Transcription
Does high cholesterol even matter anymore? It seems like a lot of people are talking about it.
Welcome to Talking with Docs. I'm Dr. Brad Weining.
I'm Dr. Paul Zozal.
Brought an old friend back, Dr. Michael Hefernick, cardiologist who's been on our channel before to share so much of his wisdom about cholesterol, blood pressure, whatever. But today, we're going to we're going to revisit a topic that is not going away regardless of what social media talks about. High cholesterol 100% is a problem. That's your first take-home message. But we're going to talk about why. are we talk about what it is, how it goes up, and why we need to get it down, and how we can do that.
So, you're going to lose some people right away. Well, fine. Judging by the comments, because a lot of people feel that cholesterol is not an an issue right now. You know, it doesn't really matter. Lifestyle is more important and it's just a number. It doesn't really make a lick of difference in your life.
So, let's kind of break it down and then if you agree or disagree, leave some comments and please subscribe to the channel. If you're watching this video, just hit subscribe. It's not a big deal. It really feeds our very fragile ego. I'm just I'm just being honest.
Okay. So, so Mike, what what is cholesterol? And first of all, like why is it important to our bodies?
Sure. I you know what, even before I do that cuz my blood pressure is already going up. Well, just go back a step. The idea that, you know, cholesterol is not important and it's just a number is a really old school thought.
Is that right? Oh yeah. I thought it was new school like like Anel Keith even before all that stuff.
Yeah, that that goes back like 20 or 30 years and that is kind of the origin for why people were a little bit mistrustful about statins. So um so that's just a little bit of history. So if somebody thinks you know this is kind of new age, this is like old school kind of redundant kind of thinking.
That's a good point because we've been thinking about cholesterol for a really long time. You know how I know? Because um I remember in Christmas Vacation, cousin Eddie stopped eating squirrels cuz they were high in cholesterol.
That's right. There you go.
Where's Eddie? He usually eats these goddamn things.
Oh, not recently, Clark. He read the squirrels were high in cholesterol.
And that was 1989, right?
There you go. Okay.
Okay.
So, we need cholesterol. Right.
Yeah. And and and I think so that's important for everybody to know. And and I think a lot of people do realize that and and maybe that's part of the criticism at times is, you know, maybe we shouldn't lower our cholesterol because we need it. So we need it to make our cell membranes. We need it for steroid synthesis. Um uh we we need it. So the problem is is that there is a series of pathways where our body makes cholesterol. I think that's the important thing. 85% of the cholesterol in your body is made by you.
It's by our liver.
By your liver, by all cells. um mostly by the liver, but all cells in the body make cholesterol. And so only a small portion, say 10, 15, 20% is governed by diet and exercise. 85% is hardwired by your DNA. Thank you, mom and dad. But you know that that's it.
Some people make a lot, some people don't make so much. We all make enough to live for our cell membranes, our steroid synthesis. The issue is not cholesterol, but it is the crappy kind of cholesterol that layers into the arteries and causes heart attacks, which is my job. Um, that's what you don't want. And so, you need the the good stuff. Um, but what you don't want are things like LDL.
You don't want a high LP little A. So, that's all the stuff that layers into the arteries, will start blocking arteries. If it blocks an artery in the heart, it's a heart attack. Blocks artery in the brain, it's a stroke. Um, and if you get, you know, blocked arteries or atherosclerosis elsewhere in the body, say the legs, then you're starting to get peripheral vascular disease where, you know, you can't walk so far because your your legs are hurting.
Okay. So, what you're saying is we most of this cholesterol is comes from us, okay? Not much uh from the diet. So you're kind of laying out the groundwork here for saying why just diet and exercise and that alone is not enough to bring down that cholesterol because such a large portion of it is made by us and not influenced by diet and exercise.
So it's it's important to you know watch what you eat, don't go crazy, exercise 150 minutes a week. You know those are the guidelines uh you know Canadian guidelines, European American guidelines. Um those are all good things. We're never going to discourage you from doing it, right? Good for your body, good for your mental health. It will lower the cholesterol a little bit, but most people who need some cholesterol lowering, they need to lower it so much more than the 15 or 20%. That's where you need a little help.
