198. Beyond LDL: The 2026 Guidelines Make Lp(a), ApoB & 30-Year Risk Essential

Welcome to Medicine Redefined. I'm Dr. Altamusharaja, and I'm Dr. Darsh Show. Let's put the help back in the healthcare. If you're a high performer who wants a clear plan for longevity, performance, and staying active with fewer setbacks, I'm now seeing patients through my telemedicine practice refining health and performance. I'm opening a limited number of founding member spots at refininghealthrx.com. All right, let's jump in. Dr. Darsh, back for another progress. How are we? Good, man. How are you doing? I'm good. I'm good. I am excited about this topic. I know as I've joked about this before, you know, you got to be, I guess, pretty lame or a certain stage in your life where you get super excited about lipidology guidelines that come in our dislippity. I've got guidelines, I should say, but I think that it's worth talking about for a couple of reasons. One, the conversations that we've had with the preventative cardiologist on here, Nicole Harkin, William Cromwell, and, you know, even Matt from a president health reports. I forget who else we've talked about this. They've been extremely popular. This is stuff that people want to hear about. Clearly, the audience have an appetite for this. But more importantly, when I actually started reading this, because there was some hype about it on social media, maybe I saw the phrase that came to mind. It was like, what's that thing that they said when they the moon landing? It was like one small step for man and one giant step. One small step for preventative medicine, one giant step for longevity medicine is kind of what the thought that I had. I thought that it would be worth it for us to unpack it a little bit, maybe inform some patients about what actually shifted. And hopefully that they can have these conversations with their primary care physicians, cardiologists that they're seeing that and go from there. Yeah, I think it nailed it. I think this is going to be an episode where it hits home for both of us. Obviously, we both have a higher risk for heart disease in our family. And this is a myth we've got a booth been on the forefront with testing and just looking at guidelines and supplements and tracking. So this is exciting for me. I'm coming into this with a clean slate. So I'm sure I'm going to have a lot of questions for you. And like you said, I think a lot of our patients hopefully can now go to their doctors and say, hey, look, these are part of the new guidelines that we feel like we've been so behind on. You know, whereas Europe has, you know, been kind of on the forefront with a lot of this testing, but yeah, hopefully they go to there. Yeah, they can at least go to their physicians and say, hey, listen to this episode medicine redefine and get with the program. Yeah, and maybe actually we'll see if you're two changes by the end of this episode or at least when you reflect on some of this, because I know this is attention that you had a while back when we were looking at your risk profile with respect to whether we should intervene pharmacologically or not. And so I guess with that, maybe I'll kind of just bring people up to the last cholesterol lipidology guidelines came on 2018. So we're eight years later and they've even just changed the name of it, right? And so they were cholesterol guidelines and eight years later, now it's called they're calling it the ACC American College of Cardiology and a J distalipidemia guidelines. And so biggest update in eight years is not cholesterol guidelines anymore. It's more of a generic or a broad umbrella term, rather, I should say, which includes the scope has been brought in right to include track list rights, Alpular lay things that people have heard about certainly long time listeners and the three words, I think that capture this update for me is a three piece. It's proactive. It's personalized and it's precise. All three words that I think that people who are in longevity medicine get off on, right? Hopefully people will get excited. I guess maybe I'll give a general overview and then, you know, feel free to ask me some questions. And then from there, I think that it makes sense to kind of dive a little bit deeper into every single segment of what I think is relevant. I'll do my best to keep this as digestible as possible. You'll tell me if that's actually the case or not, because as I mentioned, it's over 120 pages and that's struggling to kind of keep it all together. This was like there, there's six big shifts that I was able to break this down for people into number one, which is going to be no surprise to anybody who was into this or lessons here is the core philosophy has shifted from weight until risk is high enough to don't let decades of pathogenic exposure accumulate, right? And so treat earlier is kind of the idea. And they are now even more so pushing lifestyle counseling starting in youth. And I'm talking in the adolescent population much earlier on earlier, the pharmacotherapy in young adults. And so that's been the biggest change. We've talked about this with, you know, given a head nod to Dr. Alan Snyderman over from Canada before talking about 30 risk profiles. And so here are some of the new equations that we'll talk about are applicable to people as young as 30 years of age, all the way up to 79. And so anybody who has strong family history, we're going to talk about how those risk enhancing factors play in number two is, as I mentioned, we're going to estimate risk very differently. Historically, they used to these things called a pool cohort equations, which were somewhat basic. Now there's a calculator that people can readily access online, go actually calculate some of your own risk if you have these things. I encourage you to do that. Maybe we'll do it on here if you want. It's called a prevent calculator. And I think it's the, oh my god, this is preventing cardiovascular events or something like that. That's what it really stands for. And then number three is use different goals and actual target numbers to when you're treating. So the 2018 guidelines, the prior guidelines, they dropped these hard LDLC targets and the 2026 restores those specific numbers as well as the non HDLC. And we can talk about specifically what these things mean as a refresher for people at every single risk tier. And so the question is no longer, are you on a statin or are you on a lip and lowering therapy, but rather did you actually get to the biological target that we're trying to demeaning for the reduce your risk. Number four is we're measuring more than just LDL. So historically, people would say, okay, good cholesterol and bad cholesterol was LDL and putting this in quotes. We've talked about why that's very trivial and we can't reduce it to that. But things like elpular a screening, right. And all adults is now a class one category. And for those of you who don't know and not in medicine class one is really absolute recommendation, you should definitely do it. Apo B something that we've talked about a lot gets a nod as a class two A category for getting therapy. There's still a little hesitant on making a class one category like the European guidelines have, but but at least it gets the nod and there's certain nuance that they add into when it is appropriate. And so the guidelines shifts from that to looking at total authentic particle number. And then number five is escalate therapy systematically, which is good medicine. It's not just statin and done. It's statin first and add on, but you're trying to get through these goals. And then last but not least, it's take triglycerides and imaging and special populations. And seriously, caxe, right. So which is the corner artery calcium scores. You're more formally integrating that and that could be reclassifying somebody's who might be intermediate risk to high risk or low risk to moderate risk. The Vesipa, which is the only pharmacologically great EPA. I cost a pentethyl is the name for it is the only triglyceride drug with good outcomes data. So they talk about that. But they also even reclassify just the whole instead of a CVD, which is athletic cardiovascular disease to kind of look at the bigger picture. It's called cardiometabolic or cardio vascular kidney metabolic syndrome. So incorporating, you know, what is your kidney function like what's your metabolic health