The tools we've relied on for decades to predict who's going to have a heart attack and who isn't, well they're flawed.
And in some cases, they've actually been blinding us to the actual danger.
It's a profound realization, honestly, for the whole medical community.
I mean, for a long time, we thought we had a map for exactly how to snuff out cardiovascular disease.
It was perfectly drawn out, we were done.
But it turns out we were looking at proxies.
We were kind of measuring the shadows instead of the objects that were casting them.
And today, we are going to show you why that's the case.
And so,
The new ACC and AHA guidelines represent a fundamental shift in how we understand the pathophysiology of atherosclerosis, right?
So, today we are going to dive into the first actual section of this document.
Section one is a bunch of disclosures and tables of the authors, which is very important.
It shows you.
Who works for who, who consults for who, and it's helpful to see that.
And section two is a bunch of definitions, which also can be helpful.
But I'm going to start here at section three, which is where the meat of all this starts.
And so today we're going to look at the five subsections of section three, which are screening.
Standard measurements, APOB, lipoprotein little A, and monitoring.
So let's dive into it.
And I do want to make one disclaimer: these are the guidelines, but it does not mean this is how you treat every single patient, right?
I think a lot of times in medicine,
We've been guilty of the guidelines for this, so we're going to do it.
Like, we need to stop treating patients like robots and treating them like individuals.
Some people will have a high risk tolerance, others will want to be very aggressive.
And so
It's important though to know the guidelines so you can understand how you deviate from them, right?
If you don't know the guidelines, you're just winging it, that's not a good idea.
But my whole goal in this is so you have a very good understanding of the guidelines.
So then now you can have a personalized conversation with your patient and say, hey,
Do you want to be this aggressive?
Do you want to do this?
Do you want to do that?
And so that's really the main goal.
It's not to be like robots, like, oh, algorithm says this, do this.
No, it's so you can have a good understanding so you can then.
Add that nuance, use your brain, use your doctor brain, that's the most important thing, and then have a conversation with your patient.
So, that's just my disclaimer.
So, let's start with a jarring update that is pretty much guaranteed to cause a stir in the primary care world, which is about screening in pediatric populations.
And now,
On the adult side, not a whole lot changes.
The baseline is pretty familiar.
We're screening adults starting at age 19, repeating at least every five years, and tightening that interval if they have ASCV risk factors.
Nobody's going to blink at that.
That is pretty standard.
We're looking for multifactorial dyslipidemias and trying to intervene before subclinical disease actually takes place or has an event.
So that's what we're looking for.
But the pediatric side is where people are probably going to push back a little bit.
The guidelines are putting an emphasis on universal screening for children specifically between the ages of 9 and 11.
And if there's a family history of severe hypercholesterolemia,
Meaning greater than 190, or if you have familiar hypoclasteremia, they're recommending screening as early as age two.
Now, if I tell a room of clinicians that we need to stick a needle into every nine-year-old arm,
They're going to kind of think I'm crazy, right?
Or they're going to think it's overkill.
And they're going to ask, well, why can't we just rely on family history?
And the answer is that we're probably not getting the whole picture by just including family history.
That's what we're looking at.
So, first, let's tackle the age window.
So, why 9 to 11?
Well, during mid to late puberty, as a child enters tanner stages three and four, their total cholesterol and LDL actually can decline by as much as 10 to 20 percent.
And this happens because during this time, you have a massive demand for cholesterol in your body.
And cholesterol is the fundamental building block for all of our steroid hormones, right?
So, as the gonads wake up,
And it begins synthesizing massive amounts of testosterone and estrogen in teenagers to drive growth and sexual maturation, the liver has to respond by pulling in more cholesterol, right?
So it pulls more LDL into the liver to make these hormones.
So essentially, the body is just vacuuming up cholesterol to make puberty hormones.
And so, what they're saying is if you wait until someone's a little older in puberty,
Because of their increase in LDL receptors, that the clearing of cholesterol from the bloodstream may actually show artificially low cholesterol values.
