What if there was a single blood test that could reveal a hidden, lifelong risk for heart disease that one in every five people has? It's not part of the standard cholesterol screening, and this specific risk factor doesn't improve with diet exercise. It's a leading cause of heart attacks, especially in people who otherwise seem perfectly healthy. Today, we're breaking down everything you need to know about this hidden risk factor called lipop little A. And why asking your doctor for the simple once-in-a-lifetime test could be a game changer for your health. And welcome back, team, to the Building Life An podcast. Thanks so much for stopping by. I really appreciate it. We haven't had the chance to meet yet. My is Jordan Ren, and I a dual board certified physician in family and sports medicine. And the goal of this podcast to keep you active and healthy for life through actionable ev inform education. Let's dive in. So, to really understand LP little A, let's start with the basic structure. At its heart, it looks a lot like a particle we're all familiar with, a low-density lipoprotein, or LDL particle. It's got a lipid core full of cholesterol, a shell of phosphol around it, and a single molecule of apo-lip B or Ap-B. But this is where the similarity ends and the trouble begins. What makes L little A so unique and pathogenic is the addition of a big li called Apo A, or Apo. A lot of acronyms here, stick with it here. But this Ap is chemically attached to Ap by a strong dis-bide bond. This addition of the APOA creates a completely distinct particle, turning the standard LDL into something far more dangerous and ather. and it's this unique structure that's responsible for a lot of the damage that it causes. Here's one of the most critical things about L. P. Little A. Your levels are almost entirely determined by your genes. We're talking about heritability estimates that are over ninety percent. This makes it one of the most strongly inherited traits in the human genome, which is why lifestyle changes, things like diet and exercise, have a pretty negligible effect on your LPA numbers. The master controller of this gene is the actually LPA gene, so very similar there. It holds the instructions for building that unique APO protein. And then, within this gene, there's a specific section with a variable number of repeated DNA sequences, which are known as Kringle repeats. And these numbers of repeats you inherit. That's the primary factor that sets your LPA levels for life. So, with that being said, though, there are definitely some things that can affect your LPA levels outside of just genetics. So, these things include things like hormonal statuses. pregnancy, sex, hypo or hypoth, renal insufficiency, inflammatory states, medication use, and high saturated fat diets. These can all contribute, but they're really kind of a drop in the bucket compared to your genetic predisposition. Now, this is where it gets a little counterintuitive and confusing. There's a fascinating inverse relationship between the number of those Kringle repeats in your LPA gene and your actual LP little A levels in your blood. If you inherit a gene with a low number of repeats, your liver produces smaller AP proteins. These are assembled and secreted very efficiently, leading to a high circulating level of L. Conversely, if you inherit a high number of these repeats, your body produces larger, much more cumbersome APoA proteins. These are then prone to getting misfolded or degraded easier inside the liver before they can get out, which results in a lower level of Lp little A in the plasma. It's also thought that those smaller LPA particles are potentially more ather than their larger counterparts. But this genetic quirk is why we see such a massive, sometimes a thousand-fold variation in LP little A levels between individuals. It's all due to these number of Kringle repeats, which is kind of interesting. Next, let's move on to some epidemiology. So it's thought that your LP little A levels are set early in life. It's actually high when you're born, peaks around age five, and we think it stays pretty constant for the rest of your life. There are some fluctuations, but generally, we think it stays pretty stable. And this lifelong exposure to a genetically fixed risk factor is the entire rationale behind the push for a more measure once-in-a lifetime screening approach that a lot of societies are recommending. The scale of the issue is staggering. That's a big thing. It's estimated that over 20% of the entire world's population, that's over 1. 4 billion people, have elevated LPA levels that are high enough to put them at a significantly increased risk for cardiovascular events. So, think about that. One in every five patients you see likely has this hidden genetically driven risk fact that we don't know about. That 's pretty scary. When we look globally, we do see significant variation in average LPA levels across different populations. Levels are generally highest in people of African ancestry, followed by South Asians, with lower levels typically seen with European and East Asian populations. But here's the critical point for us as clinicians, right? While the specific genetic drivers might differ between those groups, the clinical danger of a given LPA level increase seems to be universal. Studies have shown that the amount of risk for a heart attack or stroke from a high LPA level is. Pretty comparable across diverse ancestries. And this gives us reassurance that results from global clinical trials