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Get the clarity you need on the hottest topics in health and wellness with Second Opinion. Hosted by Rosemarie Beltz, this podcast brings you fresh perspectives from experts, innovators, and disruptors tackling life-changing issues. Each episode unpacks the latest research, debunks the hype, and delivers insights to help you make informed decisions. If you're ready for engaging, enlightening, and occasionally unexpected takes on health and wellness, tune in and discover your second opinion.
Rosemarie - 00:00:04:
Welcome to Second Opinion. I'm Rosemarie, and if you've ever wanted a Second Opinion on some of the trending topics in health and wellness, you're in the right place. Each episode, I sit down with experts, innovators, and even a few disruptors to bring you fresh perspectives on the issues that could change your life, from age rejuvenation and brain health to the weight loss drug revolution and how to reinvent your career. Together, we'll dig into the latest research, question what's hype and what's real, and give you the insight you need to make your own choices about health and wellness. So, if you're ready for a Second Opinion that's engaging, enlightening, and maybe even a little unexpected, let's get started. Today, we're tackling a topic that affects millions of people but is often misunderstood. Cholesterol, triglycerides, and the truth behind medications like statins. We're going to touch on the topic of GLP-1 medications like Ozempic, Mounjaro, and Wegovy and ask some questions. What really causes heart disease? Is sugar more dangerous than fat? And when do cholesterol-lowering medications actually make sense? Joining us is Dr. Ian Riddock, a board-certified cardiologist with expertise in preventative cardiology, lipidology, and cardiovascular imaging. He's here to set the record straight and help us understand what's really happening inside our arteries. Ian, welcome, Dr. Riddock.
Ian - 00:01:32:
Thank you. So nice to be here. Really appreciate being a guest on your show.
Rosemarie - 00:01:38:
It's great to have you. The last, I mean, time that I've worked with you, I just remember that you were always prepared. You always delivered. You always gave me the soundbite when I was working up in Spokane, Washington at KREM 2 News. You were always, you know, right on. And I think you even did a morning show with me once.
Ian - 00:01:56:
We did, yeah. The first time I had ever been on any kind of show like that. So it was pretty nerve wracking for me, but that was a lot of fun.
Rosemarie - 00:02:04:
Yeah, and you came with props, I remember.
Ian - 00:02:06:
Yep, yep. I remember that well, too. So we were trying to get at lipoprotein particles and try to understand the difference between people that have so-called small, dense LDL particles versus more larger, buoyant. Some people don't like to even use those terms, but really getting that particle count. So we brought out a jar of blueberries. And then we brought out a jar of, I think it was like tangerines or something like that, to get a visual idea that people could see on television about, you know, they might contain the same amount of juice or Cholesterol, but there's more traffic on the freeway in the jar full of a bunch of blueberries and therefore potentially more hazardous to you. That was the point we were trying to get across.
Rosemarie - 00:03:03:
Yeah, and it worked well. And I'm going to bring this into it because I think this has a big part of it. You're very prepared. And I don't know if that has to do with your military training background or what, but I feel like people and also your cardiologist. So. How has that influenced the way you work in cardiology or does it, does it impact at all?
Ian - 00:03:27:
Yeah, I mean, I think all of that goes into play. Certainly in the military, you are trained to be prepared. You're wearing the uniform. You're dressed appropriately. If you're on time, you're late. You've got to be five minutes early, all that kind of stuff. I think cardiovascular training in general, too. We always call it high adrenaline learning. I mean, you don't show up for rounds ill-prepared. You get crushed. So there's good and bad with sleep deprivation and waking up early to round on all your patients and then facing some intimidating attending physician. And if you don't have your stuff together, boy, you find out pretty quick. So there's a lot of adrenaline going into that. But no, I think a lot of this just comes from a passion of learning. And with this kind of stuff, with lipids, with prevention, it's really exciting. It's always exciting. And retelling the stories and through repetition, maybe you get better and better at presenting it to folks, hopefully. But I think there's enthusiasm, as we talked a little bit before the show, just trying to get every little piece of information out there. Because you never know what little nugget might stick with somebody. And that helps them understand things better. And so you're like, all right. Well, in the case of the news show, though, you only have such a small amount of time to get that data out there. So hence the props and stuff like that. But trying to be prepared and hit the fine points so that you get a broad audience involved.
Rosemarie - 00:05:15:
Yeah, yeah. Well, and I feel like, too, we naturally connect it. Like when I first met you two, it's that you talked about just wanting to educate. And the more you say, the different angles of stories, too, it's like we might talk about heart health, even though we do talk about it often, which will lead really into my first question. You know, we talk about it. There's a lot of information, but somebody might hear something a little differently. They might have heard it a hundred times before that, but maybe a way that you say it, or that, you know, that day that you brought the props into the show, that could have triggered something that really made a difference. So it can't hurt by just keep, you know, just pounding in the information any which way. Weekend, so.
Ian - 00:06:02:
Yeah, a lot of what we preach in prevention, you know, a lot of that data has been out there for a while, you know, in guidelines and various publications, for instance, we'll talk about non-HDL Cholesterol in a little bit. I mean, that goes back greater than 25 years in guidelines, yet it's still challenging to get, you know, top or providers of all brands, you know, whether it's primary care, cardiology, Endocrinologists specialists to understand, and then the general population, what is non-HDL Cholesterol. So a lot of these things, you know, they just, they require repetition, they require talking about it over and over again, and basic fundamental things. That's partly also why I like lipids and things like that. It seems complex in some ways, but in other ways, it's really quite simple. A lot of things haven't really changed that much. But it's just about increasing awareness by continually educating people on these concepts.