and using that in part of the prevent calculator. So any, what do you think about that? Makes sense to me, you know, if I could summarize it, it just sounds like we're getting more aggressive. We're starting to use metrics a little bit more with harder guidelines and finding different multimodal approaches to try and reach those. Right. So the LDL less than 55 and then look at APOB again, which is last two, but then using risk calculators, right. So not only using 10 year risk, but 30 year risk. So for someone like me who's 34. Okay, I can now predict at the age of 64 I'm using that 34 risk as we know, as you said, it's an area under the curve problem. So I might not fully affects now. 30 years, I definitely will. So just like we did with hypertension and diabetes, we're starting earlier, we're getting more aggressive and we're reading and preventing things earlier. Yeah. And I think we had talked about this, right. It's not to say that the previous, we didn't have a calculator, but just to kind of drive from that point, previously, the calculator, the pool corridor calculator, I didn't even apply until the age of 40. And so for that 33 year old, such as yourself, it's South Asian ancestry myself, you know, 32 when I was arguing with my cardiologist, like how do we even put that into the framework you can't, but now you can. And so that all the one is built on this 1990's corporate data from Framingham, cardiac, these people are going to remember it included inputs like age, sex, race, just binary black versus non black. Same thing with diabetes, it was yes or no to diabetes. As a person now, you can actually put your A1C in and kind of see where and how insulin sensitive insulin resistant you are. As we've talked about the before A1C is not just a hard like it's not one day, you go to bed non diabetic the next morning, you wake up diabetic, it doesn't quite work that way, right. That thing has been building up for under the hood for months and years. Right. And so same idea there. So the new calculator called prevent. Built by the CKM model, like I talked about. It adds GFR, which is a surrogate for your kidney function. Glamour filtration lady, hemoglobin A1C, I already mentioned they also include optional your urine album and to creatinine ratio as an input that you could put all three of these I think are optional. It drops race as a variable. I think people talked about that has like some logistical and ethical problems. It gives the both 10 30 as you talks about it's validated on more than three million people from contemporary US data. So that's what's cool about this, right. So this is, I think I should mention this is not just one organization, one society guideline. The multiple societies coming together and putting this together. So there are a lot of people much smarter than you and I on here putting this together and it's really cool that there are again arguing for the things that. At least I feel like I have been fighting the most brilliant lipidologist since I guess I was 30 years old. And then last but not least, but you know the earlier age range, right. So 30 to 79 it applies to anything below 30 you got to apply a clinical judgment. The prevent calculator, I should say, I know you were giving some specific targets, the risk thresholds are like this. So less than 3% on your score, if you see that it's considered low risk. This is if you actually put your information to the prevent calculator, which again freely available we're going to link that for people between three to five percent is borderline. This is where we'll say you could consider lipid lowering therapy and I'll just call it LLT for the short for people from now on. 5% or 10% is intermediate risk. They say that it should be considered and greater than or equal to 10% is definitely higher risk and it's recommended. And you know these flag roughly the same population with the old cohort equation with 7.5 to 20% but it's a little bit better because it's now considering things that are not captured by the calculator. So they have this thing called the CPR model. So just you know short hands are always good and C is calculate we just talked about that so you'll run the prevent 10 or 30 or P my favorite part personalized. So this is where you layer on risk enhancing factors that are not in the calculator. For instance, family history of premature cardiovascular disease right that was a big one for me which is why I started really started arguing right so for those who don't know and what I've talked about this right my mom at the young age of 50 which is considered premature for females. I think for females anything under the age of 65 is going to premature for males is below below 55 so she was extremely young and she had a first MI at that range heart attack. And so that really got me down this rabbit hole that leads me to read 120 page. That's the despite not being a cardiologist L. P. Little a elevated L. P. Little a we can talk about those numbers are for me that's elevated. High sensitive CRP people have heard of CRP and in the flammatory marker able be again LDLC South Asian ancestry again that is the things that we talked about other chronic inflammatory disease HIV metabolic syndrome premature menopause preclampsia. So these are all things that that can change how you look at the problem in terms of whether or not you can intervene and last but not least in the CPR is reclassify. So there's this is where you'll selectively used imaging they specifically given not to CAC scoring to break ties for people. I think you and I can argue where CTA some of those who are again consider ourselves to practicing a little bit more aggressively truly in the longevity space will say that CT actually has a role and we can talk about that. Yeah, that's kind of the framework for this. Nice man. I got yeah, I know questions about this. I mean this this definitely makes sense. I like how it's a little bit more personalized than it's just easy to follow, right? Like you can just go down algorithmically one and then wherever you are step two input whenever you need to that step three. So I think that that gives you a more definitive kind of pathway as far as what your risk is. I guess maybe it's worth taking a step back and seeing if maybe you understand and if it's a way for audience to understand those numbers. So LDLC non HDL APO B LP like we've been throwing this around and if you go to your doctor and you get a lipid panel you'll see this number like LDL non HDL maybe they'll talk about that and they'll say hey we're going to target this. But you might have the question is like why are we targeting this and again I've emphasized as other people smarter than myself. So we shouldn't say good cholesterol, bad cholesterol, no such thing. But there are things that are authentic and can be considered bad. Do you have a clear understanding of every single one of them or how do you think about it? I guess I mean I think the LDL is what I get tripped up on most right because you hear both sides. I think with that in respect, especially like people on ketogenic diets, right? They're going to sometimes be a hyper responder and their LDL go through the roof to like 300, 350 sometimes for without any history of any type of hyper cholesterol. Leave me out. And so the argument I think with the camp that says hey you still should bring down your LDL is that you know if you look at the data, there's still a huge correlation between heart disease and elevated LDL on the other side of pushback. It's more of that correlation at this position. We'll say yeah, it's it's very much causative. Yeah, but go ahead. But no, okay, so then in that case like with the hyper responders, I guess I'll throw back to you then like what is your opinion? Because then you'll see the other side of the camp saying, you know, I mean there's a lot of people in this and the carnivore diet camp what not saying. Hey, you can still have this improvement or a rise in LDL, but when you're inflammation all your cardio, cardio metabolic factors all the other lab work looks good. You know, you're not really putting yourself too much of a risk for any type of cardiovascular events. Yeah, so this is yeah, so I think what you're talking about is the lean mass hyper responder hypothesis, right? I think it's important for people to understand just because something is causative doesn't mean it's