**EP315: Stay in Your Lane**
**Dr. Warrick Bishop:** Welcome. My name's Dr. Warrick Bishop. I'm a cardiologist, minor 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.
Now, I don't want to go into specific details because that's not really the point, but I do want to share some generalities. This particular podcast was hosted by a sports scientist, someone who had good credentials in the sporting arena. This podcast was an interview between the podcast host and, in fact, one of their lecturers from university days. Now, let's refer to the university lecturer as "the lecturer." The lecturer must have been in his 60s or thereabouts. There wasn't a mention of age, but it would be hard for this individual to not be somewhere around 60. Both these individuals are really well qualified, in fact, highly qualified in their area of specialty. And in no way do I want to diminish the value of the podcast or the podcast series in respect of that.
What I would like to do is offer some feedback on what was discussed on this podcast and how it's so important that we take what we hear in appropriate context. The conversation went on to say that he had reluctantly gone to get a coronary calcium score. Now, one could quite easily argue that that would mean that people who are listening, who were reluctant to get a coronary calcium score, could empathise, and perhaps through that, go on and get their own calcium score because for the lecturer, the score turned out to be very high and also a very high calcium score percentile, which meant for his age and for his sex, he was really at the upper extremes of what might be expected across a population.
So the lecturer went on to say that they found this incredibly disappointing and quite confusing because they had been very avid exercisers, in fact, an endurance athlete over many, many years, and even from childhood. They had eaten good food, not been overweight, had good blood pressure, no diabetes, and minimised sugar consumption. Except... there was a family history, and this was played down. There was no mention of lipid profile, which I thought was fairly interesting, and similarly, no mention about age. So when someone says, "I've got a terrible calcium score, but no risk factors," there has to be something underlying it. To say you've got no risk factors is somewhat misappropriating the origin and process of the problem.
Firstly, this male was over 60 years of age, so there's going to be calcium in the arteries by probability. The fact that it was in the higher range is often related to genetics, but it may not be. To have a conversation about plaque in the arteries without even mentioning cholesterol is really missing some major discussion points in the process of the condition. For whatever reasons, the lecturer then went on to say that they undertook their own journey in this quest for more knowledge and understanding and over several years came to the conclusion that the underlying problem was that of inflammation.
Now, at this stage, I was starting to think, how does someone who's not really across medical speak or really across the most up-to-date literature deal with this sort of summation of the situation? How does inflammation of the body come about, and what does it really mean? Well, the lecturer wanted to suggest that their particular efforts in exercise, in particular their endurance exercise, had played a major role in driving the inflammation within the coronary arteries, suggesting that exercise itself drove inflammation throughout the body. Well, as far as my understanding goes, the last time I checked, inflammation could be driven by a number of different things. One of the things that was likely to reduce inflammation was actually exercise. So, a little bit of a confounder, actually, in terms of proposed mechanisms by this lecturer of sports science, not a cardiologist.
I would then put as a question: why, if we're getting inflammation throughout the body, does it seem to be, for this patient, focused on the coronary arteries? Why is it not all of the arteries affected evenly, homogeneously, and equally? When we know, in this particular lecturer's situation, he'd received a stent, a single stent, when we know that the process of coronary artery disease is, in fact, a focal process. Therefore, it cannot be an equal distribution of a risk factor throughout an arterial tree. There's something in a specific spot that leads to narrowing in that location, and not evenly throughout the arteries. Otherwise, we would drop dead. It makes no sense if you think it through.
The conclusion from this lecturer was that the inflammation from his exercise was the culprit for his coronary artery disease. I'll give you a moment to think about that. The conclusion was that this person had exercised so much that they'd given themselves coronary artery disease. I'll let you reflect on whether you think that really is a likely cause. I'm going to put to you that I don't think it is. I think that's absolute rubbish and bollocks. If we could have people exercising an enormous amount, we would almost eradicate coronary artery disease within this country. And in fact, if we could do it broadly throughout the world, I don't think we'll see that.