Now, other people may ask: well, why can't we just rely on family history?
And ultimately, it comes down to that we're all just terrible at getting good family history.
And also, up to half of children with severely elevated LDL do not report a family history of premature cardiovascular disease or hypercholesterolemia.
So, relying strictly on family history isn't going to give us the whole picture.
It's definitely better than nothing, but it's not ideal.
And once again, I don't mean to beat a dead horse, but maybe you're asking, why are we being this aggressive?
Well, it's because the paradigm is kind of shifted in the world of lipidology.
We now think of this as a lifelong issue, and the higher levels you have for a longer period of time.
Leads to more issues and earlier cardiovascular disease.
And they get this idea from Mendelian arrangement studies.
And maybe you've heard these terms before, but aren't quite sure what that is.
So I want to take a second to explain that.
Mendelian randomizations are essentially nature's version of a randomized controlled trial.
When humans reproduce, the genes are shuffled and distributed randomly, right?
That's the Mendelian part.
We all remember that from biology.
So, we can then take a look at a massive population and find a cohort of people who won the genetic lottery.
So, for example, say they were born with mutations like a loss of function in the PCS canine gene, that naturally results in their lifetime LDL being incredibly low from the day they were born.
And when we tracked these people over a lifespan, they found that they reduced their lifetime risk of cardiovascular disease by 80 to 90% compared to the general population.
So, the idea is: if we intervene earlier in life, whether it is adolescence or early adulthood, you get a bigger bang for your buck and a greater lifetime risk reduction.
That's where all this emphasis comes from, right?
We looked at these Mendelian trials saying, hey, these people who had low LDL for their entire lifetime had a way lower risk of getting cardiovascular disease.
So that's why they're placing the emphasis now.
And on top of this, reading in the paper, they mentioned that one in five adolescents in the general population have abnormal lipids, and roughly one in 250 kids have heterozygous familial hypocholesterolemia, which to me seemed pretty darn high.
I did not expect that.
But the craziest thing is also, they've done autopsy studies on children who've died of non-cardiac causes, and they've seen a subclinical atherosclerosis in children as young as 8 to 10 years old.
And so this thing
This is starting very early in life, and that's why we're screening.
And so that's what we're looking for.
Right now, we screen about 10 to 20% of the population.
That's not a whole lot.
And so the recommendations.
are to check all children so we can try to capture these cases that could potentially lead to catastrophic incidences later in life.
We're trying to catch those earlier so we can prevent them.
Now, let's move on to talk about how we actually measure the cholesterol tests we order, right?
We all know how to order them, but now let's talk about what we're actually ordering.
And here's a few things that I think will change your practice immediately.
So, traditionally, we've always been told to get your lipid panel fasting as that's the best.
In the old guidelines, they did mention you could get non-fasting, but they hadn't really caught up to clinical practice yet.
But now, specifically, they're giving a class one recommendation that a standard non-fasting lipid panel is perfectly fine for estimating risk.
And like, that's all you really need to start.
They're saying, kind of point and period, that's all you need.
And maybe you're like me and told that we need to have fasting to make sure we have the most accurate lab.
And I was surprised to read that that may or may not have been the whole story.
Basically,
We were told to fast because eating may throw off high triglyceride values.
And although that's partly true, they found that on a population level, the vast majority of people did not have clinically significant changes in their triglycerides, even after eating food.
And more importantly, LDL and non-HGL levels varied almost 0% between fasting and non-fasting studies.
And so, overall, they found that a predicted value of a non-fasting lipid panel is identical to a fasting one.
And clinically,
A non-fasting panel may actually be better because it reflects the actual physiologic state of people, right?
Actually eating, see what it looks like.
Plus, dropping the fasting requirement could potentially increase patient compliance as they can now just get them done the same day and not have to worry about coming back after they're fasted.