absolutely 100% going to happen. That just means that we know that causes something and that cause could be tomorrow. It could be 50 years from now. It could be 80 years from now. I just don't know. And the signal is strong enough where we can go ahead and say that like smoking being the perfect example for this, right? So people again, do we have randomized control trials? Are there people who use this example to say that we have that no, but we have enough data at a level of strength strong enough where we say yes smoking causes lung cancer. Okay, hopefully I didn't piss people off with that statement right there. But I'll stick a step back and say this. I think that yes, if you have somebody who has a really high LDL just through the roof. But like you said, is of Caucasian ancestry and has an extremely low LP. It has no other adhyogenic factors has blood pressure is dialed in has no insulin resistance whatsoever. And visceral fat is like everything else that we talked about in the P for personalized is just know where on even the radar. Is that high LDL alone, okay, probably more okay than another person who has South Asian ancestry premature family history of cardiovascular disease, right? Like probably more okay. Can we ever save to anybody? You're going to have a heart attack. You're not going to have a heart attack. No, you know this and I know this is that we can never look a person in the face and say this is going to happen. Like it's all risk mitigation. We think it's going to happen and you know the other interesting about that hypothesis is the people who had the heart attack and died from that hypothesis. They're not the ones out there talking about it. You know, so this is a survivorship bias in some sense as well. And I mean, again, this is I'm not a super attuned to the whole argument from that. But this is one of those things is, you know, we can't be I guess this may be PSA for my trainees and I'm curious to get your thoughts on this is like. You and I are coming into longevity medicine in from a PM and our background. And I was thinking about this because you know, I'm in a group and I talked to people with longevity who come from internal medicine, a family medicine, nobody owns longevity. It's not it's not a specialty. It's not a field. And I think everybody who comes into the field, whatever their specialty is, they look at the longevity problem from their angle, right? I've been advocating for a lot from MSK health at least because that's the ones that I like to look at the problem from at least that's the ones that I feel most comfortable and most equipped to comment on. So when it comes to things like lipidology and cardiology, there are people that I trust more than myself on this. I just there's too much knowledge out there is too much information for me to sit there and be the subject matter expertise and lipidology while also being a subject matter expertise like I would have to trade off MSK to be able to come back then. Why am I sharing this all of this because I think that you find a lot of reputable sources and you see where that overall like overlap is and you look for the signal in that. Otherwise, if you just go to the extremes to look for the signal, that it gets really hard. I actually comment on somebody's LinkedIn, I forget this guy from primary MD, I forget his name, you know, talking about how people are using poor week alternative thinking as a we thinking as an alternative to institutional thinking that's gone wrong. And I thought about that as us because like I think about that, you know, we talk about dysfunctional thinking from an institutional standpoint all the time about how things are the way they are. But that doesn't mean we should replace lazy thinking by that metric. And so the other challenge with longevity and even this is no longer longevity because it's a guideline, but this longevity space is that it's all in the great, everything's in the great. Either shades of it, but then you know, the problem with that stuff comes is sometimes we become bolder about the evidence shows and that gets really tricky for patients. And that's why another reason I wanted to distill this down and I got super excited because this is like the first time that I can remember where the quote unquote traditional medical system is like meeting up with what a lot of people who are more proactive, primordial prevention, precise and you know, and personalized care for. So what are your thoughts about just that whole idea? I don't want to sidetrack us too much on that. Oh, yeah. No, I think I think you really nailed it. I think at the first time I'm really seeing like you said, you see the academic side of things kind of come up with a forefront of the medicine 3.0 social media people advocating and looking at research from a different angle tight mixed. If that makes sense, I again, I just think it's. It makes sense. I like how it's multimodal. It's not so black and white and I think that allows for flexibility and allows for more debate too. And I think that's what's needed in medicine is more of these type of conversations that we're having right now to kind of go through and say, hey, why is this number we're choosing or why a 30 year risk or how does this work? And I think when you start to ask these questions, you tend to go down mechanisms of, you know, certain drugs and how imaging works and you start to get exploration of all these different things that contribute to why the guidelines are the way they are. But I think that's just better for science. Yeah. Yeah. And I'll make sure I say this again at the very end, but notice that I started this whole thing by giving you the model of the CPR. And that's really important because the P in personalized is what's I think makes medicine fun. I know you like to practice medicine this way. I like to practice medicine with everybody wants to practice and a one medicine. The problem is when we're communicating a social media, when we're communicating with this podcast, if we have several hundred or thousand whatever at some time listen to this. The message is not going to be for every single person. And so that's why you kind of have to when you're ingesting information, you have to think that person actually talking to me. And sometimes the answer might be no. And the reality is we can't cover every single case. Maybe if we have time at the end, we'll do a couple of cases for people, but we're not going to be able to cover every single possible scenario. So with that said, I'll just quickly cover like LDLC low density like a protein C. This is the analogy. I was thinking about the way I think about it is their trucks, right? So all these particles are trucks. And so LDLC, which is what people use to think and we target is the cargo weight on the truck. It's the specific type of truck and that truck is the LDL particle. And it's only measuring the cargo weight on that truck, just that type of truck. And then you have non HDLC, right? So it's everything on that lipid panel that's non HDL. So you basically take your total cholesterol, right? You subtract HDL. You get your non HDLC. Now, this is the cargo weight on all of the bad trucks because more than just LDL, you have VLDLs. You have IDLs. You have triglycerides. All of these can actually be and remnants and up literally they can contribute to atler sclerosis, which can be heart disease, brain disease, that kind of stuff. So this is a simple upgrade from the standard lipid panel where non HDL goal is to actually typically even in these guidelines about 30 milligrams per deciliter more than the LDL goal, right? But it tracks pretty closely in certain instances non HDLC is a little bit better. But that matter. So that's where the non HDL is. Apo B, which we've been advocate for other people are adequate, it's actually counting the number of trucks. So LDLC cargo load on one truck, non HDL cargo load on all the bad trucks. Apo B counting the actual number of trucks. The reason that's important is people talk about particle size and particle number and they talk. It turns out that the particle number is actually more important because even the smaller trucks with less load are just as problematic as the trucks with lots of load. Right? So you actually want to get the number of trucks because that's what's going to dictate what your actual risk is. Does that make sense? Yeah, that