immune, you know, and that, and often do, so. That's what helps us prevent, like, as you said, Oh, you've got this, take a pill. It's like no, actually, if we bring this online over here, over the next six weeks to three months, it's gonna manifest differently over here. So yeah, powerful stuff.
Mary Louder:Yeah, so they definitely, the, the genes for the heart, the genes for cause, the genes for predictions, the genes for consideration, really point us in the right directions, how to evaluate somebody holistically, and give us a much better outcome. Yeah. Well, Amanda, again, this has been great fun. Great fun. We are wrapping up because we're a bit over time here, but it's great fun. I thank you again for being our guest on Since You Put It That Way. And I would encourage all of our listeners to get to my webpage, get some testing done. And if you don't want my testing, get it done locally, but I think my testing is the best, I'm just going to do a little brag--kind of brag there on that, and, and then we will see you next time we're can--we're continuing with a couple more cardiovascular things, we got a great visit with Carol Ritberger coming up again, and with the Cosmic Health and Wellness, that's been a big hit. So everybody keep enjoying what you're doing, and we shall see you next time. Thanks for being with us. Thank you for joining us on the Since You Put It That Way podcast. Today's episode was written and produced by crowded table productions, technical editing Malyn Long Lopes, sound editing Jonathan Fegel, music, the River Jordan written and performed by May Erlewine, please rate, review our podcast as well. We appreciate your feedback and hey, be positive, share the love.