Okay? And I think that's a good point. So, first of all, everybody doesn't have to lower their cholesterol. That's the first thing. So, we all have cholesterol, but most people don't have high cholesterol. So, you're going to be walking around. People don't until they have endstage symptoms. You don't know that you have high cholesterol. It's not like, oh, I feel bad today cuz my cholesterol is high until you don't. So, you see your family doctor, you might get some routine blood work as part of a a yearly or semi-early physical or whatever. And then you're identified as having high cholesterol and then we start talking about how how to lower it.
Yeah. And part of it's like when do you screen, right?
So, because you can't feel it. So, you know, when should I ask my doctor to have it done?
What's the answer to that question?
Well, it depends on where you live. Okay. Um the American guidelines were just updated uh this year. Uh in the United States they have started to say you know age 19 y and every five years after age 19 is a reasonable time. In Canada we have about age 30. Um uh unless there is you know a family history of heart disease or you have diabetes or you're a smoker. If you've got some other kind of enriching or worrisome factors we test sooner. Um and then there's a small group of people but not that small. So, one in about 250 or one in 300 people have crazy high cholesterol numbers. Okay?
Um, they have crazy high numbers because they've got some mutation, a genetic mutation, um, no fault of their own. Again, a thank you, mom and dad. Um, and so their numbers are really high. When we find those people, uh, we make sure we check their children.
Are these typically spontaneous mutation or they're they're hereditary typically? And so they would probably know because they probably have uncles and aunts and parents that have had problems or not.
Yeah, but you'd be surprised. You'd be surprised because they'll say, you know, they'll say, "Oh, yeah, I had an uncle, you know, passed away at the age of 40 and, oh, my dad had a heart attack at 55." But sometimes people don't put the, you know, the pieces of the puzzle together and go, "Oh, this is all cholesterol related."
Is there some ethnicity tied to that familial elevated cholesterol?
There it's not ethnicity, but it tends to be the this concept called founder effect.
Okay. So there are communities in the world where there was not a lot of movement of people in and out of the community. Okay. Right. So very small group of people have given rise to a population and so as a result of kind of closed families, right?
Um and uh you're more likely to have mutation. So in Canada for instance um there's a region in Quebec um where it's not one in 250 but it's like almost one in 80.
Right? So it's a really tight-knit group of people who socialize and then marry and
Yeah, there might be five families that kind of started this whole region, you know, and and there wasn't a lot of uh in and out of other uh
Right, so their genes are pretty stable and then these problems arise. So, so when we talk about screening, are we talking about so do you go and say, oh, I had like a cholesterol test? They don't say, oh, well, you have cholesterol. What what are the tests that we order and what are the numbers that we care about?
Uh, so the the panel is actually probably pretty universal globally. The units are a little different. We can talk about that. Um, but the panel, so we we look at the total cholesterol.
Yep.
The triglyceride level. Um, the LDL and the HDL
Primarily.
Okay.
Yeah. And the non-HDL.
There are other things that we do test for,
Right, which have really muddied the waters, I would say, like the the apo
Apo B and the LP little A. I think if you need to talk about one and something you really need to know about because it's a big up and comer, especially for 2026 now, will be LP little A.
And we did a video about that a couple years ago.
Yeah. The reason why this is going to be important is the very first paper will come out this August looking at treating people who have previous heart attack, stroke, you know, already have had an event. So secondary
Secondary prevention, high LP little A, and this me is a medication that has lowered it. Will these people do better?
Lowers LP little A. Now that's new because four years ago when we talked about this, there was no medication for it. So now we got one.
Yeah, so now we have one.
Because before you just used to know you had it, like, oh, sorry, what do I do now? Just be worried because we can't do anything about it.
Yeah, so this will be exciting. This will come out at the European Society of Cardiology meeting in August. You know, the results or you going to give it to you?
Well, nobody can know the. We're going to do that. Talk about studies, right? This is a double-blind, placebo-controlled study. There might be five people in the world that actually really know the results.
You're saying it's not completed yet?
No, it's completed.
Oh, it's completed. Oh, so they're analyzing the data.
Analyzing the data, but there will be only the data safety monitoring board is the only group of people who actually know what people are on and know what happened.
Are they all going on that drug? Because that'll give us a clue.