However, there are certain circumstances where facet labs are still preferred, and that is if the patient has a known personal history of a triglyceride metabolism disorder or a family history of it as well, or a genetic.
Dyslipidemia, all those other circumstances, we would want to get that.
On top of that, also, if you get a non-fasting lab and the triglycerides come back high, specifically over 400 milligrams per deciliter, you should bring those patients back for a fasting draw.
And so
In my personal practice, it's been that way for a while: saying, Hey, let's just try non-fasting.
And if it's tracheal surgery way up, we'll have to come back.
But a lot of times, it's just easier to capture patients in that time and get it right away.
So, that way, we capture more people, actually get the lab so we actually know what's going on.
I think it's a huge win.
Another topic they talk about that's pretty darn nerdy, I will admit, but actually kind of interesting, is that they recommend changing the equation we use for calculating LDL values.
So, historically, we've used something called the Free-to-Wall equation that was published back in 1972 and has been the standard for about 50 years now.
And this was created because typically we can't measure LDL or VLDL directly.
It's technically difficult and very expensive, so we came up with an equation to help us estimate the LDL and VLDL based on total cholesterol, HDL, and triglyceridin.
I won't go into all the details because they're honestly behind me and above my understanding, my simple brain.
But they found that the old equation used to have triglycerides divided by five to get the LEDL estimate.
But it turns out.
That fixed number probably isn't perfect for everybody.
It's not the most accurate thing that we use.
And so, what it did, it was overestimated the VLDL, which in turn underestimated LDL when triglycerides were higher.
But also, it didn't have a really accurate value for ALDL, even if it was very low as well.
So, if your LDL is very low, it's not going to be accurate.
If your diglycerides are high, it's not accurate.
And so
There's lots of reasons why it was an issue.
And so the guidelines now give a class one recommendation to two specific equations: the Martin-Hopkins equation and the Samson NIH equation.
The Martin Hopkins equation utilizes a massive modern database of lipid profiles.
So instead of a fixed divide by five rule, the Martin Hopkins algorithm uses a customizable denominator.
So it looks at the patient's individual.
Non-HDL, cholesterol, and their specific triglyceride levels, and selects a perfect dividing factor from a table of like 136 possibilities.
So it tries to personalize the math.
To the patient's exact metabolic state.
Pretty fancy.
And then the NIH equation is a similarly complex algorithm that is used to try to prevent and kind of find an accurate estimation, even with patients with hypertrogodemia.
So specifically.
With hydrogen, triglycerides, how do we make it better?
And this is great news for pretty much all of us, right?
So, we don't have to do this math though, like on a napkin.
There's lab software that does this automatically.
And so, the big idea is just asking what software, what equation does your lab use now, right?
So, you just have to ask and see.
I wouldn't freak out if it doesn't change because we've been doing this for so long, but change will probably gradually be coming, right?
So it's something that we can bring up if your lab's not aware of it, but it's going to be coming online.
The recommendations there, I assume it will change, but just something so you understand what's happening in the updates.
So now you may be thinking, what the heck, Jordan?
What's the point of approximating anything?
Why are we using any sort of equation?
We want to know exactly what's going in their blood.
Shouldn't we just be ordering advanced lipid testing like NMR spectroscopy or gradient gel electrophoresis to get particle size and all that detail?
While it certainly sounds logical, right?
More granular data must be better in clinical decision making, right?
Well, the guidelines would disagree and they push back on that.
In the subsection 3.
2, it gives
Advanced level protein testing like NMR, spectroscopy, all that stuff, a class three recommendation.
So, class three meaning potentially harmful and explicitly no benefit.
And that may seem strange because we've all seen clinicians on social media talking about how important it is to get particle size and whatnot.
So, why is there conflicting advice?
Well, let's look at what these tests actually look at first.
These technologies help us figure out the number and size of different subclasses of LDL, like a large buoyant LDL, small dense LDLs, et cetera.