will be widely applicable to any patient population. That's really important. But the absolute measured LPA concentration seems to be the key determinant of risk, regardless of the patient's ancestry. And so I've just been scaring you for these past few minutes about how terrifying this is. Well, what actually makes it so terrifying and what actually causes the disease? Well, we think it's due to this triad of threats. The fact that one, it's proathrogenic, two, it's pro-inflammatory, and three, it's pro-throm. So, first, it is pro, meaning it helps directly build up the plaque in the arteries. Second, that inflammation, it builds up and fuels chronic inflammation within the vessel wall, and that leads to a worsening of the plaque. And then the three is that it's proth, meaning that it interferes with our abilities. Ability to dissolve clots naturally. So the clotting one hasn't necessarily been shown in humans necessarily. It more theoretical, but the concept behind here is still very important, right? It's a big triad. And this Triad potentially explains why LPA is such a powerful driver of atheros disease, right? And also, on top of that, not just ather disease, but aortic valve sten. So it's very, very important. This can be completely independent of other risk factors like LDL. And so this unique mechanism is why we think these are so dangerous when compared to other things like just regular LDL. And so let's break these down one by one. Let's break down the first threat. Like LDL, LPA does contribute to atheroscler by getting, trapp in the artery wall, and dumping its cholesterol into the development plaque. But more importantly, L-little A is a main carrier in our blood of something called oxidized phosphol or ox. These oxidized phosphol are highly inflammatory and often are potent drivers of endothelial dysfunction and plaque formation. Carrying this extra inflammatory payload makes the LPA particle significantly more ethogen on a particle-for basis than the standard LDL partic. And take a step back here, you have way more LDL particles, way more LDL particles, but on a particle-for-particle basis, the LPA is more afrogenic. And this really is a key distinction. While we know high LDL cholesterol is strongly linked to the overall quantity or burden of plaque, recent evidence suggests that LPA plays a more specialized and sinister role related to plaque. Quality. A sub of the Pros II trial was fascinating and found that while high LDL was linked to the total volume of plaque build throughout coronary arteries, High L P little A was not. Instead, elevated L P l A was strongly and independently associated with the presence of focal vulnerable plaques, the really dangerous ones with thin caps and large lipid cores and that are prone to rupturing and causing a heart attack. This suggests a model where high LDL builds the plaque over time, but high LPA acts as a destabilizer, making that plaque much more dangerous. This helps explain the significant residual risk we see in patients with even normal LDL control, but still high LP little A levels. Now it's time for the second threat, inflammation. So, that cargo of oxidized phospholipids is a primary driver of vascular inflammation. These molecules act as danger signals that trigger the activation of endothelial cells inside the blood vessel. This leads to them expressing adhesion molecules in their surface like V and E-se. These adhesion molecules then facilitate the recruitment of immune cells, specifically monocytes, which are then drawn out from the bloodstream and into the artery wall. Once inside, these monocytes transform into macrophages, gobbl, and become foam cells, the hallmark of an early ather lesion, further driving plaque progression. However, it's not quite as simple as higher LPA, greater systemic inflammation. For years, we assumed that the potent local inflammatory reaction we saw would be reflected systemically in our blood markers like CRP. But a recent trial has kind of challenged that idea. So, the Ocean A dose trial tested a powerful new small interfering RNA drug called Olpir. It dramatically lowered both L-little A and associated oxidized phospholip by over 95%. So, that's huge. But here's a surprise. This profound reduction had absolutely no effect on circulating systemic inflammatory markers like high sensitivity CRP or inter 6. And so, this forces kind of re things, right? It strongly suggests that pro-inflammatory actions of L little A might be confined to a more local micro of the vessel and aren necessarily captured through our System blood tests. And oftentimes, people in healthcare or in the internet will say, Hey, as long as my CRP is normal, I don't have inflammation, and this is direct evidence. Against that argument, saying that, hey, even if our normal values like C or P are normal, we still might have local inflammation. So it's definitely something we have to keep an eye on. All right, so let's talk about the third and final threat, the proth pathway. L. P. little A has a remarkable structure that is so similar to a protein called plasminogen. And plasminogen is the precursor to plasmin, the main enzyme in our body that's used to dissolve blood clots in a process called fib. And because AP looks so much like it, it acts as a competitive inhibitor, thus stopping this crucial process. So far in mechanistic studies, we've seen L little A block plasminogen from binding to clot. which impairs the generation of plasmin which could affect our natural clot busting system. It also inhibits