Okay. So, now that's going to come to you. This is the Apple little A. You said
LP little A.
And an Apple B. What's the deal with that? Not as big a deal.
It it is. It is and it isn't. I think we can get most of our information from a standard cholesterol panel, right?
Um, and and now we throw on the LP little A to find out kind of what that is. But Apo B is important. It it's the protein that is linked to every molecule of uh of of the lipids that are aogenic,
Right?
So, there's an apo on LDL, there's an apo on LP little A. So, So if you count the Apo B's, then you know that you've got more aogenic particles.
Because the thought is you could theoretically have an an okay LDL but a high apo, typically not vice versa. Is that fair to say?
That's fair to say. Yeah. And I think what people didn't recognize before because they weren't checking LP a little number of particles is that yeah, you know what, you can you can have a LDL that might be reasonable or we're treating LDL and we're, you know, using a high-dose statin and maybe we're using some other medications. Like, wow, that's not going down very much.
It's not going down very much because what you're measuring has a little LP little A buried in it, and you haven't checked the LP little A.
Right.
Wow. Okay. And that and that study you said right now, uh, is good. Is going to be looking at secondary prevention, right?
Is there any data yet on primary pre? So, primary prevention versus secondary prevention. Primary prevention is trying to prevent a heart attack or a stroke in someone who's never had any sort of atherosclerotic event. Uh, secondary prevention, someone's already had a stroke or already had a heart attack. Now you're beginning a treatment to see if you can reduce the chance of something bad happening again. So my question is, Apple little A
LP little A.
LP little A. Why don't you keep saying Apple little A? You guys got to change your name. Confusing.
We'll change it.
LP little A in primary prevention. Is that, is there any evidence for that?
So that that's under investigation. So I saw a 33-year-old gentleman yesterday who has an LP little A of about 250.
Oh.
That's high. You know, upper limit of normal is 100. And so he actually came specifically to talk about, is there a study I could be in?
Right. Has not had an event.
Because he's not had an event.
Doesn't want one.
He doesn't want one. He's 33 years old. You know, he's expecting his first child or his wife is expecting the first child. And um, and I, and so those studies are ongoing. Okay.
He's not high risk enough because even in those studies, you need to have somebody who's a little bit older, maybe has a family history, uh, maybe had a coronary artery that's a little bit elevated. Um, because you can't run clinical studies for 15 years to wait for an answer, right?
So you need to kind of enrich it for people who might be a, it's primary prevention but a little bit more high risk.
Gotcha. Okay. So you can get a, so you can get a signal when you're doing your study.
Okay. So you got LP delay, Apo B, and now the role of Apo B. Are we using, are you using that clinically to help decision making?
A little bit, but rarely.
Okay. So you have an elevated LDL. Can we talk a little bit about the numbers? Yep. And like how because a lot of people like, well, yeah, the pharmaceutical companies, they just lower the number so that more people have to be on the drug. Same thing for blood pressure.
I was going to say they they lowered the cut off age for screening because that's I'm sure someone's going to make a comment when you said in the US when they lowered the screening age to 19. Someone is going to come and say, oh, that's a drug company doing that so they can sell more drugs.
Yeah. So, so what's the, what's the normal range and then what's the number that we start to to treat and how do we decide like, why do we do that? Um, and the drug companies don't sit on these advisory panels, by the way, just so you know, when, when, you know, the guidelines come out, there are about 30 people, experts in their field, national experts, whether you're Europe, Canada, Australia, the UK, the United States. Um, this is not funded by pharma.
However, what someone's going to comment and say, but those experts, maybe have contracts with pharma, but full disclosure, right? The, so, absolutely.
What you're saying is the Coca-Cola rep is not sitting on the school board to decide what drinks are served in the cafeteria. In fact, I'm doing. Yeah. And that, and we need that obviously.
Yeah.
But the expert who is
Is getting paid by Coca-Cola to do research, which does happen.
Yes. But it's fully
And that's why you have to disclose it. Yeah.
Um, that no, that's totally fair. It is tricky.
Um, so, so the units are a little bit different. So
Uh, most of the world uses SI units. So millimoles per liter. Okay. Okay. Millimoles per liter is a preferred measure, right?
Um, because it measures, because that measures the number of particles, right?
