A Functional Approach to Assessing Heart Disease

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Just for listen to a podcast, functional pharmacy listeners can also say 15% off the purchase of an unlimited membership by entering the discount code podcast 2023 that's PODCAST2023 and all caps at the checkout or by clicking the following link in the description. Welcome everyone back for yet another podcast on functional approach to all things medicine. This is another ACPE accredited one. It's kind of cool. You get to learn some functional medicine stuff, some functional pharmacy stuff, and get some CE credits, probably even on your drive. Today I want to talk about a functional approach to assessing heart disease. This is a pretty big deal. It's a really big topic. I guess we'd like also we could call this a beyond lipid approach. What we're going to do is we're going to cover like six core areas, like beyond lipids, right? A variety that we can test to really assess someone on their risk factors for heart disease that aren't just once again looking at lipids and looking at cholesterol. We are going to talk about a better way of testing cholesterol, which is critical, very important. We're also going to talk about oxidative stress and inflammation and how these two players can play a role in creating heart disease and listening to issues. We're going to talk about clotting potential, which seems to be ever so important these days. You're hearing more and more often increase in clots, which is true. We know the fact that the spiked protein, however we get it, whether it's through COVID or vaccination, can increase clotting potential amongst other things. We're going to talk about sugar and insulin markers. You've probably heard the term metabolic syndrome, and this is very much a big part of it. We know the role that metabolic syndrome can play or insulin and blood sugar in increasing risk of heart disease is pretty critical. What we're all going to talk about is hormones. We're going to talk about different hormones from our cortisol toward adrenals to our sex hormones and the role that they actually play in cardiovascular health. So the reason why when we assess a patient, we're not doing it just for hot flashes. We're actually, well, maybe we should call heart flashes. We're assessing and looking to refine or reduce their risks of issues of such as cognitive decline, cardiovascular disease, bone health. But we're going to take the focus and the view on it from the heart. All right, so let's move on here. So first of heart disease, why are we talking about heart disease? And what are we missing here? Why do I say what are we missing here? Well, heart disease is the leading cause of death for men, women, and people of most racial and ethnic groups in the United States. It is a number one cause of death. We are not winning the war on it, right? It has been for a long time. One person dies, I think these are updated stats every 36 seconds in the United States from cardiovascular disease. About 700,000 people in the United States die from heart disease each year. That's one out of every four deaths. And, you know, it seems that we're seeing in here and more of this. Heart disease costs in the United States about $363 billion each year from 2016 to 2017. This includes the cost of health care services, medicines, and loss to productivity due to death. So, you know, one thing to think about here when we say medicines, look at when you look at the pipelines, I mean, I've been in pharmacy for how long since, I don't know, 94s when I got my license. But it was all about the pipelines, right? What's coming down the pipeline? What are the new meds? What's the new antibiotics? And it certainly seems a lot of pipelines have kind of dried up, you know, over the last few decades. But cardiovascular disease, at least in the blood thinning category, right? Has definitely exploded. And it doesn't come without risks. Now, we're not going to get into medication therapy on this podcast, but just want you all to keep in mind, you know, it's there's kind of this collective awareness of heart disease at this point. And there has been, right? It's been on people's minds for a long time, like we've seen the medication pipelines such as these blood thinners explode over the last many years before COVID. Now COVID happens and, you know, we're seeing these risk factors increase. We're seeing younger populations be affected by this. Cardi may opt, my opt, but these issues like that. So very important to look at. Now, our medical system, Western medicine's number one approach in a session is test and lipids in cholesterol, as well as treatment, right? So let's just test your cholesterol. If it's high, let's give you a drug to lower it. And then we think we're going to save your life. But, you know, I think, you know, let's be honest, when we can look at the number needed to treat for drugs like stands or any cholesterol or in medication, it's a pretty paltry story, you know? There's a number, a lot of good numbers that need to be treated just to prevent in one case. So we want to talk about first off, a better approach to managing lipids. So, because, hey, maybe we're just doing the lipid equation wrong, right? And on top of that, we want to talk about the other approaches, other influence and factors to heart disease. So first of all, let's cover what lipids are and why they are. And, you know, when I sit down, I do a lot of lab readings, a lot of protocols, and I sit