was a beautiful analogy I've never heard before. I love that. Yeah, so I think they leave people looking at that way. That's why a lot of people will argue, well, why are we not getting Apo B and stuff like that? And in some cases, like I said, non HDL tracks would be very closely with a few exceptions with somebody who was insulin resistance and diabetic. That's where the discordance comes in. You and I've talked about that. I live in a triglycerides, Apo B wins every time and the guideline actually talks about this, but they still have a 2A check on this therapy that hey, let's treat it. A little egg. So this is the LDL particle. This is another big one. This is an instant interesting and this is the purely genetic thing. So just a background. This is called it's an LDL particle with a small April lipoprotein on it. I'm not going to get to the mechanisms of it, but it's 90% genetic. And the other interesting, it's stable over a lifetime. So you really just need to check it once in somebody's life. I'm pretty sure like yours is actually quite low from what I remember, right? Yeah. It's surprisingly interesting. So good for you. Mine is unfortunately not. Mine is very high and we can talk about why I chose to intervene for myself because that one reason. So there's three ways that this is actually responsible for damaging and they're independent of LDL. That's really important. Right. It's pro-atheragenic. So again, that's creating more heart disease. It's narrowing those arteries. It's pro-inflammatory because it oxidizes fast lipids and inflammation in this sense inside is not good. And it's pro-thrombic as in it causes a lot of clotting to happen. So people who have elevated levels of LPA, they're actually higher risk for clots too. That's what they're also higher risk for erotic stenosis. And these other things that are aside from quote unquote coronary artery disease. And this actually ends up being highest in African and South Asian ancestry. And about one in five people, maybe even a little bit more than that, or walk around with an elevated LPA delay. But a lot of people don't even check it. They've never even heard of this. And doctors never talked about it. You heard me talking to Cole Harkin back in the day in 2020. It was like, why the hell are we not checking it? And because people have never heard of it. But now they've made this a class one recommendation, which is super, super exciting. But what's again, what's... You could have two people with exactly identical LDL and super, super low. And everything be normal. One person, one person have an elevated LPA delay, like 1.5x. And they could be a significantly greater risk, just because it's an independent factor for contributing to adverse effects when it comes to heart. Love it. I got no questions for you. Good. Love it. So let's... Maybe the next place is... I won't spend too much time on this. I don't want to make this treatment thing. I think my hope is that people have an idea of how they can think about it. And then they can talk to their cardiologist or their family medicine doctor who can read the guidelines and talk about where the targets are. But you know, just if you are somebody who has very high risk, like the goals are... Initially, I said that we have actual targets, right? You talked about less than 55. But it's actually not just that. It's also a percent reduction. We're trying to achieve both. So for somebody who's very high risk, right? Think this is maybe your father, your mother, your grandpa, who's had a heart attack, has high blood pressure, and is already on a statin or something like that, or maybe had a stroke. Like now we're trying to get their LDL below 55. They're non-HDL below 85 and a greater than or equal to 50 percent reduction. Somebody not very high risk, 70, 150. I'm just going to mention LDL, just know that it's plus 30 for non-HDL from now on. Somebody who is intermediate risk is going to be less than 100. Somebody who's subclinical at those sclerosis, who has a CAC score greater than or equal to 100. You're trying to get less than 100. And I mentioned earlier, you know, with somebody who has... If you're using to prevent equation and the calculator, and it's for primary prevention, then it kind of really matters a lot on the P in the personalized, and the reclassified to see when you're going to intervene. And I think that point is going to be less than 100, really, what the LDLC target is goal going to be. So I think that's kind of where it is. We could quickly touch on the different agents available to us. We don't have to get into it unless you have a question, because I know other people will have a question. Statons are the tried and true, the most popular. I want to be very clear. I am not in the camp that statins should be in the drinking water. But I do think that they're one of the best drugs available to us. And we have a lot of options. They certainly have problems with them that I've personally experienced. But statins are number one almost always. Is that a mime, which is in Zedia? Is another name for it? It blocks cholesterol absorption. So statin inhibits a pathway of that cholesterol formation. Is that a mime, blocks absorption? There's a newer drug that came out after the 2018 guidelines. I think this is called bempidoic acid. Have you heard of this one? I have enough. First off, yeah. Bempidoic acid actually works this. You might remember a sentence. H-M-C-Q-E-R-D-A-C inhibitor. Remember that? Yeah. Bempidoic acid actually works in that same chain, but maybe two steps before. What's interesting and cool about bempidoic acid is it only works in the liver. So it activates only in the liver that enzyme or blocks rather. And so you don't get any muscle effects. So there's no myeloges, like you do with statins with this one. That's the indication for this is when somebody who's statin tolerant because of muscle issues. So is this now the next step after the intolerance? Because before you used to just go straight to like rapatha, right? Yeah. This could be a really good option. Unless there are some indications for a re-rapatha, what's her passive? Because repatha is still much more potent and knocks us out of the park. Like I think that data talks about alone in some of the studies that they cited that 18% bempidoic acid alone when you combine it with azetamide. There's actual pill called next lizzet. I think that's a brand name for that. That's a 38% reduction in LDLC and has clear outcomes as well. Like outcomes when we talk about as hard outcomes, quote unquote. And that's what people will say may so major adverse cardiac events. And this is did taking the medication 10 years ago to prevent a stroke. That's like the most meaningful thing. Not just did LDL get better because to your point it's like who cares if the LDL is higher low? What we're trying to eliminate is stroke, heart attack, that kind of serve. Repatha, which are a monoclonal antibodies, these are PCSK9s. They have a significant effect, 60% additional reduction if you're taking this. But the problem with them, they're very expensive. This, if you have to pack a bottle pocket, can cost $6 to $8,000 a year. This is a Q2 or Q4 week. Every two to four week injectable is sub-Q for most people. And, but the outcomes are proven. It's really good. One of the newer drugs is a SI RNA, I think inhibitor. Forget exact mechanism for this, but it's called in Clisaran. Our LEC video is under name for it. It has a similar LDL lowering advantage of this injection every six months that you have to go in. But the problem is the outcome trials are not completely there. So it works really well, but we don't have them. And so I think they gave it a nod or acknowledgement, but they didn't necessarily recommend it. So to your question, it was Stanton intolerant. The therapy, which you'd be doing is the combination. Well, maybe you could do a bit of a acid by itself. If you needed aggressive, you would do the combination with Zetamide. And then maybe add on to PCS killing. Was there any mention of supplements in the guidelines now that they're probably looking more to like medicine three out there? Absolutely was. Let's, I was going to bring that up at the very right. But if we let's do that. And we can tie into kind of your thought process because they gave, well, actually let's do this. Can we? I want to wrap up with Elpula and CAC before we go. So