And so you get a three-page printout or whatever it is of exactly how many of these dense particles you have versus large fluffy and other things of this nature.
But here's kind of where the problem starts.
First, there's a massive lack of standardization across different commercial assays.
So, an NMR from lab A might give you different cutoffs and risk percentiles than another test done at lab B, and that's hard to standardize.
Second, it creates an enormous amount of clinical noise and information overload for the patient and the clinician, and the fears that they end up treating the complex lab report instead of treating the actual patient.
However, the most convincing evidence against advanced testing is that when you actually look at outcome data, knowing the exact subclass and size of every single LDL particle rarely, if ever, changes your clinical management beyond the standard lipid panel or APOB measurement, which we'll get to in a second.
So, the guidelines logic is: let's say that the advanced testing shows the patient has predominantly small, dense LDL particles, which we know are highly athergic because they easily penetrate their terrier wall.
Does that change how we treat them?
Well, no, because they have a high number of small dense particles, their APOE measurement will also be significantly elevated, and the treatment would be the same.
Now, I know that some people will say that large buoyant LDL are less athergenic, and the small dense LDL particles is true, right?
So they're saying small dense ones probably are worse than the large buoyant ones.
But overall, the guidelines say that particle number is what we treat off of, not necessarily the LDL pattern.
And that's just what the guidelines are saying.
I'm just, hey, don't shoot the message that's what I'm saying.
But I do want to mention that speaking of ApoB, as I mentioned, the next section talks all about what this is and why we do it and why they're recommending it now.
And so let's start with physiology first.
So everyone's excited, right?
Physiology, but it's helpful to understand.
When the liver packages up triglycerides and cholesterol to send out to the body, it wraps them in a phospholipid membrane and embeds exactly one molecule of ApoB100 into that membrane.
So Apo-B.
Because of this, we know that there is one APOB molecule in every athrogenic particle, meaning LDL, IDL, VLDL, the remnants, LP little A.
In fact, the ApoB is exactly the key that brings the LDL back in.
So essentially, the key that binds the LDL receptor to get clear from the blood.
So it's actually really important.
So, if you are ordering an APOB test, what are you actually ordering?
You're measuring the concentration of the APOB proteins in the plasma.
You're performing a direct one-to-one count of the total number of atherogenic particles in circulation.
You're no longer estimating the mass of the cholesterol cargo.
You are counting the trucks carrying the cargo.
The guidelines give this a class 2A recommendation.
They state that in adults
Who are already on lipid-lowering therapy, especially those with established ASCVD, known ASCBD or type 2 diabetes, elevated triglycerides, or CKM syndrome.
Measuring Apo B is reasonable to guide therapeutic intensification once LDL goals are met.
And you might have just heard me say alphabet soup there.
Like, what do all those things mean?
I heard CCAM, that's new.
What does that mean?
Well, that's a great question because it stands for cardiovascular kidney metabolic syndrome, and it's a new term here in the guidelines.
It is a formalized framework recognizing the deep interconnectivity between obesity, insulin resistance.
Chronic kidney disease and cardiovascular risk.
So, really, this is tackling and taking metabolic syndrome to the next level, right?
Adding in kidney pathology, as we see all the time, as they are tightly related.
And the reason we mention this is because people who have insulin resistance or CCAM or medbox syndrome or what have you tend to have something called high discordance.
And what I mean by discordance is that their LDL may look normal, but their APOB is actually elevated, putting them at risk.
So let's take a clinical scenario here.
We have a 55-year-old patient who has type 2 diabetes, need a little bit of central adiposity and hypertension, and you put them on a statin.
You bring them back three months later, you check their lipid panel, and the LDL is 65.
Everyone's pumped up, they're high five and saying you're great.
But this is where ApoB really shines.
If you were to check ApoB, it might be as high as let's say 125 milligrams per deciliter.
Meaning, which is high, by the way, that this person who we thought at goals actually had a much higher risk level than previously thought.
