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Breta Alstrom: looking at like cardiac markers as a whole. If you can just outline like what those cardiac markers are that are traditionally being assessed. And then we'll talk about what we're adding on and what we're actually looking at.

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Dr Doug: Yeah, great. So when we talk about well, I shouldn't say that when most doctors talk about cardiac markers, you pretty much only hear the word cholesterol.

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Dr Doug: All right. Can I get a show of hands? Be let up? Their video on how many people all we talk about is cholesterol

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Dr Doug: should be most people. This happened. I don't know when this started, what in the 19 fifties with Doctor Keyes and this big study of what's happening with heart disease, and the only thing they could find that fit their

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Dr Doug: their bias at the time was that dietary fat and cholesterol, increases the risk of heart disease, and therefore we must reduce cholesterol, reduce dietary, fat, and measure cholesterol, and then the pharmaceutical industry jumped on board, and then it's been all downhill from there.

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Dr Doug: So we have drugs that can reduce cholesterol. Therefore there are studies that show that reduction in cholesterol can have an impact. The question is, is it really a good biomarker.

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Dr Doug: How related is it to heart disease?

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Dr Doug: Should we be lowering cholesterol with drugs like statins or other drugs? And what other things should we be looking at. And this is a really really deep topic. And just so, you know, I'm obviously not a cardiologist. But I've studied this in depth because it is so related to this concept of longevity, this concept of healthy, aging concept of health optimization.

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Dr Doug: Because if we do the things that we talk about that help us to feel better, to help us to live better, hopefully longer. But it increases our risk of heart disease, which is the number one killer for both men and women. We didn't really do ourselves any favors right?

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Dr Doug: I get worried about when I hear influencers and doctor influencers on Youtube and Instagram talk about the idea that cholesterol doesn't matter at all. All. The cholesterol stuff is wrong, and it's a big scam, and it's all about the pharmaceutical industry. And I think that's taking it too far.

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Dr Doug: So let me just summarize, then, the things that we look at include cholesterol.

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Dr Doug: It is a risk factor. It is a biomarker we can measure, but it's not the most important one.

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Dr Doug: but it is one to consider other things that we're interested in are some of the biomarkers around cholesterol. So if you consider cholesterol.

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Dr Doug: the waxy substance that is carried around in your blood to help all your cells do things. The things that carry the cholesterol. The particles that carry the cholesterol are actually more important than the cholesterol itself.

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Dr Doug: Fun facts about cholesterol is that really there's no difference between Hdl and Ldl cholesterol. It's the same molecule. It's the particles that carry it around that make it unique. So Ldl has a different particle. HTL has a different particle. The cholesterol is the same, so the particles actually matter, and we can measure the particles to some extent certain proteins on the particles we can measure which can increase or decrease risk based on whether or not you have them or don't have them. Other biomarkers like, are you developing plaque? There's a biomarker for that.

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Dr Doug: Biomarkers for inflammation are really important here. Biomarkers for oxidative stress are important here. So you start stacking together all of these different things that you can look at, and then you can come up with a case to say, Well, this person that's eating a diet that's increasing their cholesterol. They have great looking arteries. They have no other risk factors. Maybe we don't care in that circumstance, but the opposite is true, too.

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Dr Doug: If you have arteries that are showing an increase in plaque development. You have increased inflammation. You have poor metabolic health, you have all these other things, then probably your cholesterol does matter. So we really have to look at the whole picture around these biomarkers of cardiovascular health. That was a long answer. Sorry.

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Breta Alstrom: No, we're here for the long answers so I I guess this brings up a good point just about the research in general. I think a really interesting concept, too, is like the French paradox. If anyone's familiar with that which is like this idea is that the French, you know, and whatever the French are eating, they have, like a considerably lower risk of like heart. Like heart disease, and they drink wine, they eat bread, they meet like it doesn't necessarily come across, as

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Breta Alstrom: maybe what we would consider like the ideal diet. But really, as you dive deeper and deeper into the research, and like how it's presented. The the actual numbers they looked at. I think people were just classified incorrectly and like there were so many people when they looked at like cardiac events, or like deaths from cardiac events that the!

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Breta Alstrom: They were just misclassified, like people. They weren't

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Breta Alstrom: marked correctly. And then also what mattered way more was actually proximity to a hospital.

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Breta Alstrom: So, looking at those things too, and so, you know, being

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Breta Alstrom: like utilizing the research, but then, being mindful about where things might not align. Especially cause nutrition. Research is still really really young, and it's new. And although a lot of

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Breta Alstrom: a lot of. We have a lot of really great data. There's a lot of places that are lacking, too. So this is a good question from Caitlin. Would you say that cholesterol only matters in the presence of metabolic dysfunction.

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Dr Doug: Hmm.

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Dr Doug: yeah, that's that's the the

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Dr Doug: that's the line that you hear from the carnivore community people that are into eating a lot of saturated fat, regardless of genetics. They'll say that as long as your metabolic health is good, cholesterol doesn't matter.

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Dr Doug: There is evidence to support that claim. So you hear there's some really famous doctors in those communities who are citing evidence that support that. And I agree with that. But the challenge is like.

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Dr Doug: let's say you were a type 2 diabetic. For 30 years.

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Dr Doug: You have terrible cardiovascular health. Right? You have a 70% blockage in your coronary arteries. You go on a carnivore diet, and you improve your a 1 c to 5.4, and your glucose is perfect.

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Dr Doug: Does that mean that your cholesterol doesn't matter? Probably not. So you have to take it into context. So like, if you're, you know, let's use Kalin, for example, if you're very young, you've got great looking arteries. You don't have any other risk factors. You're eating a high-saturated fat diet, and your Ldl is 250. Is that a problem? Maybe not.

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Dr Doug: But we want to watch it closely. So this is where, like every person is different.

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Breta Alstrom: Yeah. And then on.

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Breta Alstrom: I think that brings up a really good point, too. Especially we go back to the research and a lot of things. It's we're gonna be looking at these massive population based studies. And when you're trying to find a common thread in a population that's actually probably not serving most people in the population. And so what's different with what we do is that we are diving really deep into stratifying risk. And we're looking at what you need individually to make the best choices for you, because what you need might be different than what Doctor Doug needs, or what I need or how that plays out.

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Breta Alstrom: You bring up a good point about the diabetic conversation as well, and a lot of times we feel like I think we pigeonhole vascular health into being like fats and cholesterol and things like that? But can you do a little bit of explanation on potentially how some of that carbohydrate metabolism can also impact vascular health.

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Dr Doug: Yeah. So we gosh, starting in the, it was 1976 when the 1st Food Guide pyramid came out, and I used to have this talk that I would do all the time that looked at obesity working with my wife's company. And I think it's funny that that food guide Pyramid came out in 1976, and I was born in 78. And you look at the like, the

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Dr Doug: the growth of obesity, and then following with it with diabetes that started in the late 19 seventies.