just because I think this is the biggest win. And so I think I've explained Elpula a little bit, but just for people again. So everybody, if you haven't had it yet, it's not medical advice, but you know, whatever. Please consider talking to your clinician about getting it just so you can assess truly what your risk is. I've already mentioned what those are. And it usually comes. You'll see it in two ways in a milligrams per deciliter or nanomoles per liter. Preferably you want a lab that's actually looking at animals per liter. There are some ways how the assay is done, but there are some, you know, they've quantified it so you can actually see the risk. So if an animal per liter anything above or equal to 125 is considered the cutoff. Like that's your high risk at that point, which would equate to 50 milligrams per deciliter. And then of course every little bit on top of that is it's multiplicative risk. It's not just an additive. That's another important. And so I talked about this. I think, you know, when I found out, you know, my mom had that issue. And my first Elpula delay was 207 nanomoles per liter at that point. I was like, okay, well, we need to consider. And that's when I started having some discussion with some preventive cardiologists. And the interesting thing about Elpula a little lay, I should say, at this juncture, we do not have drugs to address it. I mentioned it's an independent risk factor. But unfortunately, we don't have any drugs actively on the market that can directly reduce that. We've got it for LDL. We've got it for triglycerides. We do not have it. So then the question becomes, and this was the question asked of me by my wife is, well, if there's nothing you can do about it, why even check it? You might have heard this. Have you heard this? Yeah. Yeah. And the argument that I would make is it risk stratifies you as a person. Again, you've got to assess if that person in front of you, I think I talked about this with Lena Rhodes, actually, if that information is going to cripple that person, or if that's going to empower them. For instance, if you know that you are much higher risk, but there's nothing you can do about that, but you ask yourself, hey, what can you control? So interestingly, they've even talked about this, right? So they've published the anti-publishing thing called the life's essential heat, which if you optimize these, it can reduce your overall observationally, at least 60%, 67% relative risk reduction in terms of just like your overall outcomes, right? And statins, actually, even in one study, the Jupiter trial, which was a primary prevention trial way back when did cause a little bit of reduction as well. But PCSK9 is a patho in specific, can cause about 15 to 30% reduction. But in the pipeline, there's a trial right now called the horizon trial, and these things called people might hear about ASOs, so angiosense oligonucleotides, which are directly looking at this to reduce LPLLA. But to come back to that essential aid, if I remember, I mean, it's all the other things, right? Can you dial in your nutrition? Can you optimize your sleep? Can you make sure the inflammation is low? Can you make sure blood pressure is tightened up? Your kidney function is good. What are all the things that you can double down on? So for instance, like at this point, if you, what comes to mind is, let's just say somebody is, you know, sitting in that overweight obese category, they have an elevated LPLLA, and their LDLC is borderline or maybe even low. Maybe it's not that high, but they're considering whether or not they should, could GLP want for better insulin management or just insulin, you know, sensitivity and even weight loss. Maybe now, not suggesting these people should do, but maybe now your conversation changes a little bit, because now you have a stronger reason to consider something like that. You know what I mean? Hey, listen, I gotta get my, you know, a waist circumference a little bit lower, my visceral fat, that kind of stuff. So I think that's kind of like where I think that I feel strongly why this should be gotten. What do you think about that? Yeah. No, I 100% agree. I think too many people in science and medicine kind of think like direct effect, right? Like if you do a, then be automatically happens. Right. So if you can't change it, then you don't do anything. But that's not how reality works, right? Because contact exchange is everything. For me personally, I know I have a lower LPLLA. Okay. I can almost, you know, kind of effort out of find out in a way, right? I have more weight over it. I can take something. I can do more experimentation. I can see maybe what helps and what doesn't before going and jumping to a statin. Now that might change giving these new guidelines and kind of what we're talking about. But I think base of the context, it allows me to say, okay, let me double down on lifestyle activity nutrition like you're talking about, which in the long run is going to help so much more. Whereas if I had a higher LPLLA, maybe I'd be more prone to saying, okay, right off the bat, let's do a statin, but then focus less on maybe the nutrition and the exercise and what I need to do. And again, people's personalities are going to be different. Their frame of reference is going to be different, but I think it's just another tool in the toolkit that people can use. That's going to change the trajectory of their life based off, again, their reality and how they are going to essentially consume and take that number and do what they will with it. Yeah. So funny. You said that after I'm to find out because I think one of the things that I would say earlier when I found this out as, okay, I can't afford this just because, you know, it's, you know, so when I would be making a decision between Italian donut or something else, you know, those things are really good. So change the for you. Yeah. So I guess in one sentence, what I would say is knowing your LPLLA doesn't change the treatment per se, but it does change the urgency on how you might do other things around that. So, and then CAC. So CAC said, I think I had talked about that. I won't say the different cutoffs that they say what you're showing me because I don't like that matters. But what's also interesting, they even said that if you have an incidental finding of like coronary calcium on a CT, maybe you're doing a CT for lung surveillance for cancer or something like that, coming back to a smoker and you see actual calcium there, you can treat it. You know, I think it's going to be interesting if cardiologists are going to actually pull the trigger on that or they're going to say, hey, listen, I actually want a formal coronary CT. So that's TBD at this point. But I thought that was like really interesting for them to kind of be aggressive on that about the reclassification of it. Yeah. Interesting. Do you want to also explain, because I know we've talked about this, right? So a lot of people don't know about the CTA. That's somewhat new. Now you can do AI imaging for it. Kind of went to think about doing a CTA versus a CAC, because I think a lot of people will just go straight for the CAC. That's the most common thing they've heard of in the guidelines, I guess, after 40. But yeah, coronary artery calcium score. That's the CAC. And really what it's picking up is calcified plaque plaque that's already hardened. It's like scar tissue at this point. So that's indicative. If you have that, the damage is already done. In fact, you're probably lucky at this point, because that's formalized, right? What it doesn't pick up is soft plaque. The one that's fungible, the one that's amenable to changing for the better or getting cleaned up, getting reabsorbed or oxidized, or the one that's going to actually harden and lay down on those arteries, the lining of those walls and narrow those arteries, those pipes, so to speak. A CTA actually is going to pick that up. Now, it's a higher risk procedure because there's more radiation. You're actually getting contrast, so there's risks with that. I actually had one. It actually feels really weird. They did warn me that for those who had it know this experience, yeah, you have the flushing when you get the nitro, but you also feel like you feed yourself because it like drops to your system. It's so weird. It actually is a very strange feeling. I actually thought I pooped