other antic factors, further shifting the balance to a more proth state. That being said, we still haven't seen this pan out in human studies, but it definitely needs more research. But regardless, these mechanisms could create the kind of Perfect storm, right? So LP little A first helps build unstable rupture-prone plaques, then creates more inflammation, and then it simultaneously hobbles the body's ability to dissolve the very clots that form when those plaques rupture. Leading to potential catastrophic issues. And that's why we think this could be so deadly. So when you put the whole triad of threats together, this proathro, pro-inflammatory, and pro environment, you get a clear causal link to clinical disease. And this isn't just an association, it's backed by lots of research from a genetic and epidemiologic perspective as well. The first major clinical manifestations is, of course atheros cardiovascular disease or ASCBD. This includes heart attacks, ischemic strokes, peripheral artery disease, all those things. The second, though, and this is critically important to recognize as well, is it's involved in calcivic aortic valve sten. So, LP-little A is now recognized as a key causal factor in the development of progression of not just cardiovascular heart disease, but aortic sten as well. So, we are not only involving just the arteries of the heart, but the valves as well. Now let's pivot to what this means for our clinical practice. Historically, guidelines only recommended checking LPA levels in very specific high risk groups, like those with family history of early heart disease or familial hyper. However, there's been a recent shift. Recognizing that 20% of the general population has high risk levels without those classic red flags, we're moving towards a new paradigm. Leading global groups like the European Ath Growth Society and the U National Lipid Association now recommend that LPA be measured at least once in every adult's lifetime. The goal of this universal measure once strategy is simple, to identify this 20% of the population with genetically high levels that we can be more aggressive about managing their overall risk. However, the ACCAHA currently recommends checking LPA as a risk-enhancing factor to help risk sp high patients, but doesn't have a formal once-in-a-lif recommendation like other societies have. And when you order these tests, you'll see results in either one of two units: either milligrams per deciliter, which is a mass concentration, or nanomoles per liter, which is a molar concentration. And the molar concentration of the nanomoles per liter is technically the superior method because it directly reflects the number of ather LPA particles, which is actually what drives risk. So, this is kind of similar to L versus AP Ap measures these actual ethogenic lipoproteins. That's what's actually happening here with this molar concentration. And an Ice study suggests this is kind of the case and why it's better to use. It showed that. Once you account for the particle concentration, so the nanomoles per liter value, there was no residual risk left from the size of the APOA proteins, right? So when they get made, you can have varying sizes of these proteins. When you just count for concentration, that seems the most thing. So the number of particles is what matters most. Additionally, L P little A measurement is complicated by its isoform size and heterogeneity. Many traditional immunoassays use antibodies that can bind. Differently depending on the isoform size, potentially overestimating large isoforms where there's multiple binding sites, or underest smaller isoforms with fewer binding sites, right? And so this bias can lead to inaccurate measurements. And it has historically been complicated and made it difficult for us to how do we apply these values in clinical research. So, because of size variation and all these things, there is no unbiased way to convert between milligrams per deciliter and animals per liter. There's lots of variables there, and that's why it's kind of challenging. However, for clinical practice, both units can be used, but it's important to know which unit your lab uses so you can apply the correct risk thresholds, right? A rough conversion is that nanomals per liter value is about a little more than double of the milligram per dec value. But as I mentioned before, this is just a rough estimate and does not necessarily account for all the variation we see with all these LPA values. So, what are the numbers we actually need to know? Well, the most widely accepted thresholds for a high-risk LPA value are greater than 50 milligrams per decil or greater than 125 nanomoles per liter. However, oftentimes levels between 30 and 50 m per dec are considered elevated or intermediate risk. However, universally, less than 30 millig per decil or less than 75 nanomoles per liter. Are typically considered safe, whereas greater than 50 milligrams per dec or greater than 125 are risky. And so it 's also important to remember, though, that the risk is a gradient, right? It's continuous and dose-dependent. Meaning, very high levels, say above 90 milligrams per decilit, can fur lifetime risk of cardiovascular disease that is comparable to having heterozygous familial hyper. So essentially, you can be in that same risk category, which is crazy. And so, practically, what does this mean though? Well, if you have a high value, that should trigger a serious discussion with your patient about intensifying all other risks. Reduction