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Dr Doug: And if you think about that 1st food guide, pyramid, what was the big takeaway was reduced? Dietary fat.

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Dr Doug: reduce saturated fat, reduce cholesterol, eat whatever 12 servings of grains like whatever I don't even know right? But it was a very high carbohydrate low fat diet, and you saw the explosion of disease that came along with that.

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Dr Doug: What was interesting is that heart disease didn't immediately jump up.

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Dr Doug: but it did eventually follow. And what we've been able to see over the subsequent decades is that if you have poor metabolic health, then you're going to have a higher risk of heart disease. In fact, one of the biggest risk factors for having a cardiovascular event is being diabetic.

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Dr Doug: It's not cholesterol. It's being diabetic.

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Dr Doug: People that are diabetic. Have poor glucose metabolism by definition? Right? So diabetes means elevated, glucose, elevated insulin. All of those things are going to provoke plaque formation. So if you have the cholesterol problem, or even if you don't, you're still more likely, then what is it? What is it about glucose that does that? There's a lot of things here.

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Dr Doug: so glucose is a great molecule. I eat a relatively low carb diet, but I'm not a glucose hater, so I still eat carbohydrates. I encourage my patients to eat carbohydrates because carbohydrates in the form of the right foods

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Dr Doug: come with micronutrients, and as a macronutrient is a great source of energy. In fact, I consider it like jet fuel. If you look at the best athletes in the world, with some exception. But for the most part they're consuming a higher carbohydrate diet, because it is a better fuel for burning energy. Faster.

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Dr Doug: however, it is not a very clean, burning fuel, so I kind of think of it as like. This isn't a great example, but like burning Diesel versus gasoline, like Diesel is kind of like a dirty fuel. Right? So I look at carbohydrates as kind of a dirty fuel.

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Dr Doug: burning dietary, fat, or the other way burning stored energy as fat adiposity, energy in the adipocytes so burning that type of fat is going to burn very cleanly through your mitochondria versus burning glucose for fuel. So you get this sort of dirty fuel dirty burn. There's a lot of oxidative stress as a result of that, and your body has to clean that up.

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Dr Doug: Additionally, if you can't tolerate the glucose that's coming in. Then you get elevated levels of glucose. And that's when the train really goes off the rails.

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Dr Doug: So elevated glucose causes things like glycation, which is essentially glucose attaching to stuff and glucose can attach to things. It'll provoke them to not work as well get more rigid. They don't function well. And then, as glucose continues to start to climb. Insulin will start to climb. Insulin is a growth hormone. Essentially so. If you were to give somebody a lot of insulin, their blood sugar would come down. But give them enough blood, sugar, and things will start to get bigger like. There's bodybuilders that use insulin to grow. Terrible idea don't do that.

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Dr Doug: but you can use it as a growth, as a growth factor. And so if you imagine, like what's happening in obesity in a lot of people. It's this elevated insulin that starts to rise. It essentially shuts off fat burning because the fat cells feel like

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Dr Doug: they're all full of energy. Your body's full of energy, because there's a lot of insulin as a signaling molecule, and then everything needs glucose. You become glucose, dependent. Everything starts burning this dirty fuel. And then it's just this downward spiral of metabolic dysfunction that ends up with inflammation, oxidative stress, and all the stuff that goes along with that so glucose burning is not bad inherently, but glucose, as the only fuel and glucose out of control becomes very

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Dr Doug: dangerous, and that essentially is diabetes.

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Breta Alstrom: Yeah, I think you can also connect it a little bit, too, to like the idea of like, we all know that high blood pressure isn't necessarily ideal for our heart health and that pressure, like you, can only put so much stuff in your blood, and you can only put so many sugar molecules. You can only put so many insulin molecules. And it's gonna put pressure on those walls of your arteries. And that's gonna cause damage to. So just we're gonna talk a lot more about fats today. But just know that carbohydrates play a role in this conversation as well.

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Breta Alstrom: to circle back to some of the markers that we're looking at, and there's a ton of questions in the chat on imaging we're gonna get to some imaging studies a little bit later, too. So keep asking those questions. But can we talk about the use of Apo B as a cardiac.

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Dr Doug: Yeah. So I just had a great question. Gosh, who asked me that this morning?

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Dr Doug: That was one of our coaches. We were talking about somebody who was concerned about their Ldl cholesterol. Right? And so this just feeds perfectly into this.

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Dr Doug: So Apo B is a protein that lives on the surface of an Ldl particle.

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Dr Doug: This, this, like nomenclature, gets really confusing, really fast.

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Dr Doug: So I'm going to try to make it as clear as possible. But I still want to use the right terms. So apob is a protein. And these particles, these balls that carry cholesterol are essentially just. It's a ball of protein. Imagine, like a tennis ball that's just made out of protein.

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Dr Doug: one of the proteins that defines an Ldl cholesterol-containing particle is called apoe. So, instead of measuring your Ldl cholesterol, which is essentially you draw the blood, you split all the particles, and you measure the amount of cholesterol in the blood. You're actually looking for the number of Apo B proteins which tells us about the number of particles in the blood. It's a better biomarker, because if you look at studies on Ldl. Cholesterol versus

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Dr Doug: is Apo. B. Ldl. Cholesterol is not very telling of events. In fact, 50 of heart attacks occur in people that have normal Ldl. Cholesterol.

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Dr Doug: And by normal I mean actually pretty darn low.

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Dr Doug: So Ldl is not strongly associated with events. Reductions in Ldl through statins. Different conversation. But Apo. B. Is a better biomarker for looking at events. So if your apob is elevated plus or minus Ldl cholesterol, if your Apo. B. Is elevated, that is going to be more predictive of having an event. You still have to consider all the other factors, but it's a better biomarker. So I'll give you an example. So let's say.

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Dr Doug: somebody goes on, and I've seen this is interesting. I can't quote a study here, but I've seen this a couple of times.

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Dr Doug: Let's say somebody chooses to do either a saturated fat reduction or a reduction of mostly animal products, and they end up eating a lower dietary. Fat, higher, carbohydrate diet.

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Dr Doug: and their cholesterol goes down

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Dr Doug: great. So now their cardiologist is happy, their primary care doctor is happy, and they're maybe avoided going on a statin. If that was their goal. But look at all the other details. So what happens when you do? That is, your Ldl. Will come down sometimes your Apo. B. Actually goes up.

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Dr Doug: So what does that mean? It means that you have more particles carrying around less cholesterol. So if you think of this as the size of the particle and the size matters. So imagine

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Dr Doug: if you have these balls carrying around cholesterol.

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Dr Doug: if you have a bunch of volleyballs carrying around a whole lot of cholesterol versus, let's say, like a tennis ball.

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Dr Doug: much smaller, carrying around, much less cholesterol, the smaller the particle, the more dangerous they are. So

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Dr Doug: you could see a reduction in Ldl cholesterol, an increase in the number of particles. You have less cholesterol in more particles. They're going to be smaller. You can actually measure the size of the particles through a certain test called an Nmr. We used to do that test. But what we found is that different labs measure it differently, so it's hard to compare.