Rosemarie - 00:07:12:
Okay, so even with all the awareness, you know, all the, you know, February, Heart Month and all the pushes for education and technology. It's still, the heart disease is still. Right, the number one cause of death. And then in midlife, right, between the ages of 40, especially between the ages of 45 and say 65. And then according to the stats I'm looking at, one in three deaths in this age group are due to heart disease or stroke. Why are we still falling short? What do you think some of the aspects of risk and prevention are still overlooked? You kind of talked a little bit about it, but...
Ian - 00:07:51:
Yeah, so in a nutshell, I mean, we've come a long ways, you know, and what a mentor once told me is when it comes to atherosclerotic cardiovascular disease in people with established plaquing, for instance, that gets into like kind of what we call secondary prevention, where people have known disease and you know about it and you're trying to prevent it. You can really only undertreat this disease. You really can't. I mean, the evolution of therapies, you know, starting with statins, which first came online in 1989, or 1987, rather. I mix up those two years because my dad had his first event at 1989 and statins had fortunately just come out two years prior to that. These were modest or low-intensity statins, and they would shave off some Cholesterol values, which we'll get into this, why that's the most important culprit. And then as we've developed more therapies along the decades, at first we were just trying to give people some years. We are at the point where, in most people, not all people, we can actually halt the disease and its progress, and in many ways reverse it. But it requires intense therapy. That being said, however, there is still what we call in our community residual risk. And that is a product of multiple factors. One that you kind of laid out is like, how do you first of all identify these people that are at risk? There's lots of different risk calculators out there, but we are not really, and you mentioned the awareness campaigns, Heart Health Month or Women's Health in February, National Lp(a) Day. There's all these different, familiar hypercholesterolemia. We try to get at all these really hot button topics or really high risk individuals. So increasing awareness, but then also making sure that we're employing appropriate therapies to the appropriate folks and that we're actually achieving targets. And so, for instance, the National Lipid Association and others are really pushing for... An old mainstay biomarker, LDL cholesterol. It's been around for a long, long time. But it's pretty good. Why is that not a quality measure from CMS, our Centers for Medicare & Medicaid Services? We have quality measures for other things, like for hypertension and for diabetes. But why is it that we employ therapies like statins and other non-statins, and we don't ensure that we're checking the main biomarker that those therapies are impacting to make sure that patients are getting to goals that are widely published in just about every single guideline around the globe? So there's campaigns that can be towards awareness, and then there's campaigns that can be aimed at policy. But all of that is, and then we can talk about other biomarkers, which we're going to, all of that is getting at residual risk. We've done an excellent job, but there are pockets of people, pockets of patient populations. There are different phenotypes that we'll talk about in terms of lipid disorders. But there's pockets of people that are being left behind or disenfranchised. And we'll talk about how women, there are lots of different things, in particular with women, that allow them to be particularly vulnerable to residual risk. So all of those things are important to deal with. It's important to continue to educate people about. And we'll get into all of those things here.
Rosemarie - 00:11:54:
Yeah, yeah. No, I'm glad you touched on a lot of good things that will help me segue into, I really wanna just get right into metabolic health. I know heart health and metabolic health go hand in hand. You've been talking a little bit about it, but it's like you have, say two types of people, right? You've got the person that does all the right things. They go to the gym, they eat good, for the most part, like 80% of the time, right? And they turn out to be a ticking time bomb. And then you have another person where you think as you look at them, maybe they don't go to the gym, they're a little overweight and they do all the wrong things and they go through life unscathed, right? So, and then the healthy person goes and has an event and you're like, what in the world? This actually just happened to someone that we know, that I know who works at the hospital. But anyway, that it's like the picture of hell who happens to be a doctor, but yeah, who had an event at work. So could you talk a little bit about those metabolic issues that, you know, what is it? What are they and how do they affect the body?
Ian - 00:13:02:
Yeah, so I think it's really important to emphasize that when it comes to atherosclerotic cardiovascular disease or plaque formation, You know, the most predominant risk factor is your lifelong cumulative exposure to atherogenic lipoproteins. And the predominant one is LDL, low-density lipoprotein. And there's others like very low-density lipoprotein. We'll talk about Lp(a) other things. And then there are other risk factors that... So the lipoproteins are the primary driving force of atherosclerosis. And then having diabetes, having obesity, smoking, having hypertension, being sedentary, having a high-stress job, all of those things, having psoriatic arthritis, an inflammatory disorder, lupus, and things like that. Those are like kind of adding gasoline to a fire. So to what you just said there, you can be the healthiest person in the world in terms of – I mean, I live in a very healthy community here in Bend, Oregon. You know, we've got ex-Olympians and we've got, you know, people that have been triathletes for 35 years and practically a vegan. And they come in and... Either they've had an event or they went and got a screening test, like a calcium score, and their calcium score is through the roof, and they're just absolutely wrecked. You know, they're like, what gives? And a lot of the exposure to those lipoproteins throughout their life is genetically driven, you know, either polygenetic or some folks have monogenetic disorders, where it's one gene that could be like familial hypercholesterolemia, stuff like that. So while it's certainly advisable to always start with lifestyle measures and adhere to what is shown in a broad range of literature to reduce heart disease is healthy lifestyle choices, you know, exercise in terms of cardiovascular, aerobic fitness, and weight training, and eating a heart-healthy diet like a Mediterranean-style diet, and avoiding smoking and things of that sort, those are all very, very beneficial for cardiovascular health in totality. But, you know, you can be doing all of those things and still have heart disease. And even a so-called normal lipid panel or normal LDL cholesterol level throughout most of your life is still plenty to cause atherosclerosis. And so what you alluded to with some of these athletes, I kind of think of that as the healthy athlete bias, you know. And I've seen, you know, public service announcements like or ads on television where, you know, you're watching a baseball game and they break away to a health, you know, somebody promoting their health platform. And, you know, they