Dr. Vahid Yeganeh

August 18, 2026

Topic: What Lp(a) Is and Why You Should Care

Healthy Habits Episode 7

All right. Well, good evening. welcome to, to today’s talk, the Healthy Habits segment here. Thank you, TY Healthspan, for having me on. I’m Dr. Vahid Yeganeh. I’m a physician, I’m boarded in family medicine, obesity medicine, lifestyle medicine, and I love everything that has to do with cardiometabolic health.

And so today we’re gonna be talking about Lp(a), which is essentially a cholesterol related particle, excuse me, that most people haven’t had measured, although that’s changing, and I like that. and we’ll do about a ten, fifteen minute, talk here and then, jump into questions if anybody has any.

So I’ll get right into it. It’s easy to get lost in the weeds here. I will do my best to keep it light. I wanna get a few key points out there, but, let’s jump right into it here [00:01:00] And throughout the course of this talk, essentially I’m, I’m trying to answer these things for… these three things for everybody, which is, you know, first and foremost, biologically, you know, what is this thing?

What is this, Lp(a)? It’s also,… we refer to it as “Lp little a”. So I’m just gonna call it Lp(a) from here forward. You can imagine it’s, it’s got a quite a long name. And then, once we understand sort of what it is, why is this something that we should be paying attention to? And if we do have high levels of this thing, then, you know, what are we supposed to do about it?

Okay. So, that’s the goal of, of, of this talk, is to kind of be able to answer those questions for you. And so this Lp(a) that we’re gonna… that we’re talking about is essentially if you’ve ever heard of bad cholesterol, right? So if you’ve ever done a traditional lipid panel, which most adults have, and you’re looking at what we call LDL cholesterol or some people will refer to it as the bad cholesterol.

The Lp(a) is actually structurally, [00:02:00], a lot like the LD, the LDL cholesterol particle with an extra thing attached to it. Es- essentially, I call it a tail. It’s like a little tail attached to it. and that tail makes, quite a bit of a difference here. Then I’m gonna skip forward because I’m, I’m visual, and so maybe others are the same as me.

So we’re looking here on the left side of this slide, this image here, we see the yellow kind of circle. That, that yellow part is the lipid core, right? And the blue around it, that’s what we call ApoB. We don’t need to, you know, dive into that or anything. But the golden and that yellow part… sorry, the golden and the blue part is, essentially an LDL cholesterol.

You can consider it, to look like that. And then what you see on the outside of that, right? All those kind of curly squiggly lines, like coming around down, that’s the tail I’m talking about. That’s the, apolipoprotein(a), is actually what that’s called. and that is what’s making the difference. And it attaches itself to the ApoB.

[00:03:00] Again, I’m not gonna test anybody on this. We don’t have to get too much into the weeds, but I, I’m a visual person. I think it’s, it’s helpful to sort of picture, okay, I’ve got, like, this bad cholesterol thing, got an extra thing attached to it. All right? That’s what I want you to take away from that. And so this is, essentially anywhere from seventy to ninety percent, genetically determined.

and what that means is, you know, you could do everything perfectly your whole life as far as lifestyle is concerned. It’s not really gonna impact to any, considerable degree the the level of your Lp(a). And the numbers of our Lp(a) sort of the, the, the quantity we have is, essentially it stabilizes at around age five.

So this is from all the way from when we’re kids, and it stay– and it remains stable throughout, throughout our life, right? Now, different populations will have, different risk of having high Lp(a). If we looked at overall in the world, [00:04:00] you know, about one in five people, so about twenty percent of the population will have an elevated Lp(a).

And, some populations, like if you’re of African descent or Southeast Asian, or sorry, excuse me, South Asian, you can have even like one in four. And then East Asians, they have slightly less. But generally speaking, if we’re looking at, you know, population as a whole, we’re looking at about twenty percent.

but full disclosure, I’m one of those lucky, lottery winners, so I have a, an elevated Lp(a), genetically. All right? So I’m one of those twenty percent. And, obviously I got myself tested for what the reasons I’m about to explain. So question that comes to my mind, and I I feel like will probably come to, to most people’s mind is: Well, you know, if this thing is in my body, and it’s, you know, genetically determined, like what, what’s its purpose, right?

sure, someone might have a high level, someone might have a not so elevated level, [00:05:00] but what, what is the function of this thing? The truth is we’re still trying to figure that out in the scientific community. There’s a lot of good theories, but we don’t know a hundred percent. The leading theory right now is that it has to do with wound healing and tissue repair.

