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Welcome to my podcast. I am Doctor Warrick Bishop, and I want to help you to live as well as possible for as long as possible. I’m a practising cardiologist, best-selling author, keynote speaker, and the creator of The Healthy Heart Network. I have over 20 years as a specialist cardiologist and a private practice of over 10,000 patients.

Podcast Summary

Introduction

Dr. Warrick Bishop is a practicing cardiologist and author dedicated to improving patient care through cardiac health education. In this episode, he presents a provocative conceptual framework: that coronary artery disease may not be a disease itself, but rather a maladaptive physiological repair process. He explores how cholesterol's natural role in cell membrane repair, when occurring in damaged arterial areas over an extended human lifespan, could lead to plaque formation.

Key Takeaways:

  • Cholesterol serves essential bodily functions including cell membrane construction, fat-soluble vitamin transport, and hormone formation—making it necessary for human health.

  • Plaque formation in coronary arteries is highly focal and heterogeneous rather than evenly distributed throughout the arterial system, suggesting localized factors are at play.

  • Local hemodynamic stresses—such as high blood velocity at arterial branch points and shear stress on the endothelium—may trigger localized cholesterol delivery as a repair mechanism.

  • The body's cholesterol-delivery repair process may function normally in younger individuals but becomes maladaptive when humans live far beyond their evolutionary lifespan of 20-30 years.

  • Coronary artery disease parallels other maladaptive physiological responses, such as blood clot formation, which evolved protectively but can cause life-threatening complications like pulmonary embolism.

  • Individual variations in factors like inflammation, blood pressure, arterial anatomy, and cholesterol carriers (such as lipoprotein A) may determine whether the repair mechanism remains beneficial or becomes pathological.

  • The "widow maker" phenomenon—where a single small plaque in one location can be fatal if it ruptures—supports the theory of localized rather than systemic disease mechanisms.