show a bunch of people running on a trail and doing some push-ups. And that's all great, you know, because, you know, you want to promote health. I totally understand that. But in some ways, you know, and they're getting out maybe the couch potatoes, sitting there watching television, watching the ball game. They say, okay, you know, but also get off the couch and go do these things, which is great. But if you're an athlete or if you're already healthy and you're looking at that image and you're saying, well, that's me. You know, I run like that and I exercise like that and I do push-ups like that and I eat healthy, I don't have anything to worry about. And that's not necessarily true. And so we do need to be aware of that bias as well. And that's part of residual risk. There are those populations of people that are also getting undertreated or under-recognized. So we have to have... More awareness, more education, and better screening tools. And I think we have pretty good screening tools. But certainly if you know your family history or you know some of those potential genetic things, I mean, it starts with just getting a basic lipid panel done. The National Lipid Association now, as well as the Canadians and the Europeans, are recommending an Lp(a) as part of a standard lipid panel in every citizen at least once. We'll get into this, but Lp(a), do not change throughout your lifetime. So just having that baseline data to see, well, gee, do I have a genetic, either monogenetic, like familial hypercholesterolemia, where they have really high LDL cholesterol of like over 190 pretty much throughout their whole life, or if it's more of a polygenetic thing. And then they can say, all right, well, I've got some of the, I'm on top of the lifestyle stuff. Like I'm doing a pretty good job with that, or I'm working towards that. But let me also understand kind of the other genetic stuff that, well, you can't pick your parents, right? So you got to know some of that data. And all of that helps you formulate a baseline risk. And you always have to start with some sort of baseline risk before you embark on, say, therapy or something like that.
Rosemarie - 00:18:31:
Yeah. No, you said a lot of really good things. I mean, I lived in California for a long time, and I lived in a community. I lived in Manhattan Beach, so there was a lot of athletes and people were really into wellness and health. And I knew people that rode their, you know, rode by 40 miles a day and would go get fast food. For the most part, they're healthy, but then go get, you know, fast food for lunch every day. I'm thinking, this is not adding. You know, no, no, you know, I need this energy. I'm like, you don't need McDonald's. No shade. No shade to McDonald's. But I'm just saying, I'm like, you never need that. No offense. But they ride their bike. I'm like, yeah, but like your parents, like you said, the genetic thing. I'm like, but your folks had like X, Y, and Z. So, you know, and these were all really, I mean, above the bar, like in your community, like these were not, you know, these are middle-aged people that are outperforming, say people in their twenties. Right. But, you know, but then we have the whole age thing too. You know, that's the factor.
Ian - 00:19:26:
You start to develop those habits. And when you're young, you know, you can get away with a lot of that stuff, you know, but you're, but you're formulating habits and, and certain families have habits, you know, too. So, so sometimes what we might think of, of being kind of more genetic, and I hear this a lot in the clinic too, is say, oh, well. It runs in our family. Hypertension runs in our family. And diabetes runs in our family. And there are definitely an obesity and all that. There's definitely truth to that. But also habits run in family, too. So if you're not making the right healthy choices in your family, then you might grow up thinking that that's acceptable. So we have to continue to target families with our awareness campaigns and our education campaigns and making healthy food affordable and making exercise easily obtainable, having sidewalks in neighborhoods and stuff like that.
Rosemarie - 00:20:24:
Yeah. Yeah. All right. Well, I'm going to get into the science of things because I feel like we keep bringing up all these different particles, right? You're talking about the lipoproteins and so forth. And I feel like if we just get into the science, then people could understand a little bit, kind of like what we did on the show. Could you talk a little bit about the roles? Like you've got fat cells, fat molecules, Cholesterol, triglycerides, if you could talk briefly a little bit about each one and how they actually at optimized level serve the body, right? Or, you know, let's talk a little, so people can make better choices. They know more about the actual cells and molecules. Does that make sense?
Ian - 00:21:05:
Yeah. Well, let's just start maybe with how lipoproteins are manufactured and delivered and things like that. So your liver manufactures Cholesterol, and that's kind of like where statins impact things. And then you also resorb Cholesterol through recycled bile. Through your intestines. And then... You eat a little bit through dietary Cholesterol like an egg yolk, which doesn't have a tremendous contribution to your serum Cholesterol levels. But anyway, and then you have adipose tissue, fat cells. And those harbor a lot of energy and they will deliver fatty acids to your liver. And there is an enzyme there that then takes triglycerides and the Cholesterol that is in the Cholesterol pool of the liver, we call it, which is combined with what the liver makes and what was delivered to it through the intestines. And the Cholesterol and the triglycerides are packaged together initially in what's called a VLDL or a very low-density lipoprotein. And that particle is mostly triglyceride rich. It's like this big Jupiter-like particle. If you think of it like, I just like to think of these things like common things. Okay, so like you got this big planet, this big Jupiter-like particle that is a five to one ratio of triglycerides to Cholesterol. And that is secreted into the blood. And its mission is to deliver triglycerides to the tissue as energy packets. And as soon as it hits the bloodstream, you have these lipases that are cleaving off triglycerides and sending them to the tissue as those energy packets. And so whittling away that Jupiter-like planet like little piranha until, and it goes through a couple of other stages. So it becomes an IDL or intermediate density lipoprotein. And then an LDL, low-density lipoprotein. And that happens in like a matter of hours. And once that has occurred, the LDL and these lipoproteins are meant to deliver Cholesterol to the body and to bring Cholesterol back. But anyway, so when it comes to LDL, that LDL particle, it's really just at that point, it's delivered its payload. It's delivered the triglycerides to the tissue. And it's going to swim around in the bloodstream for about two to five days until one of two things happen. The liver, through these LDL receptors, is going to pick it up, bring it back into the liver, and then it releases it into the liver and it gets broken down or liver adds more triglycerides to it, sends it back out again. But if you have too much traffic on the freeway and those receptors that are clearing those LDL particles are overwhelmed, then the LDL particles like, all right, you're not picking me up. I'm tired of swimming around in the blood. I am going to go crawl into the lining of this blood vessel. And that's not supposed to be there.