Okay.
Um, in the United States, they use milligrams per deciliter.
Is it only the US? So the whole world does one thing and then just the United States.
Um, and and there's the odd country in the world that might use um, the machines purchased from the United States, right, where they'll report in milligrams per dec like Bahrain and a few. I've had people from the Middle East sometimes come back with with numbers in in non-SI units and and and that's why.
Um,
But you can just convert it. There's a conversion.
Yeah, you can convert it. Milligrams per deciliter is not considered preferred because it measures the weight of cholesterol, which we're not interested in. We're interested in the particle number. Um, and so 30 years ago, most countries shifted over to SI units and um, and the United States has not. It's just more of a legacy issue. So that's why like in our journals,
And even in the current or the recent American update, we're always expressing things in two units so that regardless of where you are in the world, at least everybody can look and go, "Okay, well, these are my units um and we can kind of be on the same page." So with that being said, I'm going to use SI units um because that's what I'm comfortable with. So um, if you've had a heart attack or a stroke, if you've had a bad event, the bare minimum is in Canada is to have an LDL below 1.8 millimoles per liter. Okay.
Okay. 1.8 bare minimum.
So, heart attack or stroke.
Yep. Or if you've got vascular disease, we have an elevated coronary calcium score study with a little plaque.
Bare minimum less than 1.8.
Okay.
Um, we will probably be updating our guidelines next year or two. You know, I'll tell you now, it's likely going to be less than 1.4.
Okay.
Okay. Um, Europe, the Europeans, less than 1.4.
The reason being, 1.8 was still allowing essentially people to have events related to high cholesterol. We just wanted lower.
Yeah. So, what happened was, if you really look and narrow down into the data, if you get to an LDL 1.8, the plaque neither progresses nor regresses. It's kind of status quo. But wouldn't you like it to go away? Sure.
Right. M.
And so if you do some subgroup analyses in some of these large studies, at around an LDL of 1.4, plaque actually starts to go away.
And and for viewers, just so you know, we're not talking about one study with 50 people. We're talking about hundreds of studies with thousands. Thousands, maybe even millions of patients if you pulled them.
Yeah. No, hundreds of thousands. Um, but in the regression studies in particular, these were kind people that allowed us to go in with a catheter into their coronary artery at time zero, measure the plaque. Wow.
And then on therapy 18 months later, say, okay, you can go back into my heart and measure again. Wow.
Um, so, you know, thankful to those those research volunteers.
Expensive, risky studies that have associated
Risk, but it has now told us 1.4 is a number. So the Europeans have said 1.4. Before the Americans have said, "Look, make it sure it's 1.4." Um, the Canadians now need to update our guidelines. We'll probably make it 1.4.
Okay.
Okay. So, um, 1.4, good number. If you're a Canadian cardiologist or a physician who's had a heart attack, they want 1.4.
Okay. And so,
That's for Sorry. And that's for, um, some that's you said that's for secondary prevent
Established event. Yeah.
Yeah. So, what about what's the number then for someone who's never had an event? So that comes into all the risk calculators. Okay. So we'll take you guys. You've never had an event. You come in. I'm, you know, I do your, you know, your age, your gender, your blood pressure,
Non-smoker.
You're not a smoker. You don't have diabetes.
Alcohol consumption. Um, any points? We're doing pretty good, right? Why blow it?
Alcohol does not come into the equation.
Um, and uh, and your cholesterol panel and, uh, weight doesn't come into to the standard calculators.
Um, you throw all of those numbers in and I will give you a score.
Okay.
Um, in general, the scores are kind of tenure scores. Here's your risk of having a heart attack, a stroke, or dying over the next 10 years. Okay?
You're either low, medium, or high. Yep.
If you're low, most people don't need a cholesterol pill. Right.
Right. If you're medium or high, you know, most people then do. And so we we try and do this risk calculation to say, okay, where do you fit? What are your numbers? Do you need something now or not? Okay. And that that's the bottom line.
Was that the Framingham?
That's a Framingham. I I have to tell you that there is a move away from using these 10-year calculators.