strategies. It's a clear signal to be more aggressive. In fact, this is how the 2018 ACCHA guidelines use LP little A. They say Hey, if you get a value at or above this certain threshold, it should be considered a risk-enhancing factor, which would then lead to a further discussion with your patient on how aggressive you want to be while controlling the other lifestyle factors. This brings us to a critical question. How do we manage these patients today in an era where we don't yet have any FDA approved drugs specifically designed to lower LP Lid? The answer and current cornerstone of management is to mitigate the patient's total cardiovascular risk by aggressively targeting every other mod risk factor that we can. This is kind of a universal recommendation. It means strict guideline-directed therapy for hypertension, diabetes, hyper, robust support for smoking cessation, and promoting a healthy lifestyle. And studies have shown that many patients with high LPA also have undertreated traditional risk factors. So this presents a clear and immediate opportunity for you to make a difference in patient lives. by making sure we're doubling down on every single risk factor. With that global risk reduction strategy, arguably the most important intervention for a patient with high LP little A today is their aggressive lowering of their LDL cholesterol. And the rationale is pretty straightforward, right? You have to reduce the total ather particle burden to compensate for your currently untreatable risk from elevated LP little A. We kind of just balancing those scales. You should view a high LP Litl level as a direct mandate to be more ambitious and aggressive with your LDL or AP reduction. And like most things with LP Lit, there's kind of some gray in the recommendations here. And there's no clear definitive guideline recommendations for Target LDLC goal with an elevated LP. There's a lot of hemming and hawing, but no rock solid recommendations. Some recommendations say you should hit your target goals for the risk level of your individual patient, but that leaves a lot to be desired. However, all the guidelines do recommend aggressive lipid lowering therapy, which could be interpreted as sub seventy milligrams per dec range, with some even referencing maybe lower than 5 milligram per deciliter for even just primary prevention. For secondary prevention, it's pretty universal. They say, hey, you should probably be under 55 milligrams per deciliter if you have elevated LP little A. But for primary, it's kind of. Up in the air. I will say that this is one area that I found lacking in literature. If you a clinician trying to help your patients, it's frustrating to not have a definitive goal or guidance. I kind of think it fits and reflects the uncertainty that we have about LP Little at this moment. So, the takeaway is that if you would normally be This is aggress with the patient, you're probably going to be a little more aggressive with a new patient, right? If they have elevated LP literally, it's just going to be a little more aggressive and it's going to come down to having discussion between you and your patient, right? And so Hopefully, future ACC H guidelines will offer more insight, but there's definitely been suggestions that it's going be reasonable to intensify therapy even if LDL is between 55 and 70. So there's some. Inkling out there that they may say, Hey, you might even go more aggressive, trying to go sub 55. We will see what that goes. There's no definitive recommendations right now, but they're saying, Hey, whatever your normal goals are, you're probably gonna be a little more aggressive in these patients. And so let's quickly run through how our current lipid drugs affect LP-little A. Statins are the foundation, right? Classic, everyone gets these. Unfortunately, they have no direct beneficial effect on L-little A and actually may increase it up to 8% to 20%. And you might be saying, like, what the heck? Like, what are we doing there? Well, it's kind of a head scratch, too. We 're not sure why, but experts do think that being on a statin still outweighs the risk. Because of the massive benefit of lowering the LDL and other athrogenic lip, right? We think getting that massive reduction outweighs the risks of a very small bump up in LP-little light. And so they're still considered standard of care. Then we also have azet as a very minor effect, reducing L little A by maybe 7%. Its main benefit is once again an add-on to statins, reducing that LDL burden. Then we have bempidoch acid, has no direct effect on L-liter that we know of. And like azetam, its role is kind of another adjunct to lower LDL. That's really what it comes down to. Usually, it's in patients who are statin tolerant or as a third-line agent. And for all three of these oral agents, the clinical benefit is usually coming from that L lowering, right? So, as we mentioned before, the main treatment is to lower all ather lipoproteins, and that's what our statins do. You know, if we do get a little Bump in LP little A, we think it's outweighed by how much we're reducing all the other ather lipoproteins. But the general rule is: hey, if we decrease those ather lipop, that's our best bet currently. Now, I do want to move on to our more powerful agents, the PCSK9 inhibitors, like Eviloc and El. So, they do provide a modest reduction in LP-little A, about 25 to 30%. However, their cardiovascular benefit in clinical trials still appears to be driven almost entirely by their profound L lowering, not necessarily