Rosemarie - 00:24:34:
Right. Okay.
Ian - 00:24:36:
So then that sets up an inflammatory reaction and your white blood cells, your monocytes will go to that area and they crawl in there and they oxidize it and it turns into what we call a foam cell and then off we go. Now we start developing atherosclerosis. And when it comes to things like triglycerides. If you, and we're going to talk about obesity and things like that, and insulin resistance and things like that. So triglycerides are there for energy. And if you are in a hypercaloric state or you are in an energy positive state, you are going to increase your adipose sites, your adipose cells. So adipose sites store fat. And so lipids are fats and oils. And so anyway, so you're storing the triglycerides in your fat cells. And your fat cells, you know, they're not inert. They have the ability to produce hormones and things like that. And they can be either, um, have a more antioxidant type of impact, or if they start to become deranged because they outstrip their blood supply, they can become pro-inflammatory, and they can contribute to more atherogenesis or atherosclerosis, and they can contribute to other things that can promote, say, plaque rupture. But what they also do, and what insulin resistance does, is it impacts the ability of those VLDL particles, those very low-density lipoprotein particles, to be hydrolyzed by those little piranha, like I was mentioning. And so, it increases the transit time of those VLDL particles. And instead of maybe several hours that it takes to have that VLDL be hydrolyzed down to that LDL, it might take many more hours or even days. And you end up having more VLDL, what we call VLDL remnants. I think of that like, I don't know, like in the movie Star Wars, where, you know, the Death Star gets destroyed, and there's still like half or three-quarters of it hanging around. So, VLDLs, when they are hanging around as remnants, they can also be incorporated into the lining of your blood vessel wall. And so, triglycerides themselves are necessary for energy. Cholesterol is very necessary for a lot of things. It is the backbone of steroid manufacturing, and it's in all of our cell membranes, and it's important for fat-soluble vitamins like vitamin D, and things like that. But it's important also to remember that all of the cells of the body, can produce their own Cholesterol. And the Cholesterol contained in the LDL particle is really just trash. And so it's important for the public to be aware that, yes, Cholesterol is super important for cellular function. But that's different than what's floating through or trafficking through the lipoproteins through your bloodstream.
Rosemarie - 00:28:17:
Okay, so lipoproteins, they definitely have their moment. I don't know if because I'm interested in them, but they keep popping up on my social media. So we love those algorithms. So I keep getting all this information, but not clearly as in-depth as we're talking about now. So what I gather, what you nicely said is basically all these cells, they all have a purpose in our body pretty much. They're giving us energy or they're the vehicle to get us the energy to our cells. Now with these lipoproteins, they are, right, when they're, it sounds like when there's no more use for them, they're going, you know, they're like the driving factor to say cardiovascular disease and heart attack. They're pretty significant, the role of them, whether they're, you know, too much, not that we don't have enough, but with the lipoproteins, if they are so critical. I don't really remember my doctor talking about lipoproteins or in a blood panel. I feel like unless you ask for these things specifically, like you did talk a little bit in the beginning that we are getting better at, or doctors are, or health providers. But why are we not looking at this more if they're so critical?