The idea is that, so structurally it looks a lot like this protein that breaks down clots, and so it can compete with that, and it’ll, essentially make it easier to make clots. and, and some of the, the ideas around this theory about the wound, wound healing essentially is that if you think about sort of earlier in human history, this could be useful, right?

That, that we would clot faster or that we would be able to heal wounds, a little bit better at the expense of, you know, maybe down the road at sixty, seventy, eighty, ninety this could be an issue, but we weren’t living that long back then. So that’s sort of the theory around that, is that this is something that probably was useful earlier in human history, and it’s just kind of [00:06:00] no longer, as useful for us, as our environments have changed, our longevity has changed.

And that’s all I will say about that. I feel like I had one more thing to say on this theory, but if it comes to me, I will, I will pop back into that idea. But let’s move on. so, you know, the title of this slide is Triple Threat. It’s just a fancy way of saying that it is having its negative effect on us, in three different ways.

One is atherogenic. What does that mean? It’s really good– This Lp(a), is really good at getting into the artery wall. It’ll jam itself into that artery wall, and that’s how plaques start, right? If you’ve ever heard the, the expression plaque in your arteries, that’s, you know, either LDL cholesterol.

There’s different types of cholesterol particles that can do that, but the Lp(a) is particularly good at that. So that’s one of the things. It’s atherogenic. It’s pro-inflammatory, excuse me. So it, it carries with it these oxidized phospholipids, and it’s, and it [00:07:00] sets off this inflammation, inflammatory process.

And so that’s not great when we are, you know, looking at the health of our vasculature. And then it’s prothrombotic. So for the same reason I, I, I mentioned a bit earlier, structurally, it, it, it does look a lot like, plasminogen, which is a, a protein that breaks down clots, and it will impact the, the body’s ability to break down blood clots.

All right? So those, those three things kind of make up its– why it’s, it’s got these negative effects. And so what could it cause? You know, it can increase your risk for a heart attack, for a, a stroke Peripheral artery disease, aortic valve stenosis, right? Now, you’ll notice these are… No, these are separate things.

But really when you think about the mechanism of what’s going on, it’s not really separate. You know, Lp(a) is gonna… If it’s elevated, it’s elevated throughout your whole, circulation, throughout all of your blood vessels. So wherever it’s kind of jamming itself into those walls and [00:08:00] creating plaque and, you know, creating inflammation, it’s gonna create an issue.

So if that happens to be the arteries that, you know, bring oxygen to your heart, then that’ll lead to a heart attack. If it happens to, be towards your brain, that would be a stroke, or if like a plaque or, you know, kind of earlier on breaks off and goes up into one of those vessels in your brain, that would cause…

This is what we call an ischemic stroke. So it’s a stroke, not where you’re bleeding, it’s where you’re, you’re not getting enough blood to that area of the brain. Peripheral artery disease, same thing. If we’re getting a bunch of plaque deposited into the arteries, around the legs, we’re impacting the blood flow to the legs, and we get peripheral artery disease.

And the aortic valve stenosis, not too dissimilar either. The aortic valve is the valve in the left side of our heart where we push this blood out to, so it can get to all the organs where it needs to get. And in that valve, if there’s, you know, this Lp(a) kind of jamming itself in there, there’s inflammation going on, that’ll eventually calcify, get like calcium deposits in it, and it could [00:09:00] impact that valve and how well it functions.

Okay. So separate things, but really similar process, similar way that we’re getting to that point, right? so why does testing matter? well, first and foremost, it is a, it’s a risk factor in and of itself. It’s a risk enhancer. So that means that, you know, if you’re wanting to know my cardiovascular risk, and you’re just getting a standard lipid panel, which gives you a lot of information.

nothing against the standard lipid panel, but you could have a completely normal standard lipid panel, as do I actually, and have an elevated Lp(a). So it’s not… It can be, it can be independent. You can have completely normal everything else and have this elevated, and that by itself can be a, a bit of a risk enhancer, depending on how high it is.

And so that’s, that’s quite important. It’s important to the point where this [00:10:00] year, March of this year, new guidelines came out that said, “Okay, yeah, you know what? We’ve decided…” And this is multiple organizations, I think like a whole panel, like 11 different organizations are supporting these guidelines, saying that we need to test this once in our lifetime.

Now, why once in our lifetime? if you remember, I mentioned that, you know, right around the age of five onwards, this number kinda stays stable. not a whole lot we can do about it when it comes to lifestyle. I’ll get into that a little bit in a moment in terms of what we can do about it. And so we just need to know, are you so- are you one of those one in five people or not, right?