down one on one with my patients, and I always like to describe to them what lipids are, what the role of cholesterol is. And I just like to bring it in a very basic form. So lipids are basically transporters, right? And I'm going to use some roadways analogies here. And for instance, LDL, and keep in mind, low density lipoprotein has been called bad cholesterol. But, let's also understand that we need all cholesterol. We just need it in the right size and the right ratios and balance. And we'll talk about that. So LDL is the mother hormone. You know, another part of our tests and services when we see our patients is a complete hormonal profile. And, you know, I'll share it with them. Be like, you know, you look at all these hormones, you look at your estrogen, your pregnant alone, your progesterone, your testosterone, all the stuff. It all comes from LDL, which is the mother hormone. So we need it. So there is some research out there that shows lower and LDL too low can affect quality of life. There is some also research that actually shows can possibly increase more, you know, mortality. So there's morbidity, mortality. Then there's some other studies that kind of go against it. So here's my thing. Hormones are great communicators. I want my material for my hormones. If my hormones are low, I want to see what the upstream efforts are to feed them. Right? And yeah, we're not going to give someone cholesterol, but we have seen people's cholesterol naturally be quite low. And there is just kind of this absence of vitality that I think we need to address. So LDL's job, very basically to take fat sivine nutrients and vitamins and get them to the cells to be utilized. Now the thing is, if we've got too much LDL compared to HDL, see after LDL does this job, there's going to be this material wasted, right? Left to side. It's almost like a disposable camera, right? But that material can lie on the vessel floor where have you. And if it becomes inflamed and oxidized, well, that's a real root cause there. Of some cardiovascular disease or some real risk factors that could become an unbored. So we want that stuff cleaned up. We want it swept up and taken out of there. That's HDL's job. HDL, aka good cholesterol's jobs to come in, clean them up and get it away. Now, so one might say that we need enough LDL to deliver the fat sivine nutrients vitamins and stuff, right, to the cells. And then we need, and not too much, right? So then we need enough HDL to clean up and get it out of the way. So that's a nice marriage of that. So when we further look at cholesterol, let's look at what a standard panel would be. So a standard panel would be assessed. And this is an estimate actually. This would be called content. So you might see it as HDL C LDLC. So it's basically plugged into a formula. So it's not always exact. And it's pretty wild because we compare this in our practice, the content, lipid content. So an LDLC compared to in the LDLP, which is a particle number, which we're going to talk about here just shortly. So, and oftentimes they're not aligned. You might see an LDL particle, which is the exact amount, being excessively high, where something can really should be done there. While the LDLC, which is that estimate, might just be a little modestly high, which the person might be told, well, you know, exercise more, eat better, which to them doesn't sound like an emergency, right? Where maybe you should be implementing some nutritional therapy, supplemental therapy, really dive into the diet and stuff like that. On the contrary, we've also seen in the case where the LDLP, right? The accurate number is a very normal number while the LDLC is excessive. So these people might be put on something like a lepator or a statin drug, which they might not really need. Where some lifestyle diet and even some modest nutritional therapy might support it as well. So good things to know. So HDL, so in a standard panel, right, you look for a cluster, it'll be about 200, note greater, HDL greater than 40, LDL less than 100. Now triglycerides I want to talk about because I like to share this with my patients as well. Treglycerides, I believe, are a wonderful respect to look at. Even on the conventional panel, this is, I feel the most important number to take a peak at. Treglycerides as I like to describe them, if you're on a bridge over a river and you're to drop a bunch of oil in that river and you see how it starts to accumulate, that would be like a triglyceride. Spilling over, spilling out of the cell cannot be stored anymore. It's not, it's, it's generally stored energy, right? Or it's coming out of its storage compartments. And it's just going into the bloodstream and it's increasing risk factors that way. Now a regular panel or average area, normals what they're looking for would be like zero to 150. So some research has been done, which in this to me is one of the main reasons we really should look at particle testing, but this does also help. So some research has been done that shows triglycerides over 150. There's a really good chance we could be having bad LDL. And what I mean by that is an over amount, too much of the small sticky type LDL, the small, right? Because it's a size. So we want to know how many we have and we also want to know the size. When triglycerides are below 70, there's really a good chance you get good LDL. You don't have too many of the small stuff and you've got just enough, you know, I mean, you've got a larger amount of the light, larger