myself, wasn't sure. I didn't though, just for those wondering. But to come back to what that actually will look up as a soft plaque. Now, the problem is, so if you think about the younger person, you 34 years old, what's the likelihood that you're going to have hard plaque? Yeah. I mean, pretty low and less depending again if you have the very high sub of your stuff and maybe, but yeah, yeah. Yeah. Because that's the other interesting. I don't people realize that this process of athlete sclerosis starts in your teenage years. It's starting to be very early on, right? Because it's a lifetime exposure, like you said earlier on. That cholesterol, that LDL is being precipitated in those artery walls much earlier on. Since you're two, three, when you're building up and so it's happening. And so depending on what kind of life you've lived and your genetic factors, that kind of stuff. Yeah, 34, you could have it, but statistically speaking, the chances are low. So in a 34 year old, a pack of zero is not that helpful because you expect it to be zero. But in a 34 year old, if you have a pack of 500, I'm really effing concern for you. So on either, if it's really high in a 34 year old, that's helpful obviously. But if it's really low, that's not helpful. So that's where a CTA I think can be more meaningful because it's going to pick up on the soft plaque. Now, if you find any soft plaque, you have evidence of disease at this point. So you got to treat at that point, right? Like you don't need to go through the whole calculator at that point. If you made that decision to go ahead and do it, then you have to treat it because you see active disease in the process. And that's coronary disease. So the problem is a lot of insurances, if you're practicing that model, they will not pay for this in the young person. You have to have a very clear reason, chest pain, shortness of breath. Like again, not a lot of 34 years, you'll get chest pain where you're considering coronary disease. So that's the challenge. So unfortunately, this is something that a lot of people have to pay cash for. Like I mean, the good news is, radiology clinics know this and you can shop around and depending on what part of the country you're in, it could be as little as, I didn't check any like somewhere in the south, but at least when I was shopping around in the greater Philadelphia area, I think the lowest I found it was like $300, right? And that was actually, okay, that's actually pretty good. You got to be very careful, though, because sometimes they'll advertise $99 and I promise you that's probably not, that's actually a cack that they're saying is CTA, but it's not. So you got to be really careful with that because I almost got tripped up. Does that make sense? I mean, yeah, there's also, I see now like cardiology clinic through CTA with AI. Do you know what that AI is? Yeah. Sure. Man, this is something called FF4. I actually don't remember what it is, but I think it's just, it's a specific way of them to just restratify. Maybe we should look this up. Like, actually look this up. Let's see here. We're going to do a little live searching. Up in CTA with FF4. CTA in the head says, I'm trying to sort about AI part of this. Yeah, so fractional flow reserve is the one that, yeah, it's a standard CTA imagery with AI driven computational fluid dynamics to evaluate blood flow restriction caused by plaque. Yeah. So it's basically, again, a better study, right, to kind of see, I guess, functionality of what you're looking for. So when you build that in and FF4 specifically, then you're looking to see is that plaque actually problematic or not? So it's actually the next level when you're checking that. It costs more money though. I'll tell you that because I know I got this. Definitely. I paid a lot more money for this. But anyways, you know, again, there's levels to this, right? Again, I feel like I've quoted Tracy Dew so much on this. The good, better best philosophy. I think at this point, you're really kind of on that whichever shade of gray and you're having that conversation. So you really need to sit down and have a lengthy conversation about the risk benefits and whether or not it's going to change your management. So I know you and I have talked about that. Maybe that could be a decision maker. I think that's all I got. But we can get into supplements now if you want. Yeah, let's do it. So they gave that whole section for supplements on this and triglycerides, especially populations. And they put supplements in a class three, no benefit. Okay, and here's what they say. They actually quoted. They talked about, I didn't know this until yesterday. There was something called the sport trial where actually compared Resuvistatin with some of the common supplements that people use for this. So, fish oil. Resuvistatin versus fish oil, cinnamon, garlic, turmeric, plant cereals, Red yeast, right? Yeah, right. Red yeast, right? Excuse me. Nature statin and placebo. And you know, it was 198 patients. It was only four weeks. Okay, only four weeks. So that's a big problem in my opinion of this. What they showed was that Resuvistatin completely blew everything out of the water. 37.9% reduction. No supplement beat the placebo. Garlic increased, actually held the LZ a little bit. Now, what are the limitations? Sure. As I mentioned, a lot of us who actually use supplementation for medical management will realize that you have to give something some time. We know this to be true for drugs as well. You know, the thing is that statins work really fast. That's the one thing. I tell people, but then three weeks there should be working. So if you're getting it, I was having this conversation with a patient the other day. You know, you had it six months later, nobody's rechecked your lipids. Why not? Yeah, we should see supplements take some more time sometimes. And so that might be one thing that I know a lot of people will argue for that. The other thing that I know people will bash this study was the study was funded by AstraZeneca, which is the supplier and producer for Resuvistatin, but they gave like an unrestricted grant for this. And I think this study, what? Don't quote me on this, but I think it was done at Cleveland Clinic. PoQ 10 was actually another thing for set myologist. They talked about this as well as class three. It actually showed that it really is not that beneficial. So that's actually something that I know. I think cardiologists and people will recommend it. I had to try this when I was using statins and I was having some issues. And they know that people a lot of times will purchase it over counter because they read about it. Turns out that it doesn't really help at least according to their conclusion here. And one exception supplementation, I mean, is the SEPA, right? And that's EPA, which is, don't ask me to say the whole thing because I don't remember the... So the main omega-3 fatty acid is the EPA and DHA. So a kind of poic, whatever acid. It's more cardio, DHA, I think about as more neurological, more brain related. But that's a prescription. And that's the one that's been studied. Reduce it is the main trial that actually looked at this. And they saw a 25% relative reduction in ASCVD. And plus in people who had ASCVD diabetes and I think triglyceride reduction as well. And you know, who are on statin. The strength trial was another one which actually looked at the EPA and DHA, which was negative. I think if I'm correct, reduce it also showed the a-fibrisc had slightly increased. This is where the conversation came up and like 21, maybe you remember that. So what are your thoughts about this? Because this is something... Is that... Why don't you... Maybe this is a good time because you and I had the conversation maybe a year ago and you looked into some supplementation. Yeah, though exactly. So I've been kind of managing my cardiovascular stuff simply or strictly I should say through supplementation as well as lifestyle factors. So I just pulled up because I've been using chat to be T a lot to kind of go through the supplements and what I'm taking. And then I also use rhythm helps. So I'll explain that as well. The supplementation wise, I mean, I'm not gonna get about a stuff. So obviously I'm multibitamin. I do take it omega-3, vitamin K2 and along with the vitamin D that's in there. CoQ-10, you know, mitochondrial hell, creatine of course, more