And when I heard this idea of discordance, it didn't quite make a lot of sense to me initially when I heard about it.
So I'm going to talk you through some of the physiology.
So hopefully, you can understand as well.
In a metabolically healthy person, insulin suppresses an enzyme in fat tissue called hormone sensitive lipase, but in an insulin resistant state like diabetes
That enzyme runs unchecked and aggressively breaks down stored fat, flooding the bloodstream with free fatty acids.
So then these free fatty acids and they head to the liver, and the liver is overwhelmed by them.
Them.
So it tries to rapidly package them into VLDL particles and pumps the VLDLs into the bloodstream.
And so now we have a massive amount of VLDL in the bloodstream.
and an exchange protein called CETP or cholesterol ester transfer protein starts swapping triglycerides out of the VDL onto LDL particles in exchange for some of its own cholesterol.
So now you have LDL molecules that are filled with triglycerides and have lost a lot of the cholesterol.
And then finally, another enzyme comes through and cleaves out those triglycerides, and you're left with a depleted particle.
So, essentially, an LDL particle that has been drained of its cholesterol and drained of its triglycerides, and it becomes a small, dense, cholesterol-depleted particle.
That doesn't have a lot of cholesterol to show for, right?
But it still has one particle of A B.
And so, because so many of these small particles aren't carrying.
Much cholesterol, it looks like LDL is quote unquote normal, but we have actually a ton of particles.
And as we've seen time and time again in literature, the number of particles is a better indicator than even just LDL, because LDL is measuring mass, right?
So, what we're saying is
These patients are at a higher risk than we would have thought.
And so here's an analogy I've used before.
I know I just said a bunch of words, and you're like, Jordan, I can't hang in there, man.
I'm losing you.
You're losing me.
But hey, hang in for a little bit.
Imagine that the bloodstream is like a highway, and you think about plaque like buildups and heart attacks or traffic jams or pileups, something like that.
So
LDL is measurement of the total weight that, let's say, transport trucks are carrying throughout the highway.
And APOB is the count of the actual trucks.
So, 10 massively fully loaded semi-trucks weigh the exact same as 100 erratic, half empty pickup trucks.
So, if you only look at the weight on the highway or the LDL, you assume the risk of an accident is the same.
But physically on the road, a hundred tiny pickups are going to cause a lot more of a traffic jam and chaos than just 10 simple trucks.
And so this is why they recommend
For patients specifically with Metabox syndrome or CKM or diabetes, to check ABOB to make sure we're not in a discordant state.
So that's a lot.
Hang with me.
Sorry about that.
Now, you might be asking, can I just measure APOB right away and deal with all this?
Yeah, you absolutely can.
The guidelines don't say that, but you absolutely can do that.
And I know people who do that.
I'm a little more aggressive in ordering Apo B, but that's not what they're saying.
And one thing is, guidelines dictate what's going to be paid for by insurance, right?
And so a lot of times it's an out-of-pocket cost.
It's not crazy expensive.
Typically, what I've seen is it runs somewhere around thirty to fifty dollars.
And so it's definitely something to consider, but the guidelines don't necessarily recommend it.
If you guys say, hey, Jordan Rennicky, how do you practice?
I order ApoB a little more aggressively because really, that's what we're titrating towards is not LDL.
And so it's kind of confusing.
I'm not going to try to put my opinion in too much, but to say, hey, ApoB is a better test.
But still use LDL, and you know, maybe they talk about non-HDL, which can be a better test than LDL, and it's just kind of confusing, I'll be honest with you.
But I understand from a cost perspective, you know, a lot of times lipid panels are covered and whatnot.
Totally get that, but that's where we're at.
Now let's move on to another biomarker that these guidelines talk about, and that is LP little A.
This one is really interesting because the guidelines now give this a class one recommendation that we measure this concentration.
At least once in a lifetime for all adults.
And so you might be asking, well, what is this molecule and why are we checking it?
Well, I'm very glad you asked.