Um, and there's a move now to going, like, we're not interested in 10 years. We're kind of knowing what's your lifetime risk, right? Um, and that in part, the new American guidelines are fantastic in that way because they said, "Look, we're more interested in this lifetime risk." And the American Heart Association has a really nice calculator called the Prevent calculator. Okay? And people can go online and look at that.
And that's what I'm going to do right after this.
It's fantastic. And so you'll enter a bunch of your data in with your updated cholesterol numbers um and you can get a more of a lifetime risk. Okay?
And then that will help decide, you know, my lifetime risk is high. Okay, maybe I'm willing to go on something.
Right.
Yeah.
And and is it a conversation, I'm assuming, with your doctor, but you get to, you get to drive the bus a little bit as a patient like
You, you actually as a patient, you should be driving the normal decision making.
So even if it's low, then I'm like, I'm just really nervous, not based on any anything that's real necessarily, but I have a lot of anxiety. I'm in that low group, but I don't want to be even in the low group. I want to be in the no risk group. So I'm like, listen, I want to be on a statin. And you say, okay, well, here's the risk of benefits of the drug, and then we decide together.
Yeah. Okay.
Yeah. And I, and you, I've had the odd patient who absolutely where you know, if it was me personally, I was like, no, I don't think I would be on something right now, but that's not their values and preferences are are a little bit different.
Okay, Brad, you, you mentioned a good point, the risks and benefits. Can we talk a little bit about the risks of being on some of these medications like
And the medications themselves too. We statins, a lot. Statins.
Yeah. So, statins, a big one. Um, so the true bill risk of having, you know, some side effect, and it's usually muscle aches and pains um, is on the on the order of about 10 or 15%. So 85% of people do very well on statins, right?
Um, we have different kind of grades of statins, kind of low, medium, and high potency. Where people are going to run into the problem, that 10 or 15% of having myalgias or muscle aches and pains is usually a higher dose of a high potency statin.
Okay. So, we don't throw the baby out with the bathwater, you know, if they if they've got that. It's like, look, okay, well, let's use something low dose, low potency, um, because we're still going to get a good bang for their buck. It's efficient and it's cheap.
And this is a, this affects an enzyme that prevents our liver from cholesterol making cholesterol. So, this knocks down the synthesis part. Okay.
What about diabetes? I've heard that sometimes statins can lead to diabetes.
So, that not just statins. Every cholesterol drug we've ever studied um, there's a small signal for uh, increasing the risk of diabetes.
Tends to be in people who are predisposed anyway.
And most of the diabetes guidelines have come out saying, we don't care.
Um, because the benefit is so overwhelmingly in favor of being on the cholesterol pill that we're uninterested in this incredibly small signal.
And because ironically, once you get diabetes, a lot of times you go on this drug anyway. Like, I mean, right? That's what I mean. So, like, even though it caused it, if you have it, you're going to be on it. So, so they kind of, they run together.
You also got to be on something else, I guess, for your diabetes. Yeah.
Presuming like a metformin or something like that.
Uh, next thing someone's going to ask is um, what about dementia? So, I'd say if you look at the data,
Right. A lot of data says it prevents or reduces your risk of dementia.
Crappy study from the early
And that's what people cling to. It was a Scottish study um early 2000s, not a randomized placebo-controlled study. Um, it was more of an editorial than anything else and it is hung on it. It is stuck to the wall.
And I feel like there's one other study we need to talk about too. Is the, hey, my the cholesterol is too low. And there was a study in these patients who were older and sicker and they had low cholesterol and they actually died more. And that study, I think, showed that really it relates to their comorbid disease. Having low cholesterol does not increase your risk of death, but being sick increases your risk of having liver problems, make your body's ability to make cholesterol. Correct.
Absolutely.
Okay. So, remove that from your argument as well as reasons to not lower your cholesterol.
We have never reached a point in any of our clinical studies where low is bad.
It's not right. There. What about, uh, there is some, and someone's going to leave a comment and possibly
Hard to predict all these comments.
Well, because usually me, it's usually me commenting. Sorry.
It's just a bug, Brad. So, um, okay. Primary prevention, never had an event,
Right?
What do the studies say about lower? I know they say they can lower the chance of an event.
Yeah.
Like a stroke or a heart attack, but all cause mortality. Is that reduced significantly by lowering your cholesterol in a primary prevention setting?