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Dr Doug: So we just use the Apoe and the Ldl Cholesterol then, and we can look at the shift. So if Ldl went up, but Apob went up as well, and they went up equivalently. If you were to do an analysis of the amount that they went up, then we know that the risk probably hasn't really changed that much. This becomes really important. We talk about dietary fat. So it's a really cool biomarker in that way.

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Breta Alstrom: Yeah. And then on the I think one of the other things that we're looking at, too, is, well, actually, I just wanna make sure, I think we might have removed it. Okay, yeah. So not

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Breta Alstrom: let me just get clear here on Lp, little, a marker that most people aren't looking at I don't think in traditional healthcare, so can you talk a little bit more about that? And then we have some good questions around that, too. So if you want to start there, and awesome.

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Dr Doug: Yeah. So so when I say Apo, B, where it is a lipoprotein, but it's called apo, B. And when we say lp, little, a. The Lp stands for lipoprotein. And again, this nomenclature like, if we could go back a couple of decades and like, let's rename these things that would have been very helpful.

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Dr Doug: But anyway, we're talking about lipoprotein little, A or LP, little, a LP, little A is another protein, so we could really call them like protein A and protein B. It'd probably be a little easier. But LP, little a is a protein that is not present on every

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Dr Doug: Apo. B. Containing particle. It is present on some of them. And this is a genetic risk factor, meaning that we don't know where the Snp is or the actual gene code, for it is, but we know that it's passed down in your family or not. So people that have a high level of LP little A are at higher risk of developing plaque and subsequent disease and events than are people that don't. So there is a specific threshold marker, and it depends on the lab that you get the lab from.

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Dr Doug: but if you are below that threshold, then you do not carry that risk. If you are above that threshold, you do carry that risk. So what does that mean? Well, it means that we need to consider this as one of the many cardiovascular risk factors. We see that people that have this LP, little a risk factor a lot of times when you ask them about their family history of cardiovascular disease are like, Oh, yeah. My dad had a heart attack at 46 my mom died of a heart attack at 60, so it becomes very clear that they're going to be at higher risk than somebody that doesn't have that.

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Breta Alstrom: Yeah, and yeah, I did post our, the our cardiac panel in the chat here. And yes, I will post that to slack as well for those who are asking, so on. Let me get back up to my Lp level a question.

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Breta Alstrom: How does elevated LP, little a play into the metabolic markers. Can you have great metabolic markers in elevated LP, little, A,

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Breta Alstrom: and what?

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Breta Alstrom: Well, yeah, we'll start there. Can you have those markers and also an elevated upload.

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Dr Doug: Yeah, totally unrelated. So if you were to, let's go on a six-month carbohydrate Bender and develop prediabetes, which is totally possible. So if you were to do that, your Lp. Little a. Wouldn't change.

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Dr Doug: You can do pretty much anything you want. Your LP, little A is not going to change. People get frustrated because we don't repeat it, and they're like, Well, I want to know if my LP little a. Went down. But it's not going to change, even if it did so. For example, taking large doses of niacin will reduce LP little, a being on a Pcs canine inhibitor drug conversation that will reduce LP, little a. But there's no evidence that reducing LP, little A actually has any impact on outcomes.

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Dr Doug: So we don't repeat it, because I just want to know if you have the risk factor, and if you do, we take it into consideration, and if you don't, we take that into consideration.

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Breta Alstrom: Speaking of that consideration like, what particular markers would you be looking at if somebody did have like? If say, they had great lipids, but they do have an lp like an elevated lp. Delay! What additional steps are you taking.

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Dr Doug: Yeah, that pushes us down the the imaging pathway. So whenever you want to talk about that.

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Breta Alstrom: Yeah, I wanna before we get to imaging here, I do wanna spend a little bit of time talking about the value of cholesterol as well, and how like, where cholesterol comes from. So I know you mentioned that cholesterol can come from different foods that we eat. There's some foods that contain cholesterol in them. We'd no longer like on the dietary guidelines. They no longer recommend restricting cholesterol, but still something, I think, a lot of people pay attention to, but pretty much if it comes from an animal product.

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Breta Alstrom: then it's gonna have some cholesterol in it. However, for most people, most cholesterol is being produced internally. But on the flip side of that, what are you looking at? If somebody is like a

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Breta Alstrom: maybe they are like a hyper absorber of cholesterol. What are their options there, and are they worth it?

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Dr Doug: Yeah. Well, let me define that for a second. So if you look at the literature from my perspective, and it's kind of fun to have right here because she reads more nutrition literature. I don't read that much nutrition literature. So from my perspective, from a cholesterol, heart disease, perspective, the recommendations to eat a reduced cholesterol diet have sort of gone by the wayside.

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Dr Doug: because dietary cholesterol is very poorly associated with serum cholesterol, or cholesterol in your blood, meaning that I could eat 100 eggs, and my blood cholesterol is unlikely to change. Maybe not at that extreme.

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Dr Doug: pretty much unlikely to change. Part of that comes in your ability of your gut to absorb cholesterol versus excrete cholesterol.

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Dr Doug: So what's really interesting about the cholesterol cycle is that cholesterol is recycled in your gut regularly. Your body needs cholesterol. So like Brett said, cholesterol is actually a really important molecule, so cholesterol is the foundation of vitamin d Cholesterol is the foundation of estrogen, of Progesterone, of Dhea, of pregnant alone, of testosterone. Right? So testosterone is a building block of all of your sex hormones, I think almost probably all of your hormones to some extent, but definitely, your sex hormones.

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Dr Doug: It is the wall of most of your cells are made of cholesterol, so cholesterol is not a bad molecule. In fact, if we didn't have cholesterol we would be a puddle on the floor. Cholesterol is that important

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Dr Doug: the challenge around cholesterol is, how much is made in the cells? If we were to remove it completely from your bloodstream.

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Dr Doug: would it actually have a negative impact? And this is where drugs like Pcsk. 9 s. Rapatha come into play because they will essentially eliminate Ldl cholesterol from your blood at the right dose.

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Dr Doug: Is that bad. Some people say Yes, some people say no.

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Dr Doug: Then going back to the question of hyperabsorbers people that absorb too much. This is a really interesting point, because there is a genetic difference between people that absorb reabsorb and absorb cholesterol

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Dr Doug: versus those that are going to put it in their gut, and then excrete it out through their stool

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Dr Doug: again. This is genetic. We can test this. And so I happen to be, and I don't know what the percentage is. I don't know if we know those numbers, Bretta, but some percentage of the population will hyperabsorb or increase absorption of dietary, cholesterol, and reabsorb cholesterol so i'm a hyperabsorber

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Dr Doug: for us. My cholesterol doesn't necessarily go up. If I eat more cholesterol it would go up if I ate more plant sterols, which a confusing topic for a lot of people. But what makes this really compelling to know is that you then become a potential patient with a target for a cholesterol blocking drug. So something like Zetia or a Zetami, which doesn't work well in the general population. But for people that are hyper absorbers, I can reduce my total cholesterol by 100 points, taking Zetia.