fluffy stuff that can just flow through the vessels. Now between this 70 and 150 is kind of this gray area, right? So we don't really know that. So there's some other things too. How you can optimize a conventional pattern, conventional panels. So that would be one way, looking at triglycerides closer to 70. Another way and usually that's going to fall in line with the diet. That's really just not a high insulin stimuli diet, to be honest with you. And also not high factory-formed fats, trans fatty acids and things like that. Now another way would be the closer your triglycerides in your HDLR, like maybe a 2-to-1 ratio, closer to a 1-to-1 ratio, the lower risk as well of heart disease and things like metabolic syndrome and insulin resistance. So a couple ways we can look at things. Now I'd like to talk about what's called advanced particle testing. So the test at we order for our patients is called NMR and is enancium, is it Mary, Ars and Robert. And this is particle testing. So this lipid profile, it's also, I think the trade name is Lippefefet. And it really comes down to the way that it's being tested, the size files that they need. So for warning, if you start doing this, check your local labs where people go because some labs aren't used to this. It's actually not very expensive either. But it provides a lot of great, a wealth of information. So I really think all practices should be doing this. So an NMR lipid profile assesses the exact amount, not the estimate of cholesterol particles in the blood. And also the size of the lipid particles. For example, we can have big buoyant ones, right? As I said, lower risk with those, or we can have the small, dense, sticky ones. So once I can kind of get into the cracks of the arteries and things like that. And there are others. So that's the generality. Now sometimes you can have a VL, LD, a very low density lipoprotein that'll be added. If that's out of whack, that's usually in line with high triglycerides as well. You can have lipoprotein A, APOB. So there's a bunch of other ones that we can look at. But I just want you to get an idea when we look at an NMR profile, you're getting the exact amount and you're finding the size. So these are all relative risk factors. And we're also looking at triglycerides. Now another analogy you can share with your patients I like to use is the tunnel effect. So now I have from Pennsylvania originally. And if you've ever driven on the Pennsylvania term pike, especially in the central to western part of it, it's when you get a little mountainous and there's a lot of tunnels. And we're heck, maybe you're driving to Manhattan where any of those tunnels. But you know, when you go through a tunnel, you look up and you see a lot of tiles, right? And on these tiles, there's a lot of scum. And this comes from the cars driving through the snow and all that stuff. And you can kind of see it on the tiles and you want to scrub it. Now that would be representative of like a plaque. And it seems that's where most people think about cholesterol, whether it's a practitioner or a patient. And they want to watch out for the plaques. Because you know, these plaques can dislodge themselves and they can cause a clot and block flow, which is, you know, it's real. But what I also want to talk about is what happens in between these cracks. So when you look at these tiles, there's little cracks, you know, you may not see it as your buzzing by, excuse me, but within those cracks, you can have lipids, little fatty deposits, find the way in there. And what can happen there? Well, oxidation can happen. So the oxidative stress triggers a cascade of free radical activity that can lead to inflammation and tissue damage. The chronic inflammation can lead to a chronic tissue breakdown, preventing the repair of the tissue while influencing various disease states, including heart disease. So think about that. So we want to see what's going on the outside and we also want to see what's going on the inside. So what are some test and options we can use for this? Well, we can use c-reactor protein. c-reactor protein is a protein where levels become elevated when the body detects an infection or need for inflammation. Now, there's normal c-reactor protein, which the levels are like less than 10 or below is what you want to look for or what they call high sensitivity c-reactor protein, which is more of a correlating factor with what's going on in the cardiovascular region. With a high sensitivity c-reactor protein, less than 3 is normal, but I'm going to give you an optimization on this one. Less than 1 is optimized. So I'll give you an example for our practice. We're very big proponents of the Mediterranean diet or any type of cardiometabolic diet. Now, if we see that there's a lot of inflammation going on, I want to look at a couple things. I want to look at the patient's vitamin D levels and I want to see that it's optimized, optimized around 60 or 80, not this normal 30 to 100, right? I want them at least 60. I also want to talk about essential fatty acids, great component, most traditional diets around the globe consume a high amount of essential fatty acids from both fish and also plant-based foods. So we're going to get people on that. So if I see a c-reactor protein that's in normal range and maybe no other elevated risk factors going on here. So normal range but not optimized. So maybe it's like two. When I see the right amidease low, I'm going to start by optimizing the vitamin D, giving them some