Ian - 00:29:30:
Oh, yeah. Good point. Yeah. So let me back up one second. And I guess we didn't really describe actually what a lipoprotein is. So as we talked about before, Cholesterol and triglycerides are fats or oils. Oil don't mix with water, which is what your blood is. And so they need to be trafficked in a vehicle that can contain both fat. So the fat is in the center, which is the Cholesterol esters and the tricylglycerols or Cholesterol and triglycerides. And then there's a phospholipid layer. Which is polar. And so it's hydrophilic on the outside and hydrophobic on the inside. So it can contain the fat on the inside and then be exposed to the water on the outside. And then there's a protein that wraps around it. So it's kind of a descriptive term, lipoprotein. So there's lipid in the middle and then there's protein on the outside. And that allows it to then float through the bloodstream. So yeah, these things are all very important. But I think, you know, what you were kind of getting at is biomarkers and using a biomarker to help us determine who is at risk for a disease. And so in the 70s, these lipid assays came out and LDL cholesterol is a calculated number. It has to be calculated. And previously, it was this thing called the Friedewald equation. And so you can measure the total cholesterol. You can measure the triglycerides. And then you can calculate LDL cholesterol concentration. And lipoproteins have become a little bit more... Heard in the common language because of other biomarkers that have started to emerge. And one is Apolipoprotein B. So, or we call it for short ApoB. So every single atherogenic lipoprotein species, of which we already kind of described VLDL, even IDL. LDL. VLDL remnants we talked about. And then another thing that we'll get into in a bit probably is Lipoprotein (a). Every single one of those lipoproteins contains exactly one apolipoprotein B protein or apolipoprotein that's wrapped around it. So if we count... Beep-o-bee. We get a better idea of amount of particles or traffic floating through the down the freeway just as we talked about on the news with the blueberries and and the tangerines now The reason that that is important is because we're all a little bit different. And when people have, like, say, metabolic syndrome, and we can talk about what that is, but it's very similar to insulin resistance and it's associated with obesity. Metabolic syndrome is basically, three out of five components. High triglycerides, low HDL Cholesterol, increased abdominal waist circumference, hypertension, and dysglycemia, meaning they've got diabetes or prediabetes. And if you have three out of those five things... Then we call it metabolic syndrome because the risk associated with it in terms of the risk of atherosclerotic cardiovascular disease is worse than the sum of its parts. So we want to identify those people. But it also speaks to a very common lipid pattern that we see in developed countries. Which is... Fueled by obesity and sedentary lifestyle and smoking and things like that, where we see high triglycerides on a lipid panel. Low HDL Cholesterol, And their LDL cholesterol might be normal. Or maybe mildly elevated. Or even in some cases, lower than most people's. You know, so where triglycerides become important as a biomarker is to, when we see somebody with elevated triglycerides. We are supposed to question the validity of the LDL cholesterol being reported in that lipid panel. Because the LDL cholesterol will be falsely reduced. I can get all nerdy as to why that is, but it gets to what you were, I think, kind of alluding to, which is why are we paying attention to these lipoproteins and the sizes and the particle numbers and stuff like that? And people that have that derangement, high triglycerides, low HDL Cholesterol, and the worse it is, the higher the triglycerides and the lower the HDL Cholesterol, the more what we call... Discordant the LDL cholesterol is in terms of reflecting actually how much traffic's on the freeway. Those people have what we call small, dense LDL particles, and they just have tons of them. In those folks, we need a better biomarker because LDL cholesterol is not telling us the full stories. LDL cholesterol works pretty good in most societies. It identifies, you know, it's pretty accurate in about 75, 80% of us. But those other folks, it may be inaccurate, and it may be inaccurate in a way that they escape detection. They go get their blood drawn, they go follow up with their provider, and they look instantaneously at their LDL cholesterol, and it's low-ish, and they pat them on the back, and they say, you're looking good, but your triglycerides are high. I want you to work on diet, exercise, stuff like that to try to reduce those triglycerides. But what they're missing is that their atherogenic particle count is elevated. So all the way back to the Cholesterol treatment education program. What we call the Adult Treatment Panel III Guidelines in 2001. And Those guidelines told us. But if your triglycerides are greater than 200 milligrams per deciliter, now we say 150, but back then even it was 200, but we knew about this. You should ignore LDL cholesterol. And you should jump immediately to non-HDL Cholesterol. What is non-HDL Cholesterol? Well, It's kind of a cumbersome term, but it's total cholesterol minus your HDL Cholesterol. And a lot of people in the lipid community hate saying this, but... For the lay person that might help them understand it. So just take your total cholesterol and subtract out the quote unquote good stuff.
Rosemarie - 00:36:29:
Okay. The happy Cholesterol.
Ian - 00:36:31:
Happy Cholesterol. And other people who might listen to this would just totally jump down my throat for saying happy or good or whatever. And we do want to try to get away from those terms, but that's going to be a work in progress. There's nothing good or bad about Cholesterol inherently, but when Cholesterol gets into your blood vessel, then that's not good. But anyway.
Rosemarie - 00:36:55:
No, but that's a good point because people use that lousy Cholesterol, LDL, and like, you know, good Cholesterol. That's the way it's sometimes translated to people in the doctor's office.
Ian - 00:37:10:
Yep. And then they pat them on the back for having a so-called good ratio. And that's the other thing that we need to start getting away from is we need to stop talking about ratios and stop using ratios. There's no use for that. And in fact, it's harmful in many cases, particularly in women who tend to have higher HDL Cholesterol. And that HDL Cholesterol does not negate or offset generally the risk of having high LDL cholesterol or high Apolipoprotein B particles. So back to that HDL Cholesterol real quick. So if in those people with the high triglycerides and the low HDL Cholesterol, whose LDL cholesterol looks okay, if you look at their non-HDL Cholesterol, it won't be okay. And it shouldn't really deviate by more than about 20 to 30 points non-HDL Cholesterol from LDL cholesterol. And the more it does deviate beyond that, the more... Excessive particles they have floating around and the more light atherogenic lipoproteins they have floating around. Now that non-HDL Cholesterol comes free, if you will, in a lipid panel. And a lot of labs don't report it, but most of them are jumping on board and they do. They should, all labs should report non-HDL Cholesterol. But if they don't, then you have to make that calculation of total cholesterol minus HDL. But then a better biomarker, not that much better, is ApoB. And ApoB can be measured very easily. It's well standardized in most labs. And that is slightly better than a non-HDL Cholesterol. And so it's a better biomarker in those people with the high triglycerides and low HDL Cholesterol.
Rosemarie - 00:38:57:
Okay, so to just kind of summarize the testing, because we talked a lot about labs and different levels. If somebody's going to their doctor, what should they be asking for? What is the full comprehensive that they should be to give them the whole story of really what's going on?