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Dr Doug: So if I wanted to reduce my cholesterol, that's the tool I would use rather than a statin, so knowing that can be really helpful, but I still don't think that it's going to increase, and maybe the nutrition literature is different bread. But I don't think that it's even knowing that you're going to increase your serum cholesterol, your blood cholesterol by consuming more dietary cholesterol.

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Breta Alstrom: Yeah, not not generally. Most of that is coming from your liver, and some people like, but it

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Breta Alstrom: there. These are more like rare cases where people are like hyper producers, so like some people produce, you know.

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Breta Alstrom: a lot which would be like, Oh, hey! Your cholesterol, slightly elevated, maybe won't have a conversation about a statin, and there's some people that produce like an insane amount like they're in the thousands for their cholesterol. But those are gonna be really rare cardiac conditions. So not too big of an issue there, but on

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Breta Alstrom: that topic of cholesterol. Yeah, like every

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Breta Alstrom: everything is built with cholesterol. So we need it. And so if you're one of those people that you're like, oh, my cholesterol is amazing. And it's really, really low. That's actually not something not to create extra stress for anybody. But it's not something we maybe don't celebrate as much. And we actually want to be investigating. Why is your cholesterol that low? Because, as Doctor Doug mentioned, it's gonna impact your hormone synthesis. It's gonna impact all of the things that we use to

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Breta Alstrom: to build with cholesterol. So do you have any tips on, or just any perspectives on, that component, on people who have extremely low cholesterol.

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Dr Doug: Yeah, a big dietary. I'm sorry, a big genetic component here. So we see people that come in with these remarkable lipid panels. I'm like, are you sure you're not on a statin because somebody's slipping a statin into your breakfast? Because your Ldl is 60 and your hdl is 60? I'm like, wow! I'm jealous of your lipid profile. But if you look at the research on cholesterol levels, actually

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Dr Doug: U, right? So at the far ends of having too much cholesterol. I guess it's a u. Not an inverse U, but at the far end of having too much cholesterol. Your risk of event goes up so risk of having a cardiac event goes up. But the same thing's true on the low end. So the lower your cholesterol actually again increased risk.

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Dr Doug: But you see this in people who are unwell. So if you follow people especially, this is like the anti-aging literature, the longevity, literature. As you follow people as they age, cholesterol levels will start to drop when they start to get sick with chronic diseases that are eventually going to kill them. So people that have a cancer diagnosis.

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Dr Doug: Cholesterol levels drop people that have chronic respiratory disease. Cholesterol levels drop. This is sort of the body kind of like wrapping things up. And so that's why I think low cholesterol is more strongly associated with death.

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Dr Doug: Is it because it is associated with disease? So it's not necessarily good to have low cholesterol. But if you've genetically always had low cholesterol, I don't think that necessarily puts you in that same group, and that's where understanding

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Dr Doug: a big study showing that low cholesterol could potentially be dangerous. Doesn't mean that if you have low cholesterol that you're going to die in the next 5 years, so you really have to understand where that data is coming from, and who the population is that they're talking about.

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Breta Alstrom: Awesome. So then, I think we bridge over into a little bit more of saturated fats from here, because that is generally what most people. They've been recommended by their cardiologist to recommend cholesterol at this point is reducing saturated fat. But most of you guys know we're preferring people to eat animal protein which is the primary source of saturated fat. For most people there's only plant based sources of saturated fats.

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Breta Alstrom: But how are we considering that in the conversation, and then I can follow that up with some things that I've shared in chronometer that I've shared in you wanna just start with the saturated fat conversation.

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Dr Doug: Yeah. So gosh! Saturated fat has been vilified for a long time, and it's because saturated fat often comes along with sources of cholesterol. I think that's where this started. So again, go back to Ansel Keys. What was the solution from the 7 country study? That is another conversation. But the answer was, reduce saturated fat. Reduce dietary fat, reduce cholesterol

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Dr Doug: over time when people in the nutrition world started realizing, like man a really high carbohydrate diet seems to be having some negative impact. We need to probably increase dietary fat. They were still like Whoa, but not saturated, fat, saturated fat is very bad.

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Dr Doug: Still, without really much compelling evidence. And so we started increasing dietary fat. We started talking. This is where the seed oils, the vegetable oils came in. That's why olive oil and avocado oil, which I like are more popular because they are different types of fat than saturated fat, still saturated fat is vilified, and there's associations of saturated fat with cardiovascular disease. When you look at this from a very

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Dr Doug: person by person unique, independent perspective, and we again used to do a lot of genetics, and we don't do as much now. But when you do a lot of genetics there are genetic variations that in theory don't do well with saturated fat, the most common one, the most well-known one, is called apoe status or apoe.

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Dr Doug: So there is a version of Apoe. The risk, the high risk version is apoe 4. And people that have this specific genetic variant in theory don't do well with saturated fat. So we used to in practice. Say, if you have apoe 4, we're going to severely restrict your saturated fat to limit your risk.

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Dr Doug: I've looked at the evidence on this.

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Dr Doug: It's compelling, but not convincing. So we've trialed it for people. We've had people that we've followed for this, and some people still choose to, because again, the evidence is compelling.

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Dr Doug: And some of these things are hard to measure, and they're very worried about dementia risk as well. And dementia risk is harder to measure than cardiovascular risk. So some people choose to stay that way.

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Dr Doug: We have, as we've especially been developing and pushing the bone health program.

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Dr Doug: we've been pushing more protein, more animal protein, which is more saturated fat. And now we're having this conversation more and more when we see aberrations in lipids. So we see Ldl cholesterol go up. So what do we do now? Well, we can trial a saturated fat reduction. But what we're finding is it's not very impressive.

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Dr Doug: So while in theory reducing saturated fat and maintaining your dietary fat, otherwise, could reduce your cholesterol. We're not finding it to be particularly compelling, and it is pretty darn restrictive, because now you're getting away from what is, from my opinion, the tastier cuts of red meat to eat a lower saturated fat cut of red meat, or potentially avoiding red meat altogether. But then you're eating less nutrient dense, like poultry and fish.

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Dr Doug: and so it just starts to erode at the quality of the diet. So then we will help people to add it back, and then we follow their lipids, and then we can talk about what we do from there. But that's sort of the saturated fat story in like saga, as it's panned out over the last decade in my practice and in my life.

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Breta Alstrom: Yeah, I think a lot of that comes down to, you know, if cardiac

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Breta Alstrom: events are something that you're worried about and deciding. You know how much you wanna learn about your body, because we'll talk about imaging in just a second. But there's definitely opportunities there to like further stratify risk, which is something we spend a lot of time doing with our patients.