fish oils as well as talking about the anti-inflammatory diet, like a Mediterranean diet. Now, if there are above three, well, I'm definitely going to be looking at something such as curcumin, curcumin phytosome, which is just a great full body anti-inflammatory. It's cardioprotective, kidney protective, liver protective, gut protective, cognitive brain protective. So that's a nice common one. And there's other things that we can measure. Interleukin 6 is a cytokine that could be measured and I wasn't going to really mention it. I'm not going to dive into it, but it does help regulate and promote the immune responses. With COVID, we heard of the cytokine storms going on. So that's what these are. These are cytokines, and they're a measure of inflammation. So they can give us good insight. So if you've got someone with the risk factors, you can definitely look at this. Now, the one thing I want you to have a take home is there's a genetic malfunction where the afflicted person can secrete more pro-inflammatory in the leucon 6 than people without, which is, you know, and it's a very potent inducer of seriactyprotein. So if we've got a seriactyprotein that's off the charts, which doesn't quite make sense, even after retesting from the lab, you might want to look at this, but how are we going to treat it anyway? We're going to treat it with the same epigenetics and lifestyle options that we would to lower the seriactyprotein anyway. So now let's talk about test and inflammation and potential wall damage. So you remember kind of how, remember kind of how, you remember how I mentioned the cracks and the tiles and that's where the oxidation and the inflammation can happen. Well, there's something we can test called, it's called MPO, M.S. and Mary P. is in Paul 0 or O. As in Othello. It's called Milo peroxidase. And it's a white blood cell derived inflammatory enzyme that measures disease activity from the arterial wall. So it's going to say what's going on with the wall structure, the integrity. You know, the walls have become so much more relevant as we've learned more in all areas of our body. Our arterial walls are as well as our intestinal walls because in that case, that's where things like leaky gut can happen, right? So when the artery wall is damaged or even inflamed, Milo peroxidase is released. Milo peroxidase mediates the vascular inflammation and plaque formation and it's linked to plaque vulnerability. So back to the tunnel, we see some plaques up on the walls and you know, honestly, maybe they don't have a lot but they have some. But if their MPO is high, that can actually make them more vulnerable to destabilize. So it's very helpful. Milo peroxidase is actively involved in the progression of atherosclerosis. So some good information there. And these can be honestly ordered with any lab. Here's the thing though, oftentimes the lab tests texts might not know what these are or the phlebotomus because they don't get these orders regularly. So sometimes it's connected with them talking to them if you're in the local community. And that is what you will see and what we see is that, you know, we've got our patients that go to their chosen labs. We'd love everyone to go to one lab and make it easy on us. But sometimes it takes a lot of educating, I guess, the lab folks. Another one, oxidation testin. We can use ox LDL. This is a potential marker of metabolic syndrome and heart disease risk. Conversion of LDL, right? We talked about that to ox LDL. Oxidized LDL appears to be an important event that helps initiate and accelerate the development of early atherosclerotic lesions or fatty streaks. Resultant issues and influence and factors of elevated ox LDL include coronary artery disease, acute myocardial infarction, stable and unstable angina, and untreated overt hypothyroidism. Which we're going to talk about because hypothyroidism is a risk of heart disease. So once again, just another good lab test that can be ordered for patients, especially as one is that, you know, you're seeing issues, you're seeing risk factors, you're seeing some destabilities, but you can't get to the root of it. Let's talk about clotting potential or stroke issues. Since we can look for this, we've got some lab tests and we even have some at home testing that we can do that could be quite helpful. Once again, we've been seeing more and more issues of this just generally in our society, right? We wouldn't have had all the zoraltos and the prodaxas and all that stuff pre-COVID if we weren't on this stint, you know? Although now it seems like it's been fast-forward. So, excuse me, there's some things that can be tested. One is something called D-dimer. D-dimer is a protein fragment in the blood that would be present after a clot is degraded by fiber and engine breakdown. So the D-dimer is actually going to show that there once was a clot, which shows there's a clot and factor in the blood that needs to be addressed, where there's a chance of. We can also measure fiber and, you know, in your individual lab that you use, they might have like a set of these together. So, fiber and engine is a fibrous protein, which is involved in the clotting of the blood. So, too much fiber and can run lead to an increased risk of clotting. Another one would be a thrombin antithromic complex. So, this is actually a protein complex of both thrombin and anti-thromin. So, thrombin leads to clotting. Antithromin, its job is to actually inhibit enzymes that lead to clotting. So, it provides a