Structurally, Lp little A begins as a standard LDL molecule and has a core of cholesterol and contains an APO B molecule.
Nothing's changed there, right?
So, however, a small covalently bonded protein called apolipoprotein A is added to the molecule and makes it LP-little.
And this little protein that they change, and it changes the entire behavior of the particle.
It turns from a standard LDL into a much more athogenic particle.
And there's three main reasons why we care about this so much.
So, first, like all other molecules containing APO-B, this can get stuck in the sub-endothelial space, contributing to atherosclerosis.
So, nothing really different here, but once again, it can contribute to the overall burden.
Reason number two, though, is interesting, and it's pro-inflammatory.
It carries a heavy payload of oxidized phospholipids.
And when this gets into the arteries around the heart, it can release oxidized phospholipids, which trigger local inflammation.
We know makes atherosclerosis worse, right?
So, like, inflammation is fuel to the fire, it's not good, and that's why another reason it's very unique.
And the third reason is very interesting because it's actually prothrombotic.
So, structurally.
It looks very similar to plasminogen, which, if you remember, plasminogen is the precursor to plasmin, which is the enzyme our body uses to break down cloth.
And so
We know this molecule that looks like plasminogen and acts like a competitive inhibitor.
So it binds to where plasminogen should normally be binding, and so we can't break down clots.
So effectively,
It's decreasing the body's ability to dissolve dangerous clots like the ones that are being formed in our hearts.
So, three big things there.
It's right: just normal, kind of pathogenic-like protein, pro-inflammatory, and
Does not help us break down clots.
So that's why it's particularly athogenic.
And so when we order this, the threshold for risk is either 125 nanomoles per liter or 50 milligrams per deciliter, depending on the lab use.
The tests that are preferred are the ones that come back in nanomoles per liter, but they did give you both just in case your lab did not have them.
And if you're at this level, this 125, it leads to a.
1.
4-fold increase in someone's cardiovascular disease.
And if it's as high as 250 nanomoles per liter, which would be about 100 milligrams per deciliter, that represents a two-fold higher increase in baseline risk, which is about equivalent of having.
Heterozygous familial hyperclostromia.
And I mentioned this because this is also a genetically inherited trait, which is kind of not a great thing.
So, LPA levels are overwhelmingly dictated by a single gene, the LPA gene.
And up to 90% of the variance in these levels is determined by genes, which is very unfortunate.
And so that's what they mentioned, at least getting it one time, right?
Because once you know it, it's unlikely to change or have a substantial change.
Because unfortunately, though, like it's just good to know, but we don't have a lot of treatments for it.
Lifestyle doesn't seem to touch it at all.
We don't have amazing treatments yet.
Statin's actually been found to sometimes paradoxically increase it.
PCSK9 inhibitors do actually decrease it maybe a little bit like 20%, but not a whole ton.
And we don't know if that's playing a significant role.
But I know they're coming down the pipeline.
Currently, we don't have anything to directly treat it.
And as I mentioned, although it's generally stable, meaning hey, it doesn't change much in lifetime, there are some physiologic states where it can fluctuate, including chronic kidney disease, liver failure, and significant thyroid dysfunction, as well as pregnancy and menopausal transition.
Currently, from a godland perspective, they say, hey, once in a lifetime, that's all we need.
Everyone should know what's going on.
And so you may be asking, why on earth are we measuring this?
Why are we making a universal screening recommendation for something we can't do anything about?
And that's a very fair question.
The guidelines say it's because it's about risk stratification.
And although, yes, as of today, we don't have any amazing medications to lower it, those are coming in the pipeline, though.
Knowing someone's true risk of cardiovascular disease helps us understand how aggressive we need to be in other aspects of our life, right?
So, let's say you know someone who has a very high L P with a.
You may be a bit more aggressive in their LDL numbers or their blood sugar or blood pressure, and so it's not supposed to be defeating, right?