Like, do you have that additional risk factor, or do you not? and so we do that just one time. Now, down the road, you know, as we develop medications that will lower this, then, you know, we could fall into a situation where now it makes sense to repeat. But for now, we only check it once, in someone’s lifetime, excuse me.

And then if you’re positive… So again, I’ll use myself as an example. So if you have that [00:11:00] positive, since it is, genetically determined, all your first-degree relatives should be tested, and you know, that siblings, parents, children. ‘Cause, it is… And I think I have this on my next slide, but it’s, you inherit a kind of one, one of these, alleles of this gene.

There’s a gene, an LPA gene, that decides who gets high levels of Lp(a) and who doesn’t, and so you get one from each parent, right? And so it, it’s important to screen first-degree relatives. So what… Let’s say you got it tested, right? So you listen to you listen to this talk, and you’re like, “Well, let me talk to my doctor and get this thing tested.”

there’s two different, sort of, not ways that it gets tested, but I guess ways because… So we have particle number and we have mass. Okay, so when we do this one, which is in nanomoles per liter, again, I’m not gonna m- make this too academic, I promise. [00:12:00], I prefer this. This is, in my opinion, is slightly, superior to doing the milligrams per deciliter.

This is looking at, mass, whereas this is looking at particles. So, I prefer this, and this is,… At least I’ve done my testing through Quest, and they seem to do this one. So again, just a small nuance. It doesn’t really matter too much as long as you get it tested. So if we’re looking at the nanomoles per liter, once we hit that one twenty five mark, that’s when the risk becomes– starts to become significant.

Like, if somebody has a hundred and twenty-five, and up, that’s– we gotta pay pretty close attention to that. when we get all the way up to two hundred and fifty, the risk actually doubles, at that, at that stage. So again, we’re, we’re, you know, hoping that, if we do find this number high, it’s not, as high as, let’s say, two fifty.

But again, that’s gonna vary from person to person, unfortunately, depending on genetics. So [00:13:00] this is, this is the hard slide to talk about because, we don’t really have medications currently in the market that can bring down your Lp(a) levels. There is a medication that’s for, lowering cholesterol in general, like your LDL cholesterol.

That class of drugs is called PCSK9 inhibitors. You might have heard like some of the commercial names like Repatha and whatnot. They’re in- injectables. that can lower it, to the tune of about twenty to thirty percent, I believe. but it’s not intended for that. So it’s not like you can say, “Hey, I have a high Lp(a).

I need my insurance to cover that.” It’s just not gonna be the case. But if for some reason you happen to be able to get on a PCSK9 and you have a high Lp(a), you will get some benefit from that. So, so what does that mean? You have a high Lp(a), there’s no drugs to treat it. What… You know, lifestyle apparently can’t touch it too much.

That’s my next slide. But, so yes, we can in fact [00:14:00] do something about it. So what we do is we, optimize for all the things we can control, so all what we call modifiable risk factors, right? So there’s non-modifiable stuff like our age, our gender, et cetera, but, risk factors that are modifiable, like if you smoke or if you’re overweight or obese or if you, you know, if you’re, type two diabetic or pre-diabetic, optimizing all those things.

Maybe your blood pressure is a little bit high. Treating those things, getting all those things to their optimal levels actually makes a difference. and on the right, this– I know that the text on this slide is a little bit small. I apologize for that. So I’ll just walk you through it. Basically what I’m saying on the right side here, there was a study done in a UK Biobank study, over four hundred thousand adults were looked at.

They looked at those people that had the highest Lp(a), right? And then they looked at those with four or more healthy lifestyle habits. I’ll, I’ll bring it full circle to the… I think these talks are called healthy habits. So four or more healthy lifestyle habits. They compared those to had only zero or so [00:15:00] none or one of those healthy habits.

The– They had forty-five percent lower risk of a coronary event, so, like, you know, a, a cardiovascular event. That’s a big deal. So Lp(a), not something they could really touch in terms of the, the levels, but they were able to, you know, utilize healthy habits to optimize the rest of the, the, the risk factors, right?

To lower the LDL cholesterol to, you know, to make sure they’re exercising, et cetera, et cetera. moving along. So I did say there’s no medications so far. However, there are several in phase III trials, phase III that it’s, you know, getting ready to come out into the market. of those, you know, I, I don’t really see the point in reading off all of the names to you, but I’ll say Pelacarsen, the first one you see there, we are waiting for results of that, the trial.