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Breta Alstrom: And then in you know, I've I've looked at a lot of chronometer data and most people that we're looking at on saturated fats. And in that reduction

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Breta Alstrom: the cool thing. And I, I posted a video in the nutrition channel there, and I might have pinned it on the canvas. But, you can see a lot of the the saturated fats that are pushing you over are generally not coming from that whole foods diet, even if you are gonna be eating, you know some of those red meats or higher protein diet. So most of it when I've reviewed stuff with people is actually coming from. You know, the time that we stop at

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Breta Alstrom: Chick-fil-a, or you know, we're stopping out for for fast food and cutting that one thing for that day. It keeps them under their levels that we would recommend for that. And that's going to be based on, you know, the only time

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Breta Alstrom: we're ever seeing, like a saturated fat restriction is if they potentially have the genetic component. For, like Apoe.

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Breta Alstrom: like an apoe. 44. We might be looking at that. But again, we can stratify risk in other ways, and some people find that more important to reduce saturated fats than other people. So it's definitely a personal decision with your healthcare team guidance. But there's for the most part it's not necessarily coming from that whole foods diet that you're eating, unless you're pipelining coconut oil. And that's like a whole other conversation that should not be your 1st line choice for fats. If you're worried about saturated fats. But

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Breta Alstrom: some good questions. Here is apoe the snip, for how quickly you use. Mk, 7.

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Breta Alstrom: I don't believe so.

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Dr Doug: Yeah, I wouldn't. I wouldn't change.

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Dr Doug: So we don't have enough data for Apoe specifically to talk about. Are we going to update our supplement stack around Vitamin K. There's some other things that you could potentially do there, but it wouldn't necessarily change that. The things that we do around Apoe probably we could do in another topic, because it's a full thing in and of itself.

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Breta Alstrom: Yeah.

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Breta Alstrom: awesome. We'll we'll dive into that. And then just so you guys know, if you guys want some genetic testing within the next week or so, we're gonna be able to offer that you guys to order. So just send me a message on slack. Just a personal message. If that's something you're interested in, and then we'll kind of live launch like a little beta test. But you'll be able to get our full genetics panel. So you guys can have some of the data that you're looking for here. I know I've had a couple of people

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Breta Alstrom: in that. So these things will be there. Okay? So then let's talk about just a few more community questions here on

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Breta Alstrom: some of the biomarkers before we get to imaging. How do you reduce small Ldl particles and increase the large Ldl particles.

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Dr Doug: Yeah, kind of a.

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Dr Doug: We don't have a great answer to that other than it's lifestyle driven. So we see small Ldl particles when you have increased levels of inflammation when you have poor metabolic health, if you have increased insulin, increased a 1 c increased oxidative stress, poor sleep. Basically all the things that are bad for you will provoke small Ldl particles smoking. All these things are associated. And I think it's because

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Dr Doug: it's this weird shift in the body, where, when it's exposed to a lot of bad things, all the bad things pop up. So basically, all the lifestyle stuff that you would want to do like for your bone health, or for longevity. All those things are going to likely push you in the direction of having bigger fluffier particles.

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Breta Alstrom: Yeah. And then what about the ratio of Hdl to Ldl to total cholesterol? All the things.

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Dr Doug: Yeah. So the ratio question has been in play for a long time.

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Dr Doug: Early on again going back into the fifties. All they had at that time was total cholesterol. We know total cholesterol is a terrible biomarker. The only way that Ansel Keys could even find an association was by eliminating countries that didn't fit his bias. So that's the details of the 7 country study. But when you start to break down cholesterol, then you do actually see some of the associations. That's where Ldl and Hdl come in.

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Dr Doug: And so if you look at the 3 primary breakdown products of total cholesterol, you have Ldl, the quote-unquote, bad cholesterol, hdl, the quote-unquote, good cholesterol, and then Triglycerides, which is essentially fat, being carried around in the bloodstream.

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Dr Doug: The original data said, let's just look at Ldl.

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Dr Doug: and that was all that data. And then Hdl started to become the good risk factor because we found that people, that we

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Dr Doug: they found that people that had higher levels of HTL. And this number has changed over time. But like over 30 was good. And then it's over 50. And now we say 60, and then some people say, Oh, it should be 100. But Hdl is associate. High levels of Hdl. Is associated with better health

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Dr Doug: or lower risk, I should say.

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Dr Doug: But what you can see now, as you start to break this down is that you can look at Hdl to total cholesterol. You can look at Hdl to Ldl Cholesterol. Most important one, and I think has the best data to support. It is the Hdl to Triglyceride. So this sort of excludes Ldl altogether, and the reason why you do that is that Triglycerides, even though it is fat, being carried around in the bloodstream

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Dr Doug: Triglyceride, is really a marker of carbohydrate metabolism.

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Dr Doug: Hdl is a marker of metabolic health. And so when you look in an Hdl to triglyceride ratio, then you're looking at metabolic health.

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Dr Doug: And this is where that conversation that Kayla mentioned earlier. If your metabolic health is in check, does Ldl matter. So I'll just give an example. So let's say someone's Hdl is 80, and their triglycerides are just call it 80 to make it simple. So they have a ratio of one, and their Ldl. Is 200.

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Dr Doug: Am I concerned about their Ldl.

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Dr Doug: Not as much as if they had low Hdl. And high Triglyceride.

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Dr Doug: We know that those people that have sorry, Hdl. Of 20 so low hdl triglyceride of 300 and an Ldl. Of 100 are at much higher risk than the 1st person that I just demonstrated, because their metabolic health is in question.

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Breta Alstrom: Sleeping with

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Breta Alstrom: awesome. So just wanna wrap up something at the that was asked at the beginning, just to make sure that we have clarity here. So if somebody has a family history,

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Breta Alstrom: do we need to be doing something to manage and counter this? And if your liver is just making a bunch of cholesterol. Is there anything that you can actually do for that.

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Dr Doug: So family history of high cholesterol. I'm not as concerned as family history, of heart disease and events.

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Dr Doug: I'm a great example. I have a family history of high cholesterol. I have high cholesterol. My dad had a heart attack at whatever 58, so I'm more concerned about his heart attack than I am about his high cholesterol.

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Dr Doug: He also weighs 350 pounds. So different metabolic question there.

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Dr Doug: But the family history of risk is much more strongly associated with your own risk than is the cholesterol. Because we see lots of people with high cholesterol that don't have events.

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Dr Doug: So it's something to consider, because if somebody, let's say both my parents had high cholesterol, I have high cholesterol. I'm going to whatever go on a Vegan diet to reduce my cholesterol. How much is it actually going to go down?

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Dr Doug: Probably not that much. It would go down, but not as much as someone who had a lower level or less family history, of having higher cholesterol levels.

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Breta Alstrom: Yeah.