As a primary endpoint. Yeah. All cause mortality. Yeah. No. Like that's impossible to obtain, right? All cause mortality.
All cause mortality is a primary endpoint in a low-risk population.
You need hundreds of thousands of people in the clinical study to prove that. So
That that will never be shown. So endpoints in the clinical studies are always combined in place, right? Heart attack, stroke, or death. Because if you choose one endpoint, you're going to need to kind of triple or quadruple the number of people that you need for the study to
And that's what the average person doesn't understand, right? That's why they fixate on that. Well, look, statins hasn't shown it's going to make me live longer, so why would I bother taking it? This is the trouble.
So,
You're saying it's not that statins don't help you live longer. It's just that it's difficult to prove that.
It's difficult to prove all cause mortality in in a randomized placebo-controlled clinical study. Absolutely. Like good quality data.
Because that that sort of plays into a, I've seen people on physicians on social media say, "I would never take a statin." Uh, because they, they often look at the number needed to treat and they'll say, because that, because the flip side of that, if you have such a low reduction in all cause mortality because of the logistics of running an experiment like that.
So your number needed to treat goes so high. I have to treat three or two or 300 people before I can save one person.
That's a little bogus though, right? So we're worried more, we're worried about more than just all cause mortality. Um, if you were hospitalized with a heart attack, that's meaningful. You develop heart failure as a result, meaningful. If you had a stroke.
So number needed to treat for those events is like 25.
And so, you know, now death shouldn't be, death is not the most important thing here. There are a lot of bad things that happen before death, and you don't want to live with those bad comorbidities. And so those numbers needed to treat are fantastic.
20 to 25.
Yeah. And I, maybe people might not understand or be familiar with number needed to treat, but you know, number needed to treat of like anything less than 50 is a fantastic, good bang for your buck.
Yeah. So, number needed to treat is just a statistical experiment or statistical way of presenting the data. Uh, that looks at how many people you'd have to put on the medication before you reduce, stopped one event from happening. That's basically number needed to treat. So that's pretty low for for events.
No, it's really good.
Okay. Okay. So,
You're on a statin. It's either I couldn't tolerate the side effects or it was not lowering my cholesterol enough. What would be next to either add or to substitute?
Um, yes. So, I, I'm going to rather than do it sequentially, I'm going to tell you there are options because the national guidelines are going to differ a little bit, you know, depending on where you live.
Um, I think an easy one is a brand name's Ezetrol. Um, so you'll get about a 20% lowering of your cholesterol with that. By the way, with the statins, you get about a 50% lowering. Yeah.
Um, so now we're kind of going down the road.
And and is the, the mechanism of that one is that it increases the LDL receptors and then it is that the one that actually all of them will increase LDL receptors. Yeah. And so if you have more LDL receptors sitting on your liver like garbage trucks, then you'll just have more garbage trucks kind of taking stuff away out of your bloodstream.
Okay.
Um, so, yeah, reducing statins will increase LDL receptors by lowering cholesterol. Ezetrol stops you from reabsorbing cholesterol in your gut.
Okay?
And so more of it goes out into the toilet, and so then you have less LDL.
Um, there's another medication available in Europe and the United States since 2020, just available in Canada now. Bempedoic acid.
Uh, no. So, Bempedoic acid is a really cool molecule. It also works on the cholesterol synthesis pathway, but it will never work in your muscles.
It can't work in the muscles the way it's been created. It will only work in the liver. So its claim to fame is it has no muscle aches and pains side effects. Um, again, modest lowering, about Ezetrol, like like 20%.
Okay.
Um, we have the PCSK9 inhibitors. So those are injectable medications once every two weeks, once a month, once every six months.
Um, they lower something actually in the liver um called PCSK9. Um, and that will reduce the LDL 50%. Oh.
Um, so
So they work very well.
They work very, I'm assuming they're just expensive because they're injectable and
Yeah.
Yep. So, PCSK9 inhibitors, statins, Ezetrol, Bempedoic acid. Okay.
Um, so those are all traditional stuff. European guidelines that came out last year has a fantastic figure. People can Google it and get the PDF. But if you're on all of this stuff, you can lower your cholesterol like 90%.
Wow.
And everyone needs that. But the odd person where, you know, they are options.