Ian - 00:39:16:
Yeah, so they need to have a standard lipid panel. I would argue that having a baseline Apolipoprotein B is very helpful. And then the other is that Lp(a), that we talked about that. Now, real quick, Lp(a) as an LDL-like particle. It behaves and acts just like LDL, but it's got this other little apo A that wraps around it and it has a few regions on it that are homologous to something called plasminogen. Plasminogen is part of the yin and yang of the body. You want this Goldilocks situation where you're not bleeding too much, not clotting too much. Plasminogen helps break down clot or helps prevent clot from forming. So some people and about one in five, one in four, one in five of us in the population have an overabundance of Lp(a). And most of us, it's a minority particle. It definitely just like LDL contributes to atherosclerosis and it's not really worth that much attention because LDL is the predominant thing. But in those people that have that genetic disorder where they have an overabundance of Lp(a), can contribute significantly. And then it tends to promote when it does manifest in heart disease, it tends to promote more clotting in the form of heart attack, stroke. And you might see that in some of their family history and stuff like that. So a lipid panel, an Apolipoprotein B and an Lp(a) make sure that they're not one of those one in four, one in five that have really high levels. And that can help establish their risk. And then if they're like a lot of people listening to your show and they're on the forties and fifties and sixties and they really want to refine things, then a calcium score is very helpful. Anyone over the age of 40 really with at least one risk factor might benefit from a calcium score. And that's a CT scan that just takes thin slices through your heart and it looks for bits and specks of calcification in their coronaries. And calcification is a byproduct of inflamed plaquing over the years. The earlier you start to develop that and the more of it you have, the more inflamed plaque you've already got. And the more likely you are to have an untoward event.
Rosemarie - 00:41:27:
Just a lot of controversy around medications when it comes to your Cholesterol. There's so many sides to it, right? There's a debate, statin, no statin. Who would benefit? Who doesn't? If you could touch upon that, why the pushback? Why the controversy? A lot of different things, even in midlife women because of the hormone situation and things like that. So if we could touch upon that.
Ian - 00:41:49:
Yeah.
Rosemarie - 00:41:49:
Thank you. I didn't mean to cut you off on the last question.
Ian - 00:41:51:
No, no, no. I always end up talking a lot on all these things. There's so much to cover.
Rosemarie - 00:41:56:
There's a lot to talk about.
Ian - 00:41:57:
Right. Now, you know, I don't understand totally why statins have such... You know, polarizing discussions like on social media and the internet, whatever, and why there is so much pushback. But that being said, you know, you always, again, have to start with baseline risk. I think that putting statins in the water. Or statins are the cause of every plague to mankind, those are like two opposing and ridiculous things. You know, no, we shouldn't be putting statins in the water. And no, statins are not the root of all evil. You have to appropriately risk assess folks. And so there's lots of different risk calculators out there. You know, there's the pool cohort equation, which is the American College of cardiology American Heart Association and you can calculate somebody's 10-year risk and If it's greater than 7.5% 10-year risk, then you should consider a statin. If it's less than 5, then statins may not benefit. Between 5 and 7.5, you know, it's a gray area, reasonable to start a statin. And then you can use other adjuncts like we talked about with a calcium score. And then you want to, so the problem with tenure risks is that it doesn't really take into account a lot of people's family history and their genetics. And so, you know, if I have a 40-year-old that walks in and they, you know, most of them are going to have a low tenure risk, well, I'm not really concerned about whether they're going to have a heart attack or stroke by the age of 50, but I do want to know whether they're going to have one by the age of 70. And so you also want to calculate a lifetime risk and think of that like a 30-year risk. And you can use those same calculators and just pretend that you're 30 years older and put that number in. That's one way of doing it. Or you can look at either a calcium score. If I've got a 35-year-old in my clinic who went and got a calcium score and it's even one, you want a score of zero and it goes all the way up into the thousands. But if they've got a score of one, they are already high lifetime risk. And that person, you shouldn't mess around with them. The earlier that you start preventive therapy, the better. And the best, you know, tools that we have are statins because they've been around since we talked about since 87. We have more data with statins than just about any other medicine known to mankind because of how common atherosclerotic cardiovascular disease is. How many clinical trials we've performed? Thousands, tens, hundreds of thousands. I mean, these clinical trials were like 10,000 to 20,000 patients over, you know, five to, in some cases, 10 years. And the side effects of statins are very low. That being said, people can have them. And it's overblown in either direction. We know that clinical trials tend to kind of have a roster of patients and cherry-pick patients a little bit. And they tend to be folks that can tolerate medications. And in clinical trials, about 1 in 1,000 patients had to stop their statins because of adverse side effects. Clinical practice, it's more like 10% to 15%. But 90% of that is up here or it's other things because when we've done trials on them, we make them serve as their own control and do a double crossover trial. You give them a statin, wash it out, give them a placebo, wash it out, mix up the order. You know, 90% of their statin complaints go away or they can't pinpoint them. But it exists. But we have other non-statins, like Ezetimibe is a wonderful agent as well. And it inhibits Cholesterol absorption through the intestine. When you add it to even the lowest dose of a statin, you get 20% to 25% additional Cholesterol reduction. By itself, it's not very effective, only 10% to 15% lowering. So in the old days, I say the old days, but we still kind of do this, it was like max out your statin. You got to max out your statin. Well... Not everyone practices that way. You'll still find that in a lot of guidelines, but you can actually achieve the same lipid lowering with a low dose of a high-intensity statin. So like rosuvastatin or atorvastatin, 5 milligrams of rosuva, 10 of atorva. Antenna of ezetimibe. Is equivalent to the highest dose of those statins. So it's a great combination therapy to achieve very good lipid lowering and stay at the shallow end of the side effect profile. Now, beyond that, then you're getting into branded drugs like PCSK9 inhibitors, which are injectable. They're very good. They're humanized monoclonal, or excuse me, not humanized. They're fully human monoclonal antibodies. You inject them every two weeks or some, actually, there's another messenger RNA drug that's in the doctor's office every twice a year in the doctor's office. The first year is three years. But yeah, you can get 50% to 70% reduction with these PCSK9 inhibitors, but they're very expensive. They cost about $6,000 a year. And the insurance companies, the payers are going to push back unless you've really established that you're statin intolerant or that you can't take those drugs or that you just haven't been able to achieve therapy. So again, it all depends on risk that you're starting with. So if you have a high-risk individual, you want to treat those people early in life. And even lower is even better for even longer. That's kind of the mantra in our highest-risk folks.