the L-little reduction. High LP little A, however, is a strong factor favoring their use to get LDL as low as possible, right? And that's kind of why we use this, once again, just trying to get all our ethogenic burden as low as possible. We also have ic ethyl, which essentially prescription-grade omega-3 fatty acids, has no direct effect on L-little A levels. But a key analysis from the Red trial showed that it reduces cardiovascular events. Considerably across people with all L little A levels. So, this means that you should consider this potentially in appropriate patients, those with high triglycerides or established cardiovascular disease or diabetes. Regardless of the L P little A status. And its benefit seems to be separate but additive. Maybe this is due to the anti-inflammatory effects of the omega-3 in the pro-inflammatory setting elevated LP little A. Not sure that's yet to be seen, but it seems like it may be helpful. It's also critical to know what not to use, right? So let's talk about niacin. Niacin actually does lower L L a little bit by about 25%, but large clinical trials like the AIM High showed it provides No additional cardiovascular benefit when added to a statin and actually can cause harm. And so they did recommend that it should be avoided. And this is by the National Lip Association. Aspirin has no effect on L P-little A levels, and there's no evidence to support using it for primary prevention solely because a patient has high LP-little A. It should be used guided by standard secondary prevention guidelines, or how you would typically prescribe aspirin. And finally, there's lipop apheresis. And actually, this procedure physically removes lipop from the blood and can lower LPA dramatically. However, Due to the cost and invasive nature, it's reserved for kind of extreme high-risk cases with progressive disease despite maximal medical therapy. And so I wouldn't say that you Have to avoid this, meaning it doesn't work. It definitely works, it's very, very effective, but it's just not clinically something you're going to start with, right? You're definitely going to have to have a lipid specialist involved. This is not run in the middle, so this is not our first line. Typically, if you're starting therapy for someone with this situation, like this is not where you're going. It's going be later down the line. And while current management is indirect. The field is on the verge of a massive paradigm shift. Several highly specific and incredibly potent therapies are in the final stages of development. These agents represent the next frontier and the promise to finally give us a way to directly treat and neutralize this causal risk factor. The most advanced therapies use RNA-based mechanisms. They work essentially by silencing that LPA gene inside the liver. Preventing the AP protein from ever being made in the first place. That's predominantly what's going on. There are a couple other variants as well, but the two main approaches are anti-sense oulon or ASOs and small interfering RNAs or SI RNAs. And we'll talk more about those. The leading antis olon is called pellic. So it is designed to find and bind to the messenger RNA that codes for that AP. This binding event flags the mRNA for destruction by an enzyme, which stops the protein from being made and prevents new L p lil particles from forming. Phase two trials were impressive, showing pellic reduced LP lil by about 80%, with 98% of patients getting below the high-risk threshold. So that's pretty huge. The definitive test, though, is going to be the massive L L Horizon out trial. The study will tell us if this 80% reduction actually prevents heart attacks and strokes from happening, right? So the top line results are expected in 2026. And so we see these massive reductions, a common theme here. Massive reductions, but we don know if they're clinically meaningful yet, and that's why we need more research. The other major RNA approach is with small interfering RNAs. And these are medications that have very complicated names. One specifically they talk about is Olparic, and there's also le and xer. I sure butchered those, but those are the names. And these drugs tap into the body's natural RNA interference pathway to find and literally splice up the APO messenger RNA, again silencing that gene. The results here are even more profound. In the Phase two Ocean A dose trial of op, it showed a 9% reduction in L p litole, which is incredible. And what's more though is that this effect seemed pretty durable. A huge reduction of 40 to 50 percent. Was still seen almost a full year after the last dose. And the large Oce Al trial is now underway to test, once again, if this has effect on clinical events. But we are seeing these have profound impact on lowering L P-liter levels. And while injectable RNA therapies are huge and exciting, a big breakthrough has recently happened with the development of Mol, a first-in-class oral small molecule inhibitor of L-little A. The drug works by a completely different mechanism. Instead of stopping the Ap protein from being made, it stops the final assembly of the LP little A particle. It basically blocks the Ap protein from attaching to the Ap on the LDL particle and preventing the complete dangerous LP particle from ever forming. This development is going in oral pill form and could be a massive game changer for patient acc and adherence. And it will be a major advance if we get going. But once again, we have a lot more research to still do, but it's down the pipeline. And