balance, like it checks the balances. So, it's essentially a marker of net activation of coagulation. So, all these can be very, very helpful. And if you've got patients that have had COVID, have long COVID, have had the vaccinations, have had cardiovascular risk and issues, these all should be tested. Excuse me. Something else could be nitric oxide status. So, nitric oxide, right? It's a vasodilator. If we don't have that, or blood can be thick, right? If things aren't dilated enough, and that could be an increased risk factor as well. We have seen, this has been an issue post-COVID as well. The test for this, you can just get nitric oxide test and strip, so that it can be a valid amount. How would you balance that out? Well, you can give someone supplements that actually increase nitric oxide. So, things like certain amino acids that can support it, beat as a source that can help support it as well. So, yeah, so a couple things to check marks to put down there. There's a coronary calcium scan. So, this is basically a specialized X-ray that provides an early look at levels of plaque. Hearts scan might help guide treatment if you have a load of moderate risk of heart disease, or maybe it's just not clear. So, once again, it's going to give us a better idea of what's going on with plaque, right? But now, do we want to stop there? Because what are we going to do with a plaque, right? And is it oxidized? Like, what's the level of damage that one might be experiencing? All right, so I'm going to pause for a second and I'm going to be right back with you. All right, welcome back. So, now we're going to step into yet another level of tensile. And then we're going to talk about insulin blood sugar, insulin resistance, and prediabetes in the world of this place. And what we can look to assess these. So, you know, I guess this whole thing is more of a like a cardiometabolic. So, elevated insulin is a risk for heart disease. Elevated blood sugar is a risk for heart disease. For many different ways, these can increase inflammation. They can increase clot and potential. They can affect lipid levels. And that's probably another thing that I should put in mind here. When we look at lipid levels, lipid levels are not just affected by chance, by genetics, or by diet. Only about 25% of the cholesterol in our body comes from diet. So, it's really important we look at things like insulin blood sugar, hormones, thyroid, right? And all this, which we're covered. So, this is part of the reason we're covering all this stuff. So, first of all, let's give you a little little lesson. So, other levels that we check on our conventional serum lab panels with patients, it's not going to just be HBA, one say, all right? We're going to just check a fast and glucose as well as an insulin. We could do leptin, we don't, but we could. And I'll explain that. And we can also can do an insulin response test, which we generally don't either. But I want to talk to you about the optimization of numbers. So, the path of insulin resistance. So, when someone eats a carbohydrate, and honestly, it doesn't matter the source, right? I don't care if it's whole wheat bread. I don't care if it is a carbohydrate from, you know, a gluten-free whatever, or even a carbohydrate from a fruit or vegetable. That carbohydrate dumps into sugar in the bloodstream. Now, if there's more fiber, it will slow the release. So, yes, the amount as well as things like fiber matters. So, you consume a carbohydrate, it transforms into blood sugar, glucose, right? And then the body looks down the body, you know, in its wisdom. It only likes about a teaspoon of sugar running through the blood in any given time. So, when it starts to see that rise, it's like, yo, insulin, come on in, need you to grab it, usher it out of here. Get it to the cell, store it for energy when I need it later. And keep in mind this, the body can only store about 350 to about 500 grams of carbohydrates in the form of glycogen, which is stored glucose. So, as far as energy is concerned, the lesser the need we have for external carbohydrates is how we are designed. We're designed to be fat burners, to access our fat stores, much more efficient. There's 3500 calories per pound of fat. And for every gram of fat, it's nine calories. So, that's very efficient. That's a lot of energy. We're protein in carbs, early five. So, keep that in mind, right? So, what happens is we consume the carbohydrate, glistubled sugar, insulin is called upon it. If we keep doing this, our insulin levels can go up. And what happens is we can develop this thing, one called glucose and tolerance, but also insulin, or glucose resistance, or glucose and tolerance, or insulin resistance. Now insulin resistance, it's kind of like if you walk into a room in this particular odor, and you notice it at first, but then you don't notice it anymore. Well, that's the way the body is when it produces pump seven insulin. So, it might be doing the insulin in a great response to remove the carbohydrate from the bloodstream, but then it might lose its ability for the read. And it might just keep pumping it up. So, insulin elevates. So, first thing that's going to, so once insulin elevates, we might often see insulin elevate before glucose does. So, we can often see a patient that's got a fast and glucose of like 85. Looks great, but their insulin is like 14 or 15 or 20 or 21, or even over 24, right? So, a lot of times we'll see insulin rise first. The resistance happens first. Same with