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Breta Alstrom: awesome. I think that's helpful. And now I wanna I do wanna switch gears into some of the imaging. So 2 of the things that we'll do. Do some more than others, but a Cac and a Cct, so could we just start with the cac in those. So which is a coronary artery calcium score. How are we using this? What is it? What's the.

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Dr Doug: Yeah, let me just hit like hit the big players here because we we get there's a lot of confusion around this.

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Dr Doug: So the 2 major tests that we talk about are the coronary artery, calcium score, which we'll just call CAC versus the Ccta, which is the coronary Ct

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Dr Doug: angiogram coronary ct, angiogram ccta. So those are the 2 major things other things that people talk about, they say. Well, I want to get an echo. I want to get an Ekg, I want to get an ultrasound of my carotid arteries.

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Dr Doug: So all of those things tell us data. But I don't rely on Ekg, because that's only looking at the rhythm of the electrical circuits of your heart. So unless you are actively having a heart attack or worried about some kind of an electrical event, a weird rhythm, or whatever. That's when you get an Ekg, it's not. Gonna tell me about your risk.

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Dr Doug: What was that? The one I mentioned. Oh, stress test. I don't know if I mentioned that, but I hear this all the time. My cardiologist ordered a stress test because I was concerned about my cardiovascular health.

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Dr Doug: I can't say that everybody here would pass a stress test, but I can tell by looking at people pretty quickly whether or not they're going to pass a stress test. A stress test is only going to be positive. If you have significant stenosis or narrowing of one of the arteries that feeds blood to your heart. So we're talking like 70 80%, something would be considered a critical stenosis. So what the cardiologists are looking at is is there an indication here for a procedure

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Dr Doug: meaning like, does this person need a Stent? Does this person need an operation? This is not what we're looking for because anybody that's in that category they're already. I could probably already identify that they're at high risk. Right? So like stress test pretty much never answers my question. So we don't rely on that

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Dr Doug: carotid ultrasound provides some information. It feels easier because it's an ultrasound. There's no radiation. It's cheaper. But the problem is, we don't have as good information of what to do with the test of the carotids as we do with the test of the coronary arteries, and they also sound similar, which is really confusing for people. So while I will look at data from the carotid arteries, I still want to know what's going on in the heart.

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Dr Doug: So then we get to the heart test. So the true heart test, the Cac and the Ccta, the Cac. We generally will get first, st because it is cheaper, it's easier. There's lower radiation insurance still, plus or minus may not cover it, but even if they don't cover it, it is not terribly expensive, generally like 200 to $300 should be less than $100. But

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Dr Doug: insurances, health care whatever.

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Dr Doug: So the Cac. Tells us. If you have calcification of the plaque in your arteries, assuming that you have any.

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Dr Doug: this is really telling, because we know that it takes decades generally to develop plaque. It takes more time than to calcify that plaque. That's part of the healing process of developing plaque in those arteries. So if you were, let's just use an example of a woman who is 60 years old. She's 10 years out from menopause

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Dr Doug: talking about using Hrt. We want to know what her cardiovascular risk. Looks like we're going to look at her biomarkers. We're going to ask about her family. But then we're going to consider getting imaging. In that imaging. We would start with a cac. If the Cac. Comes back positive, meaning any number other than 0. That means she has calcification of plaque in her arteries. That means that she's been developing plaque for at least a decade or more.

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Dr Doug: That would be a potentially a red flag, maybe like an orange flag. To say, this individual might be at higher risk than somebody that had a level of 0 on a coronary calcium score. So it helps us to identify longstanding, calcified plaque

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Dr Doug: which would be great if that's all that we worried about. But it's not

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Dr Doug: so actually that plaque is not the plaque that I'm most worried about the plaque that I'm most worried about is the soft, uncalcified plaque which has likely been there for not as long, and is actually a bigger risk for developing an event.

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Dr Doug: So when Cac got very popular, I don't know. Maybe 15 years ago, everybody was ordering Cac and the longevity health space. And then you started hearing these stories of like a Marathon runner, a guy and is 50 years old, had a 0 cac. And then had a heart attack the next day. How could that be? And it's because it's the soft plaque that actually is the plaque that's going to rupture and provoke a heart attack.

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Dr Doug: You can't see that on Cac, but you can see it on what's called Ccta. So Ccta. And then the version we use has an additional add-on algorithm software program that runs

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Dr Doug: on top of it tells us about the soft plaque, and it tells us about the amount of narrowing to a very, very significant, tiny degree. So like, for example, I have a 6% stenosis in one of the arteries of my heart.

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Dr Doug: so that would not have shown up on any other test, but it tells me that I have some plaque, but it also tells me that I don't have much plaque, and I've had high cholesterol my entire life, and my father had a heart attack. So it actually did change the way that I treat myself.

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Dr Doug: And we use the same data in patients. So let's go back to that sixty-year-old patient. She has a cac. Let's say it's you know, whatever it's 15, or even if it's 0. And she says, Gosh, but I have a family history. I'm worried about it. Okay, let's get a Ccta. She gets the Ccta. And let's say she has a 30% stenosis. She has a lot of unstable looking plaque. Is this a person? I'm going to put on estrogen? Probably not.

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Dr Doug: We wouldn't have known that

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Dr Doug: unless we did that test. Not everybody wants to do that test, because that test is more expensive. Insurance might cover part of it, but it's at least a thousand dollars, and it could potentially be $4,000. And that's the challenges in our system that we have to deal with. But the data is extremely valuable if you can get it.

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Breta Alstrom: So just to clarify somebody has a cap of 0. When would you recommend they would get a Cct. If at all.

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Dr Doug: Yeah, this is such a challenging question, because it honestly just depends on resources. So like, if you have a Cac, that's 0.

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Dr Doug: And you have $4,000 you can spend to get more information, I'd like to know.

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Dr Doug: But I can't make that call. So basically, a patient gets a Cac. It's 0.

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Dr Doug: The follow-up is man. I'd love to see a Ccta. It's probably not going to change what I do, meaning that generally, if somebody, let's say, use that sixty-year-old, for example, she has a Cac. That's 0. Would I make her get a Ccta before I prescribe estrogen? No, because her statistically her increased risk is extremely low and actually potentially not even there. So it wouldn't stop me from prescribing for her. But I'll say, look.

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Dr Doug: we might not know about soft plaque. You might have some risk here that's not been uncovered. If you're okay with the expense I would recommend going down this pathway. If her answer is, I just can't afford that right now. It's not a priority for me right now. It's not going to stop what we do, but I still generally would recommend it, and if I could wave a magic wand, say this to every patient, if I could wave a magic wand and get that data, I would get that data in a second.

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Breta Alstrom: Yeah.

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Breta Alstrom: Sorry. Just cleaning up some of the chat questions here. A couple of really good ones from the beginning. How often in a population over 65 do you find cac. Scores 0. But stenosis on Ccta.

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Dr Doug: But I don't have enough data here to say confidently that we would see it very often. My thought is that you wouldn't see it very often.