as we get closer to these powerful new therapies, some nuanced questions are emerging. However, one of the most fascinating is the LPA and type 2 diabetes paradox. Large genetic studies have shown this previously, and they've shown a strange link. People with genetically very low or absent Lp-l A levels have a slightly increased risk for developing type 2 diabetes. This genetic signal was echoed in the Oce A dose trial of O, which reported a small, non-significant increase in hyperglycemia in the treatment groups. This raises a Critical long-term safety question, right? Similar to the small diabetes risk increase we see with statins. The ongoing outcome trials are powered to assess this, and it'll be Very helpful, and it's most likely that there are going to be a net benefit taking these medications, even with the bump up and things. But it's just definitely something worth mentioning and wanting to keep an eye on. And it's, you know, there's no free lunch. That's the takeaway here is that there's no free lunch in anything we do. It's also clear that the harmful impact of LP-letla is magnified in certain high-risk groups as well. And so, specifically, I want to talk about a couple groups that have a higher-risk status than someone else. So, in patients with familial hypocholesterolemia or FH. Who are already at a high risk from high LDL, the high LPA creates a kind of dual hit of ather particles, right? Creating an exceptionally high risk state. Elevated L is also very common in findings in younger people who have heart attacks or strokes or without the usual risk factors. So the relative impact seems to be greatest in those For the premature causes of AS, this is probably the most classic thing I see in my clinic: someone with either a strong ham family history or they had an earlier cardiovascular disease. You're wondering what's going on, and it may be due to this elevated L-little A. And finally, and this is critical, you can have elevated alkal in children and adolescents. Usually, if they're above 30 milligrams per dec, they've been linked to an increased risk of ischemic stroke. This is not something they recommend you're routinely screening for, just something that if you see this in a patient, you may want to check for this. Understanding this risk factor may exist in our pediatric population as well. D all of this incredible progress, several key questions remain that will shape the next decade of research. First, what is the optimal therape target? Should we aim for a more specific number, like less than fifty milligrams per dec? Or maybe a percentage-based reduction. We're not sure. Second, will these therapies be beneficial in primary prevention? We're not sure. That's what the studies will show. And third, will the measure once approach, will that hold, right? Or will we need to do serial monitoring as we guide? We're not sure. The takeaway here is that we have learned so much about this, but we still have so much more to learn. So things are going to change. And don't be caught off guard if things do change in the future. All right, so let's wrap this up here with some key takeaways. So, what are the key clinical takeaways for clinical practice? Well, first, the era of ignoring LP little A is over, and maybe we're ignoring it. Maybe we just didn't know it existed. But either way, that's gone. It's a common, independent, and causal risk factor for ASCBD and aortic sten. It's a mainstream topic of conversation now, and it's not going anywhere. Second, it seems like it'll be inevitable that universal screening of all adult patients at least once in a lifetime will become commonplace. The goal is to find that one in five people with levels over fifty milligrams per dec so we can try and prevent a future cardiovascular event. And third, for any patient that you do find with high L-little del, the primary strategy today is aggressive management of all other modifiable risk factors. And finally, looking ahead, a new era of specific targeted therapy is right around the corner. These RNA-based drugs like thul and olpir are capable of lowering L by an incredible 80% to 95%. The results of the LP Little A Horizon trial, which we expect to see in 202, are set to be a landmark event in cardiology. It will likely deliver the first ever approved treatment to directly neutralize this high-risk form of LP Little A. However, Before we get too excited, we need to see if those medications actually lead to clinically meaningful outcomes. However, the bottom line is that the scientific and therapeutic landscape for L L is moving at an incredible pace. And the next few years are going to be completely transformed the way we do preventative cardiology, giving us new tools to protect our highest risk patients. So it's absolutely essential to stay informed. All right, that brings us to the end of our discussion. As we've seen, LP little A has moved from a niche research topic to a very important and clinically meaningful risk factor we should all be aware of. In the next few years, our approach to preventative cardiology is set to be completely transformed. All right, and that's going to be it for today. Thanks so much for stopping by. I really appreciate it. If you enjoyed this podcast, it would mean the world to me if you either. Share this with a friend, left a five-star review on your podcast platform or choice, or subscribed on YouTube. But that's going to be it for today. Now get off your phone and get outside, have a great rest of your day, and we'll see you next time.