leptin, that's the other hormone that I was talking about. We can measure which would give you even further insight on what to take action, because that's what this is all about. As far as preventive medicine, first of all, we want to find what we're looking for that's going to be a virus factor. And then we want to be able to take action, because it's a lot easier to take action before we get ourselves into a state of disease. So, factors that insulin that influences thing called insulin resistance. Yes, genetic stats, but we got to remember we like to look at things through epigenetics. It's the influence that we put on our body and ourselves, which is stress, diet, joy, power of play, all these things that I can influence it. So, if we give the right messages to our genes, then a potential mutation that we have might, doesn't have to turn on, right? Not all mutations turn on, and they don't have to. So, we can influence whether we turn on good genes or turn off bad genes, turn on bad genes or turn off bad genes. Obviously, a high insulin producing diet can influence insulin resistance. And what's interesting, such as the work that Rob Wufted in his book, "Wire to Eat." Some people might react differently to a said carbohydrate source than others. For instance, you know, Mr. Smith, his blood sugar might rise a lot to an apple, where Mrs. Smith might not rise at all. So, these can be individualized. And that's, I think, where some people find benefits with continuous glucose monotone. I'm not a big fan of wearables and like this over connection to data. I think it kind of can stress on nervous system out a bit. Lifestyle elements play a role. Factors of insulin resistance. Are we sleeping? What's our exercise like? Are we managing our stress? How's our diet? Dietary and environmental toxins, nutrient deficiencies. The gut plays a super big role. Altered gut microbiota. That can affect insulin resistance. That's why we actually check gut health in our practice. Chronic stress and adequate sleep in said in our early lifestyle. So, what about testing? Let's talk about blood sugar first. We want to have it a fast and excuse me. 126 and above is diabetes. Boom. Now, there's this real big gray area, which we don't want to wait for 126. I saw that happen way too often. It's the 125. This is considered very high. It's in paired glucose tolerance. This is pre-diabetes. So, if we, if this is our fast and sugar at the state here, this is when we need to act or even before this. We don't want to be at 105 and be like, let's just wait and see. Exercise more eat better, right? 85 to 100. This would be normal. So, that's a normal range. Now, 70 to 85, that's optimal range. Now, I'm also going to say, this is individualized for the patients. You might have a patient that is diabetic, a type 2 diabetic, and maybe they're blood sugar levels, and maybe they're even on insulin. Maybe normal for them's like 170. If you try to bring them down to 70, they're not going to be feeling really good. So, I really, you know, you need to individualize all of this per the patient. HBA 1C, 7 or above, increased risk for diabetes, 59 to 69, that's elevated. 56 to 58 is good. 54 or less is optimal. Yeah, sure people win. So, 5.4 or less is going to be optimal on this one. And that would fall online with that blood sugar we're looking at would be 70 to 85. You know, when you see someone in the 5, 6 to 5, 8, they do their estimated glucose over that time. It's usually 95 to 105. So, it's kind of interesting to see that. Insulin, very, very important. I think everyone really should look at this, looking at metabolic conditions or prevention of. So, fast and insulin normal is going to be like 3 to 24. When we get above 10, we want, we start making changes with people. We want, you know, optimize, we look at this less than 9. When you look at someone who's say in the state of ketosis or in a ketogenic diet, which there's like no insulin stimulation because they've got a very low carbohydrate content, which is usually 20 grams a day of carbs or below or even 50. You know, we might see them about a two. Now, you can also do an insulin response test. So, insulin levels are measured fast and then one to two hours after drinking a sugary drink. So, if we feel as an instability, we can do this. Leptin, I talked about the resistance is often a precursor to insulin resistance. So, if we really want to cue in there, we can check left and levels. Optimal is going to be between four and six. Optin 9 is okay. 10 plus is bad. All right. So, how about we just chat a bit about hormones here? A lot of people don't realize hormones play a very, very, very big role in cardiovascular health. So, and you know, as I said, when we measure people and we are balancing the hormones, we'll look at what's considered a premenopausal range, which is essentially like age 12 or whatever to like 50, right? While someone's in reproductive errors, reproductive ages, maybe not 12, maybe a little older, but we need larger hormones for things that the body wants to repair, reproductive abilities and things like that. When we get into the menopausal state, repost menopausal state, well, we don't need it for that. So, we don't need as many hormones. So, you know, I think with hormonal and biodontical hormonal application, there needs to be really a judicious approach for the benefit of the patients. Because what are we looking for? We're not looking to make so many teen again or 25 again. We're looking to reduce the risk of heart