There are options. You have a lot of options. Now, how is it going, how is this uh
Reduction of LP little A going to affect this whole algorithm?
It's independent.
Okay.
Cuz LP little A is an independent risk factor. So, we need to lower LDL. We've got all these tools to do it. We've never had a tool to lower LP little A. There are four companies that have molecules to lower LP little A and the first will be presented in August. So, hopefully we'll have some data there.
Now, for sure, I'm predicting comments now. Now, I've got you in this game. Well, what what natural things can I take? Right. That that's fair.
Yes.
Mostly none. Um, that's the bottom line.
Um, so red yeast rice.
Yes. Read a lot about this.
So if you're taking red yeast rice, you're taking a statin.
No. Okay. Okay.
It's just a natural statin.
It's lovastatin.
Oh, okay.
So, so red yeast rice actually makes lovastatin. Okay.
So you get about a 20% lowering.
And so a pharmaceutical company then said, "Let's just make this molecule and remove the red yeast part from Okay. and let's be highly regulated and make sure that when we say it's 20 milligrams, it's 20 milligrams. Let's make sure no impurities in it and let's make sure nobody dies from the contaminants."
So if you're on a statin, then you should you or should you not add red yeast rice?
Don't add red yeast rice. More statin. That's a lot of statin. You're more likely to get muscle aches and pains. You have no idea what's in that bottle, uh, because it's a food supplement and it's not regulated.
Okay. I know your next one, it's going to be nice. Has to be nice. Is that you're going to talk about
We don't use niacin, right? I know. But a lot of people talk about it, right? Oh, it's going to lower my cholesterol, blah, blah, blah, and forget about the flush and forget about this. But it, it's dangerous, right?
Uh, yeah, niacin can definitely increase risk of myalgias, risk of muscle breakdown.
Um, there has never been a study that's proven that niacin, and there have been a lot of studies, uh, placebo-controlled, randomized studies, uh, that showed that niacin adds anything on top of a statin. So, niacin's a wash. There are no guidelines that really recommend it at all anymore.
Mix the niacin.
Yeah. Uh, plant sterols.
Yum. Again, so they, uh, they're modestly effective. Maybe like 10% or so. Um, so not, not terrible, just not very effective.
You can take those on top of a statin.
You could, you could. The thing is, I guess my comment to patients is, yes, you know, there, there are some things that will provide some small benefit. So, if you're in that low-risk group that's not going to need medication anyway, maybe that will help.
Yeah. Um, it would be really nice that, you know, try and land on something that you're not ordering online, um, that you know, it's a reputable company, um, that, uh, that you can, you know, you can be confident that, you know, what's the label in the bottle is what's in the bottle,
Right?
Yeah.
Okay. Wow. So, we've talked about cholesterol, what it is, what having a high cholesterol means to you.
We've talked about how to lower it. Yeah.
We talked about the fact that probably going to need some kind of medication. This is not one that lifestyle alone is going to do, but of course, it will help. And we talked about some of the adjunct things or some food supplement type things that you can do as well.
Anything else?
That's like a PhD in cholesterol.
We didn't do diet.
Okay.
So, um, fiber.
Like the DASH diet or a Mediterranean diet.
Um,
So, whole, so whole foods, mostly plants, you know, fiber-rich.
We kind of did. We said, but you're only going to get
10 to 20%.
But if you want to, if you want to lean on one particular, we hate the word diet, but kind of like food choices.
Yeah.
That that's that's what you should leave.
I always say never go on a diet, but change your diet. So that's kind of my
I do say that a lot.
Say that a lot.
Other things.
Okay. Now, now you know if if you had questions about cholesterol, I think this is going to be answered. It's going to empower you to go have a conversation, a thoughtful conversation with your doctor and say, "Listen, here's what I'm thinking." And then you guys can talk about it together. And if you like this video, please like it. Please subscribe to our channel. Share it with someone who maybe is telling you some stuff that's not totally true about cholesterol. And you likely know someone.
Or if you've likely seen someone online talking about it too. There's lots of different uh people online that are slamming cholesterol lowering practices right now.
I know.
Remember, you are in charge of your own health.
And thanks Dr. Hefernick for joining us as usual. We'll see you next time.