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Dr Doug: but I've never seen a big study looking at this, and we just don't have enough patience for me to say with any certainty what that would be. I've seen it. I don't see it very often.

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Breta Alstrom: Another great question, since we're talking about Hrt. And I know that obviously like this question is important for everyone because of longevity. Most people in our practice, though, have a lot of these significant questions, and are going through imaging studies to see if they're a good fit for Hrt. But how long after menopause would

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Breta Alstrom: where they

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Breta Alstrom: let me? Would you be concerned about estrogen and heart health like? How long without estrogen, would be a concern that you would really be pushing this versus like, if or and would it vary if somebody was maybe in menopause and wanting to start? Hrt.

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Dr Doug: Yeah, it does vary.

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Dr Doug: And we've had to really look at this in a lot of depth, because our patient population in general is women that are 10 to 20 years out from menopause. If you were to look at our average age, this is our average patient.

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Dr Doug: and the reason for that is, that most of these women have gone through menopause have either not been offered Hrt. Or refused it, for whatever reason, and didn't do anything about their bone likely hadn't been screened, and they lost a tremendous amount of bone. And now they have osteoporosis, and they're 60 years old, so it's a very easy pathway to go down if you're not aware of it. So we've looked at this in a lot of depth, because when I was trained I was trained in I don't know. It was

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Dr Doug: forward thinking, but still stuck in some of the traditional dogma which is a woman's 10 years after menopause. She doesn't need Hrt. And I hate that mindset because it avoids it just doesn't even consider all the benefits of all 3 of the sex hormones. If you're considering all 3 outside of the potential benefits for hot flashes and night sweats

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Dr Doug: right like it just ignores all of it, which is crazy even that because this was in like an anti-aging fellowship, you know, but it's it was an obgyn

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Dr Doug: dogma related thing.

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Dr Doug: So

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Dr Doug: from the estrogen perspective, from the cardiovascular risk, perspective, we can avoid all the other conversation. We just need to know what is the risk of me starting estrogen in a woman who is 60 years old 10 years out from menopause and then repeat that question for a woman who's 65, 70, 75, 80, even 85.

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Dr Doug: There's some great data. Actually, if you look at the recent twenty-year follow-up from the Whi.

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Dr Doug: there are multiple studies that have gone back and look at what's happened with the cohort of women that were on even. They weren't great forms of Hrt. But they were on Hrt. And they were older, to begin with. So the average age of the women and the combined

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Dr Doug: hormone group from the WHI was 66.

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Dr Doug: So we can look at data then from women that are in that 1st ten-year group, the 10 to Twenty-year group and the over 20 year group.

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Dr Doug: Again, I was trained over 10 years out. There's too much risk. It's not worth the benefit.

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Dr Doug: Even if that were true in our population that has osteoporosis, you could argue that that risk benefit ratio is different.

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Dr Doug: But the thing is when you look at the newer data, it's not true.

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Dr Doug: There was a cardiovascular protective

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Dr Doug: mechanism, even with the oral estrogen that they used.

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Dr Doug: But with that oral estrogen. If women started within that ten-year window, and some studies would say, the four-year window is the magic window. But even in 10 years, up to 10 years. It was protective

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Dr Doug: of heart disease, both development and events.

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Dr Doug: So that's obviously clear. But what was really interesting about this study is that the 10 to 20 Year Group there was no increased risk.

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Dr Doug: There was no longer a clear benefit.

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Dr Doug: but there was no increased risk. So when it comes to me, starting estrogen in a 60 five-year-old woman who's 15 years out from menopause. Statistically, there's no increased risk.

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Dr Doug: So why not? If she has osteoporosis.

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Dr Doug: and then we get into the individual variations over 20 years out, though over 20 years out, the risk does start to climb.

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Dr Doug: But we're still talking a very small amount, not statistically significant. Just a trend.

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Dr Doug: So for us, if we have a woman who's 70 years old, 75 years old, even 80 years old, I'll have the conversation. We'll go down the pathway. But the problem is, when you start getting to 30 years out 30 years without estrogen, they are likely going to have cardiovascular disease. They're likely going to have unfavorable biomarkers, metabolic dysfunction, etc. So then, we start to say, look, this is probably not the right pathway. Here, but we've had multiple patients well into their seventies. Have a ccta that looks better than mine.

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Dr Doug: so would I deny her estrogen because she's in her mid seventies. No, no way.

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Dr Doug: So that's why this process is so different than the oh, well, you're 60 years out. You don't need it.

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Dr Doug: Just such a different mindset.

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Breta Alstrom: Yeah. And then, just due to time, I have one last question and guys, if we didn't, we'll

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Breta Alstrom: we'll take a couple of questions from the audience after this last question, but if you have other questions, drop them in the live session, follow up in slack, and we'll get to them there. One, I think of the biggest things is, if you have done a Cct.

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Breta Alstrom: And you have soft plaque, can you reduce that soft plaque.

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Dr Doug: Yeah. So the answer from the preventive cardiologist would be, yes.

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Dr Doug: the challenge is with what? And so there's some evidence to say that vitamin K can have an impact here. So like K, 2 is mk, 7. There's some studies on that. I'd love to look deeper at what they were actually measuring.

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Dr Doug: There are advocates for plant-based diets would say that you can reverse plaque with a plant-based diet. If you reduce cholesterol, you could do the same thing with statins, Pcsk. Inhibitors, etc. But the question I have is, so are you?

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Dr Doug: Are you reducing the plaque? Are you just remodeling the plaque? Are you calcifying old plaque. I think there's a lot of stuff in here that we don't know. It sounds great to reduce plaque. I don't know that that should necessarily be our goal, though. But again, I'm not a

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Dr Doug: I don't know. There's I did an interview.

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Dr Doug: I'm blanking on his name.

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Dr Doug: It'll come to me in a second, with an integration.

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Breta Alstrom: Just fine.

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Dr Doug: Yeah. Yeah. So Michael Twyman. So I did an interview with Michael Twyman. And if you're really interested in this stuff, check out his Youtube channel. He does live Instagram, I think, every day. So he just loves this. It is his bread and butter. So if you want to follow Michael Twyman. It would be a cool follow to just really dig into this stuff because he's just such an advocate for this type of information.

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Breta Alstrom: Okay, well, that's the end of the questions I'm gonna ask. So again, if your questions didn't get answered, specifically, if there's specific numbers for yourself. We really can't answer a ton of like specific healthcare questions in this platform.

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Breta Alstrom: But if you guys have questions, put those in the live session. Follow up for today in slack, and then I'll just open the floor up if anybody wants to to raise their hand, and I see a hand raised. Shelley, if you want to pop on and ask your question. Unmute yourself. You're not, maybe not muted. But yeah, go ahead, Shelley. You can ask a question.

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Shelly’s iPad: Hello, guys.