Rosemarie - 00:47:56:
Okay. So we've talked, we just, you gave a great description of statins and some alternatives of this, you know, targeting the same, right? Your Cholesterol. Now I'm going to go to a newer drugs. This is classic. Well, they've been around, but that's now in fashion, the GLP-1s real quickly. Are you seeing with your patients who are on these medications, a decrease in say some of the metabolic disorders or cardiovascular risk with these patients that are on GLP-1s and just the debate, sugar versus fat. So if you want to talk a little bit about GLP-1s and what's, what should we be looking at sugar or fat?
Ian - 00:48:38:
Well-
Rosemarie - 00:48:38:
Everything.
Ian - 00:48:39:
Everything, right. I mean, I think, you know, what's interesting is I'll try to make this quick, you know, in diabetes, you know, we were so focused on, on glycemic control for so many years, you know, reducing the A1C, getting their blood sugar down. All right. Well, what's, what's the most common demise of a diabetic patient? It's macrovascular complications, atherosclerotic cardiovascular disease complications, heart attack, stroke, big things like that. Right. And, and microvascular complications like retinopathy, neuropathy, nephropathy, or kidney issues are important. They're very important, but that's really what the glycemic kind of stuff does. So, but one would stand to think that if the focus of our attention and diabetics was to lower their blood sugar. And in so doing, you would expect to see a reduction in cardiovascular events. We didn't see that. We had never seen that. The UKPDS trial and then in the early or the mid-2000s, there was some studies looking at intense glycemic control. And it actually, in some of those trials, led to worse outcomes in the ACCORD trial and other things like that. And then some of the therapies that were around were associated with worsening heart function. So like Rosiglitazone was removed from the market because it worsened heart failure. And cardiovascular events. So appropriately, the Institute of Medicine and the FDA said in 2008, they said, all right, any other diabetes drugs that you guys want to bring to the market, you need to do cardiovascular event trials to at least show that they are not harmful. They can be net neutral. So like the first kind of kids that came out were the DPP-4s and they were kind of more net neutral. And then the GLP-1 agonists, the SGLT2s and the GLP-1 agonists came on board. And it was just this like almost by accident, you know, like a lot of things in innovation and science and where you stumble upon something that has an off-target effect that is actually beneficial. And so GLP-1 agonists are just, they are showing a lot of really good promise in cardiovascular medicine at getting at this residual risk, but importantly attacking a lot of the issues of obesity, but also a lot of the metabolic derangements of metabolic syndrome and insulin resistance. And so a lot of the cardiovascular benefits. Are due to a conglomeration of all of those things, weight loss. Yes, I have anecdotally and just, you know, and in the clinical trials, but significant weight reduction. And significant improvement in their diabetes and in just dysglycemia and in insulin resistance. And as we talked earlier about, there is a connection of that in terms of lipids too, right? So reducing triglycerides and reducing VLDLs that are just overwhelmed with triglycerides, which is also reducing their clearance from the blood and reducing that lipid derangement of the high triglycerides, low HDL Cholesterol, and reducing blood pressure. And so all of those things have an effect on both plaque stabilization. But also on other things that are related more to the hypertensive renal and obesity problems that we see in heart disease, i.e., heart failure, heart failure with preserved ejection fraction. Now we're starting to see some data with the GLP-1s on heart failure with a preserved ejection fraction. The STEP-HFpEF trial, I think it was, I might be screwing up the name of that trial, but really showing that there were... Improvements in some of the measures that we use for heart failure with a preserved ejection fraction, like Kansas City questionnaire and six-minute walk times and stuff like that. So those are legitimate endpoints for heart failure patients that they showed a statistically significant reduction in with these GLP-1s. And then just looking at overweight and obesity, and that's a great, you know, aside from diabetes, just looking at people that have overweight and obesity with established atherosclerotic cardiovascular disease and showing a significant reduction in cardiovascular events in people simply because, well, not simply because, but showing a significant reduction in weight. And we don't think that it's all just related to the weight loss. There are other things, as we had touched upon a little bit, that is influencing cardiovascular disease. So yeah, if you're a cardiologist out there, which is tough for us as cardiologists, you know, to wade back into these drugs that treat diabetes and obesity and stuff like that, but we can't just leave it up to the Endocrinologists or to the primary care doctors to it to be the ones to prescribe these drugs. And in fact, historically, they've looked up to us.
Rosemarie - 00:54:05:
All right. So final questions. If somebody's watching or listening and they've taken in all this information, what are... A couple of action steps that they can do starting today to empower their heart health moving forward.