for weightlifting. Iron, it's been deficient in giving them a vegetarian. Let's see, NAD supplement. I just added on, you know, obviously just listen to kind of podcasts. Here are the interesting ones. Bergamot and black seed oil. Now according to chat to you, I'm looking at examined and stuff. These are two supplements that actually have more reduction in terms of apopie. And then at night time, I have been using... What's the first one? Bergamot. Bergamot. Yeah. It's like almost an oil. That's how I always hear it. Oil or plant? Yeah, it's a plant. It's a plant that they use at Bergamot orange. But they, yeah, they crush it up, use it in supplement form. And then at night time, the red yeast from Thor and Burberry, mainly for the reducing inflammation. So with that, that's kind of my stack for the morning of that night. I've been using rhythm health. So people probably have heard of function. I think they're probably the most popular precision medicine type lab company. Rhythm is somewhat similar. They use way less labs. So I think they only check about maybe 12 to 15 labs, but you check it monthly. So I pay a subscription monthly. It's at home test. But the reason I like that is I get more motivation from data that I get more frequently. And therefore, if I am adding a new supplement or taking something away, I can then see over the next two, three months and didn't have maybe somewhat of an effect. Now my apopie, when I was, you know, originally testing last year in the summer or earlier last year, was hovering around 110 to like 115 since I've been doing this now for about, I'd say, three, four months, which I agree with you. I think supplements do take a little bit longer than four weeks to kind of set it and work. I've dropped my apopie to an average around 85 to 90. Still not ideal, right, to kind of where we want to hit the target. But now it's at least let me really focus on driving down my weight. So I'm still, I feel like I'm over muscleed a little bit right now. So I'm still kind of pushing thing, right? There is. You're right. I have too much muscle. These are real problems. I'm trying to cut down Mike Isertel. It's just losing his mind right now. So I'm cutting down from like trying to cut down from one 85 to around 175, get at a better weight for tennis. And then high rocks is coming up in October. So I try to train for that as well. But being around 17 175 is just like an easier way to move around. And you know, we'll see kind of how that does too. Hopefully keeping that body fat low. I think that's going to be the biggest challenge, right? As you cut how you preserve that muscle mass. But especially as I'm playing more tennis, I definitely need a cut down board to keep up with some of these better players. But yeah, no, after talking to you though, I mean, I think next step, I've always been wanting to get a CTA. So that's going to probably happen in the next couple months, looking at Texas scans, kind of seeing where I'm at. I'm also interested in getting a VO2 mass test actually, and kind of seeing where I am for that. But I think the CTA will be important. They'll get me more information. And then, you know, if I need to cut down some of these supplements, because again, a lot of people look at like cost. And these supplements can cost more than the actual statin. And I think a lot of people forget that. A lot more. Yeah, not covered by insurance. Exactly. And people forget that. And so they want to go down this natural brow, which is fine. I mean, if you're going through good brands that we can trust and stuff. But the question becomes like, are you doing it just because of this fallacy? That something is more natural versus doing a statin. That's cheaper and probably more effective. So that's kind of the next decision tree. So then all that note, like that's what I want to ask you. Talk me through your thought process of, well, actually before I do that, some of the earlier mentioned supplements of vitamin K are, and vitamin D, those are not for your APOB management. Right. Specifically the bergamot and black seagulls. Black seagulls. And the red yeast. Red yeast. Right. The other ones are just for other things that you mentioned, mitochondrial health, that kind of stuff. Just for general health. Okay. Are you taking an official ill too or no? I did the LG Omega 3. Okay. So talk through the lot process of why did you decide to go this right? Because I know you had a conversation with a colleague. But I think a lot of people arrive at this. And I know you highlighted the appeal to nature fallacy. But I'm just curious to getting it in your thought process. And like why not just go to something that you know a channel? What was your strategy? Yeah. Has it in C? Yeah. I think the biggest thing is hesitancy, right? Like, if you've listened to drug story podcast on statin. Yeah. And kind of like, you know, the one who's actually really good. Yeah. So like, you know, when you look at think about the general public, I think like in medicine, sometimes we have oversight in terms of like, Oh, we have the data. Statins are great. Boom. You know, my father's taking statins. He's also had the myopathy, you know, from those things. That's always kind of played a role in my mind. And I always spelled, I'm the type of person where if I take the medication, and this is just my reality for some reason, I take the medication or the supplement. It allows me to slack off a little bit more with the lifestyle modification. Almost like how I feel TLP ones do. So people I feel like, you know, now that GLP ones exist, it allows people to become obese or allows people to live maybe not a healthier lifestyle because they know what pill exists. And therefore they can live a certain way and then say, oh, well, it works for a lot of people. So let me take it. Whatever it's pretty innocuous, right? I think statins are marketed the same way in terms of this pretty like an innocuous cost effective medication that works. But it's funny because that's just the way I feel like my brain works when it comes to. That's fascinating. Knowing how I work with lifestyle modification. Yeah, this is what I love about the variance in people's psychology, because I find myself to be the exact opposite, where if I have to take a medication, I'm more incentivized to get off the medication and therefore be even stricter and be even healthier. And actually have these conversations with people and they're like, because sometimes you can say, that's the other thing is, you know, if somebody, like, here's how I have this conversation with somebody, and say, listen, I don't really want to be on duck. Can we do this without drugs? Can we do this? Otherwise, I'm like, sure we can't. Yeah. It's going to be harder and it's going to take longer to get there. The medication is the most effective. At least the support trial had a bunch of issues, but it still shows that. I think if you stress this out to 12 weeks, you're probably still getting a similar effect that it's knocking them out of the park. And so I ask them, I'm like, well, can we start a statin? And then get it down, and then you get really dialed in, and then maybe you lose some weight. Maybe your visceral fat goes down. Your inflammatory HSCRP goes down, and then we get you off. There's no rule that you start a statin or any medication for that. And you're only for the rest of life. Like this is the conversation that I know of. Pediatrics, same thing with EDHU drugs. We talk about this all the time. It's like you have to be able to de-prescribe just as much as you prescribe these drugs. Because if we agree, which I think you and I did earlier, that it is a lifelong cumulative area under their curve thing, it's like anything that I can do, to reduce that risk over time is a why not even over the next six months reduce it. That's how I have the conversation. But I think it's just, to your point, it's like you really have to kind of know what type of person you are. Some people are just really averse to the pill burden. Like as you were saying, all those supplements, I know you're only taking three for specific it will be, but that's three extra pills. Like for somebody who's already taking a bunch of pills, like you got three more pills or I can add one pill. That cognitive overload of taking extra pills, you know, feeling sick. Nobody likes feeling sick, even if you are sick. Like