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Transcript English

Welcome to Dr. Warrick's podcast channel. Warrick is a practicing cardiologist and author with a passion for improving care by helping patients understand their heart health through education. Warrick believes educated patients get the best health care. Discover and understand the latest approaches and technology in heart care and how this might apply to you or someone you love. Hi, my name is Dr. Warrick Bishop and I'd like to welcome you to my podcast and videocast station. Today I'd like to talk about what I think is conceptually a really interesting concept. What I'd like to put out there is the possibility that coronary artery disease is not a disease at all. What I'd like to put out there is that coronary artery disease may in fact be a maladaptive physiological process, a process that is meant to happen, but in certain situations goes wrong. Well, why would I say that? Well, let's roll back and think a little bit about what cholesterol does and why it's transported around the body. Well, cholesterol does a couple of things. It is central in the construction of cell membranes, so it's a building block. for all the cells in the body. So we really need it. It helps in the transport of fat soluble vitamins. Really important. No issue with that. It also helps in the formation of the particular hormones that really the adrenal glands that tend to produce. And those hormones can be sex hormones, but they can also be the hormones that control or regulate salt and blood pressure within the body so pretty important. Well let's wind back to the first of those roles that cholesterol has in the body and that is for cell membrane construction. So now let's think through that just a little bit. If we were to imagine an area in the body that was damaged that there might be stress or wear and tear or degradation of cells in that area then it makes sense that cholesterol may be delivered to that area to facilitate the construction or rebuilding of cell walls that have been damaged or be available for generation of new cells to replace those old cells. Well let's think about that in a bit more detail. If we now think about the arteries per se then there are spots of wear and tear within the arteries and these are very focal and localized. One of the things that made that most apparent to me was my own area of expertise and interest is in cardiac CT imaging. And when we look at the arteries of individuals with plaque in their arteries, we do not see that plaque or cholesterol deposited evenly right throughout the artery. We do not. It is not homogenous. process of plaque formation is incredibly heterogeneous and focal. In fact, it can be so focal that a single plaque of little more than a centimetre in length in the very beginning part of the major artery that runs down the front of the heart can be the only plaque in an entire person's coronary circulation. Yet, if that single plaque ruptures, That individual will die. And in fact, that situation is so common that it is called a widow maker lesion. Let's stop, step back from that and think about that a bit more. Why would this process only be occurring in one space? And in that particular space, how does that work? I don't know the answer, but what I'm going to do is speculate that it's something to do with local factors. Because if it weren't local factors, that cholesterol would be evenly deposited right through all the coronary arteries, smoothly, evenly, homogeneously. But it's not. Let's think about briefly that proximal part of the artery that runs down the front of the heart, just by way of example. Well, if we think about it, blood coming out of the aorta shoots into that artery and potentially is at its highest velocity and could create sheer stress at that location. Sheer stress meaning that the viscosity of the blood passing over that part of the artery literally causes wear and tear on the lining of the artery wall, the internal lining that we call the endothelium. It may also be that the movement of the heart with each contraction may impact the integrity of the wear and tear of that artery at that certain location. The whole point about this discussion is to try and raise the possibility that what we're seeing is not the development of a disease in that particular location, but what we're seeing. Is the body trying to repair or heal what it has detected as wear and tear and stress and strain on a particular part of the vasculature and in trying to repair that area, the body has really directed cholesterol into that space so that Cell walls may be repaired or cell walls may be generated for new cells that are created. I think that it is possible that coronary artery disease may be simply a maladaptive repair mechanism that we haven't really come to terms with in our current environment where we now live with average life expectancy is far beyond what our evolutionary blueprint ever dictated. You see, when we evolved on the African plains four million years ago, we were never designed to live to the sort of ages we live to now. We were only expected to live to maybe 20... tops absolutely 30 years of age and if you think about people at 20 or 30 years of age they don't have heart attacks except for the very rare group of people who have genetically extraordinarily high cholesterol levels but let's put them out of the equation the average bear the average human being doesn't have heart attacks at 20 and 30 years of age so that repair mechanism may be acting and functioning perfectly well because that repair mechanism may also be exactly what goes on at a site where there's damage to the artery through trauma in the periphery so that the cells within that area that's damaged can be regenerated or new cells created and cholesterol is central for cell wall formation. Well, I'm perhaps throwing a concept out there that could get me into trouble. I don't think so because I think it's a really, really interesting idea. But I think it is not alone because we see maladaptive normal or physiological responses leading to problems in other areas. And specifically... The maladaptive problem that I think of that first comes to mind for me is clotting. We know clots form within the body to protect the bloodstream from pouring out if there's damage to the blood vessel. It stops us bleeding to death if we get a small nick, which is protective. It's fantastic. But that propensity for the body to form clots can sometimes go wrong. If you damage a vein in your leg, for example, or you're immobile for a period of time, then a clot might form in the veins of your legs. That clot forms thinking that there could have been damage or some problem within the legs or even the stasis, the lack of blood flow may mean that the components that come together to form a clot have a chance to interact. A clot in the leg can become dislodged, break off, go back to the heart and be pumped out to the lungs where it creates an absolute disaster called a pulmonary embolism and that can be life-threatening. Clotting within the body being a maladaptive physiological response. So could coronary artery disease not be a disease at all? Could it simply be a maladaptive physiological? response which is driven by different components within individuals who may have more inflammation for some reason or another, who may have more blood pressure and therefore more stress and wear and tear on their blood vessels and therefore greater propensity for trying to heal and repair where that blood pressure has had an effect. Perhaps it's just to do with the anatomy of arteries, whether there's a slight kink here or there that makes a difference in where the wear and tear occurs within that arteries think of the bends in a river as it travels down an open plain their twists and turns alter the shear stresses and the forces on the bends in that river no different in the arteries and there may even be within individuals variances within the carriers of cholesterol that could impact and derange or help derail this particular physiological attempt at repair. Things like lipoprotein A. Things like very high cholesterol may drive the process off the tracks. Well, I hope you found that an interesting concept to mull over. I think it's absolutely fascinating. I would be interested if you have any questions, drop us a line at members at drWarrickbishop.online. If you have any suggestions for future podcasts, of course, let us know. As always, thank you so much for joining us. I really appreciate you listening. If you've enjoyed this podcast, please share it. I really am excited with the feedback I've had from these podcasts. So please share it with others who you think might be interested. Till next time, I wish you the very best and please don't die from a heart attack. Goodbye. You have been listening to another podcast from Dr. Warrick. Visit his website at drWarrickbishop.com for the latest news on heart disease. If you love this podcast, feel free to leave us a review.