Welcome, my name's Dr. Warrick Bishop. I'm a cardiologist, an author and a keynote speaker. I'm CEO of the Healthy Heart Network. I'm all about trying to help people live as well as possible for as long as possible. Heart disease is huge in Australia. Every 20 minutes someone suffers a heart attack. Most of these could probably have been avoided if only we knew what to do. This podcast is all about helping you understand. blood pressure, weight, cholesterol, for better health. If you enjoy this podcast, I would be honoured for a five-star review. You can share it with your family and friends. It may well save someone you love. G'day, my name is Dr. Oric Bishop and welcome to my podcast and videocast station. I'm really delighted you've tuned in and today I'm pretty keen to talk about some language or ideas or concepts. which I think hinder the conversation around cholesterol. And I think these concepts are really, really important as foundational pieces of understanding if we are going to think and talk about cholesterol and its impact on cardiovascular health. Let me start off with the first bit of bad language, if you like, that I think needs to be addressed. I think the term coronary artery disease is a little bit misrepresentative. The process, a disease by definition, is something that alters function or causes symptoms. And one of the really important things that we know from coronary artery disease is that people are symptomless, are unaware until the moment that something happens. This means that the concept coronary artery disease misses the point that this is a process that occurs over not hours or minutes or days, but over years and decades. And really what we need to be thinking about is a progression of atherosclerosis. Let me share that as an image for those who are watching this as a video, for those who are not looking as a video, try and imagine an artery where in maybe as young as your teens, some cholesterol can end up in the artery and then gradually build up over decades to a point where it eventually leads to a plaque that will rupture and cause an event. Well, labeling that process coronary artery disease focuses on the very last step or stage of it. And that just doesn't make sense. It really then throws an enormous amount of confusion into the conversation about where cholesterol can be beneficial. There is robust data that tells us over and over that secondary prevention, i.e. treating people with cholesterol lowering, If those people have had coronary artery events or cerebrovascular events, for that matter, treating those people is without doubt supported and proven scientifically. So if you've had a problem, then no question to reduce the risk of subsequent problems treating with cholesterol-lowering medication works. and has been scientifically proven. But here's the confusion. When we talk about primary prevention, and that word primary prevention alludes to individuals who have not yet had an event. When we talk about primary prevention, there's lots of mystery, lots of confusion, lots of opinion about whether cholesterol therapy is important. And when you look at the data around primary prevention, it's much harder to put a finger on it. If we were to change our language from managing coronary artery disease to managing the process of atherosclerosis, then that would make an absolutely enormous difference because then we could start to identify people who many years before an event occurs may have evidence of plaque building up in their arteries to a substantial degree. Those individuals, if we are treating for atherosclerosis, would be considered at unacceptably high risk if left without therapy or without attention, and those individuals would be treated. No question, no confusion. One of the other concepts that I think we have to be so careful with is this concept of low risk when it comes to cardiovascular disease. with one in four people being impacted by coronary artery disease, I think we have to all accept that we're all potentially at risk. We're all potentially at risk of car accident. We're all potentially at risk of drowning if we go swimming. We're all potentially at risk of coronary artery disease because it affects so many people. And the reason why I think that language of low risk is such a problem is because it can provide a false sense of security and it misses the concept I've just talked about, which is atherosclerosis being a progressive and potentially lifelong problem. Decades. So imagine a 45-year-old man who believes he's low risk because the risk calculator that the GP put him through indicates low risk. Well, that low risk, believe it or not, generally only relates to the next five years. This is a 45-year-old man. I would put to you that that 45-year-old man wants to live probably to 85, 90, maybe even 100 if you asked him. He might say, well, my grandpa lived to 101 and I told him I wanted to pip him by a couple of years. So a five-year risk calculation that says he's low risk, is somewhat meaningless for this man who's actually got a lifetime journey, which is not at 50, but twice those many years. You see, when we start to reduce the distance we're looking down the road when it comes to risk, we can under-represent risk dramatically compared to longer durations and lifetime risk. concerned that