disease, cognitive decline, and osteoporosis, right? So, hormones we're going to look at on their effect of the cardiovascular health, our cortisol, thyroid, estrogen, progesterone, and testosterone. Adrenal testin, everyone gets it in our practice. It's so important. Regardless of your stage in life, regardless how old you are, you know, a little thing with this, we're designed on a fight or flight response, right? But it's acute stress, short-term stressors. Our bodies, we have the same genes that we had when we were designed 160,000 years ago. We were living a completely different life. The fight or flight realm back then would be forging through the serringetti, looking for food, and then a tiger sees us, wants us to be their food. Excuse me, starts to chase us. So, we need the energy. We need the cortisol, we need the adrenaline. We need to release the glucose and the blood sugar to get to our muscles, to our brains, right? To get out of danger. We are in fight or flight. And the body deems this still these days, even if it's like, oh my god, a bill is due, but I don't have the money or whatever it might be, a life or death experience. This is how our nervous system is seeing this to be, which is really important thing to think about. Because a lot of people might think, ah, stress, I'm not stressed, but, and we might look at their cortisol, or here on the contrary, we might look at their cortisol levels and things don't look horrible, but they're really stressed and their nervous system is tweaked, they're not sleeping, right? So, that's all well and good, but on the opposite side of fight or flight is rest and digest. We need to dive into that, one for a digestive health, but two, to hop into the parasympathetic, because that's our nervous system. We've got our sympathetic, right, nervous system, which is fight or flight, then the parasympathetic, which is rest and digest or rest and repair. You know, our bodies naturally work this way. We like the adaptiveness of stress. We like to be challenged, but stress and inflammation are like double ed swords. They can make it stronger, but we need periods of rest from them to break down to allow ourselves to rebuild and get stronger. So, when we talk to our patients, we like to explain chronic stress in three different phases, and we'll have another podcast that dies more into this. But stage one would be, you know, this is chronically, we're not giving ourselves the period of rest and, rest and digest, which can lead to a lot of issues, but the important thing is to recognize that right now we are, what our globe or world just went through, we're kind of in this collective state of PTSD. So, I don't know of anyone that life didn't change through COVID, and stress does play a role. Stage one cortisol rises, DHA rise. They're the two primary stress hormones. Now, if chronic stress continues and continues, then you go into what would be called stage two. And I'm just simplifying this for you. I know there's a lot of different explanations on this. Stage two is going to be the body wants to keep cortisol alive because it keeps us alive. Remember, this is life or death. So, it's going to start stealing it from other hormones. It's going to steal from progesterone. It's going to steal from pre-ninalone. It's going to steal from all of the DHA, right? So, that's what stage two is. Now, a lot of adults can live in stage two for decades. Just different degrees of it. That's why we like to measure all hormones. Now, stage three is like the bottom falls out. This is freeze. Fight, flight, freeze. Yeah, this is when we're trying to peel ourselves out of bed in the morning time. We're just too tired because our adrenals have taken the hit. So, when you can kind of break it down that way, it can be helpful for patients. But, let's talk about the influence on the cardiovascular health. So, cortisol, if it's elevated or even any of these stress hormones can increase blood pressure, increase insulin resistance, increase blood sugar, increase insulin levels, increase insulin resistance, increase inflammation, increase potential to clot. So, this is why it's really important to measure stress. Heart rate variability is something that you can order, measure. And I kind of like this because, you know, I talked about the sympathetic and the paramedic nervous system. So, the amount of time between your heartbeats, even though these fluctuations are undetectable, except with specialized devices, can still indicate current or future health problems, including heart conditions and mental health issues like anxiety and depression. So, we can measure our HRV or heart rate variability. This sympathetic, as I mentioned, this is where you're in fight or flight. That's where that response comes from. Parasympathetic, this helps balance it out. Controls the natural relaxation response. How do you maximize your heart rate variability? Well, healthy diet, hydration, enough fluids, water. Not too much alcohol. Definitely getting in the sunshine. Sunlight will give it, we'll help maximize it. Proper sleep, sleeps a big one. Stress management, being in nature, cold water, the cold water plunges or even a shower. Breathing exercises and strategies, the right to exercise, right? So, you know, not into a chronic cardio, we're overstressing the heart. Burst type exercises like sprints, things like that can help maximize as well. Not every day, maybe once a week. Meditation. As well as train the heart rate above chronic cardio, we want