Ian - 00:54:22:
I'm really a big fan of the patient being their own advocate. And in fact, I even am trying to work on my own website for it. But be your own advocate and learn as much as you can. I don't mind if people have gone. People come into my office and they're like, oh, I did the whole Dr. Google search thing. You probably don't like that. I don't care if you did the whole Dr. Google search thing. That's great. Let's get down to it. Some of it might be good information. Some of it might not be. But the thing, too, about, I mean, we can have a whole other discussion about AI and all of that. But there. There are some good resources out there. Be your own advocate. Go in with a set of questions to your doctor and a set of goals in mind. But use your provider to help guide you through some of the misinformation and trust your providers. We have really good doctors out there and they want to do a really good job, but they only have a short amount of time to see you. And so, you know, listen to things like your podcast, the whole thing about-
Rosemarie - 00:55:37:
Thanks to the plug.
Ian - 00:55:38:
Well, you know, I mean, it's important. I love the concept of that Second Opinion because, I mean, it's actually, it's funny because we're almost going to name our website something very similar to that because, people need to have, when they go to see their provider, they understand the constraints of the healthcare system and they only have a few minutes to see their doctor and their doctors or their providers are well-intentioned, but they don't have time sometimes. And there are knowledge gaps. We don't, we can't all know everything. So AI and some of these other tools can help us identify where to put our attention or where to put place our risk. But when they leave the doctor's office, they might kind of say to themselves, huh, you know, I wonder if I really. Got what I came for. And having another resource where they can... I kind of need a Second Opinion sort of thing. And you need to go to the experts, which is why you're inviting experts, which I feel very honored to be on here and you consider me that. But yes, we need to lean on our experts and we need to have resources where we have a checklist of things that – and why are we not allowing the public to have access to a lot of these guidelines and things like that? They should be at their fingertips too. They should be armed with this information as well. So they can go in with a set of questions and expectations. But do a little bit of reading. Do a little bit of research. And then go in and what you really want to do is try to establish what's your short-term risk. Disease, what's your long-term risk? What's your lifetime risk? Always be mindful of the lifetime risk, especially if you're a younger person. And the earlier when it comes to prevention, that you start to kind of address these things, the better off you're going to be. And always, drugs are in many cases necessary. If we don't need to use them, great. But if we need to use them... Don't necessarily be afraid. You always want to have a high benefit to risk ratio. And I know, you know, we had talked about just briefly, I think you had mentioned on some of the notes to me beforehand, other things like I'll give an example of Red Yeast Rice. You know, Red Yeast Rice, it's a statin. And it's a supplement, and it is molecularly the same thing as lovastatin, which was the first statin that came out in 1987. But it's a weak statin. And it's not really, it's a supplement, so it's not regulated at all. You don't know what's in it. And because it's weak, the benefit derived from it is going to be small. And the risk... That you're exposing yourself to is going to be relatively higher than things that have gone through the intense scrutiny of FDA application and peer review and all that kind of stuff. So just always bear in mind that any therapy that you're going to expose yourself to, you want to have a high benefit, low risk ratio. And that always starts with baseline risk. The higher the risk you are, the more likely you're to benefit from a therapy. The lower the risk you are, you may not benefit quite as much. So you want to start with that 10-year risk and that lifetime risk and decide for yourself. Where am I in there? And is now the time to pull the trigger? And if you need those ancillary biomarkers or studies, like for instance, the calcium score, the Lp(a) a help you out, then that's advisable.
Rosemarie - 00:59:45:
Great. Well, you shared so much information today. We will probably have another conversation because there's lots of things that I wanted to talk about. AI was one of them. There's just, we could go on and on, but just to wrap things up, how can you But just to wrap things up, how can people find you or work with you? I know you're kind of working on a website. I don't know if it's up yet. But if, say, somebody just wanted to track you down, how can they find you?
Ian - 01:00:09:
Yeah, well, I'm in Bend, Oregon, and I'm with a group called Summit Health. And by the way, I guess for legally, I speak for myself and not for anybody else. But yeah, that's where I'm at in Central Oregon. The National Lipid Association, lipid.org, is a good website for people looking for lipidologists. They have a thing on there called like Find my Doc or something like that. It's like a find a lipidologist. That's one. The website, yes, it is available. It's very much a work in progress. It's called cardioadvocate.com. I'm still trying to make it look nicer and prettier and stuff like that. It's got some articles on there. But I'm super busy, so I don't have a lot of time to invest in it. And it's really, if I can get awareness out there and people learn something from it, great. It really kind of started off as just a resource for my patients instead of giving them the patient instructions. I know patients leave the office and have lots of questions. So I thought, well, I might as well start writing some of this stuff down. So it's got some articles on there kind of going into depth about what we've talked about here. But, I appreciate that.
Rosemarie - 01:01:27:
Great. No, you're welcome. Thank you for your time. It's been so great being in contact with you again and having these conversations and hopefully we'll have more.
Ian - 01:01:37:
Yeah, I appreciate your insightful questions. And, you know, I love chatting with people that are really passionate about all the things that we've talked about over the years and trying to educate the public and, you know, and educate other providers, too. Hopefully there's a lot to learn and, you know, we try to we want to talk in great depth, but also try to talk kind of fundamentally as well for everybody.
Rosemarie - 01:02:11:
Yep. And that's a wrap for today's episode of Second Opinion. A big thank you to Dr. Ian Riddock for sharing his insight from lipoproteins and lab tests to statins, stress, and sugar. I hope this episode helped clear up some of the confusion around Cholesterol, triglycerides, and metabolic health, and what it really takes to protect your heart and midlife. If you've enjoyed today's conversation, don't forget to subscribe, rate, and leave a review. It helps others find the show. And if there's a topic or expert you'd like for us to explore next, reach out. We love hearing from you. I'm Rosemarie Beltz. Until next time, stay well, stay curious, and remember, it never hurts to get a Second Opinion.