The, the name of that trial is called the HORIZON, and it’s due at any moment. I’m, like… I’m checking the news every day actually, waiting for this data, because it’s real [00:16:00] world data on the, outcomes of this is, if you think about it this way. So, you know, these medications in the studies I’ve been looking at, they all have been bringing down Lp(a).

So that’s great news. They’re, you know, they’re finalizing a few things obviously. But once we can bring that number down, then the question is, okay, so we take someone like Dr. Yeganeh who has a high Lp(a), we give him this drug, we brought the number down. Did he actually have less of a chance of a heart attack or, you know?

So we’re looking at these studies and saying, by lowering this, are people having less heart attack, less strokes, they’re dying less, or, or, you know, less, like at a later age versus, if we hadn’t given them this drug? And so that’s why the data on these studies is really, really eagerly awaited because it’s- I have a que- I have a question you want to ask?

Yeah, go, go ahead. I’m sorry. Yeah. I was gonna interrupt with a question that might be- Yeah… with, with you right here. Yeah, absolutely. Yeah. so looking through the lens of, let’s [00:17:00] say, longevity and healthy habits combined, how does Lp(a) compare as a marker to know for longevity reasons versus like ApoB or fasted glucose levels?

How does it compare? So it, it’s valuable in that if you, if you test it and you don’t have an elevated number, well, then you know you don’t have that risk factor, right? If you test it and it’s high, it would just make it that much more important to optimize everything up. And we have clear data that that makes a difference.

So, for example, like ApoB, ApoB is attached to, to essentially every- everything that can cause plaque, right? And so that’s a very useful number to track, right? To just see, do I have a high level of, you know, any of these particles, whether it’s LDL [00:18:00] cholesterol, IDL, VLDL, whether, you know, Lp(a) that, that is causing plaque.

And so that’s something you’d wanna track over time. Mm-hmm. fasting blood sugar, fasting blood sugar similarly. With Lp(a), you’re just doing a one-time to say, “Do I have this risk factor or not?” Currently, today, right? In today’s world, like up until what we know now. Now, once these m- medications come out and perhaps we- we’re able to, lower it and then track as well.

But right now it is,… I would look at it like this. It’s like having an extra data point. It’s like having a broader picture of your- Yeah… cardiovascular risk. And so if you, if you, if you wanna put it in the context of longevity, the number one thing that’s killing US adults is heart disease, right? So- Mm-hmm

Lp(a) is directly related to heart disease, and so I would wanna know. That’s why I tested mine. I hope that, that- It seem… Yeah… answers the question. Yeah. It seems like a… It, it does. It seems like it’s an important factor to know, and you need- Yes… to get it [00:19:00] known at least once in your lifetime. Yeah. In this, in this space, I mean, I’m not, board certified in lipidology, but I, I, I love the topic, so I end up going to a lot of their conferences and following lots of this stuff.

So in that space, we’ve known about Lp(a) for a very, very long time. it’s just never been part of the guidelines until this year. So as of this year, it’s… And, and what that means, bottom line, is more and more physicians that were perhaps, less aware of this before, or, or not just physicians, any healthcare provider that could be ordering you blood work, right?

now that it’s part of the guidelines means much more or many more healthcare professionals are gonna be knowledgeable about these things. Whereas before it was only cardiologists, and even, you know, some years ago, maybe even certain, certain cardiologists, but usually it’s, it’s just cardiologists who follow that space closely.

So this being more now mainstream guideline this year [00:20:00] makes it so that, maybe, you know, as I talk about it today, it’s not as well known, but I’m sure a year from now, two years from now, it’s, it’s going to start becoming part of your standard cardiovascular, risk assessment. Thank you. It’s very helpful.

You’re welcome. Absolutely, no problem. and I’m, and I’m winding down here. I, I know, I promised that we wouldn’t, we wouldn’t keep you too long. But, yeah, so this, this is a- actually my last slide. So if you take anything away from this, it’s the following: Consider getting tested for Lp(a). Talk to your, you know, to your doctor about that.

insurance-wise, like, does insurance cover for it? That’s a question that comes up a lot. it’s kind of all over the place. I feel that that is going to improve because of the guidelines now that it’s, you know, it’s something that, you can hang your hat on. Like, “Hey, this is part of guidelines, so, you know, it, it’s recommended.”

But it’s still kind of all over the place. There are… If you Google Lp(a), I believe there’s a [00:21:00] foundation, I can’t remember their name. I wanna say maybe heart something, family heart, that I think offered, like, a home test kit for it. I’ve never used it, so I can’t really speak to it. you know, I think you can also participate in research and get that tested, because there’s a lot of ongoing research, on this topic, as you can imagine.