there are these little things that I think are really important in their conversation. It's true, man. Yeah, it's fascinating. And I think you're so right. I think, you know, for people listening to this that are in healthcare, resident training or whoever you might be, I think it's so important to understand the person in front of you, like you said, right? And having that discussion and seeing kind of what they appeal to, whether it's nature fallacy or difficulty doing things. I mean, understanding that human psyche is so important. So, you know, I want to actually flip the script and I'm going to share a personal story here and come back and now maybe speak to some of my colleagues and because I think one of the things that happens, and especially a lot of the cardiologists will say, listen, sad has great data, the whole myologist stuff. I mean, I see this all the time. And so they'll talk about the no-cebo effect. You're familiar with the no-cebo effect, right? Yeah. For those who are not, basically what that will say is, you know, when, let's say I give you sugar pill or placebo medicine, and I tell you it's a statin, and you as a person start having some of the side of frittrumasatin. That's called a no-cebo effect. Right. Did I describe that correctly? I think it did. Yeah. It's something that will have it be in more awful effect. Yeah. And so they'll cite these studies, which actually happened, and I was saying they're making it up. They'll cite these studies, which actually showed that people or a placebo had these effects like myalgias. Okay. And they'll say, oh, look, the rate of myalgias was no different than from on placebos as opposed to statins, and therefore, you know, statins aren't really causing them. However, if you prescribe that, and you have a patient in front of you on that medication, and they're telling you they have these things happening to them, whether or not it's no-cebo, plus-cebo, or an actual side effect, whatever it is, it's a very real experience that you're going through. And I think dismissing them for, look, it doesn't really happen. This and that kind of stuff is a way to gaslight somebody. And I think that's kind of what makes, or at least one of the things that makes people distrust. And now they're more likely to go listen to the influencer who was promising them to, I don't know, you know, sit in the sun without their pants so they can kind of whatever they're thinking. Maybe what I thought of before he said it. That's to reduce the air, it will be instead, or red light therapy to reduce the air, it will be that's wild. But that's the kind of shit, so I guess what I'm talking to, and here's where I'll share my story, right? So my experience, when I first got on, and I tried multiple statins before, I couldn't tolerate them. The first time I had the experience is I felt, and I sort of would receive a statin. You know, we hit the targets, I was happy with that, but probably about three to four weeks in, after a really intense lower body workout, I would be incredibly sore the next morning. You know, I happened two or three times, but I remember at least twice, you know, when you're in so much pain that you were walking up from your sleep type situation, that happened to me two times, and I remember having a conversation with my cardiologist, and I said, hey, Doc, like, here's the situation, here's what happened, and I was very clear that it only happened after my lower body workout. His conclusion, well, it's not the statin, it's your lower body workout. No shit, yes, it is my lower body workout, but what I'm telling you is that the statin is reducing my threshold for having this intense pain. So, yeah, one answer could be, don't work out, which is not a good answer, and I'm not doing that, right? Or the other answer is, let's look at the drug that is decreasing my threshold for that such intense symptoms to happen. And, you know, like, both things were true. Yes, it was my workout, and yes, it was the statin, but just that conversation with the cardiologist was so difficult that ultimately, he was great, actually. Otherwise, he was good, he's, you know, a good thought process, and you know, Doc, if you're listening, you know, please, no offense here, no hard feelings, but I ended up not going back, and so it's just these little things that we have in conversation, and then we try to different one with the different cardiologists, and that almost took me to the ER at one point. You know, I think these things to speaking to my colleagues is really important. Let's not dismiss the symptoms. The experience that person is having is actually a very real experience, and it's like pain, right? You know, talk about this. Yeah, truly pain is in your head. Yes, but the experience is real. Like, we're not saying it's not there, but technically you're interpreting it in your head. You know what I mean? So, that's my little PSA for my residents and fellows or students, whoever's listening. Yeah, nice man. This has been awesome. Anything else you want to add in there? I think, um, No, I think, I think so. I kind of wanted to do a couple of cases, but honestly, I mean, this has gotten up in, at this point, people might be sick of this. So, maybe just some closing thoughts. If, is this going to change your management, your personal stuff, anything? Yeah, no, I think, I think I'm going to be a little bit more hasty in terms of getting those imaging done and just really being on top of this. Again, like, to me, I know that's an area under the problem curve, but I still feel, you know what I mean? Like, I feel like I'm 20, and I think that's an issue as well, and that's dangerous. So, it's dangerous. But yeah, no, I think, um, taking more control of my health, right, in terms of this cardiovascular disease. I mean, this is the biggest thing in my family that I know of runs. Obviously, I've been blessed genetically somehow, because my brother is obviously the opposite, you know, with his LP LA. So, it's very interesting, um, how he got a higher one. I got a lower one. My mom doesn't have any heart risk. My dad does. So, it's kind of like, you know, I don't know where I fall in that, but getting this imaging will at least help. And, you know, that family thing is not uncommon, because interestingly, both of my parents who corner on the CAD, they're both LP LA is normal or low. Really? Wow. Even my mom. I, for sure. But, you know, before this happened, I learned about it. I mean, my cardiologist ordered it from my mom, and I was like, that's got to be it, and it wasn't. So, again, this is, this is interesting. No, I made this wrong case about it being independent, but it's like, yeah. What caused it for her? Like, she, you know, other than from hypertension and hyperlipidemia, which is just high cholesterol, she never had anything wrong with it. So, we don't have all the answers. Like, we have strong signals, but there are no absolutes, and there's exceptions to every rule. So, this is not to say that if you have a high LDL and high this, you for sure are getting a heart attack. That's not to say that. You might be that unicorn who can go on for the rest of your life. But, you know, usually, it's the whole cut, like, the thing that we talk about. You know, people are so preoccupied with microplastics when we know so little about microplastic, and they so boldly claim, they're willing to do that, yet we have a strong signal here, and they're not. So, hopefully, this is the framework. Remember, CPR, P and personalized, really important. Re-calcify. Re-calcify. So much. Re-classify. Excuse me, right? And I think that's going to be good, and then remember just you can go calculate. Just at the very least, please have the conversation, take agency into your own hands. It's your health. You have to be the advocate for it. I know you and I've talked about this for six years now. Yeah, yeah. I'll leave it there for people. Yeah, hey, maybe, if people are hanging around for this long, join our newsletter, maybe we do a newsletter with our cases, and can kind of talk about that about that for people. There you go. That could be a cool thing. So sign up at www.mettisonredefine.com. Medicine Redefine. There you go. Awesome. All right, man. Let's sign off. All right, man. Cool. Thank you. Thanks for listening to the other episode of Medicine Redefine. 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