we use the term low risk and this individual may well take that on board and instead of being checked again at five years, may with false reassurance not be checked for 10 or even 15 years or have an event before he gets checked again. So low risk, I think, is a terminology we have to be super careful with and probably not use. I think we have to recognize anyone, everyone can be at risk of coronary artery disease. Some people more than others. The next bit of language that I think we really, really have to be careful about is cholesterol. We think about cholesterol and the term is thrown around an awful lot. What is cholesterol? Well, it's an organic molecule. It's a fat. But the chemical compound cholesterol is not the cholesterol that we measure in blood and that we relate to risk of heart attack. These are two different things. This is absolutely critical to understand. When we talk about cholesterol in the blood, we talk about cholesterol, being associated with the proteins that carry cholesterol around the blood. There are two main proteins that do that. There's ApoB and ApoA. Now, this is super duper important because cholesterol, just the molecule, is... required for all sorts of aspects of human health membrane integrity hormone production it helps in digestion it helps with vitamin d formation so cholesterol is an important molecule but when we talk about cholesterol measurements when we talk about cholesterol in the blood when we talk about cholesterol related to coronary artery disease, we're talking about cholesterol in the particles moving around the bloodstream. And when we look at those particles, there's a number of different types. There's the cholesterol particle that comes in from the gut. This is called a chylomicron. This probably doesn't feed into the cholesterol conversation around cardiovascular risk. Then at the other end of the scale or spectrum is the cholesterol that we find in HDL cholesterol or high density lipoprotein. This HDL cholesterol is linked to the apolipoprotein or protein ApoA1. This is at the other end of the spectrum of the chylomicron. Remember the chylomicron. probably not tied in with cardiovascular disease. The HDL, the high-density lipoprotein with APOA, probably is protective or at least not contributory to cardiovascular risk. So we've got two ends of the spectrum. Neither are those appearing from our research to be directly linked to cardiovascular risk, yet both of them carry cholesterol. Well, what leaves, what's in between? What's in the middle of that spectrum? What fills that spectrum? Well, we have very low density lipoprotein, which the liver can produce. And that's a way of getting energy around the body. As the very low density lipoprotein gives up components of its liver to the tissue, it becomes a intermediate density lipoprotein, which also can give up cholesterol to the tissues. And if it loses more cholesterol out of its structure, it can become a low-density lipoprotein. Those three particles, the very low-density lipoprotein, the intermediate-density lipoprotein, and the LDL, or low-density lipoprotein, are associated with ApoB100. This is the cholesterol. That is the concern. So interchangeably, we're talking about concern with particles that carry the cholesterol around. Do you see the shift? I'm moving from talking about cholesterol as a molecule, which of course has a role. And now I'm talking about cholesterol, how it moves around the body and the company it keeps. When cholesterol keeps the company of a chylomicron, it's not necessarily problematic to cardiovascular risk. When the cholesterol keeps the company of an HDL cholesterol with ApoA1 as the protein that holds it together, it doesn't seem to cause a risk. But when cholesterol hangs out with ApoB100, the apolipoprotein that's... associated with very low density lipoprotein, intermediate density lipoprotein and LDL lipoprotein, when cholesterol hangs out with APO B100, that's when it can get into mischief. And that's where we need to have that distinction. Cholesterol is not cholesterol, is not cholesterol. Lastly, in terms of trying to bring A little bit of better language to our communication. Let's talk about high cholesterol. And this is also really, really important. When we talk about cardiovascular risk high cholesterol, we're talking about those particles, the APOB particles that appear to be linked to coronary artery disease or interaction with the vascular wall and giving up their cholesterol to those sites that end up becoming atherosclerotic. Well, let's think of those ApoB particles, the VDL, the IDL, and the LDL. And LDL is the one that we see the most of. LDL is the one that we've got most of our research over. But let's think of those cholesterol particles in a slightly different way. Let's think of them as mischievous particles of salt, as we might consider salt in sea air, if we parked our car near the beach. If we parked our car near the beach, we'd all agree that those particles of salt flying around in the atmosphere would create the environment for rust to form. And the more salt you have, the greater the chance of that rust forming. So APO B, 100 particles, VLDL, IDL, and particularly and really importantly, LDL, these are the particles that create the environment for rust to form. How do we then classify