What's really troubling for me is there were no comments about other things that could drive significant elevation of calcium within the arteries. Even the most simple things like risk factors around cholesterol. What was his LDL cholesterol, for example? What was his HDL cholesterol, for example? Things that the average man on the street would be able to relate to. Cholesterol particles that we talk about these days as a recognised risk factor is lipoprotein A. Now, this is like the so-called bad cholesterol, LDL cholesterol, but is a bit more aggressive in its approach. This can be tied to people who have a significant propensity to put calcium in their arteries. There wasn't a mention about vitamin D, homocysteine, or really even blood pressure for that matter.
So I felt compelled to do this podcast and share with you what I believe is an enormous frustration I have that people at times will like to share what they believe they know with good intent and with a desire to help. But it's not right. It's wrong. This particular lecturer on this particular podcast probably should have stayed in his own lane and been more interested in asking questions rather than suggesting mechanisms in a process that we don't fully understand. I would be one of the first to admit that the complexity of coronary artery disease is way beyond my understanding, but that's from a position of knowing an awful lot about it and being in close quarters with some of the world leaders in the space, and they don't fully understand the process. It is more complicated than increasing exercise leads to inflammation, leads to coronary artery disease. That is a sadly and concerningly misdirected simplification of the facts.
Let me add a couple of other bits in there. Remember, when we look at people with plaque, we actually find that calcium can act as a stabiliser. So sometimes increasing calcium scores may actually be telling us that the fatty plaque within the plaque, the fatty cholesterol dominant component of the plaque, is being converted to a calcific component of the plaque, and that calcific component of the plaque is less likely to rupture, less likely to be inflamed, in fact. We actually know that endurance athletes will, on average, show higher levels of calcification within their arteries compared to an age-matched equivalent population. And why is that? Well, they probably put fatty material cholesterol into their arteries, but because of their exercise, go on and stabilise it. So they have potentially the same amount of plaque in their arteries as the age-matched equivalent, but because of their exercise, that plaque has been stabilised; therefore, their calcium score is higher.
I even came across a paper recently which confirmed that very high-intensity exercise led to increased calcification within the arteries, even over and above high-intensity exercise alone. Meaning that that very high intensity leads to wear and tear within the arteries, leading to the process of fat deposition for repair, leading to subsequent calcification and stabilisation because that individual exercised at a high degree, and the environment of exercise leads to stabilisation of plaque.
So there you go. Some of my comments based on the suggestions about plaque and exercise from this podcast; you've now got my take on it. Well, I listened to a bit more of this podcast, and I have to say the next bit, as it occurred, was the bit that made me turn it off. The lecturer was asked by the podcast host to tell him about the Widowmaker. Now, the lecturer was happy to oblige and started to talk about rhythm disturbance within the heart, leading to sudden death, with "widow-maker" being the term given to, obviously, men who die young.
And suddenly, of course, the widow-maker is not a primary electrical problem at all. In fact, this is misleading. The widow-maker is related to plaque, to coronary artery disease. The term "widow-maker," used by cardiologists, is the term to describe a plaque or a lesion or a blockage or a narrowing at the very beginning of the left anterior descending artery, the artery that runs down the front of the heart. So, the widow-maker is not a primary electrical problem; it's primarily a coronary artery disease problem. Of course, blocked arteries can lead to electrical problems, and sudden cardiac death, by definition, is a chaotic rhythm of the heart. But a widow-maker is a lesion in the left anterior descending artery.
I could talk about this for over 300 podcasts. Goodness, I already have. But what I do want to finish on is that at times you have to be so careful about what you listen to. The very reason I started sharing podcasts and sharing information is I became frustrated at the sound bites of information that people were getting and the misleading information that people were being offered. Well, this particular situation, with two highly qualified individuals in their field, should probably stay in their lane.
Well, I don't want to sound like I was too cranky or a grumpy old man, but I really, really think it's important that people be given the best possible information to allow them to live as well as possible for as long as possible. And with that, I am going to wish you the very best. Take care and bye for now.
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