to watch out. So, we don't want our maximum heart rate. This is the work from Dr. Phil Maffatone. To be over 180 minus your age, that should be the maxed. So, if you're used to running, this might be a neat little experiment for you to do. Try to keep your heart rate at a max of 180 minus your age. See how slow you might run compared to what you're used to. Thyroid is a biggie. I like to talk about hypothyroidism and the role that it plays. Hypothyroidism. So, first of all, thyroid is, and we've had a couple podcasts on this so far, that are also CE accredited ones. Thyroid is often under addressed and under assessed. Oftentimes, what's happens or what's tested is a free T4 as well as a TSH. Now, we want more because T4 is storage thyroid. It converts to T3, which is active thyroid, but people might not convert due to elevated cortisol levels or even some nutrient efficiencies or impairments there. TSH, yes, is important, but we want to also, as I said, so we want TSH, free T4, free T3, and a body so important. What if we have Hashimoto's? We're working against it. So, we need to optimize it that way. Vitamin D is very important. Optimized to be 1680, between 1680, as well as ferritin, a measure for iron stores. We like to have that close to 90 to 110. This is what helps drive the active T3 to the nucleus of the cell. So, it's really important to refine and dial in people's thyroid health that way. And if we do have elevated antibodies to treat them, talked about that in previous podcast, you can go back there. So, hypothyroidism can lead to increased risks of cardiovascular events, elevated cholesterol, increased arterial sclerosis and heart attacks. It's believed to be a contributive factor in 60% of heart attacks. Why aren't we looking at this completely? A 2.2-fold increased risk of coronary artery disease and a 1.5-fold increased risk of death from heart disease. Estrogen? Many people don't realize too little estrogen can be bad for the heart. Well, too much can be too. But the appropriate level of estrogen leads to a dilation of blood vessels and reduced plaque. Also, reduce inflammation. Roots of therapy matters. You can overdoze via those estradiol patches or the pellets. The patches might say there's like what, 0.1 micrograms or something like that per patch or 0.1 milligrams. Which in fact, that's their measuring what goes into the serum, but they're not looking at metabolites. There's a lot more in that patch that they put in there to get their serum level. So, they're not looking at what's going on at tissue level. So, what happens is the body can be taken in a lot more. There could be milligrams and milligrams of estadial in those patches. Same thing with pellets. Oral form of estrogen can lead to inflammation, increased potential for clots, as well as nutrient depletion such as co-insum ketone, which is so important part. Dr. Robert Jastron, too little. Too little progesterone can lead to a low HDL. Remember, HDL's job is to come in and clean up what's left beyond. So, it doesn't oxidize and inflame. So, optimize progesterone for that. Appropriate progesterone helps you sleep, provides a calming effect. All these have benefits to cardiovascular health, right? Reduces risk of type 2 diabetes. Blood pressure supports estrogen's ability to dilate the blood vessels and reduce plaques. That's huge. Estrogen and progesterone always work together. You should never give estrogen without opposition of progesterone. Too much progesterone can actually influence type 2 diabetes. Let's talk about testosterone. So, too high of testosterone, which we generally see from medication therapy. Testosterone naturally can be in the high side due to stress. Cortisol, popping basically. It seems like there's this rampant issue of younger men in their 20s having low testosterone. And, you know, still trying to figure the whole thing out. Sometimes it is associated with low cortisol levels to be honest with you. In adrenal health. So, we do want to watch out on testosterone therapy. Don't overdose people. Don't even inappropriately give it to someone who doesn't need it yet. Let's look deeper. Let's look what's going on with the adrenal glands and everything. Two low levels of testosterone can lead to excess weight gain, decreased muscle mass, increased risk of insulin resistance. For women, testosterone without estrogen therapy can increase risk of heart disease. So, that's a good need to know as well. So, there you have it folks. What I wanted to provide to you was an overview of how we can test a little broader. So, we stop missing the boat on this heart disease thing. You know, getting caught up in this lipid, this only lipid approach, taking this beyond lipid approach, which is absolutely critical. So, love to hear from you. Reach out to me. [email protected]. You'll find me online, social media, Instagram and Twitter, RobcressFRX. You'll even find me on Facebook. FunctionalFarmacy. That's my website, FunctionalFarmacy.com. Got a lot of great stuff. There are a lot of great ways you can actually enhance your practice as well as courses with farm con and free CE to further expand your FunctionalFarmacy, Functional Medicine and the Pharmacy Knowledge and Database. So, I just want to thank you so much for tuning in. Yeah, and I will see you in the next podcast or we'll listen to each other. Take care. And for those of you looking to get CE's for this podcast, you can use the code heart health, H-E-A-R-T-H-E-A-L-T-H and capital letters over at freece.com.