that? Well, we talk about high, borderline high, very high. But we're talking about this in context of other individuals and what sort of levels that they may be seeing. So for LDL cholesterol, there are very high levels. Right up to 4.9 millimoles per litre and above would define very high levels. High, 4.1 millimoles per litre. Up to 4.9 is high. 3.4 to 4.1. as borderline high. Now what I want you to get here is that there isn't a cutoff at one point where, if you like, the rust stops and the car is safe. You drive your car away from the ocean, you reduce the number of particles, you see lower levels of ApoB particles in the bloodstream, lower levels of LDL in particular, as you see lower, lower levels, your risk of plaque, your risk of rust gradually reduces, but it doesn't become zero. You can't get to a point easily at all where there's a zero risk of rust. There's always a small risk, but as you get closer... to that environment where that environment is more toxic if you like because of those particles your risk increases when we talk about high cholesterol we have to be clearer in our distinction are we talking about borderline high cholesterol which affects a huge number of the population or are we talking about high cholesterol or are we talking about very high cholesterol? Well, when it comes to very high cholesterol, you're basically parking your car on the beach. These people, without question, are going to need something to modify their future risk of plaque formation. When we then talk about the next step and then the next step and the next step, these are not all high. This is a continuum. And so I think we have to be really cautious about using the term high cholesterol because it encompasses borderline high, high and very high. And they're very different clinical pictures. The very high group, the high group, without question, they're going to need some sort of modification of risk over that lifetime if we're going to prevent rust in their pipes, if we're going to alter the progression of atherosclerosis in their arteries. Our confusion in the broader sense, the controversy begins at borderline high and below. And at borderline high and below, these are the groups of people where advocates for cholesterol being good for you, people who are non-statin promoters will make the case that the medications are not valuable. But because they're using the term high, they're creating confusion with the true high and very high individuals. I think we've got to be super careful, but we do need to respect the language and get that language right. I think we have to be cautious about using the term coronary artery disease because it negates the process that leads up to it. I think we have to be really cautious about using the term low risk because it's often for risk calculators that only last five years. And let's face it, we want to be living much longer than five years. So that just doesn't cut the mustard for me. We almost need to accept everyone is at risk. Some people at higher risk than others. Remember, not all cholesterol is the same. There's cholesterol, the molecule, and then there's cholesterol who hangs out with different mischievous parties. And that cholesterol, it's the company that it keeps that defines whether it's going to be problematic or not to the arteries. Apo B100 is the company that it keeps when it's really getting up to mischief. When it is the company of Apo A1, or when it's in a chylomicron, we don't see the same problem. So cholesterol is not cholesterol. Cholesterol is all about the company it keeps. And what is high? Well, high is a continuum. And it can be from very, very high, right down to borderline high. And even optimal levels of cholesterol can leave us finding individuals with plaque in the arteries. But the term high just negates. and causes confusion because it generally is used to represent those people who are borderline high and allows non-cholesterol believers a wedge to knock, sorry, a crack to knock a wedge in. That's me banging on about a bit of language. I think this is super important stuff though, because I'm dealing regularly with people who have a real issue or concern around cholesterol and cardiovascular risk. And a lot of the conversation we have revolves around me trying to peel back some of the misinformation, which is from some of that bad language I just shared. I really do hope that's made some sense to you. I've gone on a little longer than usual. You could say I've almost ranted. I don't think so. I really have been appreciating people's questions. I am putting out that weekly email. So if you're tuning into that or reading that, that's fantastic. I hope you enjoy it. I'm getting feedback from that as well. If you found this beneficial, please subscribe. Please feel free to share it. For now though, I am going to say goodbye. I'm going to wish you the very best. I do hope you live as well as possible for as long as possible. Take care and bye for now. Did you know that coronary artery disease kills one in four people? So most of us are likely to carry some risk or know someone who does. If you're interested in finding out more about how to evaluate that risk, check out. www.virtualheartcheck.com.au It will give you information about risk and what else can be done to be even more precise.