Like, oh shoot, I'm stuck with this for life.
It's supposed to be empowering so we can understand risk and we can pick up the slack anywhere else we need to.
All right, moving on to the last section.
If you're still with me, you are awesome because this is deep stuff, but props to you.
But we're going to talk about monitoring and follow-up now.
And this is important because this has changed a lot from previous years.
As it used to be, we used to kind of just like start a medication and you set it and forget it.
That's it.
Well, the guidelines have changed.
Now they're asking for.
Two specific things.
The percent reduction LDL, which was recommended in previous guidelines, but now they're also looking at hard LDL, non-HDL, or APOB goals.
Because previously, as I mentioned, if someone was at high risk, you'd just start them on a statin and hope that their LDL will drop by 50% and just kind of call it good.
But in reality, like were a lot of people checking that we were dropping 50%, and even then.
If you still had LDL that was high, but you decreased by 50, was that just good?
You'd kind of say, Yep, we're fine.
So we had a lot of people who were still at risk without knowing it.
And on top of that,
Human beings are not randomized controlled trials, right?
They're individual people, they're individualized patients with unique genetic variations.
So, for example, statins we know are metabolized through the cytochrome P450 pathway, which gives a ton
Of genetic variants.
In fact, statins are typically pulled into the liver by a specific transport protein called the OATP1B1.
Doesn't matter what it is, but that's what it does.
But if you have a genetic polymorphism, right, that makes that transport slow or inefficient, then the statins can back up in the bloodstream.
Which means they're maybe circulating around the blood, which can penetrate muscle tissues and cause some of the unintended side effects that we know and we commonly see.
So, I guess
What I'm saying is that we won't know how someone will respond to a medication until they're actually on, unfortunately.
At least, not yet.
Hopefully, in the future, we have personalized medicines, but at this time, that's not reality.
And so, overall recommendations are to follow up and repeat labs in 4 to 12 weeks and then make a dose adjustment or add additional therapies as needed.
And so we've covered a lot in just this one section.
Let's real quick do a rapid fire summary about what we talked about.
So, number one, universal screening in patients 9 to 11 is now recommended to try to catch someone's true genetic baseline before puberty drops.
We don't think family history is sufficient, and so we're looking for specific blood tests now.
On top of that, adults still start at 19, get them at least every five years, but that really hasn't changed much.
Number two, we have changed the equations we use for determining LDL.
And because of that, thresholds have also changed for treatment, which we'll talk about in future videos.
This doesn't affect you so much today, but I understand it's coming.
Three is the rise of APOB and non-HDL cholesterol.
All recommendations are still talking about LDL cholesterol.
But I think we're starting to see the shift where, if I had to guess, one day we'll be talking about LDL as an old remnants.
Meaning, we don't talk about it.
We'll look specifically at ApoB.
Or non-HDL.
And I will step back here.
Non-HDL, just to clarify, non-HDL is the stuff that's not the HDL, right?
So it includes all those things I mentioned.
LDL, the VLDL, the IDL, the remnants, the LPLA.
So essentially, it's a proxy for ApoB.
There's lots of data showing that non-HDL is probably even better than LDL.
So if I had to guess in the future, LDL will kind of.
Follow the wayside, we'll bring up non-HDL and APOB, but they're in the guidelines now, so that's not it.
But the guidelines currently talk about incorporating APOB specifically when we're looking for discords, like patients with CKM.
Insome resistance or diabetes.
And finally, it's now recommended that every adult gets their L P little A checked at least once in their lifetime.
So that was a lot.
We are done with this section.
We will continue to move on through these guidelines.
That's my main goal here is to go through each section of the guidelines.
So at the end of the day,
You'll have a very good understanding of what the guidelines say.
But if you'd enjoyed this, it would mean the world to me if you share this with a colleague or a friend.
But that's going to be it today.
Thank you so much for stopping by.
Now get off your phone, get outside, have a great rest of your day.
We'll see you next time.