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Shelly’s iPad: I have a question because you mentioned Vitamin K earlier. I'm on the Algecald 3, and then also just the plus. And I see that I understand that vitamin K 2 and vitamin K. Just regular K. When it comes to blood clotting issues and things like that. One of these has just vitamin K in it, which I've never had been taken before, so I don't think it's the K. 2.

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Shelly’s iPad: Is there, and it's at a high. It's like 833% of the daily value. What does this mean?

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Dr Doug: Yeah, yeah, this is super confusing. And I like that. They did this with Al Jacal prior to switching back to using the algecal products. I wasn't recommending vitamin k. 1 in supplementation, because people are going to generally get plenty of k. 1 through diet. There is value in k. 1 and a lot of the early research was on k. 1. But the problem with k, 1 is that you have to convert it to K. 2. If you want. K. 2 and K 2 is

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Dr Doug: the one that has most of the impact of what we're looking for. So I don't mind people taking k 1, obviously, because I support using the product. But I also don't worry about the k 1 in supplementation and blood clot risk.

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Dr Doug: I've looked into this in a lot of depth because we talk a lot about vitamin K. And so unless you're on the drug, and by you, I mean anybody, unless someone is on the drug coumadin, or warfarin that works through the vitamin K pathway to prevent blood clots. Vitamin K, through supplementation or through diet, has never been shown to increase the risk of blood clot. And it's been studied in massive doses. So you're looking at 833%. I'm talking like 80,000%.

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Dr Doug: I'm not worried that through supplementation you're going to increase your risk of clot. Doctors have been taught that because of just the historic use of Coumadin, everybody was on Coumadin back in the old days, and in my training in orthopedics we used Coumadin as blood thinners after surgery. So in my mind I get this gut like. Oh, God! I can't give a vitamin K. They're going to clot, but there's no evidence to support that. But that's where that comes from.

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Shelly’s iPad: Okay. So K, just K is actually k 1,

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Shelly’s iPad: there's not a KK 1 and K, 2.

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Dr Doug: Correct. Well, there, there are lots of K's. But I'm assuming that they're talking about k. 1. And I think it's listed in there somewhere in tiny print.

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Shelly’s iPad: Okay. Alright. So they're fine to do together. And you're you're still recommending.

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Dr Doug: And that's and that's how we generally recommend them together. Yeah.

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Shelly’s iPad: Okay. Thank you.

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Dr Doug: I think it's I think it's Helen.

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Breta Alstrom: Helen. Yeah, let's go.

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Helen: I wonder that you have mentioned the Ccta. Add on.

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Helen: And what what is that, Nick?

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Dr Doug: What is that thing? Yeah. So it's a company called clearly. So CLEERLY, and maybe Bretta, we can drop a link to their patient-facing website. It's a really cool company that uses the data from the Ccta and creates a 3D. And maybe even next time I can actually have this loaded. And I can show what that test actually shows. The data is so cool.

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Dr Doug: But when you look at it, it basically allows me to look at every fraction of a millimeter of the artery, the stenosis, the plaque, all of it. It's such cool data, but the ccta by itself won't show you that the Ccta by itself just shows you

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Dr Doug: from a big picture perspective stenosis. It's read by a radiologist or cardiologist, and they'll say mild, moderate, severe. That's not really that helpful unless it's severe. If it's severe, then I want to know. But if it's moderate, it's like, Well, is that like 20? Or is that like 60, because the difference there for me matters.

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Helen: And how do you get access.

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Dr Doug: Right. So the way that we and we have like, I think we have multiple team members, like all they do is to help people do this. And so you get the Ccta at the hospital and you have to go in. Get the thing that's iv contrast. It's a whole rigmarole. But you get the data, and then you cannot leave without a disc in your hand.

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Dr Doug: And this is like people like, don't hear me say that, but do not leave without a disk in your hand, and then you send that to us. We send it to clearly, or you send it to clearly, and then they upload it into their system, getting it after the fact is nearly impossible.

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Helen: Thank you.

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Helen: Yeah.

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Breta Alstrom: Awesome. Does anybody else wanna raise their hand.

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Dr Doug: Cheryl has her hand raised.

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Breta Alstrom: Aye.

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Cheryl Edwards: Hi! What is an optimal fasting? Blood, glucose.

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Dr Doug: That's a good question. I think by definition, it's under 90, I think 89. And below is what what is on our.

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Dr Doug: what our optimal level is.

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Dr Doug: But the truth is, fasting glucose is the least important of the glucose markers from my perspective, because a lot of things will have an impact on fasting glucose. The most important one from a morning fasting. Glucose test is going to be cortisol.

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Dr Doug: So if your cortisol is elevated from a stress perspective. For whatever reason, your glucose is going to be elevated. And so again, I'll just use myself as an example, because I have dozens and dozens of data points. When I'm stressed out and I wake up in the morning, my fasting glucose is always in the one-teens which would be really concerning if I didn't know that my a. 1 c was like 4, 8,

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Dr Doug: which is very low. So I have high fasting glucose in the morning because I wake up, and I am ready to conquer the world, and as a result of that my glucose goes up because it's expecting me to fight tigers or something, but so I don't worry too much about fasting glucose.

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Cheryl Edwards: Is it better to have an a 1? c.

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Dr Doug: Always. Yeah. But even that has to be taken into context, because a 1 c can be falsely elevated if someone's carbohydrate restricted. And that's where the use of like a Cgm comes into play. And then, also knowing fasting insulin is the 3rd part of that.

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Cheryl Edwards: Thank you.

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Breta Alstrom: Yeah.

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Breta Alstrom: Just a quick question. If somebody had a ccta in 2020, but wanted to do clearly now, should they get a repeat Angiogram.

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Dr Doug: Sorry. Sit one more time I was reading.

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Breta Alstrom: They had a.

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Dr Doug: It!

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Breta Alstrom: If they had a ccta in 2020, would it be worth it to run it through.

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Breta Alstrom: Now.

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Dr Doug: If you can get the data. Yeah, you know, we're 4 years out. So could it change, of course, but at least knowing that starting point. Because, let's say, it was beautiful, it was pristine. Would that change the the frequency at which we would repeat the Cctta? Probably. But let's say it was 50, you know. Would I want to know 4 years later? Probably.

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Dr Doug: So yeah, I would love to see that data. And it's the the cost. The cash part of that is a little under a thousand dollars. We don't like when we do it. That's what we pay. We don't have any profit off of that. So you could I?

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Dr Doug: I'd be curious if you could do that directly as a consumer, I think you might be able to question is, what would you do with it?

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Dr Doug: You gotta read it.

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Breta Alstrom: Yeah.

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Breta Alstrom: awesome. Okay? Well, we're at time, everyone. And Doctor Doug has to go see patients. So we're gonna let him go again. I have like an extra 5 min to stay on and answer any tech questions for you guys. Oh, you guys, some updated tutorials. But thanks for your time, Doctor Doug, and we'll catch you later.

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