So getting or at least being curious about maybe getting tested, my first line of recommendation would be talk to your doctor. “Hey, what’s Lp(a)? I heard about it. Should I be getting tested for it?” Right? That, that’s, that’s one thing. If you do get it tested and it’s elevated- Consider the same thing for first-degree relatives, okay?

And then if it is elevated, optimize for everything else. And so again, kind of, adding on to the answer to your, to your question, Fred, is that if you never test for it, and you’re always having a normal lipid panel, it can, you know, it can give you that false sense of, oh, I’m fine. I don’t have to be as, you know, as aggressive about, what kind of [00:22:00] lifestyle I’m leading because my LDL cholesterol is always really low, right?

that’s actually ties also into, you mentioned ApoB. I’ll order an ApoB alongside the standard lipid panel because some people will have really small, dense, LDL cholesterol particles that won’t necessarily show up as elevated on the standard lipid panel but will have a high ApoB. It’s what we call a discordance there.

And so that’s a– that and then you combine to that, with that the Lp(a), all of a sudden I have this bigger picture, right? And then as science advances, we’ll probably have bigger and bigger picture to look at. But right now, I feel that Lp(a) test definitely adds a useful, actionable part of that picture.

and yeah, talking about, so for example, if your Lp(a) is high and you’re kind of on the fence about, about taking a drug to lower your LDL cholesterol. Let’s say your LDL cholesterol was kind of high but kind of borderline, and your doctor was like, “Well, we can try lifestyle for a little bit, and then maybe we have to end up on a medication.”

If you happen to have [00:23:00] an Lp(a) test done and that’s high, well, that’s, that’s shifting the weight towards, well, let’s be more aggressive about lowering this. Maybe we do need to consider medication, right? Or maybe we instead of just casually thinking about, dietary pattern change or more exercise, really making a plan around that.

So it makes a difference in the decision-making around somebody’s health, specifically when it comes to risk reduction, longevity, all of that ties into it. and then keep an eye on this space. There are medications, like, on the verge of coming out into the market that will impact this. And so who knows?

Maybe at another healthy habits talk, I’ll come in and talk, you know, about those horizon results if anybody’s interested. But, I will, I will, I will leave it at that. If there’s any, if there’s any other questions, happy to address them. Thank you for, for your time.

Yeah. Thank you, thank you, Dr. Vahid. This is very helpful. I think what you’re underscoring is more marker information, more data, more [00:24:00] robust picture can actually help you with your decisions around healthy habits or around medication or around a combination of those things if you’re finding yourself with high Lp(a) scores or high ApoB scores.

Yes. Absolutely. I think it’s… it definitely plays a part, in essentially, getting an objective data point, right? So this is, just more information that you can use, to make your health, health decisions, I guess, along with your doctor. Yeah. Is there anything more you wanna say that would leave us feeling hopeful after hearing this?

Yeah. ‘Cause that’s a, that’s a good note to, to end on, actually. This is… I don’t want this to feel all doom and gloom. Oh no, if I have it high, there’s no medication to lower it. I would say think about that study I mentioned where having, you know, those four or more healthy habits when they [00:25:00] compared it to just as high Lp(a), forty-five percent less risk of, of heart attacks.

Like, I, I go to sleep well at night with a high Lp(a), you know, because I’m, you know, I, I know I’m optimizing all these other factors. and so, it’s not all doom and gloom. Things will get better as we get, you know, these medications out in the market and kind of understand them a bit, bit better and see what they do in the real world.

but it’s just information. It’s not something to necessarily lose sleep over. I, I, I’m of the thinking the more information we have, we can make more informed decisions around our health. Excellent. That’s a great way to summarize it. Thank you so much, Dr. Vahid, for contributing to Healthy Habits. We do this every Tuesday night with TY Healthspan, and, you’re definitely gonna be invited to come back and speak some more.

But we’ll see. I appreciate it. Thank you. And for, and for everyone out there who’s checking this out on YouTube, go ahead and continue to like and subscribe, share this with your friends. You’ll be seeing more of this content [00:26:00] in social media, on our website, in our blog posts, and thank you for showing up for Healthy Habits and making yourself healthier.

I’m I’m Fred Spring with TY Healthspan. Dr. Vahid, welcome, and welcome to the core. I’m glad you’re part of this team, and, we look forward to more information from you. Thank you. Bye for now